Sleep habits, food intake, and physical activity levels in normal and overweight and obese Malaysian children.

PubMed

Firouzi, Somayyeh; Poh, Bee Koon; Ismail, Mohd Noor; Sadeghilar, Aidin

2014-01-01

This study aimed to determine the association between sleep habits (including bedtime, wake up time, sleep duration, and sleep disorder score) and physical characteristics, physical activity level, and food pattern in overweight and obese versus normal weight children. Case control study. 164 Malaysian boys and girls aged 6-€“12 years. Anthropometric measurements included weight, height, waist circumference, and body fat percentage. Subjects divided into normal weight (n = 82) and overweight/obese (n = 82) group based on World Health Organization 2007 BMI-for-age criteria and were matched one by one based on ethnicity, gender, and age plus minus one year. Questionnaires related to sleep habits, physical activity, and food frequency were proxy-reported by parents. Sleep disorder score was measured by Children Sleep Habit Questionnaire. Sleep disorder score and carbohydrate intake (%) to total energy intake were significantly higher in overweight/obese group (p < 0.01 and p < 0.05, respectively). After adjusting for age and gender, sleep disorder score was correlated with BMI (r = 0.275, p < 0.001), weight (r = 0.253, p < 0.001), and WC (r = 0.293, p < 0.001). Based on adjusted odd ratio, children with shortest sleep duration were found to have 4.5 times higher odds of being overweight/obese (odd ratio: 4.536, 95% CI: 1.912-€“8.898) compared to children with normal sleep duration. The odds of being overweight/obese in children with sleep disorder score higher than 48 were 2.17 times more than children with sleep disorder score less than 48. Children who sleep lees than normal amount, had poor sleep quality, and consumed more carbohydrates were at higher risk of overweight/obesity. © 2014 Asian Oceanian Association for the Study of Obesity . Published by Elsevier Ltd. All rights reserved.

Effects of Sleep Fragmentation on Glucose Metabolism in Normal Subjects

PubMed Central

Stamatakis, Katherine A.

2010-01-01

Background: Sleep disorders are increasingly associated with insulin resistance, glucose intolerance, and type 2 diabetes mellitus. Whether the metabolic toll imposed by sleep-related disorders is caused by poor-quality sleep or due to other confounding factors is not known. The objective of this study was to examine whether experimental sleep fragmentation across all sleep stages would alter glucose metabolism, adrenocortical function, and sympathovagal balance. Methods: Sleep was experimentally fragmented across all stages in 11 healthy, normal volunteers for two nights using auditory and mechanical stimuli. Primary outcomes included insulin sensitivity (SI), glucose effectiveness (SG), and insulin secretion, as determined by the intravenous glucose tolerance test. Secondary outcomes included measures of sympathovagal balance and serum levels of inflammatory markers, adipokines, and cortisol. Results: Following two nights of sleep fragmentation, SI decreased from 5.02 to 3.76 (mU/L)−1min−1 (P < .0001). SG, which is the ability of glucose to mobilize itself independent of an insulin response, also decreased from 2.73 × 10−2 min−1 to 2.16 × 10−2 min−1 (P < .01). Sleep fragmentation led to an increase in morning cortisol levels and a shift in sympathovagal balance toward an increase in sympathetic nervous system activity. Markers of systemic inflammation and serum adipokines were unchanged with sleep fragmentation. Conclusions: Fragmentation of sleep across all stages is associated with a decrease in SI and SG. Increases in sympathetic nervous system and adrenocortical activity likely mediate the adverse metabolic effects of poor sleep quality. PMID:19542260

How are normal sleeping controls selected? A systematic review of cross-sectional insomnia studies and a standardized method to select healthy controls for sleep research.

PubMed

Beattie, Louise; Espie, Colin A; Kyle, Simon D; Biello, Stephany M

2015-06-01

There appears to be some inconsistency in how normal sleepers (controls) are selected and screened for participation in research studies for comparison with insomnia patients. The purpose of the current study is to assess and compare methods of identifying normal sleepers in insomnia studies, with reference to published standards. We systematically reviewed the literature on insomnia patients, which included control subjects. The resulting 37 articles were systematically reviewed with reference to the five criteria for normal sleep specified by Edinger et al. In summary, these criteria are as follows: evidence of sleep disruption, sleep scheduling, general health, substance/medication use, and other sleep disorders. We found sleep diaries, polysomnography (PSG), and clinical screening examinations to be widely used with both control subjects and insomnia participants. However, there are differences between research groups in the precise definitions applied to the components of normal sleep. We found that none of the reviewed studies applied all of the Edinger et al. criteria, and 16% met four criteria. In general, screening is applied most rigorously at the level of a clinical disorder, whether physical, psychiatric, or sleep. While the Edinger et al. criteria seem to be applied in some form by most researchers, there is scope to improve standards and definitions in this area. Ideally, different methods such as sleep diaries and questionnaires would be used concurrently with objective measures to ensure normal sleepers are identified, and descriptive information for control subjects would be reported. Here, we have devised working criteria and methods to be used for the assessment of normal sleepers. This would help clarify the nature of the control group, in contrast to insomnia subjects and other patient groups. Copyright © 2015 The Authors. Published by Elsevier B.V. All rights reserved.

Neurofeedback in ADHD and insomnia: vigilance stabilization through sleep spindles and circadian networks.

PubMed

Arns, Martijn; Kenemans, J Leon

2014-07-01

In this review article an overview of the history and current status of neurofeedback for the treatment of ADHD and insomnia is provided. Recent insights suggest a central role of circadian phase delay, resulting in sleep onset insomnia (SOI) in a sub-group of ADHD patients. Chronobiological treatments, such as melatonin and early morning bright light, affect the suprachiasmatic nucleus. This nucleus has been shown to project to the noradrenergic locus coeruleus (LC) thereby explaining the vigilance stabilizing effects of such treatments in ADHD. It is hypothesized that both Sensori-Motor Rhythm (SMR) and Slow-Cortical Potential (SCP) neurofeedback impact on the sleep spindle circuitry resulting in increased sleep spindle density, normalization of SOI and thereby affect the noradrenergic LC, resulting in vigilance stabilization. After SOI is normalized, improvements on ADHD symptoms will occur with a delayed onset of effect. Therefore, clinical trials investigating new treatments in ADHD should include assessments at follow-up as their primary endpoint rather than assessments at outtake. Furthermore, an implication requiring further study is that neurofeedback could be stopped when SOI is normalized, which might result in fewer sessions. Copyright © 2012 Elsevier Ltd. All rights reserved.

Functions and Mechanisms of Sleep

PubMed Central

Zielinski, Mark R.; McKenna, James T.; McCarley, Robert W.

2017-01-01

Sleep is a complex physiological process that is regulated globally, regionally, and locally by both cellular and molecular mechanisms. It occurs to some extent in all animals, although sleep expression in lower animals may be co-extensive with rest. Sleep regulation plays an intrinsic part in many behavioral and physiological functions. Currently, all researchers agree there is no single physiological role sleep serves. Nevertheless, it is quite evident that sleep is essential for many vital functions including development, energy conservation, brain waste clearance, modulation of immune responses, cognition, performance, vigilance, disease, and psychological state. This review details the physiological processes involved in sleep regulation and the possible functions that sleep may serve. This description of the brain circuitry, cell types, and molecules involved in sleep regulation is intended to further the reader’s understanding of the functions of sleep. PMID:28413828

The Biology of REM Sleep

PubMed Central

Peever, John; Fuller, Patrick M.

2018-01-01

Considerable advances in our understanding of the mechanisms and functions of rapid-eye-movement (REM) sleep have occurred over the past decade. Much of this progress can be attributed to the development of new neuroscience tools that have enabled high-precision interrogation of brain circuitry linked with REM sleep control, in turn revealing how REM sleep mechanisms themselves impact processes such as sensorimotor function. This review is intended to update the general scientific community about the recent mechanistic, functional and conceptual developments in our current understanding of REM sleep biology and pathobiology. Specifically, this review outlines the historical origins of the discovery of REM sleep, the diversity of REM sleep expression across and within species, the potential functions of REM sleep (e.g., memory consolidation), the neural circuits that control REM sleep, and how dysfunction of REM sleep mechanisms underlie debilitating sleep disorders such as REM sleep behaviour disorder and narcolepsy. PMID:26766231

Individual Differences in Sleep Timing Relate to Melanopsin-Based Phototransduction in Healthy Adolescents and Young Adults.

PubMed

van der Meijden, Wisse P; Van Someren, Jamie L; Te Lindert, Bart H W; Bruijel, Jessica; van Oosterhout, Floor; Coppens, Joris E; Kalsbeek, Andries; Cajochen, Christian; Bourgin, Patrice; Van Someren, Eus J W

2016-06-01

Individual differences in sleep timing have been widely recognized and are of particular relevance in adolescents and young adults who often show mild to severely delayed sleep. The biological mechanisms underlying the between-subject variance remain to be determined. Recent human genetics studies showed an association between sleep timing and melanopsin gene variation, but support for functional effects on downstream pathways and behavior was not demonstrated before. We therefore investigated the association between the autonomic (i.e., pupil diameter) and behavioral (i.e., sleep timing) readouts of two different downstream brain areas, both affected by the same melanopsin-dependent retinal phototransduction: the olivary pretectal nucleus (OPN) and the suprachiasmatic nucleus (SCN). Our study population included 71 healthy individuals within an age range with known vulnerability to a delayed sleep phase (16.8-35.7 y, 37 males, 34 females). Pupillometry was performed to estimate functionality of the intrinsic melanopsin-signaling circuitry based on the OPN-mediated post-illumination pupil response (PIPR) to blue light. Sleep timing was quantified by estimating the SCN-mediated mid-sleep timing in three different ways in parallel: using a chronotype questionnaire, a sleep diary, and actigraphy. All three measures consistently showed that those individuals with a later mid-sleep timing had a more pronounced PIPR (0.03 < P < 0.05), indicating a stronger blue-light responsiveness of the intrinsic melanopsin-based phototransduction circuitry. Trait-like individual differences in the melanopsin phototransduction circuitry contribute to individual differences in sleep timing. Blue light-sensitive young individuals are more prone to delayed sleep. © 2016 Associated Professional Sleep Societies, LLC.

Tumor Necrosis Factor Antagonism Normalizes Rapid Eye Movement Sleep in Alcohol Dependence

PubMed Central

Irwin, Michael R.; Olmstead, Richard; Valladares, Edwin M.; Breen, Elizabeth Crabb; Ehlers, Cindy L.

2009-01-01

Background In alcohol dependence, markers of inflammation are associated with increases in rapid eye movement (REM) sleep, which is thought to be a prognostic indicator of alcohol relapse. This study was undertaken to test whether blockade of biologically active tumor necrosis factor-α (TNF-α) normalizes REM sleep in alcohol-dependent adults. Methods In a randomized, placebo-controlled, double-blind, crossover trial, 18 abstinent alcohol-dependent male adults received a single dose of etanercept (25 mg) versus placebo in a counterbalanced order. Polysomnographic sleep was measured at baseline and for 3 nights after the acute dose of etanercept or placebo. Results Compared with placebo, administration of etanercept produced significant decreases in the amount and percentage of REM sleep. Decreases in REM sleep were robust and approached low levels typically found in age-comparable control subjects. Individual differences in biologically active drug as indexed by circulating levels of soluble tumor necrosis factor receptor II negatively correlated with the percentage of REM sleep. Conclusions Pharmacologic neutralization of TNF-α activity is associated with significant reductions in REM sleep in abstinent alcohol-dependent patients. These data suggest that circulating levels of TNF-α may have a physiologic role in the regulation of REM sleep in humans. PMID:19185287

Normal sleep on mechanical ventilation in adult patients with congenital central alveolar hypoventilation (Ondine's curse syndrome).

PubMed

Attali, Valérie; Straus, Christian; Pottier, Michel; Buzare, Marie-Annick; Morélot-Panzini, Capucine; Arnulf, Isabelle; Similowski, Thomas

2017-01-23

The purpose of this study was to describe the sleep structure (especially slow wave sleep) in adults with congenital central hypoventilation syndrome (CCHS), a rare genetic disease due to mutations in the PHOX2B gene. Fourteen patients aged 23 (19.0; 24.8) years old (median [1 rst -3rd quartiles]) with CCHS underwent a sleep interview and night-time attended polysomnography with their ventilatory support. Their sleep variables were compared to those collected in 15 healthy control subjects matched for age, sex and body mass index. The latency to N3 sleep was shorter in patients (26.3 min [24.0; 30.1]) than in controls (49.5 min [34.3; 66.9]; P = 0.005), and sleep onset latency tended to be shorter in patients (14.0 min [7.0; 20.5]) than in controls (33.0 min [18.0; 49.0]; P = 0.052). Total sleep time, sleep stage percentages, sleep fragmentation as well as respiratory and movement index were within normal ranges and not different between groups. Normal sleep in adult patients with CCHS and adequate ventilator support indicates that the PHOX2 gene mutations do not affect brain sleep networks. Consequently, any complaint of disrupted sleep should prompt clinicians to look for the usual causes of sleep disorders, primarily inadequate mechanical ventilation. Shorter N3 latency may indicate a higher need for slow wave sleep, to compensate for the abnormal respiratory-related cortical activity during awake quiet breathing observed in patients with CCH.

New Data Pre-processing on Assessing of Obstructive Sleep Apnea Syndrome: Line Based Normalization Method (LBNM)

NASA Astrophysics Data System (ADS)

Akdemir, Bayram; Güneş, Salih; Yosunkaya, Şebnem

Sleep disorders are a very common unawareness illness among public. Obstructive Sleep Apnea Syndrome (OSAS) is characterized with decreased oxygen saturation level and repetitive upper respiratory tract obstruction episodes during full night sleep. In the present study, we have proposed a novel data normalization method called Line Based Normalization Method (LBNM) to evaluate OSAS using real data set obtained from Polysomnography device as a diagnostic tool in patients and clinically suspected of suffering OSAS. Here, we have combined the LBNM and classification methods comprising C4.5 decision tree classifier and Artificial Neural Network (ANN) to diagnose the OSAS. Firstly, each clinical feature in OSAS dataset is scaled by LBNM method in the range of [0,1]. Secondly, normalized OSAS dataset is classified using different classifier algorithms including C4.5 decision tree classifier and ANN, respectively. The proposed normalization method was compared with min-max normalization, z-score normalization, and decimal scaling methods existing in literature on the diagnosis of OSAS. LBNM has produced very promising results on the assessing of OSAS. Also, this method could be applied to other biomedical datasets.

The neuropeptide NLP-22 regulates a sleep-like state in Caenorhabditis elegans

PubMed Central

Nelson, MD; Trojanowski, NF; George-Raizen, JB; Smith, CJ; Yu, C-C; Fang-Yen, C; Raizen, DM

2013-01-01

Neuropeptides play central roles in the regulation of homeostatic behaviors such as sleep and feeding. Caenorhabditis elegans displays sleep-like quiescence of locomotion and feeding during a larval transition stage called lethargus and feeds during active larval and adult stages. Here we show that the neuropeptide NLP-22 is a regulator of Caenorhabditis elegans sleep-like quiescence observed during lethargus. nlp-22 shows cyclical mRNA expression in synchrony with lethargus; it is regulated by LIN-42, an orthologue of the core circadian protein PERIOD; and it is expressed solely in the two RIA interneurons. nlp-22 and the RIA interneurons are required for normal lethargus quiescence, and forced expression of nlp-22 during active stages causes anachronistic locomotion and feeding quiescence. Optogenetic stimulation of RIA interneurons has a movement-promoting effect, demonstrating functional complexity in a single neuron type. Our work defines a quiescence-regulating role for NLP-22 and expands our knowledge of the neural circuitry controlling Caenorhabditis elegans behavioral quiescence. PMID:24301180

The neuropeptide NLP-22 regulates a sleep-like state in Caenorhabditis elegans.

PubMed

Nelson, M D; Trojanowski, N F; George-Raizen, J B; Smith, C J; Yu, C-C; Fang-Yen, C; Raizen, D M

2013-01-01

Neuropeptides have central roles in the regulation of homoeostatic behaviours such as sleep and feeding. Caenorhabditis elegans displays sleep-like quiescence of locomotion and feeding during a larval transition stage called lethargus and feeds during active larval and adult stages. Here we show that the neuropeptide NLP-22 is a regulator of Caenorhabditis elegans sleep-like quiescence observed during lethargus. nlp-22 shows cyclical mRNA expression in synchrony with lethargus; it is regulated by LIN-42, an orthologue of the core circadian protein PERIOD; and it is expressed solely in the two RIA interneurons. nlp-22 and the RIA interneurons are required for normal lethargus quiescence, and forced expression of nlp-22 during active stages causes anachronistic locomotion and feeding quiescence. Optogenetic stimulation of the RIA interneurons has a movement-promoting effect, demonstrating functional complexity in a single-neuron type. Our work defines a quiescence-regulating role for NLP-22 and expands our knowledge of the neural circuitry controlling Caenorhabditis elegans behavioural quiescence.

The role of serotonin and norepinephrine in sleep-waking activity.

PubMed

Morgane, P J; Stern, W C

1975-11-01

A critical review of the evidences relating the biogenic amines serotonin and norepinephrine to the states of slow-wave and rapid eye movement (REM) sleep is presented. Various alternative explanations for specific chemical regulation of the individual sleep states, including the phasic events of REM sleep, are evaluated within the overall framework of the monoamine theory of sleep. Several critical neuropsychopharmacological studies relating to metabolsim of the amines in relation to sleep-waking behavior are presented. Models of the chemical neuronal circuitry involved in sleep-waking activity are derived and interactions between several brainstem nuclei, particularly the raphé complex and locus coeruleus, are discussed. Activity in these aminergic systems in relation to oscillations in the sleep-waking cycles is evaluated. In particular, the assessment of single cell activity in specific chemical systems in relations to chemical models of sleep is reviewed. Overall, it appears that the biogenic amines, especially serotonin and norepinephrine, play key roles in the generation and maintenance of the sleep states. These neurotransmitters participate in some manner in the "triggering" processes necessary for actuating each sleep phase and in regulating the transitions from sleep to waking activity. The biogenic amines are, however, probably not "sleep factors" or direct inducers of the sleep states. Rather, they appear to be components of a multiplicity of interacting chemical circuitry in the brain whose activity maintains various chemical balances in different brain regions. Shifts in these balances appear to be involved in the triggering and maintenance of the various states comprising the vigilance continuum.

Obstructive Sleep Apnea Severity Affects Amyloid Burden in Cognitively Normal Elderly. A Longitudinal Study.

PubMed

Sharma, Ram A; Varga, Andrew W; Bubu, Omonigho M; Pirraglia, Elizabeth; Kam, Korey; Parekh, Ankit; Wohlleber, Margaret; Miller, Margo D; Andrade, Andreia; Lewis, Clifton; Tweardy, Samuel; Buj, Maja; Yau, Po L; Sadda, Reem; Mosconi, Lisa; Li, Yi; Butler, Tracy; Glodzik, Lidia; Fieremans, Els; Babb, James S; Blennow, Kaj; Zetterberg, Henrik; Lu, Shou E; Badia, Sandra G; Romero, Sergio; Rosenzweig, Ivana; Gosselin, Nadia; Jean-Louis, Girardin; Rapoport, David M; de Leon, Mony J; Ayappa, Indu; Osorio, Ricardo S

2018-04-01

Recent evidence suggests that obstructive sleep apnea (OSA) may be a risk factor for developing mild cognitive impairment and Alzheimer's disease. However, how sleep apnea affects longitudinal risk for Alzheimer's disease is less well understood. To test the hypothesis that there is an association between severity of OSA and longitudinal increase in amyloid burden in cognitively normal elderly. Data were derived from a 2-year prospective longitudinal study that sampled community-dwelling healthy cognitively normal elderly. Subjects were healthy volunteers between the ages of 55 and 90, were nondepressed, and had a consensus clinical diagnosis of cognitively normal. Cerebrospinal fluid amyloid β was measured using ELISA. Subjects received Pittsburgh compound B positron emission tomography scans following standardized procedures. Monitoring of OSA was completed using a home sleep recording device. We found that severity of OSA indices (AHIall [F 1,88  = 4.26; P < 0.05] and AHI4% [F 1,87  = 4.36; P < 0.05]) were associated with annual rate of change of cerebrospinal fluid amyloid β 42 using linear regression after adjusting for age, sex, body mass index, and apolipoprotein E4 status. AHIall and AHI4% were not associated with increases in AD PiB -mask (Alzheimer's disease vulnerable regions of interest Pittsburg compound B positron emission tomography mask) most likely because of the small sample size, although there was a trend for AHIall (F 1,28  = 2.96, P = 0.09; and F 1,28  = 2.32, not significant, respectively). In a sample of cognitively normal elderly, OSA was associated with markers of increased amyloid burden over the 2-year follow-up. Sleep fragmentation and/or intermittent hypoxia from OSA are likely candidate mechanisms. If confirmed, clinical interventions for OSA may be useful in preventing amyloid build-up in cognitively normal elderly.

The effect of sleep restriction on neurobehavioural functioning in normally developing children and adolescents: insights from the Attention, Behaviour and Sleep Laboratory.

PubMed

Cassoff, J; Bhatti, J A; Gruber, R

2014-10-01

In the current paper, we first introduce the research themes of the attention, behaviour and sleep (ABS) laboratory, namely, sleep and ADHD, sleep and obesity, and sleep and academic performance. We then focus in on the topic to be reviewed in the current paper - the association between sleep restriction and neurobehavioral functioning (NBF) in typically developing children. We review the research thus far conducted by the ABS lab specific to this topic and posit the unique methodological contributions of the ABS lab (e.g. home-based assessment of sleep architecture and patterns, extensive phenotyping, etc.) in terms of advancing this research area. In the second section of the paper, we review 13 studies investigating the causal association between experimental sleep restriction and NBF in normally developing pediatric populations. Eight of the 13 studies found that sleep restriction causes impairments in neurobehavioural functioning. However, given the inconsistency in outcome measures, experimental protocols and statistical power, the studies reviewed herein are difficult to interpret. Strategies used by the ABS including implementing home assessments of sleep, restricting sleep relative to the participants' typical sleep schedules, blinding raters who assess NBF, and using valid and reliable NBF assessments are an attempt to address the gaps in this research area and clarify the causal relationship between sleep restriction and NBF in typically developing children and adolescents. Copyright © 2014. Published by Elsevier SAS.

Determinants of perceived sleep quality in normal sleepers.

PubMed

Goelema, M S; Regis, M; Haakma, R; van den Heuvel, E R; Markopoulos, P; Overeem, S

2017-09-20

This study aimed to establish the determinants of perceived sleep quality over a longer period of time, taking into account the separate contributions of actigraphy-based sleep measures and self-reported sleep indices. Fifty participants (52 ± 6.6 years; 27 females) completed two consecutive weeks of home monitoring, during which they kept a sleep-wake diary while their sleep was monitored using a wrist-worn actigraph. The diary included questions on perceived sleep quality, sleep-wake information, and additional factors such as well-being and stress. The data were analyzed using multilevel models to compare a model that included only actigraphy-based sleep measures (model Acti) to a model that included only self-reported sleep measures to explain perceived sleep quality (model Self). In addition, a model based on the self-reported sleep measures and extended with nonsleep-related factors was analyzed to find the most significant determinants of perceived sleep quality (model Extended). Self-reported sleep measures (model Self) explained 61% of the total variance, while actigraphy-based sleep measures (model Acti) only accounted for 41% of the perceived sleep quality. The main predictors in the self-reported model were number of awakenings during the night, sleep onset latency, and wake time after sleep onset. In the extended model, the number of awakenings during the night and total sleep time of the previous night were the strongest determinants of perceived sleep quality, with 64% of the variance explained. In our cohort, perceived sleep quality was mainly determined by self-reported sleep measures and less by actigraphy-based sleep indices. These data further stress the importance of taking multiple nights into account when trying to understand perceived sleep quality.

Sleep disorders in Latin-American children with asthma and/or allergic rhinitis and normal controls.

PubMed

Urrutia-Pereira, M; Solé, D; Chong Neto, H J; Acosta, V; Cepeda, A M; Álvarez-Castelló, M; Almendarez, C F; Lozano-Saenz, J; Sisul-Alvariza, J C; Rosario, N A; Castillo, A J; Valentin-Rostan, M; Badellino, H; Castro-Almarales, R L; González-León, M; Sanchez-Silot, C; Avalos, M M; Fernandez, C; Berroa, F; De la Cruz, M M; Sarni, R O S

Asthma and/or allergic rhinitis have been associated with sleep disorders. The aim of this study was to evaluate sleep disorders in Latin-American children (4-10 years) from nine countries, with persistent asthma (A) and/or allergic rhinitis (AR) and in normal controls (C). Parents from 454 C children and 700 A and/or AR children followed up in allergy reference clinics completed the Children's Sleep Habits Questionnaire (CSHQ) which is a retrospective one-week questionnaire composed of 33 questions composed of seven subscales (bedtime resistance, sleep duration, sleep anxiety, night wakings, parasomnias, sleep-disordered breathing and daytime sleepiness). The total scale of CSHQ and the subscales were compared between groups C and A+AR, A (n=285) vs. AR (n=390), and between controlled A (CA, n=103) vs. partially controlled/uncontrolled A (UA, n=182). The comparison between C and A+AR showed no significant differences in age (6.7 years vs. 7.0 years, respectively), mean Body Mass Index and total scale of CSHQ (53.3 vs. 63.2, respectively) and the subscales were significantly higher in the A+AR group. Comparison between groups A and AR, except for sleep anxiety, showed significantly higher values for CSHQ total scale (66.9 vs. 61.0, respectively) and subscales for group A. The UA group showed significantly higher values for total CSHQ scale and subscales in comparison to CA (71.1 vs. 59.4, respectively). Latin-American children with asthma and/or allergic rhinitis showed sleep disorders identified by the CSHQ when compared to normal controls. Despite being treated, asthma causes sleep impairment, especially when uncontrolled. Copyright © 2016 SEICAP. Published by Elsevier España, S.L.U. All rights reserved.

Operational testing of system for automatic sleep analysis

NASA Technical Reports Server (NTRS)

Kellaway, P.

1972-01-01

Tables on the performance, under operational conditions, of an automatic sleep monitoring system are presented. Data are recorded from patients who were undergoing heart and great vessel surgery. This study resulted in cap, electrode, and preamplifier improvements. Children were used to test the sleep analyzer and medical console write out units. From these data, an automatic voltage control circuit for the analyzer was developed. A special circuitry for obviating the possibility of incorrect sleep staging due to the presence of a movement artifact was also developed as a result of the study.

Acquired auditory agnosia in childhood and normal sleep electroencephalography subsequently diagnosed as Landau-Kleffner syndrome: a report of three cases.

PubMed

van Bogaert, Patrick; King, Mary D; Paquier, Philippe; Wetzburger, Catherine; Labasse, Catherine; Dubru, Jean-Marie; Deonna, Thierry

2013-06-01

  We report three cases of Landau-Kleffner syndrome (LKS) in children (two females, one male) in whom diagnosis was delayed because the sleep electroencephalography (EEG) was initially normal.   Case histories including EEG, positron emission tomography findings, and long-term outcome were reviewed.   Auditory agnosia occurred between the age of 2 years and 3 years 6 months, after a period of normal language development. Initial awake and sleep EEG, recorded weeks to months after the onset of language regression, during a nap period in two cases and during a full night of sleep in the third case, was normal. Repeat EEG between 2 months and 2 years later showed epileptiform discharges during wakefulness and strongly activated by sleep, with a pattern of continuous spike-waves during slow-wave sleep in two patients. Patients were diagnosed with LKS and treated with various antiepileptic regimens, including corticosteroids. One patient in whom EEG became normal on hydrocortisone is making significant recovery. The other two patients did not exhibit a sustained response to treatment and remained severely impaired.   Sleep EEG may be normal in the early phase of acquired auditory agnosia. EEG should be repeated frequently in individuals in whom a firm clinical diagnosis is made to facilitate early treatment. © The Authors. Developmental Medicine & Child Neurology © 2012 Mac Keith Press.

The preproghrelin gene is required for the normal integration of thermoregulation and sleep in mice

PubMed Central

Szentirmai, Éva; Kapás, Levente; Sun, Yuxiang; Smith, Roy G.; Krueger, James M.

2009-01-01

Peptidergic mechanisms controlling feeding, metabolism, thermoregulation, and sleep overlap in the hypothalamus. Low ambient temperatures and food restriction induce hypothermic (torpor) bouts and characteristic metabolic and sleep changes in mice. We report that mice lacking the preproghrelin gene, but not those lacking the ghrelin receptor, have impaired abilities to manifest and integrate normal sleep and thermoregulatory responses to metabolic challenges. In response to fasting at 17 °C (a subthermoneutral ambient temperature), preproghrelin knockout mice enter hypothermic bouts associated with reduced sleep, culminating in a marked drop in body temperature to near-ambient levels. Prior treatment with obestatin, another preproghrelin gene product, attenuates the hypothermic response of preproghrelin knockout mice. Results suggest that obestatin is a component in the coordinated regulation of metabolism and sleep during torpor. PMID:19666521

Individual Differences in Sleep Timing Relate to Melanopsin-Based Phototransduction in Healthy Adolescents and Young Adults

PubMed Central

van der Meijden, Wisse P.; Van Someren, Jamie L.; te Lindert, Bart H.W.; Bruijel, Jessica; van Oosterhout, Floor; Coppens, Joris E.; Kalsbeek, Andries; Cajochen, Christian; Bourgin, Patrice; Van Someren, Eus J.W.

2016-01-01

Study Objectives: Individual differences in sleep timing have been widely recognized and are of particular relevance in adolescents and young adults who often show mild to severely delayed sleep. The biological mechanisms underlying the between-subject variance remain to be determined. Recent human genetics studies showed an association between sleep timing and melanopsin gene variation, but support for functional effects on downstream pathways and behavior was not demonstrated before. We therefore investigated the association between the autonomic (i.e., pupil diameter) and behavioral (i.e., sleep timing) readouts of two different downstream brain areas, both affected by the same melanopsin-dependent retinal phototransduction: the olivary pretectal nucleus (OPN) and the suprachiasmatic nucleus (SCN). Methods: Our study population included 71 healthy individuals within an age range with known vulnerability to a delayed sleep phase (16.8–35.7 y, 37 males, 34 females). Pupillometry was performed to estimate functionality of the intrinsic melanopsin-signaling circuitry based on the OPN-mediated post-illumination pupil response (PIPR) to blue light. Sleep timing was quantified by estimating the SCN-mediated mid-sleep timing in three different ways in parallel: using a chronotype questionnaire, a sleep diary, and actigraphy. Results: All three measures consistently showed that those individuals with a later mid-sleep timing had a more pronounced PIPR (0.03 < P < 0.05), indicating a stronger blue-light responsiveness of the intrinsic melanopsin-based phototransduction circuitry. Conclusions: Trait-like individual differences in the melanopsin phototransduction circuitry contribute to individual differences in sleep timing. Blue light-sensitive young individuals are more prone to delayed sleep. Citation: van der Meijden WP, Van Someren JL; te Lindert BH, Bruijel J, van Oosterhout F, Coppens JE, Kalsbeek A, Cajochen C, Bourgin P, Van Someren EJ. Individual differences in

Role of Basal Ganglia in Sleep–Wake Regulation: Neural Circuitry and Clinical Significance

PubMed Central

Vetrivelan, Ramalingam; Qiu, Mei-Hong; Chang, Celene; Lu, Jun

2010-01-01

Researchers over the last decade have made substantial progress toward understanding the roles of dopamine and the basal ganglia (BG) in the control of sleep–wake behavior. In this review, we outline recent advancements regarding dopaminergic modulation of sleep through the BG and extra-BG sites. Our main hypothesis is that dopamine promotes sleep by its action on the D2 receptors in the BG and promotes wakefulness by its action on D1 and D2 receptors in the extra-BG sites. This hypothesis implicates dopamine depletion in the BG (such as in Parkinson's disease) in causing frequent nighttime arousal and overall insomnia. Furthermore, the arousal effects of psychostimulants (methamphetamine, cocaine, and modafinil) may be linked to the ventral periaquductal gray (vPAG) dopaminergic circuitry targeting the extra-BG sleep–wake network. PMID:21151379

Developmental Changes in Ultradian Sleep Cycles across Early Childhood.

PubMed

Lopp, Sean; Navidi, William; Achermann, Peter; LeBourgeois, Monique; Diniz Behn, Cecilia

2017-02-01

Nocturnal human sleep is composed of cycles between rapid eye movement (REM) sleep and non-REM (NREM) sleep. In adults, the structure of ultradian cycles between NREM and REM sleep is well characterized; however, less is known about the developmental trajectories of ultradian sleep cycles across early childhood. Cross-sectional studies indicate that the rapid ultradian cycling of active-quiet sleep in infancy shifts to a more adult-like pattern of NREM-REM sleep cycling by the school-age years, yet longitudinal studies elucidating the details of this transition are scarce. To address this gap, we examined ultradian cycling during nocturnal sleep following 13 h of prior wakefulness in 8 healthy children at 3 longitudinal points: 2Y (2.5-3.0 years of age), 3Y (3.5-4.0 years of age), and 5Y (5.5-6.0 years of age). We found that the length of ultradian cycles increased with age as a result of increased NREM sleep episode duration. In addition, we observed a significant decrease in the number of NREM sleep episodes as well as a nonsignificant trend for a decrease in the number of cycles with increasing age. Together, these findings suggest a concurrent change in which cycle duration increases and the number of cycles decreases across development. We also found that, consistent with data from adolescents and adults, the duration of NREM sleep episodes decreased with time since lights-off whereas the duration of REM sleep episodes increased over this time period. These results indicate the presence of circadian modulation of nocturnal sleep in preschool children. In addition to characterizing changes in ultradian cycling in healthy children ages 2 to 5 years, this work describes a developmental model that may provide insights into the emergence of normal adult REM sleep regulatory circuitry as well as potential trajectories of dysregulated ultradian cycles such as those associated with affective disorders.

Perspectives on the rapid eye movement sleep switch in rapid eye movement sleep behavior disorder.

PubMed

Ramaligam, Vetrivelan; Chen, Michael C; Saper, Clifford B; Lu, Jun

2013-08-01

Rapid eye movement (REM) sleep in mammals is associated with wakelike cortical and hippocampal activation and concurrent postural muscle atonia. Research during the past 5 decades has revealed the details of the neural circuitry regulating REM sleep and muscle atonia during this state. REM-active glutamatergic neurons in the sublaterodorsal nucleus (SLD) of the dorsal pons are critical for generation for REM sleep atonia. Descending projections from SLD glutamatergic neurons activate inhibitory premotor neurons in the ventromedial medulla (VMM) and in the spinal cord to antagonize the glutamatergic supraspinal inputs on the motor neurons during REM sleep. REM sleep behavior disorder (RBD) consists of simple behaviors (i.e., twitching, jerking) and complex behaviors (i.e., defensive behavior, talking). Animal research has lead to the hypothesis that complex behaviors in RBD are due to SLD pathology, while simple behaviors of RBD may be due to less severe SLD pathology or dysfunction of the VMM, ventral pons, or spinal cord. Copyright © 2013 Elsevier B.V. All rights reserved.

Use-dependent plasticity in clock neurons regulates sleep need in Drosophila.

PubMed

Donlea, Jeffrey M; Ramanan, Narendrakumar; Shaw, Paul J

2009-04-03

Sleep is important for memory consolidation and is responsive to waking experience. Clock circuitry is uniquely positioned to coordinate interactions between processes underlying memory and sleep need. Flies increase sleep both after exposure to an enriched social environment and after protocols that induce long-term memory. We found that flies mutant for rutabaga, period, and blistered were deficient for experience-dependent increases in sleep. Rescue of each of these genes within the ventral lateral neurons (LNVs) restores increased sleep after social enrichment. Social experiences that induce increased sleep were associated with an increase in the number of synaptic terminals in the LNV projections into the medulla. The number of synaptic terminals was reduced during sleep and this decline was prevented by sleep deprivation.

Gut microbiota and glucometabolic alterations in response to recurrent partial sleep deprivation in normal-weight young individuals.

PubMed

Benedict, Christian; Vogel, Heike; Jonas, Wenke; Woting, Anni; Blaut, Michael; Schürmann, Annette; Cedernaes, Jonathan

2016-12-01

Changes to the microbial community in the human gut have been proposed to promote metabolic disturbances that also occur after short periods of sleep loss (including insulin resistance). However, whether sleep loss affects the gut microbiota remains unknown. In a randomized within-subject crossover study utilizing a standardized in-lab protocol (with fixed meal times and exercise schedules), we studied nine normal-weight men at two occasions: after two nights of partial sleep deprivation (PSD; sleep opportunity 02:45-07:00 h), and after two nights of normal sleep (NS; sleep opportunity 22:30-07:00 h). Fecal samples were collected within 24 h before, and after two in-lab nights, of either NS or PSD. In addition, participants underwent an oral glucose tolerance test following each sleep intervention. Microbiota composition analysis (V4 16S rRNA gene sequencing) revealed that after two days of PSD vs. after two days of NS, individuals exhibited an increased Firmicutes:Bacteroidetes ratio, higher abundances of the families Coriobacteriaceae and Erysipelotrichaceae, and lower abundance of Tenericutes (all P < 0.05) - previously all associated with metabolic perturbations in animal or human models. However, no PSD vs. NS effect on beta diversity or on fecal short-chain fatty acid concentrations was found. Fasting and postprandial insulin sensitivity decreased after PSD vs. NS (all P < 0.05). Our findings demonstrate that short-term sleep loss induces subtle effects on human microbiota. To what extent the observed changes to the microbial community contribute to metabolic consequences of sleep loss warrants further investigations in larger and more prolonged sleep studies, to also assess how sleep loss impacts the microbiota in individuals who already are metabolically compromised.

Poor sleep is associated with CSF biomarkers of amyloid pathology in cognitively normal adults

PubMed Central

Koscik, Rebecca L.; Carlsson, Cynthia M.; Zetterberg, Henrik; Blennow, Kaj; Okonkwo, Ozioma C.; Sager, Mark A.; Asthana, Sanjay; Johnson, Sterling C.; Benca, Ruth M.; Bendlin, Barbara B.

2017-01-01

Objective: To determine the relationship between sleep quality and CSF markers of Alzheimer disease (AD) pathology in late midlife. Methods: We investigated the relationship between sleep quality and CSF AD biomarkers in a cohort enriched for parental history of sporadic AD, the Wisconsin Registry for Alzheimer's Prevention. A total of 101 participants (mean age 62.9 ± 6.2 years, 65.3% female) completed sleep assessments and CSF collection and were cognitively normal. Sleep quality was measured with the Medical Outcomes Study Sleep Scale. CSF was assayed for biomarkers of amyloid metabolism and plaques (β-amyloid 42 [Aβ42]), tau pathology (phosphorylated tau [p-tau] 181), neuronal/axonal degeneration (total tau [t-tau], neurofilament light [NFL]), neuroinflammation/astroglial activation (monocyte chemoattractant protein–1 [MCP-1], chitinase-3-like protein 1 [YKL-40]), and synaptic dysfunction/degeneration (neurogranin). To adjust for individual differences in total amyloid production, Aβ42 was expressed relative to Aβ40. To assess cumulative pathology, CSF biomarkers were expressed in ratio to Aβ42. Relationships among sleep scores and CSF biomarkers were assessed with multiple regression, controlling for age, sex, time between sleep and CSF measurements, and CSF assay batch. Results: Worse subjective sleep quality, more sleep problems, and daytime somnolence were associated with greater AD pathology, indicated by lower CSF Aβ42/Aβ40 and higher t-tau/Aβ42, p-tau/Aβ42, MCP-1/Aβ42, and YKL-40/Aβ42. There were no significant associations between sleep and NFL or neurogranin. Conclusions: Self-report of poor sleep was associated with greater AD-related pathology in cognitively healthy adults at risk for AD. Effective strategies exist for improving sleep; therefore sleep health may be a tractable target for early intervention to attenuate AD pathogenesis. PMID:28679595

Sleep in space as a new medical frontier: the challenge of preserving normal sleep in the abnormal environment of space missions.

PubMed

Pandi-Perumal, Seithikurippu R; Gonfalone, Alain A

2016-01-01

Space agencies such as the National Aeronautics and Space Administration of the United States, the Russian Federal Space Agency, the European Space Agency, the China National Space Administration, the Japan Aerospace Exploration Agency, and Indian Space Research Organization, although differing in their local political agendas, have a common interest in promoting all applied sciences that may facilitate man's adaptation to life beyond the earth. One of man's most important adaptations has been the evolutionary development of sleep cycles in response to the 24 hour rotation of the earth. Less well understood has been man's biological response to gravity. Before humans ventured into space, many questioned whether sleep was possible at all in microgravity environments. It is now known that, in fact, space travelers can sleep once they leave the pull of the earth's gravity, but that the sleep they do get is not completely refreshing and that the associated sleep disturbances can be elaborate and variable. According to astronauts' subjective reports, the duration of sleep is shorter than that on earth and there is an increased incidence of disturbed sleep. Objective sleep recordings carried out during various missions including the Skylab missions, space shuttle missions, and Mir missions all support the conclusion that, compared to sleep on earth, the duration in human sleep in space is shorter, averaging about six hours. In the new frontier of space exploration, one of the great practical problems to be solved relates to how man can preserve "normal" sleep in a very abnormal environment. The challenge of managing fatigue and sleep loss during space mission has critical importance for the mental efficiency and safety of the crew and ultimately for the success of the mission itself. Numerous "earthly" examples now show that crew fatigue on ships, trucks, and long-haul jetliners can lead to inadequate performance and sometimes fatal consequences, a reality which has

Sleep and its disorders in translational medicine.

PubMed

Paterson, Louise M; Nutt, David J; Wilson, Sue J

2011-09-01

The study of sleep is a useful approach to studying the brain in psychiatric disorders and in investigating the effects of psychotropic drugs. Sleep physiology lends itself well to pharmacological and physiological manipulation, as it has the advantage of a functional output, the electroencephalograph, which is common to all mammals, and can be measured in freely moving (or naturally sleeping) animals under controlled laboratory conditions or in a naturalistic home environment. The complexity of sleep architecture varies between species but all share features which are comparable. In addition, sleep architecture is sensitive to changes in brain neurotransmitters such as serotonin, so cross-species sleep measurement can be combined with pharmacological manipulation to investigate the receptor mechanisms controlling sleep-wake regulation and sleep architecture in response to known and novel agents. Translational approaches such as these have improved our understanding of sleep circuitry and facilitated the development of new treatments for sleep disorders, particularly insomnia. This review provides examples of how research findings within the sleep field have been translated between animal models, healthy volunteers and patient populations with particular focus on the serotonergic system.

Upper-airway flow limitation and transcutaneous carbon dioxide during sleep in normal pregnancy.

PubMed

Rimpilä, Ville; Jernman, Riina; Lassila, Katariina; Uotila, Jukka; Huhtala, Heini; Mäenpää, Johanna; Polo, Olli

2017-08-01

Sleep during pregnancy involves a physiological challenge to provide sufficient gas exchange to the fetus. Enhanced ventilatory responses to hypercapnia and hypoxia may protect from deficient gas exchange, but sleep-disordered breathing (SDB) may predispose to adverse events. The aim of this study was to analyze sleep and breathing in healthy pregnant women compared to non-pregnant controls, with a focus on CO 2 changes and upper-airway flow limitation. Healthy women in the third trimester and healthy non-pregnant women with normal body mass index (BMI) were recruited for polysomnography. Conventional analysis of sleep and breathing was performed. Transcutaneous carbon dioxide (TcCO 2 ) was determined for each sleep stage. Flow-limitation was analyzed using the flattening index and TcCO 2 values were recorded for every inspiration. Eighteen pregnant women and 12 controls were studied. Pregnancy was associated with shorter sleep duration and more superficial sleep. Apnea-hypopnea index, arterial oxyhemoglobin desaturation, flow-limitation, snoring or periodic leg movements were similar in the two groups. Mean SaO 2 and minimum SaO 2 were lower and average heart rate was higher in the pregnant group. TcCO 2 levels did not differ between groups but variance of TcCO 2 was smaller in pregnant women during non-rapid eye movement (NREM). TcCO 2 profiles showed transient TcCO 2 peaks, which seem specific to pregnancy. Healthy pregnancy does not predispose to SDB. Enhanced ventilatory control manifests as narrowing threshold of TcCO 2 between wakefulness and sleep. Pregnant women have a tendency for rapid CO 2 increases during sleep which might have harmful consequences if not properly compensated. Copyright © 2017 Elsevier B.V. All rights reserved.

Role of the pedunculopontine nucleus in controlling gait and sleep in normal and parkinsonian monkeys.

PubMed

Karachi, C; Francois, Chantal

2018-03-01

Patients with Parkinson's disease (PD) develop cardinal motor symptoms, including akinesia, rigidity, and tremor, that are alleviated by dopaminergic medication and/or subthalamic deep brain stimulation. Over the time course of the disease, gait and balance disorders worsen and become resistant to pharmacological and surgical treatments. These disorders generate debilitating motor symptoms leading to increased dependency, morbidity, and mortality. PD patients also experience sleep disturbance that raise the question of a common physiological basis. An extensive experimental and clinical body of work has highlighted the crucial role of the pedunculopontine nucleus (PPN) in the control of gait and sleep, and its potential major role in PD. Here, we summarise our investigations in the monkey PPN in the normal and parkinsonian states. We first examined the anatomy and connectivity of the PPN and the cuneiform nucleus which both belong to the mesencephalic locomotor region. Second, we conducted experiments to demonstrate the specific effects of PPN cholinergic lesions on locomotion in the normal and parkinsonian monkey. Third, we aimed to understand how PPN cholinergic lesions impair sleep in parkinsonian monkeys. Our final goal was to develop a novel model of advanced PD with gait and sleep disorders. We believe that this monkey model, even if it does not attempt to reproduce the exact human disease with all its complexities, represents a good biomedical model to characterise locomotion and sleep in the context of PD.

Heart rate variability in normal and pathological sleep.

PubMed

Tobaldini, Eleonora; Nobili, Lino; Strada, Silvia; Casali, Karina R; Braghiroli, Alberto; Montano, Nicola

2013-10-16

Sleep is a physiological process involving different biological systems, from molecular to organ level; its integrity is essential for maintaining health and homeostasis in human beings. Although in the past sleep has been considered a state of quiet, experimental and clinical evidences suggest a noteworthy activation of different biological systems during sleep. A key role is played by the autonomic nervous system (ANS), whose modulation regulates cardiovascular functions during sleep onset and different sleep stages. Therefore, an interest on the evaluation of autonomic cardiovascular control in health and disease is growing by means of linear and non-linear heart rate variability (HRV) analyses. The application of classical tools for ANS analysis, such as HRV during physiological sleep, showed that the rapid eye movement (REM) stage is characterized by a likely sympathetic predominance associated with a vagal withdrawal, while the opposite trend is observed during non-REM sleep. More recently, the use of non-linear tools, such as entropy-derived indices, have provided new insight on the cardiac autonomic regulation, revealing for instance changes in the cardiovascular complexity during REM sleep, supporting the hypothesis of a reduced capability of the cardiovascular system to deal with stress challenges. Interestingly, different HRV tools have been applied to characterize autonomic cardiac control in different pathological conditions, from neurological sleep disorders to sleep disordered breathing (SDB). In summary, linear and non-linear analysis of HRV are reliable approaches to assess changes of autonomic cardiac modulation during sleep both in health and diseases. The use of these tools could provide important information of clinical and prognostic relevance.

Normal weight children have higher cognitive performance - Independent of physical activity, sleep, and diet.

PubMed

Hjorth, Mads F; Sørensen, Louise B; Andersen, Rikke; Dyssegaard, Camilla B; Ritz, Christian; Tetens, Inge; Michaelsen, Kim F; Astrup, Arne; Egelund, Niels; Sjödin, Anders

2016-10-15

Aside from the health consequences, observational studies indicate that being overweight may also negatively affect cognitive function. However, existing evidence has to a large extent not controlled for the possible confounding effect of having different lifestyles. Therefore, the objective was to examine the independent associations between weight status and lifestyle indicators with cognitive performance in 8-11year old Danish children. The analyses included 828 children (measured in 2011-2012) each having one to three measurement occasions separated by approximately 100days. Dietary intake, physical activity, sedentary time, and sleep duration were measured using dietary records and accelerometers. The Children's Sleep Habits Questionnaire was used to access sleep problems and the Andersen test was carried out to estimate cardio-respiratory fitness (CRF). Weight status (underweight, normal weight, and overweight/obese) was defined according to body mass index and cognitive performance was assessed using the d2-test of attention, a reading test, and a math test. A linear mixed model including a number of fixed and random effects was used to test associations between lifestyle indicators as well as BMI category and cognitive performance. After adjustment for demographics, socioeconomics, and multiple lifestyle indicators, normal weight children had higher cognitive test scores than overweight/obese and underweight children of up to 89% and 48% of expected learning within one school year (P<0.05). Daily breakfast consumption, fewer sleep problems, higher CRF, less total physical activity, more sedentary time, and less light physical activity were associated with higher cognitive performance independently of each other in at least one of the three cognitive tests (P<0.05). Normal weight children had higher cognitive performance compared to overweight/obese as well as underweight children, independent of multiple lifestyle indicators. Copyright © 2016 Elsevier Inc

A sleep state in Drosophila larvae required for neural stem cell proliferation

PubMed Central

Szuperak, Milan; Churgin, Matthew A; Borja, Austin J; Raizen, David M; Fang-Yen, Christopher

2018-01-01

Sleep during development is involved in refining brain circuitry, but a role for sleep in the earliest periods of nervous system elaboration, when neurons are first being born, has not been explored. Here we identify a sleep state in Drosophila larvae that coincides with a major wave of neurogenesis. Mechanisms controlling larval sleep are partially distinct from adult sleep: octopamine, the Drosophila analog of mammalian norepinephrine, is the major arousal neuromodulator in larvae, but dopamine is not required. Using real-time behavioral monitoring in a closed-loop sleep deprivation system, we find that sleep loss in larvae impairs cell division of neural progenitors. This work establishes a system uniquely suited for studying sleep during nascent periods, and demonstrates that sleep in early life regulates neural stem cell proliferation. PMID:29424688

Developmental Changes in Ultradian Sleep Cycles across Early Childhood: Preliminary Insights

PubMed Central

Lopp, Sean; Navidi, William; Achermann, Peter; LeBourgeois, Monique; Diniz Behn, Cecilia

2017-01-01

Nocturnal human sleep is composed of cycles between rapid eye movement (REM) sleep and non-REM (NREM) sleep. In adults, the structure of ultradian cycles between NREM and REM sleep is well characterized; however, less is known about the developmental trajectories of ultradian sleep cycles across early childhood. Cross-sectional studies indicate that the rapid ultradian cycling of active-quiet sleep in infancy shifts to a more adult-like pattern of NREM-REM sleep cycling by the school-age years, yet longitudinal studies elucidating the details of this transition are scarce. To address this gap, we examined ultradian cycling during nocturnal sleep following 13 h of prior wakefulness in 8 healthy children at 3 longitudinal points: 2Y (2.5-3.0 years of age), 3Y (3.5-4.0 years of age), and 5Y (5.5-6.0 years of age). We found that the length of ultradian cycles increased with age as a result of increased NREM sleep episode duration. In addition, we observed a significant decrease in the number of NREM sleep episodes as well as a nonsignificant trend for a decrease in the number of cycles with increasing age. Together, these findings suggest a concurrent change in which cycle duration increases and the number of cycles decreases across development. We also found that, consistent with data from adolescents and adults, the duration of NREM sleep episodes decreased with time since lights-off whereas the duration of REM sleep episodes increased over this time period. These results indicate the presence of circadian modulation of nocturnal sleep in preschool children. In addition to characterizing changes in ultradian cycling in healthy children ages 2 to 5 years, this work describes a developmental model that may provide insights into the emergence of normal adult REM sleep regulatory circuitry as well as potential trajectories of dysregulated ultradian cycles such as those associated with affective disorders. PMID:28088873

[Clinical correlation of hypnagogic hypersynchrony during sleep in normal children and those with learning disability].

PubMed

Olmos G de Alba, G; Fraire-Martínez, M I; Valenzuela-Romero, R

One of the electroencephalographic (EEG) patterns that can be mistaken for paroxysmal clinical activity, when not taken into account and especially in children, is hypnagogic hypersynchrony (HH). This consists in generalised, paroxysmal, synchronic, symmetrical, slow, high voltage waves lasting 2 8 seconds, which appear in drowsiness and in stage I. It was observed that this pattern often appeared in children with learning disability (LD). AIMS. To correlate clinical data with the presence of HH during sleep in normal children and those with LD. We assessed 180 children between the ages of 6 12 years with normal neurological development, 130 of which suffered LD and 50 who did not have LD. EEG was performed with sleep deprivation, following the International Federation of Clinical Neurophysiology guidelines. The presence or absence of HH, together with its characteristics, was assessed. Of the children with LD, 35.38% displayed HH and of the children without LD, only 4% displayed HH. Since the characteristics of HH in the children with LD were different to previous descriptions, we put forward criteria with which to evaluate those differences. HH appeared more often in children with LD than in normal children. Qualitative, quantitative (p< 0.05) and morphological changes were found in the paroxysmal activity of HH during the stages of sleep in children with LD.

Oscillatory brain activity in spontaneous and induced sleep stages in flies.

PubMed

Yap, Melvyn H W; Grabowska, Martyna J; Rohrscheib, Chelsie; Jeans, Rhiannon; Troup, Michael; Paulk, Angelique C; van Alphen, Bart; Shaw, Paul J; van Swinderen, Bruno

2017-11-28

Sleep is a dynamic process comprising multiple stages, each associated with distinct electrophysiological properties and potentially serving different functions. While these phenomena are well described in vertebrates, it is unclear if invertebrates have distinct sleep stages. We perform local field potential (LFP) recordings on flies spontaneously sleeping, and compare their brain activity to flies induced to sleep using either genetic activation of sleep-promoting circuitry or the GABA A agonist Gaboxadol. We find a transitional sleep stage associated with a 7-10 Hz oscillation in the central brain during spontaneous sleep. Oscillatory activity is also evident when we acutely activate sleep-promoting neurons in the dorsal fan-shaped body (dFB) of Drosophila. In contrast, sleep following Gaboxadol exposure is characterized by low-amplitude LFPs, during which dFB-induced effects are suppressed. Sleep in flies thus appears to involve at least two distinct stages: increased oscillatory activity, particularly during sleep induction, followed by desynchronized or decreased brain activity.

New assessment tools that measure sleep vital signs: the SleepMed Insomnia Index and the Sleep Matrix

PubMed Central

Bogan, Richard K; Turner, Jo Anne

2007-01-01

Insomnia is the leading sleep disorder in the US; however, diagnosis is often problematic. This pilot study assessed the clinical value of a novel diagnostic insomnia questionnaire. The SleepMed Insomnia Index (SMI) was administered to 543 consecutive patients and 50 normal control subjects during a pilot study. Mean SMI scores were assessed based on subsequent sleep-related diagnoses. The SMI scores for patients with sleep-related disorders were significantly higher than those for the control group (p < 0.001) and highest for the 90 patients comprising the insomnia group. Analysis of the SMI scores from the 90 insomnia patients indicates a high degree of reliability (Cronbach’s alpha: 0.7). These data support our clinical experience with this diagnostic tool which indicates a strong likelihood of disrupted nighttime sleep in patients with high SMI scores. Following further validation, the SMI may prove to be a valuable tool for evaluating sleep disorders, specifically as an aid in the diagnosis of insomnia. The Sleep Matrix is a visual tool that quantifies a sleep complaint by combining scores from the Epworth Sleepiness Scale (ESS) and the SMI. The SMI measures an insomnia component while the ESS is an accepted measure of daytime sleepiness. The Sleep Matrix visually displays the complexity of the sleep complaint in an effort to differentiate insomnia with differing etiologies from other sleep disorders and measure treatment outcomes. To pilot test the Sleep Matrix, the tool was administered to 90 patients with insomnia and to 22 normal controls. Plots from the insomnia patients were concentrated into the “insomnia zone” while scores from the normal controls were located in the “normal zone” located in the lower left quadrant. Additional research using the Sleep Matrix could provide data that the tool could be utilized to visually aid the clinician in the diagnosis of unknown sleep complaints. PMID:19300579

A role for clock genes in sleep homeostasis.

PubMed

Franken, Paul

2013-10-01

The timing and quality of both sleep and wakefulness are thought to be regulated by the interaction of two processes. One of these two processes keeps track of the prior sleep-wake history and controls the homeostatic need for sleep while the other sets the time-of-day that sleep preferably occurs. The molecular pathways underlying the latter, circadian process have been studied in detail and their key role in physiological time-keeping has been well established. Analyses of sleep in mice and flies lacking core circadian clock gene proteins have demonstrated, however, that besides disrupting circadian rhythms, also sleep homeostatic processes were affected. Subsequent studies revealed that sleep loss alters both the mRNA levels and the specific DNA-binding of the key circadian transcriptional regulators to their target sequences in the mouse brain. The fact that sleep loss impinges on the very core of the molecular circadian circuitry might explain why both inadequate sleep and disrupted circadian rhythms can similarly lead to metabolic pathology. The evidence for a role for clock genes in sleep homeostasis will be reviewed here. Copyright © 2013 Elsevier Ltd. All rights reserved.

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

PubMed

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

2014-10-01

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

Method for integrating microelectromechanical devices with electronic circuitry

DOEpatents

Montague, Stephen; Smith, James H.; Sniegowski, Jeffry J.; McWhorter, Paul J.

1998-01-01

A method for integrating one or more microelectromechanical (MEM) devices with electronic circuitry. The method comprises the steps of forming each MEM device within a cavity below a device surface of the substrate; encapsulating the MEM device prior to forming electronic circuitry on the substrate; and releasing the MEM device for operation after fabrication of the electronic circuitry. Planarization of the encapsulated MEM device prior to formation of the electronic circuitry allows the use of standard processing steps for fabrication of the electronic circuitry.

Sleep-disordered breathing in patients with atrial fibrillation and normal systolic left ventricular function.

PubMed

Bitter, Thomas; Langer, Christoph; Vogt, Jürgen; Lange, Mathias; Horstkotte, Dieter; Oldenburg, Olaf

2009-03-01

Obstructive sleep apnea (OSA) is more common in patients with atrial fibrillation (AFib). Recently, an additional association between central sleep apnea/Cheyne-Stokes respiration (CSA/CSR) and AFib has been described. The aim of this study was to investigate the prevalence and type of sleep-disordered breathing in patients with AFib and normal systolic left ventricular function. 150 patients (110 men and 40 women, aged 66.1 +/- 1.7 years) underwent cardiorespiratory polygraphy, capillary blood gas analysis, measurement of NT-proBNP, and echocardiography to determine the diameter of the left atrium (LAD) and the peak systolic pulmonary artery pressure (PAP). Sleep-disordered breathing was documented in 74% of all patients with AFib (43% had OSA and 31% had CSA/CSR). Patients with CSA/CSR had a higher PAP, a higher apnea-hypopnea index, a greater LAD, and a lower capillary blood pCO(2) than patients with OSA. Patients with AFib were found to have not only a high prevalence of obstructive sleep apnea, as has been described previously, but also a high prevalence of CSA/CSR. It remains unknown whether CSA/CSR is more common in AFib because of diastolic dysfunction or whether phenomena associated with CSA/CSR predispose to AFib. Further research on this question is needed.

Method for integrating microelectromechanical devices with electronic circuitry

DOEpatents

Montague, S.; Smith, J.H.; Sniegowski, J.J.; McWhorter, P.J.

1998-08-25

A method is disclosed for integrating one or more microelectromechanical (MEM) devices with electronic circuitry. The method comprises the steps of forming each MEM device within a cavity below a device surface of the substrate; encapsulating the MEM device prior to forming electronic circuitry on the substrate; and releasing the MEM device for operation after fabrication of the electronic circuitry. Planarization of the encapsulated MEM device prior to formation of the electronic circuitry allows the use of standard processing steps for fabrication of the electronic circuitry. 13 figs.

Baseline Levels of Rapid Eye Movement Sleep May Protect Against Excessive Activity in Fear-Related Neural Circuitry.

PubMed

Lerner, Itamar; Lupkin, Shira M; Sinha, Neha; Tsai, Alan; Gluck, Mark A

2017-11-15

Sleep, and particularly rapid eye movement sleep (REM), has been implicated in the modulation of neural activity following fear conditioning and extinction in both human and animal studies. It has long been presumed that such effects play a role in the formation and persistence of posttraumatic stress disorder, of which sleep impairments are a core feature. However, to date, few studies have thoroughly examined the potential effects of sleep prior to conditioning on subsequent acquisition of fear learning in humans. Furthermore, these studies have been restricted to analyzing the effects of a single night of sleep-thus assuming a state-like relationship between the two. In the current study, we used long-term mobile sleep monitoring and functional neuroimaging (fMRI) to explore whether trait-like variations in sleep patterns, measured in advance in both male and female participants, predict subsequent patterns of neural activity during fear learning. Our results indicate that higher baseline levels of REM sleep predict reduced fear-related activity in, and connectivity between, the hippocampus, amygdala and ventromedial PFC during conditioning. Additionally, skin conductance responses (SCRs) were weakly correlated to the activity in the amygdala. Conversely, there was no direct correlation between REM sleep and SCRs, indicating that REM may only modulate fear acquisition indirectly. In a follow-up experiment, we show that these results are replicable, though to a lesser extent, when measuring sleep over a single night just before conditioning. As such, baseline sleep parameters may be able to serve as biomarkers for resilience, or lack thereof, to trauma. SIGNIFICANCE STATEMENT Numerous studies over the past two decades have established a clear role of sleep in fear-learning processes. However, previous work has focused on the effects of sleep following fear acquisition, thus neglecting the potential effects of baseline sleep levels on the acquisition itself. The

Dynamics of sleep/wake determination--Normal and abnormal

NASA Astrophysics Data System (ADS)

Mahowald, Mark W.; Schenck, Carlos H.; O'Connor, Kevin A.

1991-10-01

Virtually all members of the animal kingdom experience a relentless and powerful cycling of states of being: wakefulness, rapid eye movement sleep, and nonrapid eye movement sleep. Each of these states is composed of a number of physiologic variables generated in a variety of neural structures. The predictable oscillations of these states are driven by presumed neural pacemakers which are entrained to the 24 h geophysical environment by the light/dark cycle. Experiments in nature have indicated that wake/sleep rhythm perturbations may occur either involving desynchronization of the basic 24 h wake/sleep cycle within the geophysical 24 h cycle (circadian rhythm disturbances) or involving the rapid oscillation or incomplete declaration of state (such as narcolepsy). The use of phase spaces to describe states of being may be of interest in the description of state determination in both illness and health. Some fascinating clinical and experimental phenomena may represent bifurcations in the sleep/wake control system.

Polysomnography (Sleep Study)

MedlinePlus

... it's done Polysomnography monitors your sleep stages and cycles to identify if or when your sleep patterns ... You normally go through four to six sleep cycles a night, cycling between NREM and REM sleep ...

Advanced Data Acquisition Systems with Self-Healing Circuitry

NASA Technical Reports Server (NTRS)

Larson, William E.; Ihlefeld, Curtis M.; Medelius, Pedro J.; Delgado, H. (Technical Monitor)

2001-01-01

Kennedy Space Center's Spaceport Engineering & Technology Directorate has developed a data acquisition system that will help drive down the cost of ground launch operations. This system automates both the physical measurement set-up function as well as configuration management documentation. The key element of the system is a self-configuring, self-calibrating, signal-conditioning amplifier that automatically adapts to any sensor to which it is connected. This paper will describe the core technology behind this device and the automated data system in which it has been integrated. The paper will also describe the revolutionary enhancements that are planned for this innovative measurement technology. All measurement electronics devices contain circuitry that, if it fails or degrades, requires the unit to be replaced, adding to the cost of operations. Kennedy Space Center is now developing analog circuits that will be able to detect their own failure and dynamically reconfigure their circuitry to restore themselves to normal operation. This technology will have wide ranging application in all electronic devices used in space and ground systems.

Sleep and executive functions in older adults: A systematic review

PubMed Central

Holanda, Francisco Wilson Nogueira; de Almondes, Katie Moraes

2016-01-01

ABSTRACT Introduction: A recent increase in studies suggests a role of age-related sleep changes in executive functions (EF). However, this relationship remains unclear and mixed results have emerged. Objective: To investigate how age-related sleep changes may play an important role in the extent to which healthy older adults exhibit decline in EF. Methods: A systematic strategy was employed to identify the available literature on age-related sleep changes and EF. Results: Of the 465 studies identified, 26 were included. Results suggest that multiple sleep parameters differ in the way they benefit or impair EF. Parameters such as greater wake after sleep onset and lower sleep efficiency, in addition to circadian fragmentation of sleep, showed more consistent results and are potentially correlated with worsening in EF measures. However, other results seem inconclusive. Conclusion: These findings were discussed based on the prefrontal circuitry vulnerability model, in which sleep has been identified as a beneficial factor for prefrontal cortex functioning and hence for EF, which relies mostly on this brain area and its related networks. PMID:29213454

Heritability of Craniofacial Structures in Normal Subjects and Patients with Sleep Apnea

PubMed Central

Chi, Luqi; Comyn, Francois-Louis; Keenan, Brendan T.; Cater, Jacqueline; Maislin, Greg; Pack, Allan I.; Schwab, Richard J.

2014-01-01

Objectives: Accumulating evidence has shown that there is a genetic contribution to obstructive sleep apnea (OSA).The objectives were to use magnetic resonance imaging (MRI) cephalometry to (1) confirm heritability of craniofacial risk factors for OSA previously shown by cephalometrics; and (2) examine the heritability of new craniofacial structures that are measurable with MRI. Design: A sib pair “quad” design examining apneics, apneic siblings, controls, and control siblings. The study design used exact matching on ethnicity and sex, frequency matching on age, and statistical control for differences in age, sex, ethnicity, height, and weight. Setting: Academic medical center. Patients: We examined 55 apneic probands (apnea-hypopnea index [AHI]: 46.8 ± 33.5 events/h), 55 proband siblings (AHI: 11.1 ± 15.9 events/h), 55 controls (AHI: 2.2 ± 1.7 events/h), and 55 control siblings (AHI: 4.1 ± 4.0 events/h). Interventions: N/A. Measurements and Results: Five independent domains reflecting different aspects of the craniofacial structure were examined. We confirmed heritability of sella–nasion–subspinale (38%, P = 0.002), saddle angle (55%, P < 0.0001), mandibular length (24%, P = 0.02) and lower facial height (33%, P = 0.006) previously measured by cephalometry. In addition, the current study added new insights by demonstrating significant heritability of mandibular width (30%, P = 0.005), maxillary width (47%, P < 0.0001), distance from the hyoid bone to the retropogonion (36%, P = 0.0018) and size of the oropharyngeal space (31%, P = 0.004). Finally, our data indicate that heritability of the craniofacial structures is similar in normal patients and those with apnea. Conclusions: The data support our a priori hypothesis that the craniofacial structures that have been associated with obstructive sleep apnea (OSA) are heritable. We have demonstrated heritability for several intermediate craniofacial phenotypes for OSA. Thus, we believe that future studies

Obstructive sleep apnea in normal weight patients: characteristics and comparison with overweight and obese patients.

PubMed

Dacal Quintas, Raquel; Tumbeiro Novoa, Manuel; Alves Pérez, María Teresa; Santalla Martínez, Mari Luz; Acuña Fernández, Adela; Marcos Velázquez, Pedro

2013-12-01

To determine the frequency of obstructive sleep apnoea (OSA) and metabolic syndrome (MS) in normal weight patients and their characteristics, and to compare these with overweight and obese patients. We studied all patients with suspected OSA referred to the sleep laboratory from January to December 2009. OSA was diagnosed when the apnoea-hypopnoea index (AHI) was >5 and symptoms were present. MS was diagnosed according to International Diabetes Federation (IDF) criteria. The patients were distributed into 3 groups according to body mass index (BMI): normal weight (<25kg/m(2)), overweight (25-29.9kg/m(2)) and obese (≥30kg/m(2)). We studied 475 patients: 7.60% normal weight and 56.4% obese. Most patients in the normal weight group were women, snorers, non-smokers, non-drinkers and were significantly younger and with a smaller neck and waist circumference than obese and overweight patients. OSA was diagnosed in 90.10%: 77.70% normal weight. OSA in these patients was mostly mild, and there were differences between the diagnosis of OSA and the BMI classified. MS was diagnosed in 64.40%: 33.33% normal weight. There was a higher probability of MS as the BMI increased. OSA and MS frequency in normal weight patients was 22% and in obese patients was 70.52%. OSA in normal weight patients was related with gender and age. There was no relationship between OSA and MS, or between otorhinolaryngological malformations and OSA in normal weight patients. Eight normal weight patients with OSA were treated with continuous positive airway pressure (CPAP) therapy. The frequency of OSA in normal weight patients was lower than in overweight and obese patients. The frequency of concomitant OSA and MS was lower in normal weight patients than in obese subjects. Normal weight patients were mostly women, younger and had no toxic habits. In normal weight patients, age and gender were predictive factors for OSA, but OSA and MS were not related. Copyright © 2013 SEPAR. Published by Elsevier

The Development of Micromachined Gyroscope Structure and Circuitry Technology

PubMed Central

Xia, Dunzhu; Yu, Cheng; Kong, Lun

2014-01-01

This review surveys micromachined gyroscope structure and circuitry technology. The principle of micromachined gyroscopes is first introduced. Then, different kinds of MEMS gyroscope structures, materials and fabrication technologies are illustrated. Micromachined gyroscopes are mainly categorized into micromachined vibrating gyroscopes (MVGs), piezoelectric vibrating gyroscopes (PVGs), surface acoustic wave (SAW) gyroscopes, bulk acoustic wave (BAW) gyroscopes, micromachined electrostatically suspended gyroscopes (MESGs), magnetically suspended gyroscopes (MSGs), micro fiber optic gyroscopes (MFOGs), micro fluid gyroscopes (MFGs), micro atom gyroscopes (MAGs), and special micromachined gyroscopes. Next, the control electronics of micromachined gyroscopes are analyzed. The control circuits are categorized into typical circuitry and special circuitry technologies. The typical circuitry technologies include typical analog circuitry and digital circuitry, while the special circuitry consists of sigma delta, mode matching, temperature/quadrature compensation and novel special technologies. Finally, the characteristics of various typical gyroscopes and their development tendency are discussed and investigated in detail. PMID:24424468

Scale-free dynamics of the synchronization between sleep EEG power bands and the high frequency component of heart rate variability in normal men and patients with sleep apnea-hypopnea syndrome.

PubMed

Dumont, Martine; Jurysta, Fabrice; Lanquart, Jean-Pol; Noseda, André; van de Borne, Philippe; Linkowski, Paul

2007-12-01

To investigate the dynamics of the synchronization between heart rate variability and sleep electroencephalogram power spectra and the effect of sleep apnea-hypopnea syndrome. Heart rate and sleep electroencephalogram signals were recorded in controls and patients with sleep apnea-hypopnea syndrome that were matched for age, gender, sleep parameters, and blood pressure. Spectral analysis was applied to electrocardiogram and electroencephalogram sleep recordings to obtain power values every 20s. Synchronization likelihood was computed between time series of the normalized high frequency spectral component of RR-intervals and all electroencephalographic frequency bands. Detrended fluctuation analysis was applied to the synchronizations in order to qualify their dynamic behaviors. For all sleep bands, the fluctuations of the synchronization between sleep EEG and heart activity appear scale free and the scaling exponent is close to one as for 1/f noise. We could not detect any effect due to sleep apnea-hypopnea syndrome. The synchronizations between the high frequency component of heart rate variability and all sleep power bands exhibited robust fluctuations characterized by self-similar temporal behavior of 1/f noise type. No effects of sleep apnea-hypopnea syndrome were observed in these synchronizations. Sleep apnea-hypopnea syndrome does not affect the interdependence between the high frequency component of heart rate variability and all sleep power bands as measured by synchronization likelihood.

Lighting up the brain's reward circuitry.

PubMed

Lobo, Mary Kay

2012-07-01

The brain's reward circuit is critical for mediating natural reward behaviors including food, sex, and social interaction. Drugs of abuse take over this circuit and produce persistent molecular and cellular alterations in the brain regions and their neural circuitry that make up the reward pathway. Recent use of optogenetic technologies has provided novel insights into the functional and molecular role of the circuitry and cell subtypes within these circuits that constitute this pathway. This perspective will address the current and future use of light-activated proteins, including those involved in modulating neuronal activity, cellular signaling, and molecular properties in the neural circuitry mediating rewarding stimuli and maladaptive responses to drugs of abuse. © 2012 New York Academy of Sciences.

Phospholipase C-beta4 is essential for the progression of the normal sleep sequence and ultradian body temperature rhythms in mice.

PubMed

Ikeda, Masayuki; Hirono, Moritoshi; Sugiyama, Takashi; Moriya, Takahiro; Ikeda-Sagara, Masami; Eguchi, Naomi; Urade, Yoshihiro; Yoshioka, Tohru

2009-11-09

THE SLEEP SEQUENCE: i) non-REM sleep, ii) REM sleep, and iii) wakefulness, is stable and widely preserved in mammals, but the underlying mechanisms are unknown. It has been shown that this sequence is disrupted by sudden REM sleep onset during active wakefulness (i.e., narcolepsy) in orexin-deficient mutant animals. Phospholipase C (PLC) mediates the signaling of numerous metabotropic receptors, including orexin receptors. Among the several PLC subtypes, the beta4 subtype is uniquely localized in the geniculate nucleus of thalamus which is hypothesized to have a critical role in the transition and maintenance of sleep stages. In fact, we have reported irregular theta wave frequency during REM sleep in PLC-beta4-deficient mutant (PLC-beta4-/-) mice. Daily behavioral phenotypes and metabotropic receptors involved have not been analyzed in detail in PLC-beta4-/- mice, however. Therefore, we analyzed 24-h sleep electroencephalogram in PLC-beta4-/- mice. PLC-beta4-/- mice exhibited normal non-REM sleep both during the day and nighttime. PLC-beta4-/- mice, however, exhibited increased REM sleep during the night, their active period. Also, their sleep was fragmented with unusual wake-to-REM sleep transitions, both during the day and nighttime. In addition, PLC-beta4-/- mice reduced ultradian body temperature rhythms and elevated body temperatures during the daytime, but had normal homeothermal response to acute shifts in ambient temperatures (22 degrees C-4 degrees C). Within the most likely brain areas to produce these behavioral phenotypes, we found that, not orexin, but group-1 metabotropic glutamate receptor (mGluR)-mediated Ca(2+) mobilization was significantly reduced in the dorsal lateral geniculate nucleus (LGNd) of PLC-beta4-/- mice. Voltage clamp recordings revealed that group-1 mGluR-mediated currents in LGNd relay neurons (inward in wild-type mice) were outward in PLC-beta4-/- mice. These lines of evidence indicate that impaired LGNd relay, possibly mediated

Sleep and emotions: a focus on insomnia.

PubMed

Baglioni, Chiara; Spiegelhalder, Kai; Lombardo, Caterina; Riemann, Dieter

2010-08-01

Insomnia disorder is defined as difficulties in initiating/maintaining sleep and/or non-restorative sleep accompanied by decreased daytime functioning, persisting for at least four weeks. For many patients suffering from depression and anxiety, insomnia is a pervasive problem. Many of the aetiological theories of insomnia postulate that heightened emotional reactivity contributes to the maintenance of symptoms. This review focuses on the role of emotional reactivity in insomnia, and how the relationship between insomnia and depression and anxiety may be mediated by emotional reactivity. Furthermore, studies investigating the valence of emotions in insomnia are reviewed. Overall, there is empirical evidence that dysfunctional emotional reactivity might mediate the interaction between cognitive and autonomic hyperarousal, thus contributing to the maintenance of insomnia. Moreover, dysfunctions in sleep-wake regulating neural circuitries seem to be able to reinforce emotional disturbances. It seems plausible that dysfunctional emotional reactivity modulates the relationship between insomnia and depression and anxiety. Considering the interaction between sleep and emotional valence, poor sleep quality seems to correlate with high negative and low positive emotions, both in clinical and subclinical samples. Good sleep seems to be associated with high positive emotions, but not necessarily with low negative emotions. This review underlines the need for future research on emotions in insomnia. (c) 2009 Elsevier Ltd. All rights reserved.

Glucose Induces Slow-Wave Sleep by Exciting the Sleep-Promoting Neurons in the Ventrolateral Preoptic Nucleus: A New Link between Sleep and Metabolism.

PubMed

Varin, Christophe; Rancillac, Armelle; Geoffroy, Hélène; Arthaud, Sébastien; Fort, Patrice; Gallopin, Thierry

2015-07-08

Sleep-active neurons located in the ventrolateral preoptic nucleus (VLPO) play a crucial role in the induction and maintenance of slow-wave sleep (SWS). However, the cellular and molecular mechanisms responsible for their activation at sleep onset remain poorly understood. Here, we test the hypothesis that a rise in extracellular glucose concentration in the VLPO can promote sleep by increasing the activity of sleep-promoting VLPO neurons. We find that infusion of a glucose concentration into the VLPO of mice promotes SWS and increases the density of c-Fos-labeled neurons selectively in the VLPO. Moreover, we show in patch-clamp recordings from brain slices that VLPO neurons exhibiting properties of sleep-promoting neurons are selectively excited by glucose within physiological range. This glucose-induced excitation implies the catabolism of glucose, leading to a closure of ATP-sensitive potassium (KATP) channels. The extracellular glucose concentration monitors the gating of KATP channels of sleep-promoting neurons, highlighting that these neurons can adapt their excitability according to the extracellular energy status. Together, these results provide evidence that glucose may participate in the mechanisms of SWS promotion and/or consolidation. Although the brain circuitry underlying vigilance states is well described, the molecular mechanisms responsible for sleep onset remain largely unknown. Combining in vitro and in vivo experiments, we demonstrate that glucose likely contributes to sleep onset facilitation by increasing the excitability of sleep-promoting neurons in the ventrolateral preoptic nucleus (VLPO). We find here that these neurons integrate energetic signals such as ambient glucose directly to regulate vigilance states accordingly. Glucose-induced excitation of sleep-promoting VLPO neurons should therefore be involved in the drowsiness that one feels after a high-sugar meal. This novel mechanism regulating the activity of VLPO neurons reinforces the

Frequency of EEG arousals from nocturnal sleep in normal subjects.

PubMed

Mathur, R; Douglas, N J

1995-06-01

Brief arousals are clinically important and increasingly scored during polysomnography. However, the frequency of arousals during routine polysomnography in the normal population is unknown. We performed overnight polysomnography in the 55 of 59 control subjects from a family practice list who were approached and agreed to undergo polysomnography. Awakenings were scored according to the criteria of Rechtschaffen and Kales and briefer arousals according to three different criteria, including the American Sleep Disorders Association (ASDA) definition. There was a mean of 4 [95% confidence interval (CI), 1-15) Rechtschaffen and Kales awakenings per hour, whereas the ASDA definition gave 21 (95% CI, 7-56) per hour slept. Arousal frequencies increased significantly (p < 0.001) with age in our subjects, who ranged from the late teens to early 70s. The high upper limit of the frequency of brief arousals was not altered by exclusion of patients who snored or had witnessed apneas or daytime sleepiness. It is important that those scoring arousals on routine polysomnography recognize that high arousal frequencies occur in the normal population on 1-night polysomnography.

Comparison of ambulatory and polysomnographic recording of jaw muscle activity during sleep in normal subjects.

PubMed

Yamaguchi, T; Abe, S; Rompré, P H; Manzini, C; Lavigne, G J

2012-01-01

Clinicians and investigators need a simple and reliable recording device to diagnose or monitor sleep bruxism (SB). The aim of this study was to compare recordings made with an ambulatory electromyographic telemetry recorder (TEL-EMG) with those made with standard sleep laboratory polysomnography with synchronised audio-visual recording (PSG-AV). Eight volunteer subjects without current history of tooth grinding spent one night in a sleep laboratory. Simultaneous bilateral masseter EMG recordings were made with a TEL-EMG and standard PSG. All types of oromotor activity and rhythmic masseter muscle activity (RMMA), typical of SB, were independently scored by two individuals. Correlation and intra-class coefficient (ICC) were estimated for scores on each system. The TEL-EMG was highly sensitive to detect RMMA (0·988), but with low positive predictive value (0·231) because of a high rate of oromotor activity detection (e.g. swallowing and scratching). Almost 72% of false-positive oromotor activity scored with the TEL-EMG occurred during the transient wake period of sleep. A non-significant correlation between recording systems was found (r = 0·49). Because of the high frequency of wake periods during sleep, ICC was low (0·47), and the removal of the influence of wake periods improved the detection reliability of the TEL-EMG (ICC = 0·88). The TEL-EMG is sensitive to detect RMMA in normal subjects. However, it obtained a high rate of false-positive detections because of the presence of frequent oromotor activities and transient wake periods of sleep. New algorithms are needed to improve the validity of TEL-EMG recordings. © 2011 Blackwell Publishing Ltd.

Sleep Misperception and Chronic Insomnia in the General Population: The Role of Objective Sleep Duration and Psychological Profiles

PubMed Central

Fernandez-Mendoza, Julio; Calhoun, Susan L.; Bixler, Edward O.; Karataraki, Maria; Liao, Duanping; Vela-Bueno, Antonio; Ramos-Platon, María Jose; Sauder, Katherine A.; Basta, Maria; Vgontzas, Alexandros N.

2011-01-01

Objective Sleep misperception is considered by some investigators a common characteristic of chronic insomnia, whereas others propose it as a separate diagnosis. The frequency and the determinants of sleep misperception in general population samples are unknown. In this study we examined the role of objective sleep duration, a novel marker in phenotyping insomnia, and psychological profiles on sleep misperception in a large, general population sample. Methods 142 insomniacs and 724 controls selected from a general random sample of 1,741 individuals (age ≥ 20 years) underwent a polysomnographic evaluation, completed the Minnesota Multiphasic Personality Inventory-2, and were split into two groups based on their objective sleep duration: “normal sleep duration” (≥ 6 hours) and “short sleep duration” (< 6 hours). Results The discrepancy between subjective and objective sleep duration was determined by two independent factors. Short sleepers reported more sleep than they objectively had and insomniacs reported less sleep than controls with similar objective sleep duration. The additive effect of these two factors resulted in underestimation only in insomniacs with normal sleep duration. Insomniacs with normal sleep duration showed a MMPI-2 profile of high depression and anxiety, and low ego strength, whereas insomniacs with short sleep duration showed a profile of a medical disorder. Conclusions Underestimation of sleep duration is prevalent among insomniacs with objective normal sleep duration. Anxious-ruminative traits and poor resources for coping with stress appear to mediate the underestimation of sleep duration. These data further support the validity and clinical utility of objective sleep measures in phenotyping insomnia. PMID:20978224

Polysomnographic study of nocturnal sleep in idiopathic hypersomnia without long sleep time.

PubMed

Pizza, Fabio; Ferri, Raffaele; Poli, Francesca; Vandi, Stefano; Cosentino, Filomena I I; Plazzi, Giuseppe

2013-04-01

We investigated nocturnal sleep abnormalities in 19 patients with idiopathic hypersomnia without long sleep time (IH) in comparison with two age- and sex- matched control groups of 13 normal subjects (C) and of 17 patients with narcolepsy with cataplexy (NC), the latter considered as the extreme of excessive daytime sleepiness (EDS). Sleep macro- and micro- (i.e. cyclic alternating pattern, CAP) structure as well as quantitative analysis of EEG, of periodic leg movements during sleep (PLMS), and of muscle tone during REM sleep were compared across groups. IH and NC patients slept more than C subjects, but IH showed the highest levels of sleep fragmentation (e.g. awakenings), associated with a CAP rate higher than NC during lighter sleep stages and lower than C during slow wave sleep respectively, and with the highest relative amount of A3 and the lowest of A1 subtypes. IH showed a delta power in between C and NC groups, whereas muscle tone and PLMS had normal characteristics. A peculiar profile of microstructural sleep abnormalities may contribute to sleep fragmentation and, possibly, EDS in IH. © 2012 European Sleep Research Society.

Brain serotonergic circuitries

PubMed Central

Charnay, Yves; Leger, Lucienne

2010-01-01

Brain serotonergic circuitries interact with other neurotransmitter systems on a multitude of different molecular levels. In humans, as in other mammalian species, serotonin (5-HT) plays a modulatory role in almost every physiological function. Furthermore, serotonergic dysfunction is thought to be implicated in several psychiatric and neurodegenerative disorders. We describe the neuroanatomy and neurochemistry of brain serotonergic circuitries. The contribution of emergent in vivo imaging methods to the regional localization of binding site receptors and certain aspects of their functional connectivity in correlation to behavior is also discussed. 5-HT cell bodies, mainly localized in the raphe nuclei, send axons to almost every brain region. It is argued that the specificity of the local chemocommunication between 5-HT and other neuronal elements mainly depends on mechanisms regulating the extracellular concentration of 5-HT, the diversity of high-affinity membrane receptors, and their specific transduction modalities. PMID:21319493

Evolution of the circuitry for conscious color vision in primates

PubMed Central

Neitz, J; Neitz, M

2017-01-01

There are many ganglion cell types and subtypes in our retina that carry color information. These have appeared at different times over the history of the evolution of the vertebrate visual system. They project to several different places in the brain and serve a variety of purposes allowing wavelength information to contribute to diverse visual functions. These include circadian photoentrainment, regulation of sleep and mood, guidance of orienting movements, detection and segmentation of objects. Predecessors to some of the circuits serving these purposes presumably arose before mammals evolved and different functions are represented by distinct ganglion cell types. However, while other animals use color information to elicit motor movements and regulate activity rhythms, as do humans, using phylogenetically ancient circuitry, the ability to appreciate color appearance may have been refined in ancestors to primates, mediated by a special set of ganglion cells that serve only that purpose. Understanding the circuitry for color vision has implications for the possibility of treating color blindness using gene therapy by recapitulating evolution. In addition, understanding how color is encoded, including how chromatic and achromatic percepts are separated is a step toward developing a complete picture of the diversity of ganglion cell types and their functions. Such knowledge could be useful in developing therapeutic strategies for blinding eye disorders that rely on stimulating elements in the retina, where more than 50 different neuron types are organized into circuits that transform signals from photoreceptors into specialized detectors many of which are not directly involved in conscious vision. PMID:27935605

Evolution of the circuitry for conscious color vision in primates.

PubMed

Neitz, J; Neitz, M

2017-02-01

There are many ganglion cell types and subtypes in our retina that carry color information. These have appeared at different times over the history of the evolution of the vertebrate visual system. They project to several different places in the brain and serve a variety of purposes allowing wavelength information to contribute to diverse visual functions. These include circadian photoentrainment, regulation of sleep and mood, guidance of orienting movements, detection and segmentation of objects. Predecessors to some of the circuits serving these purposes presumably arose before mammals evolved and different functions are represented by distinct ganglion cell types. However, while other animals use color information to elicit motor movements and regulate activity rhythms, as do humans, using phylogenetically ancient circuitry, the ability to appreciate color appearance may have been refined in ancestors to primates, mediated by a special set of ganglion cells that serve only that purpose. Understanding the circuitry for color vision has implications for the possibility of treating color blindness using gene therapy by recapitulating evolution. In addition, understanding how color is encoded, including how chromatic and achromatic percepts are separated is a step toward developing a complete picture of the diversity of ganglion cell types and their functions. Such knowledge could be useful in developing therapeutic strategies for blinding eye disorders that rely on stimulating elements in the retina, where more than 50 different neuron types are organized into circuits that transform signals from photoreceptors into specialized detectors many of which are not directly involved in conscious vision.

Phospholipase C-β4 Is Essential for the Progression of the Normal Sleep Sequence and Ultradian Body Temperature Rhythms in Mice

PubMed Central

Ikeda, Masayuki; Hirono, Moritoshi; Sugiyama, Takashi; Moriya, Takahiro; Ikeda-Sagara, Masami; Eguchi, Naomi; Urade, Yoshihiro; Yoshioka, Tohru

2009-01-01

Background The sleep sequence: i) non-REM sleep, ii) REM sleep, and iii) wakefulness, is stable and widely preserved in mammals, but the underlying mechanisms are unknown. It has been shown that this sequence is disrupted by sudden REM sleep onset during active wakefulness (i.e., narcolepsy) in orexin-deficient mutant animals. Phospholipase C (PLC) mediates the signaling of numerous metabotropic receptors, including orexin receptors. Among the several PLC subtypes, the β4 subtype is uniquely localized in the geniculate nucleus of thalamus which is hypothesized to have a critical role in the transition and maintenance of sleep stages. In fact, we have reported irregular theta wave frequency during REM sleep in PLC-β4-deficient mutant (PLC-β4−/−) mice. Daily behavioral phenotypes and metabotropic receptors involved have not been analyzed in detail in PLC-β4−/− mice, however. Methodology/Principal Findings Therefore, we analyzed 24-h sleep electroencephalogram in PLC-β4−/− mice. PLC-β4−/− mice exhibited normal non-REM sleep both during the day and nighttime. PLC-β4−/− mice, however, exhibited increased REM sleep during the night, their active period. Also, their sleep was fragmented with unusual wake-to-REM sleep transitions, both during the day and nighttime. In addition, PLC-β4−/− mice reduced ultradian body temperature rhythms and elevated body temperatures during the daytime, but had normal homeothermal response to acute shifts in ambient temperatures (22°C–4°C). Within the most likely brain areas to produce these behavioral phenotypes, we found that, not orexin, but group-1 metabotropic glutamate receptor (mGluR)-mediated Ca2+ mobilization was significantly reduced in the dorsal lateral geniculate nucleus (LGNd) of PLC-β4−/− mice. Voltage clamp recordings revealed that group-1 mGluR-mediated currents in LGNd relay neurons (inward in wild-type mice) were outward in PLC-β4−/− mice. Conclusions/Significance These lines

Method for integrating microelectromechanical devices with electronic circuitry

DOEpatents

Barron, Carole C.; Fleming, James G.; Montague, Stephen

1999-01-01

A method is disclosed for integrating one or more microelectromechanical (MEM) devices with electronic circuitry on a common substrate. The MEM device can be fabricated within a substrate cavity and encapsulated with a sacrificial material. This allows the MEM device to be annealed and the substrate planarized prior to forming electronic circuitry on the substrate using a series of standard processing steps. After fabrication of the electronic circuitry, the electronic circuitry can be protected by a two-ply protection layer of titanium nitride (TiN) and tungsten (W) during an etch release process whereby the MEM device is released for operation by etching away a portion of a sacrificial material (e.g. silicon dioxide or a silicate glass) that encapsulates the MEM device. The etch release process is preferably performed using a mixture of hydrofluoric acid (HF) and hydrochloric acid (HCI) which reduces the time for releasing the MEM device compared to use of a buffered oxide etchant. After release of the MEM device, the TiN:W protection layer can be removed with a peroxide-based etchant without damaging the electronic circuitry.

Associations between sleep duration, sleep quality and diabetic retinopathy.

PubMed

Tan, Nicholas Y Q; Chew, Merwyn; Tham, Yih-Chung; Nguyen, Quang Duc; Yasuda, Masayuki; Cheng, Ching-Yu; Wong, Tien Yin; Sabanayagam, Charumathi

2018-01-01

Abnormal durations of sleep have been associated with risk of diabetes. However, it is not clear if sleep duration is associated with diabetic retinopathy (DR). In a cross-sectional study, we included 1,231 (Malay, n = 395; Indian, n = 836) adults (mean age 64.4 ± 9.0 years, 50.4% female) with diabetes from the second visit of two independent population-based cohort studies (2011-15) in Singapore. Self-reported habitual sleep duration was categorized as short (<6 h), normal (6≤ h <8), and long (≥8 h). Questionnaires were administered to detect risk of obstructive sleep apnea (OSA), excessive daytime sleepiness, and insomnia, all of which may indicate poor quality of sleep. The associations between sleep-related characteristics with moderate DR and vision-threatening DR (VTDR) were analysed using logistic regression models adjusted for potential confounders. Prevalence of moderate DR and VTDR in the study population were 10.5% and 6.3% respectively. The mean duration of sleep was 6.4 ± 1.5 h. Compared to normal sleep duration, both short and long sleep durations were associated with moderate DR with multivariable odds ratio (95% confidence interval) of 1.73 (1.03-2.89) and 2.17 (1.28-3.66) respectively. Long sleep duration (2.37 [1.16-4.89]), high risk of OSA (2.24 [1.09-4.75]), and excessive daytime sleepiness (3.27 [1.02-10.30]) were separately associated with VTDR. Sleep duration had a U-shaped association with moderate DR; long sleep duration, excessive daytime sleepiness and high risk of OSA were positively associated with VTDR.

Chronic sleep loss and risk-taking behavior: Does the origin of sleep loss matter?

PubMed

Rusnac, Natalia; Spitzenstetter, Florence; Tassi, Patricia

2018-06-20

Many adolescents and young adults get insufficient sleep. A link between sleep loss and risk-taking behavior has been consistently found in the literature, but surprisingly, the role played by the origin of sleep loss in this link has never been investigated. Sleep loss can be voluntary (instead of sleeping, a significant amount of time is devoted to other activities) or involuntary (caused by a sleep disorder, for example, insomnia). The aim of this research was to investigate whether both types of sleep loss are associated to the same extent with risky behavior. Five hundred thirty-six university students between 19 and 25 years old participated in this study. Three groups were selected: participants with voluntary sleep loss, participants with insomnia, and normal sleepers. We assessed risk-taking behavior in virtual driving situations, as well as drinking habits in terms of quantity and frequency. To further explore the differences between the groups, we also measured sensation seeking, a personality trait related to risk-taking behavior. Compared to participants with insomnia and normal sleepers, participants with voluntary sleep loss take more risks in dangerous driving situations, drink more alcohol, and have higher disinhibition scores on the Sensation-Seeking Scale. On the other hand, no such differences were found between participants with insomnia and normal sleepers, suggesting that sleep loss is not always associated with risk taking. Whether sleep loss is associated with risk-taking behavior or not could depend on the origin of sleep loss and the underlying personality traits.

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

PubMed

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

2010-12-14

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

Epigenetics of sleep and chronobiology.

PubMed

Qureshi, Irfan A; Mehler, Mark F

2014-03-01

The circadian clock choreographs fundamental biological rhythms. This system is comprised of the master circadian pacemaker in the suprachiasmatic nucleus and associated pacemakers in other tissues that coordinate complex physiological processes and behaviors, such as sleep, feeding, and metabolism. The molecular circuitry that underlies these clocks and orchestrates circadian gene expression has been the focus of intensive investigation, and it is becoming clear that epigenetic factors are highly integrated into these networks. In this review, we draw attention to the fundamental roles played by epigenetic mechanisms in transcriptional and post-transcriptional regulation within the circadian clock system. We also highlight how alterations in epigenetic factors and mechanisms are being linked with sleep-wake disorders. These observations provide important insights into the pathogenesis and potential treatment of these disorders and implicate epigenetic deregulation in the significant but poorly understood interconnections now emerging between circadian processes and neurodegeneration, metabolic diseases, cancer, and aging.

Gender differences in brain regional homogeneity of healthy subjects after normal sleep and after sleep deprivation: a resting-state fMRI study.

PubMed

Dai, Xi-Jian; Gong, Hong-Han; Wang, Yi-Xiang; Zhou, Fu-Qing; Min, You-Jiang; Zhao, Feng; Wang, Si-Yong; Liu, Bi-Xia; Xiao, Xiang-Zuo

2012-06-01

To explore the gender differences of brain regional homogeneity (ReHo) in healthy subjects during the resting-state, after normal sleep, and after sleep deprivation (SD) using functional magnetic resonance imaging (fMRI) and the ReHo method. Sixteen healthy subjects (eight males and eight females) each underwent the resting-state fMRI exams twice, i.e., once after normal sleep and again after 24h's SD. According to the gender and sleep, 16 subjects were all measured twice and divided into four groups: the male control group (MC), female control group (FC), male SD group (MSD), and female SD group (FSD). The ReHo method was used to calculate and analyze the data, SPM5 software was used to perform a two-sample T-test and a two-pair T-test with a P value <0.001, and cluster volume ≥ 270 mm(3) was used to determine statistical significance. Compared with the MC, the MSD showed significantly higher ReHo in the right paracentral lobule (BA3/6), but in no obviously lower regions. Compared with the FC, the FSD showed significantly higher ReHo in bilateral parietal lobes (BA2/3), bilateral vision-related regions of occipital lobes (BA17/18/19), right frontal lobe (BA4/6), and lower ReHo in the right frontal lobe. Compared with the FC, the MC showed significantly higher ReHo in the left occipital lobe (BA18/19), and left temporal lobe (BA21), left frontal lobe, and lower ReHo in the right insula and in the left parietal lobe. Compared with the FSD, the MSD showed significantly higher ReHo in the left cerebellum posterior lobe (uvula/declive of vermis), left parietal lobe, and bilateral frontal lobes, and lower ReHo in the right occipital lobe (BA17) and right frontal lobe (BA4). The differences of brain activity in the resting state can be widely found not only between the control and SD group in a same gender group, but also between the male group and female group. Thus, we should take the gender differences into consideration in future fMRI studies, especially the

REM Sleep EEG Instability in REM Sleep Behavior Disorder and Clonazepam Effects.

PubMed

Ferri, Raffaele; Rundo, Francesco; Silvani, Alessandro; Zucconi, Marco; Bruni, Oliviero; Ferini-Strambi, Luigi; Plazzi, Giuseppe; Manconi, Mauro

2017-08-01

We aimed to analyze quantitatively rapid eye movement (REM) sleep electroencephalogram (EEG) in controls, drug-naïve idiopathic REM sleep behavior disorder patients (iRBD), and iRBD patients treated with clonazepam. Twenty-nine drug-naïve iRBD patients (mean age 68.2 years), 14 iRBD patients under chronic clonazepam therapy (mean age 66.3 years), and 21 controls (mean age 66.8 years) were recruited. Power spectra were obtained from sleep EEG (central derivation), using a 2-second sliding window, with 1-second steps. The power values of each REM sleep EEG spectral band (one every second) were normalized with respect to the average power value obtained during sleep stage 2 in the same individual. In drug-naïve patients, the normalized power values showed a less pronounced REM-related decrease of power in all bands with frequency <15 Hz than controls and an increase in the beta band, negatively correlated with muscle atonia; in patients treated with clonazepam there was a partial return of all bands <15 Hz toward the control values. The standard deviation values of the normalized power were higher for untreated patients in all EEG bands and were almost completely normalized in patients treated with clonazepam. The REM sleep EEG structure changes found in this study disclose subtle but significant alterations in the cortical electrophysiology of RBD that might represent the early expression of the supposed neurodegenerative processes already taking place at this stage of the disease and might be the target of better and effective future therapeutic strategies for this condition. © 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.

Sex Differences in Stress Response Circuitry Activation Dependent on Female Hormonal Cycle

PubMed Central

Goldstein, Jill M.; Jerram, Matthew; Abbs, Brandon; Whitfield-Gabrieli, Susan; Makris, Nikos

2010-01-01

Understanding sex differences in stress regulation has important implications for understanding basic physiological differences in the male and female brain and their impact on vulnerability to sex differences in chronic medical disorders associated with stress response circuitry. In this fMRI study, we demonstrated that significant sex differences in brain activity in stress response circuitry were dependent on women's menstrual cycle phase. Twelve healthy Caucasian premenopausal women were compared to a group of healthy men from the same population, based on age, ethnicity, education, and right-handedness. Subjects were scanned using negative valence/high arousal versus neutral visual stimuli that we demonstrated activated stress response circuitry (amygdala, hypothalamus, hippocampus, brainstem, orbitofrontal and medial prefrontal cortices (OFC and mPFC), and anterior cingulate gyrus (ACG). Women were scanned twice based on normal variation in menstrual cycle hormones (i.e., early follicular (EF) compared with late follicular-midcycle menstrual phases (LF/MC)). Using SPM8b, there were few significant differences in BOLD signal changes in men compared to EF women, except ventromedial (VMN) and lateral (LHA) hypothalamus, left amygdala, and ACG. In contrast, men exhibited significantly greater BOLD signal changes compared to LF/MC women on bilateral ACG and OFC, mPFC, LHA, VMN, hippocampus, and periaqueductal gray, with largest effect sizes in mPFC and OFC. Findings suggest that sex differences in stress response circuitry are hormonally regulated via the impact of subcortical brain activity on the cortical control of arousal, and demonstrate that females have been endowed with a natural hormonal capacity to regulate the stress response that differs from males. PMID:20071507

Sex differences in stress response circuitry activation dependent on female hormonal cycle.

PubMed

Goldstein, Jill M; Jerram, Matthew; Abbs, Brandon; Whitfield-Gabrieli, Susan; Makris, Nikos

2010-01-13

Understanding sex differences in stress regulation has important implications for understanding basic physiological differences in the male and female brain and their impact on vulnerability to sex differences in chronic medical disorders associated with stress response circuitry. In this functional magnetic resonance imaging study, we demonstrated that significant sex differences in brain activity in stress response circuitry were dependent on women's menstrual cycle phase. Twelve healthy Caucasian premenopausal women were compared to a group of healthy men from the same population, based on age, ethnicity, education, and right handedness. Subjects were scanned using negative valence/high arousal versus neutral visual stimuli that we demonstrated activated stress response circuitry [amygdala, hypothalamus, hippocampus, brainstem, orbitofrontal cortex (OFC), medial prefrontal cortex (mPFC), and anterior cingulate gyrus (ACG)]. Women were scanned twice based on normal variation in menstrual cycle hormones [i.e., early follicular (EF) compared with late follicular-midcycle (LF/MC) menstrual phases]. Using SPM8b, there were few significant differences in blood oxygenation level-dependent (BOLD) signal changes in men compared to EF women, except ventromedial nucleus (VMN), lateral hypothalamic area (LHA), left amygdala, and ACG. In contrast, men exhibited significantly greater BOLD signal changes compared to LF/MC women on bilateral ACG and OFC, mPFC, LHA, VMN, hippocampus, and periaqueductal gray, with largest effect sizes in mPFC and OFC. Findings suggest that sex differences in stress response circuitry are hormonally regulated via the impact of subcortical brain activity on the cortical control of arousal, and demonstrate that females have been endowed with a natural hormonal capacity to regulate the stress response that differs from males.

Normal Morning Melanin-Concentrating Hormone Levels and No Association with Rapid Eye Movement or Non-Rapid Eye Movement Sleep Parameters in Narcolepsy Type 1 and Type 2

PubMed Central

Schrölkamp, Maren; Jennum, Poul J.; Gammeltoft, Steen; Holm, Anja; Kornum, Birgitte R.; Knudsen, Stine

2017-01-01

Study Objectives: Other than hypocretin-1 (HCRT-1) deficiency in narcolepsy type 1 (NT1), the neurochemical imbalance of NT1 and narcolepsy type 2 (NT2) with normal HCRT-1 levels is largely unknown. The neuropeptide melanin-concentrating hormone (MCH) is mainly secreted during sleep and is involved in rapid eye movement (REM) and non-rapid eye movement (NREM) sleep regulation. Hypocretin neurons reciprocally interact with MCH neurons. We hypothesized that altered MCH secretion contributes to the symptoms and sleep abnormalities of narcolepsy and that this is reflected in morning cerebrospinal fluid (CSF) MCH levels, in contrast to previously reported normal evening/afternoon levels. Methods: Lumbar CSF and plasma were collected from 07:00 to 10:00 from 57 patients with narcolepsy (subtypes: 47 NT1; 10 NT2) diagnosed according to International Classification of Sleep Disorders, Third Edition (ICSD-3) and 20 healthy controls. HCRT-1 and MCH levels were quantified by radioimmunoassay and correlated with clinical symptoms, polysomnography (PSG), and Multiple Sleep Latency Test (MSLT) parameters. Results: CSF and plasma MCH levels were not significantly different between narcolepsy patients regardless of ICSD-3 subtype, HCRT-1 levels, or compared to controls. CSF MCH and HCRT-1 levels were not significantly correlated. Multivariate regression models of CSF MCH levels, age, sex, and body mass index predicting clinical, PSG, and MSLT parameters did not reveal any significant associations to CSF MCH levels. Conclusions: Our study shows that MCH levels in CSF collected in the morning are normal in narcolepsy and not associated with the clinical symptoms, REM sleep abnormalities, nor number of muscle movements during REM or NREM sleep of the patients. We conclude that morning lumbar CSF MCH measurement is not an informative diagnostic marker for narcolepsy. Citation: Schrölkamp M, Jennum PJ, Gammeltoft S, Holm A, Kornum BR, Knudsen S. Normal morning melanin

Sleep for cognitive enhancement.

PubMed

Diekelmann, Susanne

2014-01-01

Sleep is essential for effective cognitive functioning. Loosing even a few hours of sleep can have detrimental effects on a wide variety of cognitive processes such as attention, language, reasoning, decision making, learning and memory. While sleep is necessary to ensure normal healthy cognitive functioning, it can also enhance performance beyond the boundaries of the normal condition. This article discusses the enhancing potential of sleep, mainly focusing on the domain of learning and memory. Sleep is known to facilitate the consolidation of memories learned before sleep as well as the acquisition of new memories to be learned after sleep. According to a widely held model this beneficial effect of sleep relies on the neuronal reactivation of memories during sleep that is associated with sleep-specific brain oscillations (slow oscillations, spindles, ripples) as well as a characteristic neurotransmitter milieu. Recent research indicates that memory processing during sleep can be boosted by (i) cueing memory reactivation during sleep; (ii) stimulating sleep-specific brain oscillations; and (iii) targeting specific neurotransmitter systems pharmacologically. Olfactory and auditory cues can be used, for example, to increase reactivation of associated memories during post-learning sleep. Intensifying neocortical slow oscillations (the hallmark of slow wave sleep (SWS)) by electrical or auditory stimulation and modulating specific neurotransmitters such as noradrenaline and glutamate likewise facilitates memory processing during sleep. With this evidence in mind, this article concludes by discussing different methodological caveats and ethical issues that should be considered when thinking about using sleep for cognitive enhancement in everyday applications.

Sleep for cognitive enhancement

PubMed Central

Diekelmann, Susanne

2014-01-01

Sleep is essential for effective cognitive functioning. Loosing even a few hours of sleep can have detrimental effects on a wide variety of cognitive processes such as attention, language, reasoning, decision making, learning and memory. While sleep is necessary to ensure normal healthy cognitive functioning, it can also enhance performance beyond the boundaries of the normal condition. This article discusses the enhancing potential of sleep, mainly focusing on the domain of learning and memory. Sleep is known to facilitate the consolidation of memories learned before sleep as well as the acquisition of new memories to be learned after sleep. According to a widely held model this beneficial effect of sleep relies on the neuronal reactivation of memories during sleep that is associated with sleep-specific brain oscillations (slow oscillations, spindles, ripples) as well as a characteristic neurotransmitter milieu. Recent research indicates that memory processing during sleep can be boosted by (i) cueing memory reactivation during sleep; (ii) stimulating sleep-specific brain oscillations; and (iii) targeting specific neurotransmitter systems pharmacologically. Olfactory and auditory cues can be used, for example, to increase reactivation of associated memories during post-learning sleep. Intensifying neocortical slow oscillations (the hallmark of slow wave sleep (SWS)) by electrical or auditory stimulation and modulating specific neurotransmitters such as noradrenaline and glutamate likewise facilitates memory processing during sleep. With this evidence in mind, this article concludes by discussing different methodological caveats and ethical issues that should be considered when thinking about using sleep for cognitive enhancement in everyday applications. PMID:24765066

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

NASA Technical Reports Server (NTRS)

Carskadon, Mary A.

1997-01-01

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

Reward Circuitry in Addiction.

PubMed

Cooper, Sarah; Robison, A J; Mazei-Robison, Michelle S

2017-07-01

Understanding the brain circuitry that underlies reward is critical to improve treatment for many common health issues, including obesity, depression, and addiction. Here we focus on insights into the organization and function of reward circuitry and its synaptic and structural adaptations in response to cocaine exposure. While the importance of certain circuits, such as the mesocorticolimbic dopamine pathway, are well established in drug reward, recent studies using genetics-based tools have revealed functional changes throughout the reward circuitry that contribute to different facets of addiction, such as relapse and craving. The ability to observe and manipulate neuronal activity within specific cell types and circuits has led to new insight into not only the basic connections between brain regions, but also the molecular changes within these specific microcircuits, such as neurotrophic factor and GTPase signaling or α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor function, that underlie synaptic and structural plasticity evoked by drugs of abuse. Excitingly, these insights from preclinical rodent work are now being translated into the clinic, where transcranial magnetic simulation and deep brain stimulation therapies are being piloted in human cocaine dependence. Thus, this review seeks to summarize current understanding of the major brain regions implicated in drug-related behaviors and the molecular mechanisms that contribute to altered connectivity between these regions, with the postulation that increased knowledge of the plasticity within the drug reward circuit will lead to new and improved treatments for addiction.

Perceptual alternation in obsessive compulsive disorder--implications for a role of the cortico-striatal circuitry in mediating awareness.

PubMed

Li, C S; Chen, M C; Yang, Y Y; Chang, H L; Liu, C Y; Shen, S; Chen, C Y

2000-06-15

Mounting evidence suggests that obsessive compulsive disorder (OCD) results from functional aberrations of the fronto-striatal circuitry. However, empirical studies of the behavioral manifestations of OCD have been relatively lacking. The present study employs a behavioral task that allows a quantitative measure of how alternative percepts are formed from one moment to another, a process mimicking the brain state in which different thoughts and imageries compete for access to awareness. Eighteen patients with OCD, 12 with generalized anxiety disorder, and 18 normal subjects participated in the experiment, in which they viewed one of the three Schröder staircases and responded by pressing a key to each perceptual reversal. The results demonstrate that the patients with OCD have a higher perceptual alternation rate than the normal controls. Moreover, the frequency of perceptual alternation is significantly correlated with the Yale-Brown obsessive compulsive and the Hamilton anxiety scores. The increase in the frequency of perceptual reversals cannot easily be accounted for by learning or by different patterns of eye fixations on the task. These results provide further evidence that an impairment of the inhibitory function of the cortico-striatal circuitry might underlie the etiology of OCD. The implications of the results for a general role of the cortico-striatal circuitry in mediating awareness are discussed.

Neuroimmunologic aspects of sleep and sleep loss

NASA Technical Reports Server (NTRS)

Rogers, N. L.; Szuba, M. P.; Staab, J. P.; Evans, D. L.; Dinges, D. F.

2001-01-01

The complex and intimate interactions between the sleep and immune systems have been the focus of study for several years. Immune factors, particularly the interleukins, regulate sleep and in turn are altered by sleep and sleep deprivation. The sleep-wake cycle likewise regulates normal functioning of the immune system. Although a large number of studies have focused on the relationship between the immune system and sleep, relatively few studies have examined the effects of sleep deprivation on immune parameters. Studies of sleep deprivation's effects are important for several reasons. First, in the 21st century, various societal pressures require humans to work longer and sleep less. Sleep deprivation is becoming an occupational hazard in many industries. Second, to garner a greater understanding of the regulatory effects of sleep on the immune system, one must understand the consequences of sleep deprivation on the immune system. Significant detrimental effects on immune functioning can be seen after a few days of total sleep deprivation or even several days of partial sleep deprivation. Interestingly, not all of the changes in immune physiology that occur as a result of sleep deprivation appear to be negative. Numerous medical disorders involving the immune system are associated with changes in the sleep-wake physiology--either being caused by sleep dysfunction or being exacerbated by sleep disruption. These disorders include infectious diseases, fibromyalgia, cancers, and major depressive disorder. In this article, we will describe the relationships between sleep physiology and the immune system, in states of health and disease. Interspersed will be proposals for future research that may illuminate the clinical relevance of the relationships between sleeping, sleep loss and immune function in humans. Copyright 2001 by W.B. Saunders Company.

Sleep-wake cycle effects on sleep stages, and plasma cortisol and growth secretions

NASA Technical Reports Server (NTRS)

1971-01-01

Studies were made of the effects of various stimuli on sleep stages and of secretion of a number of different hormones during sleep in human subjects. Among the stimuli were vestibular stimulation, the action of L-Dopa, and a three-hour sleep-wake cycle. Hormones observed included plasma cortisol, growth hormone, dehydroisoandrosterone, and luteinizing hormone. Relationships between sleep onset, the presence of Cushing's syndrome or sleep disorders, and ultradian rhythmicity, and hormone secretion were investigated. Sleep patterns and hormone secretion in normal subjects were also studied.

Electroencephalogram spindle activity during dexmedetomidine sedation and physiological sleep.

PubMed

Huupponen, E; Maksimow, A; Lapinlampi, P; Särkelä, M; Saastamoinen, A; Snapir, A; Scheinin, H; Scheinin, M; Meriläinen, P; Himanen, S-L; Jääskeläinen, S

2008-02-01

Dexmedetomidine, a selective alpha(2)-adrenoceptor agonist, induces a unique, sleep-like state of sedation. The objective of the present work was to study human electroencephalogram (EEG) sleep spindles during dexmedetomidine sedation and compare them with spindles during normal physiological sleep, to test the hypothesis that dexmedetomidine exerts its effects via normal sleep-promoting pathways. EEG was continuously recorded from a bipolar frontopolar-laterofrontal derivation with Entropy Module (GE Healthcare) during light and deep dexmedetomidine sedation (target-controlled infusions set at 0.5 and 3.2 ng/ml) in 11 healthy subjects, and during physiological sleep in 10 healthy control subjects. Sleep spindles were visually scored and quantitatively analyzed for density, duration, amplitude (band-pass filtering) and frequency content (matching pursuit approach), and compared between the two groups. In visual analysis, EEG activity during dexmedetomidine sedation was similar to physiological stage 2 (S2) sleep with slight to moderate amount of slow-wave activity and abundant sleep spindle activity. In quantitative EEG analyses, sleep spindles were similar during dexmedetomidine sedation and normal sleep. No statistically significant differences were found in spindle density, amplitude or frequency content, but the spindles during dexmedetomidine sedation had longer duration (mean 1.11 s, SD 0.14 s) than spindles in normal sleep (mean 0.88 s, SD 0.14 s; P=0.0014). Analysis of sleep spindles shows that dexmedetomidine produces a state closely resembling physiological S2 sleep in humans, which gives further support to earlier experimental evidence for activation of normal non-rapid eye movement sleep-promoting pathways by this sedative agent.

Sleeping while disabled, disabled while sleeping.

PubMed

Reiss, Benjamin

2016-09-01

This essay considers areas in which the study of sleep and sleep disorders might profit from the perspective of disability studies, as practiced in the humanities and social sciences. This interdisciplinary perspective considers the social and cultural dimensions of bodily and mental states and conditions that a particular society deems abnormal or impaired, as well as the lived consequences of those determinations. Some sleep disorders are considered disabilities, but almost all disabilities entail some disruption from normal sleeping patterns--whether because of physical pain, exhaustion, and emotional stress of facing obstacles in work and other areas of waking life, or challenging sleeping environments in which many disabled people live. Despite these disruptions, finding adequate nighttime care is often difficult for people with disabilities, and consequently, night is often when social isolation and vulnerability are most profound. In addition, caretakers themselves often find their own sleep profoundly disrupted, whether this occurs in a family setting or an institutional space. Finally, the essay suggests that a disability studies perspective can help us to see that disordered sleep--whether primary or secondary to a disabling condition--can both impact and be shaped by social relationships. Copyright © 2016 National Sleep Foundation. Published by Elsevier Inc. All rights reserved.

Insomnia with objective short sleep duration is associated with longer duration of insomnia in the Freiburg Insomnia Cohort compared to insomnia with normal sleep duration, but not with hypertension

PubMed Central

Johann, Anna F.; Hertenstein, Elisabeth; Kyle, Simon D.; Baglioni, Chiara; Feige, Bernd; Nissen, Christoph; McGinness, Alastair J.; Riemann, Dieter; Spiegelhalder, Kai

2017-01-01

Study objectives To replicate the association between insomnia with objective short sleep duration and hypertension, type 2 diabetes and duration of insomnia. Design Retrospective case-control study. Setting Department of Psychiatry and Psychotherapy, Medical Center—University of Freiburg. Participants 328 patients with primary insomnia classified according to DSM-IV criteria (125 males, 203 females, 44.3 ± 12.2 years). Interventions N/A Measurements All participants were investigated using polysomnography, blood pressure measurements, and fasting routine laboratory. Results Insomnia patients with short sleep duration (< 6 hours) in the first night of laboratory sleep presented with a longer duration of insomnia compared to those with normal sleep duration (≥ 6 hours) in the first night of laboratory sleep. Insomnia patients who were categorised as short sleepers in either night were not more likely to suffer from hypertension (systolic blood pressure of ≥ 140 mm Hg, diastolic blood pressure of ≥ 90 mm Hg, or a previously established diagnosis). Data analysis showed that insomnia patients with objective short sleep duration were not more likely to suffer from type 2 diabetes (fasting plasma glucose level of ≥ 126 mg/dl, or a previously established diagnosis). However, the diabetes analysis was only based on a very small number of diabetes cases. As a new finding, insomnia patients who were categorised as short sleepers in either night presented with increases in liver enzyme levels. Conclusions The finding on insomnia duration supports the concept of two distinct sub-groups of insomnia, namely insomnia with, and without, objectively determined short sleep duration. However, our data challenges previous findings that insomnia patients with short sleep duration are more likely to suffer from hypertension. PMID:28746413

Insomnia with objective short sleep duration is associated with longer duration of insomnia in the Freiburg Insomnia Cohort compared to insomnia with normal sleep duration, but not with hypertension.

PubMed

Johann, Anna F; Hertenstein, Elisabeth; Kyle, Simon D; Baglioni, Chiara; Feige, Bernd; Nissen, Christoph; McGinness, Alastair J; Riemann, Dieter; Spiegelhalder, Kai

2017-01-01

To replicate the association between insomnia with objective short sleep duration and hypertension, type 2 diabetes and duration of insomnia. Retrospective case-control study. Department of Psychiatry and Psychotherapy, Medical Center-University of Freiburg. 328 patients with primary insomnia classified according to DSM-IV criteria (125 males, 203 females, 44.3 ± 12.2 years). N/A. All participants were investigated using polysomnography, blood pressure measurements, and fasting routine laboratory. Insomnia patients with short sleep duration (< 6 hours) in the first night of laboratory sleep presented with a longer duration of insomnia compared to those with normal sleep duration (≥ 6 hours) in the first night of laboratory sleep. Insomnia patients who were categorised as short sleepers in either night were not more likely to suffer from hypertension (systolic blood pressure of ≥ 140 mm Hg, diastolic blood pressure of ≥ 90 mm Hg, or a previously established diagnosis). Data analysis showed that insomnia patients with objective short sleep duration were not more likely to suffer from type 2 diabetes (fasting plasma glucose level of ≥ 126 mg/dl, or a previously established diagnosis). However, the diabetes analysis was only based on a very small number of diabetes cases. As a new finding, insomnia patients who were categorised as short sleepers in either night presented with increases in liver enzyme levels. The finding on insomnia duration supports the concept of two distinct sub-groups of insomnia, namely insomnia with, and without, objectively determined short sleep duration. However, our data challenges previous findings that insomnia patients with short sleep duration are more likely to suffer from hypertension.

24-h actigraphic monitoring of motor activity, sleeping and eating behaviors in underweight, normal weight, overweight and obese children.

PubMed

Martoni, Monica; Carissimi, Alicia; Fabbri, Marco; Filardi, Marco; Tonetti, Lorenzo; Natale, Vincenzo

2016-12-01

Within a chronobiological perspective, the present study aimed to describe 24 h of sleep-wake cycle, motor activity, and food intake patterns in different body mass index (BMI) categories of children through 7 days of actigraphic recording. Height and weight were objectively measured for BMI calculation in a sample of 115 Italian primary schoolchildren (10.21 ± 0.48 years, 62.61 % females). According to BMI values, 2.60 % were underweight, 61.70 % were of normal weight, 29.60 % were overweight and 6.10 % were obese. Participants wore a wrist actigraph continuously for 7 days to record motor activity and describe sleep-wake patterns. In addition, participants were requested to push the event-marker button of the actigraph each time they consumed food to describe their circadian eating patterns. BMI group differences were found for sleep quantity (i.e. midpoint of sleep and amplitude), while sleep quality, 24-h motor activity and food intake patterns were similar between groups. Regression analyses showed that BMI was negatively predicted by sleep duration on schooldays. BMI was also predicted by motor activity and by food intake frequencies recorded at particular times of day during schooldays and at the weekend. The circadian perspective seems to provide promising insight into childhood obesity, but this aspect needs to be further explored.

Acetylcholine Neuromodulation in Normal and Abnormal Learning and Memory: Vigilance Control in Waking, Sleep, Autism, Amnesia and Alzheimer’s Disease

PubMed Central

Grossberg, Stephen

2017-01-01

Adaptive Resonance Theory, or ART, is a neural model that explains how normal and abnormal brains may learn to categorize and recognize objects and events in a changing world, and how these learned categories may be remembered for a long time. This article uses ART to propose and unify the explanation of diverse data about normal and abnormal modulation of learning and memory by acetylcholine (ACh). In ART, vigilance control determines whether learned categories will be general and abstract, or specific and concrete. ART models how vigilance may be regulated by ACh release in layer 5 neocortical cells by influencing after-hyperpolarization (AHP) currents. This phasic ACh release is mediated by cells in the nucleus basalis (NB) of Meynert that are activated by unexpected events. The article additionally discusses data about ACh-mediated tonic control of vigilance. ART proposes that there are often dynamic breakdowns of tonic control in mental disorders such as autism, where vigilance remains high, and medial temporal amnesia, where vigilance remains low. Tonic control also occurs during sleep-wake cycles. Properties of Up and Down states during slow wave sleep arise in ACh-modulated laminar cortical ART circuits that carry out processes in awake individuals of contrast normalization, attentional modulation, decision-making, activity-dependent habituation, and mismatch-mediated reset. These slow wave sleep circuits interact with circuits that control circadian rhythms and memory consolidation. Tonic control properties also clarify how Alzheimer’s disease symptoms follow from a massive structural degeneration that includes undermining vigilance control by ACh in cortical layers 3 and 5. Sleep disruptions before and during Alzheimer’s disease, and how they contribute to a vicious cycle of plaque formation in layers 3 and 5, are also clarified from this perspective. PMID:29163063

Effects of sleep on memory for conditioned fear and fear extinction.

PubMed

Pace-Schott, Edward F; Germain, Anne; Milad, Mohammed R

2015-07-01

Learning and memory for extinction of conditioned fear is a basic mammalian mechanism for regulating negative emotion. Sleep promotes both the consolidation of memory and the regulation of emotion. Sleep can influence consolidation and modification of memories associated with both fear and its extinction. After brief overviews of the behavior and neural circuitry associated with fear conditioning, extinction learning, and extinction memory in the rodent and human, interactions of sleep with these processes will be examined. Animal and human studies suggest that sleep can serve to consolidate both fear and extinction memory. In humans, sleep also promotes generalization of extinction memory. Time-of-day effects on extinction learning and generalization are also seen. Rapid eye movement (REM) may be a sleep stage of particular importance for the consolidation of both fear and extinction memory as evidenced by selective REM deprivation experiments. REM sleep is accompanied by selective activation of the same limbic structures implicated in the learning and memory of fear and extinction. Preliminary evidence also suggests extinction learning can take place during slow wave sleep. Study of low-level processes such as conditioning, extinction, and habituation may allow sleep effects on emotional memory to be identified and inform study of sleep's effects on more complex, emotionally salient declarative memories. Anxiety disorders are marked by impairments of both sleep and extinction memory. Improving sleep quality may ameliorate anxiety disorders by strengthening naturally acquired extinction. Strategically timed sleep may be used to enhance treatment of anxiety by strengthening therapeutic extinction learned via exposure therapy. (PsycINFO Database Record (c) 2015 APA, all rights reserved).

Sleep less and bite more: sleep disorders associated with occlusal loads during sleep.

PubMed

Kato, Takafumi; Yamaguchi, Taihiko; Okura, Kazuo; Abe, Susumu; Lavigne, Gilles J

2013-04-01

Occlusal overload during sleep is a significant clinical issue that has negative impacts on the maintenance of teeth and the longevity of dental prostheses. Sleep is usually viewed as an 'out-of-functional' mode for masticatory muscles. However, orodental structures and prostheses are not free from occlusal loads during sleep since masticatory muscles can be activated at a low level within normal sleep continuity. Thus, an increase in masticatory muscle contractions, by whatever the cause, can be associated with a risk of increased occlusal loads during sleep. Among such conditions, sleep bruxism (SB) is a type of sleep-related movement disorders with potential load challenge to the tooth and orofacial structures. Patients with SB usually report frequent tooth grinding noises during sleep and there is a consecutive increase in number and strength of rhythmic masticatory muscle activity (RMMA). Other types of masticatory muscle contractions can be non-specifically activated during sleep, such as brief contractions with tooth tapping, sleep talking, non-rhythmic contractions related to non-specific body movements, etc.; these occur more frequently in sleep disorders. Studies have shown that clinical signs and symptoms of SB can be found in patients with sleep disorders. In addition, sleep becomes compromised with aging process, and a prevalence of most sleep disorders is high in the elderly populations, in which prosthodontic rehabilitations are more required. Therefore, the recognition and understanding of the role of sleep disorders can provide a comprehensive vision for prosthodontic rehabilitations when prosthodontists manage complex orodental cases needing interdisciplinary collaborations between dentistry and sleep medicine. Copyright © 2013 Japan Prosthodontic Society. Published by Elsevier Ltd. All rights reserved.

The anatomical, cellular and synaptic basis of motor atonia during rapid eye movement sleep

PubMed Central

Chen, Michael C.

2016-01-01

Abstract Rapid eye movement (REM) sleep is a recurring part of the sleep–wake cycle characterized by fast, desynchronized rhythms in the electroencephalogram (EEG), hippocampal theta activity, rapid eye movements, autonomic activation and loss of postural muscle tone (atonia). The brain circuitry governing REM sleep is located in the pontine and medullary brainstem and includes ascending and descending projections that regulate the EEG and motor components of REM sleep. The descending signal for postural muscle atonia during REM sleep is thought to originate from glutamatergic neurons of the sublaterodorsal nucleus (SLD), which in turn activate glycinergic pre‐motor neurons in the spinal cord and/or ventromedial medulla to inhibit motor neurons. Despite work over the past two decades on many neurotransmitter systems that regulate the SLD, gaps remain in our knowledge of the synaptic basis by which SLD REM neurons are regulated and in turn produce REM sleep atonia. Elucidating the anatomical, cellular and synaptic basis of REM sleep atonia control is a critical step for treating many sleep‐related disorders including obstructive sleep apnoea (apnea), REM sleep behaviour disorder (RBD) and narcolepsy with cataplexy. PMID:27060683

Sleep, Cognition, and Normal Aging: Integrating a Half-Century of Multidisciplinary Research

PubMed Central

Scullin, Michael K.; Bliwise, Donald L.

2014-01-01

Sleep is implicated in cognitive functioning in young adults. With increasing age there are substantial changes to sleep quantity and quality including changes to slow wave sleep, spindle density, and sleep continuity/fragmentation. A provocative question for the field of cognitive aging is whether such changes in sleep physiology affect cognition (e.g., memory consolidation). We review nearly a half-century of research studies across 7 diverse correlational and experimental literature domains, which historically have had little crosstalk. Broadly speaking, sleep and cognitive functions are often related in advancing age, though the prevalence of null effects (including correlations in the unexpected, negative direction) in healthy older adults indicates that age may be an effect modifier of these associations. We interpret the literature as suggesting that maintaining good sleep quality, at least in young adulthood and middle age, promotes better cognitive functioning and serves to protect against age-related cognitive declines. PMID:25620997

Normal Morning Melanin-Concentrating Hormone Levels and No Association with Rapid Eye Movement or Non-Rapid Eye Movement Sleep Parameters in Narcolepsy Type 1 and Type 2.

PubMed

Schrölkamp, Maren; Jennum, Poul J; Gammeltoft, Steen; Holm, Anja; Kornum, Birgitte R; Knudsen, Stine

2017-02-15

Other than hypocretin-1 (HCRT-1) deficiency in narcolepsy type 1 (NT1), the neurochemical imbalance of NT1 and narcolepsy type 2 (NT2) with normal HCRT-1 levels is largely unknown. The neuropeptide melanin-concentrating hormone (MCH) is mainly secreted during sleep and is involved in rapid eye movement (REM) and non-rapid eye movement (NREM) sleep regulation. Hypocretin neurons reciprocally interact with MCH neurons. We hypothesized that altered MCH secretion contributes to the symptoms and sleep abnormalities of narcolepsy and that this is reflected in morning cerebrospinal fluid (CSF) MCH levels, in contrast to previously reported normal evening/afternoon levels. Lumbar CSF and plasma were collected from 07:00 to 10:00 from 57 patients with narcolepsy (subtypes: 47 NT1; 10 NT2) diagnosed according to International Classification of Sleep Disorders, Third Edition (ICSD-3) and 20 healthy controls. HCRT-1 and MCH levels were quantified by radioimmunoassay and correlated with clinical symptoms, polysomnography (PSG), and Multiple Sleep Latency Test (MSLT) parameters. CSF and plasma MCH levels were not significantly different between narcolepsy patients regardless of ICSD-3 subtype, HCRT-1 levels, or compared to controls. CSF MCH and HCRT-1 levels were not significantly correlated. Multivariate regression models of CSF MCH levels, age, sex, and body mass index predicting clinical, PSG, and MSLT parameters did not reveal any significant associations to CSF MCH levels. Our study shows that MCH levels in CSF collected in the morning are normal in narcolepsy and not associated with the clinical symptoms, REM sleep abnormalities, nor number of muscle movements during REM or NREM sleep of the patients. We conclude that morning lumbar CSF MCH measurement is not an informative diagnostic marker for narcolepsy. © 2017 American Academy of Sleep Medicine

Science and Teachers: Cardboard Circuitry

ERIC Educational Resources Information Center

Science and Children, 1977

1977-01-01

Diagrams a quick, improvised cardboard circuitry for battery holder, bulb socket, and switches. Materials include corrugated cardboard, paper clips, and rubber bands. Assembly useful in determining the electrical conductivity of substances. (CS)

The Sleep Disorder in Anti-lgLON5 Disease.

PubMed

Gaig, Carles; Iranzo, Alex; Santamaria, Joan; Graus, Francesc

2018-05-23

To review the clinical and polysomnographic features of the sleep disorder occurring in the recently described anti-IgLON5 disease. The hallmark of the disease is the presence of antibodies against IgLON5, a neural cell adhesion molecule of unknown function. The disease presents a robust HLA association, and the neuropathological examination shows a novel neuronal tauopathy with predominant hypothalamic and brainstem involvement. Most patients (> 80%) present sleep-related vocalizations with movements and behaviors and sleep-disordered breathing. Polysomnographic studies show (1) a complex NREM sleep parasomnia at sleep initiation characterized by undifferentiated NREM or poorly structured N2 sleep with sleep-talking or mumbling, and simple or finalistic movements followed by normal periods of N3 or N2 NREM sleep, (2) REM sleep behavior disorder (RBD), and (3) obstructive sleep apnea with stridor. The last two features appear mainly in periods where NREM sleep normalizes. Identification of the anti-IgLON5 sleep disorder is important to suspect the disease. The combination of abnormal NREM sleep initiation, followed by normal periods of NREM sleep and RBD, represents a novel parasomnia.

Effects of sleep on memory for conditioned fear and fear extinction

PubMed Central

Pace-Schott, Edward F.; Germain, Anne; Milad, Mohammed R.

2015-01-01

Learning and memory for extinction of conditioned fear is a basic mammalian mechanism for regulating negative emotion. Sleep promotes both the consolidation of memory and the regulation of emotion. Sleep can influence consolidation and modification of memories associated with both fear and its extinction. After brief overviews of the behavior and neural circuitry associated with fear conditioning, extinction learning and extinction memory in the rodent and human, interactions of sleep with these processes will be examined. Animal and human studies suggest that sleep can serve to consolidate both fear and extinction memory. In humans, sleep also promotes generalization of extinction memory. Time-of-day effects on extinction learning and generalization are also seen. REM may be a sleep stage of particular importance for the consolidation of both fear and extinction memory as evidenced by selective REM deprivation experiments. REM sleep is accompanied by selective activation of the same limbic structures implicated in the learning and memory of fear and extinction. Preliminary evidence also suggests extinction learning can take place during slow wave sleep. Study of low-level processes such as conditioning, extinction and habituation may allow sleep effects on emotional memory to be identified and inform study of sleep’s effects on more complex, emotionally salient declarative memories. Anxiety disorders are marked by impairments of both sleep and extinction memory. Improving sleep quality may ameliorate anxiety disorders by strengthening naturally acquired extinction. Strategically timed sleep may be used to enhance treatment of anxiety by strengthening therapeutic extinction learned via exposure therapy. PMID:25894546

Hypaphorine, an indole alkaloid from Erythrina velutina, induced sleep on normal mice.

PubMed

Ozawa, Masaaki; Honda, Kazuki; Nakai, Izumi; Kishida, Akio; Ohsaki, Ayumi

2008-07-15

An indole alkaloid (hypaphorine (1)) was isolated from Brazilian medicinal plant, Erythrina velutina (Leguminosae). This compound was investigated for sleep promoting effects in mice, and the results showed that it significantly increased non-rapid eye movement (NREM) sleep time during the first hour after its administration. The NREM sleep time was enhanced by 33% in the experimental mice when compared to that of the controls. This study therefore confirmed its sleep promoting property.

Sleep and Human Aging

PubMed Central

Mander, Bryce A.; Winer, Joseph R.; Walker, Matthew P.

2017-01-01

Older adults do not sleep as well as younger adults. Why? What alterations in sleep quantity and quality occur as we age, and are there functional consequences? What are the underlying neural mechanisms that explain age-related sleep disruption? This review tackles these questions. First, we describe canonical changes in human sleep quantity and quality in cognitively normal older adults. Second, we explore the underlying neurobiological mechanisms that may account for these human sleep alterations. Third, we consider the functional consequences of age-related sleep disruption, focusing on memory impairment as an exemplar. We conclude with a discussion of a still-debated question: do older adults simply need less sleep, or rather, are they unable to generate the sleep that they still need? PMID:28384471

Circuitry, systems and methods for detecting magnetic fields

DOEpatents

Kotter, Dale K [Shelley, ID; Spencer, David F [Idaho Falls, ID; Roybal, Lyle G [Idaho Falls, ID; Rohrbaugh, David T [Idaho Falls, ID

2010-09-14

Circuitry for detecting magnetic fields includes a first magnetoresistive sensor and a second magnetoresistive sensor configured to form a gradiometer. The circuitry includes a digital signal processor and a first feedback loop coupled between the first magnetoresistive sensor and the digital signal processor. A second feedback loop which is discrete from the first feedback loop is coupled between the second magnetoresistive sensor and the digital signal processor.

Transitional circuitry for studying the properties of DNA

NASA Astrophysics Data System (ADS)

Trubochkina, N.

2018-01-01

The article is devoted to a new view of the structure of DNA as an intellectual scheme possessing the properties of logic and memory. The theory of transient circuitry, developed by the author for optimal computer circuits, revealed an amazing structural similarity between mathematical models of transition silicon elements and logic and memory circuits of solid state transient circuitry and atomic models of parts of DNA.

Insomnia, metabolic rate and sleep restoration.

PubMed

Bonnet, M H; Arand, D L

2003-07-01

Studies have shown occasional evidence of increased physiological activity in patients with primary insomnia. We hypothesized that metabolic rate, as measured by overall oxygen use (VO2), might be a more general index of increased physiological activity. An initial experiment found elevated VO2 both at night and during the day in patients with primary insomnia as compared with matched normal sleepers. A second experiment found significant but more modest increases in VO2 in patients with Sleep State Misperception Insomnia [who complain of poor sleep but who had normal sleep by electroencephalographic (EEG) criteria]. In a third experiment, normal young adults were given caffeine 400 mg three times per day (TID) for 1 week as a means of increasing VO2 and possibly producing other symptoms of insomnia. Participants developed many symptoms consistent with those seen in patients with primary insomnia (poor sleep, increased latency on the Multiple Sleep Latency Test, increasing fatigue despite physiological activation, and increased anxiety on the Minnesota Multiphasic Personality Inventory (MMPI)). In a final experiment, physiological arousal was again produced by caffeine to determine if sleep with elevated arousal would be less restorative. All subjects (Ss) slept for 3.5 h after being given 400 mg of caffeine. During 41 h of sleep deprivation that followed, there was no significant condition difference for the Multiple Sleep Latency Test or mood measures. The results provided only weak support for the idea that sleep is less restorative after physiological arousal.

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

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.

Sporadic occurrence of completely lateralized vertex sharp transients of sleep is a normal phenomenon: a retrospective, blinded, case-control study.

PubMed

Brenton, J Nicholas; Mytinger, John R

2015-04-01

Vertex sharp transients (VSTs) of sleep often lateralize to the left or right frontocentral regions and can be mistaken as epileptiform. The aim of this study was to determine the prevalence of completely lateralized VSTs in pediatric-aged individuals and to assess their significance by comparing cohorts with and without epilepsy. The authors hypothesized that completely lateralized VSTs are normal and occur with similar frequencies in patients with and without epilepsy. The authors conducted a retrospective, blinded, case-control study comparing completely lateralized VSTs within a 5-minute EEG sleep epoch between cohorts of 100 patients with epilepsy and 100 age- and gender-matched controls. The number of patients with completely lateralized VSTs was not significantly different between cases (62%) and controls (65%) (P = 0.66). The median number of completely lateralized VSTs was small but not significantly different between cases (median 3) and controls (median 4) (P = 0.11). The presence of completely lateralized VSTs in cases (generalized vs. focal epilepsy) was not significantly different (P > 0.95). This is the first systematic study of the prevalence and significance of completely lateralized VSTs of sleep. This study provides class III evidence that completely lateralized VSTs, occurring in a sporadic fashion, are a normal phenomenon and should not be confused with epileptiform discharges.

Sleep in the Aging Population.

PubMed

Miner, Brienne; Kryger, Meir H

2017-03-01

There are normal changes to sleep architecture throughout the lifespan. There is not, however, a decreased need for sleep and sleep disturbance is not an inherent part of the aging process. Sleep disturbance is common in older adults because aging is associated with an increasing prevalence of multimorbidity, polypharmacy, psychosocial factors affecting sleep, and certain primary sleep disorders. It is also associated with morbidity and mortality. Because many older adults have several factors from different domains affecting their sleep, these complaints are best approached as a multifactorial geriatric health condition, necessitating a multifaceted treatment approach. Copyright © 2016 Elsevier Inc. All rights reserved.

Sleep and Human Aging.

PubMed

Mander, Bryce A; Winer, Joseph R; Walker, Matthew P

2017-04-05

Older adults do not sleep as well as younger adults. Why? What alterations in sleep quantity and quality occur as we age, and are there functional consequences? What are the underlying neural mechanisms that explain age-related sleep disruption? This review tackles these questions. First, we describe canonical changes in human sleep quantity and quality in cognitively normal older adults. Second, we explore the underlying neurobiological mechanisms that may account for these human sleep alterations. Third, we consider the functional consequences of age-related sleep disruption, focusing on memory impairment as an exemplar. We conclude with a discussion of a still-debated question: do older adults simply need less sleep, or rather, are they unable to generate the sleep that they still need? Copyright © 2017. Published by Elsevier Inc.

Sleep and Development in Genetically Tractable Model Organisms

PubMed Central

Kayser, Matthew S.; Biron, David

2016-01-01

Sleep is widely recognized as essential, but without a clear singular function. Inadequate sleep impairs cognition, metabolism, immune function, and many other processes. Work in genetic model systems has greatly expanded our understanding of basic sleep neurobiology as well as introduced new concepts for why we sleep. Among these is an idea with its roots in human work nearly 50 years old: sleep in early life is crucial for normal brain maturation. Nearly all known species that sleep do so more while immature, and this increased sleep coincides with a period of exuberant synaptogenesis and massive neural circuit remodeling. Adequate sleep also appears critical for normal neurodevelopmental progression. This article describes recent findings regarding molecular and circuit mechanisms of sleep, with a focus on development and the insights garnered from models amenable to detailed genetic analyses. PMID:27183564

Connectivity of Sleep- and Wake-Promoting Regions of the Human Hypothalamus During Resting Wakefulness.

PubMed

Boes, Aaron D; Fischer, David; Geerling, Joel C; Bruss, Joel; Saper, Clifford B; Fox, Michael D

2018-05-29

The hypothalamus is a central hub for regulating sleep-wake patterns, the circuitry of which has been investigated extensively in experimental animals. This work has identified a wake-promoting region in the posterior hypothalamus, with connections to other wake-promoting regions, and a sleep-promoting region in the anterior hypothalamus, with inhibitory projections to the posterior hypothalamus. It is unclear whether a similar organization exists in humans. Here, we use anatomical landmarks to identify homologous sleep and wake-promoting regions of the human hypothalamus and investigate their functional relationships using resting-state functional connectivity MRI in healthy awake participants. First, we identify a negative correlation (anticorrelation) between the anterior and posterior hypothalamus, two regions with opposing roles in sleep-wake regulation. Next, we show that hypothalamic connectivity predicts a pattern of regional sleep-wake changes previously observed in humans. Specifically, regions that are more positively correlated with the posterior hypothalamus and more negatively correlated with the anterior hypothalamus correspond to regions with the greatest change in cerebral blood flow between sleep-wake states. Taken together, these findings provide preliminary evidence relating a hypothalamic circuit investigated in animals to sleep-wake neuroimaging results in humans, with implications for our understanding of human sleep-wake regulation and the functional significance of anticorrelations.

Conic section function neural network circuitry for offline signature recognition.

PubMed

Erkmen, Burcu; Kahraman, Nihan; Vural, Revna A; Yildirim, Tulay

2010-04-01

In this brief, conic section function neural network (CSFNN) circuitry was designed for offline signature recognition. CSFNN is a unified framework for multilayer perceptron (MLP) and radial basis function (RBF) networks to make simultaneous use of advantages of both. The CSFNN circuitry architecture was developed using a mixed mode circuit implementation. The designed circuit system is problem independent. Hence, the general purpose neural network circuit system could be applied to various pattern recognition problems with different network sizes on condition with the maximum network size of 16-16-8. In this brief, CSFNN circuitry system has been applied to two different signature recognition problems. CSFNN circuitry was trained with chip-in-the-loop learning technique in order to compensate typical analog process variations. CSFNN hardware achieved highly comparable computational performances with CSFNN software for nonlinear signature recognition problems.

Alternative neural circuitry that might be impaired in the development of Alzheimer disease.

PubMed

Avila, Jesus; Perry, George; Strange, Bryan A; Hernandez, Felix

2015-01-01

It is well established that some individuals with normal cognitive capacity have abundant senile plaques in their brains. It has been proposed that those individuals are resilient or have compensation factors to prevent cognitive decline. In this comment, we explore an alternative mechanism through which cognitive capacity is maintained. This mechanism could involve the impairment of alternative neural circuitry. Also, the proportion of molecules such as Aβ or tau protein present in different areas of the brain could be important.

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.

Optogenetic dissection of medial prefrontal cortex circuitry

PubMed Central

Riga, Danai; Matos, Mariana R.; Glas, Annet; Smit, August B.; Spijker, Sabine; Van den Oever, Michel C.

2014-01-01

The medial prefrontal cortex (mPFC) is critically involved in numerous cognitive functions, including attention, inhibitory control, habit formation, working memory and long-term memory. Moreover, through its dense interconnectivity with subcortical regions (e.g., thalamus, striatum, amygdala and hippocampus), the mPFC is thought to exert top-down executive control over the processing of aversive and appetitive stimuli. Because the mPFC has been implicated in the processing of a wide range of cognitive and emotional stimuli, it is thought to function as a central hub in the brain circuitry mediating symptoms of psychiatric disorders. New optogenetics technology enables anatomical and functional dissection of mPFC circuitry with unprecedented spatial and temporal resolution. This provides important novel insights in the contribution of specific neuronal subpopulations and their connectivity to mPFC function in health and disease states. In this review, we present the current knowledge obtained with optogenetic methods concerning mPFC function and dysfunction and integrate this with findings from traditional intervention approaches used to investigate the mPFC circuitry in animal models of cognitive processing and psychiatric disorders. PMID:25538574

Optogenetic dissection of medial prefrontal cortex circuitry.

PubMed

Riga, Danai; Matos, Mariana R; Glas, Annet; Smit, August B; Spijker, Sabine; Van den Oever, Michel C

2014-01-01

The medial prefrontal cortex (mPFC) is critically involved in numerous cognitive functions, including attention, inhibitory control, habit formation, working memory and long-term memory. Moreover, through its dense interconnectivity with subcortical regions (e.g., thalamus, striatum, amygdala and hippocampus), the mPFC is thought to exert top-down executive control over the processing of aversive and appetitive stimuli. Because the mPFC has been implicated in the processing of a wide range of cognitive and emotional stimuli, it is thought to function as a central hub in the brain circuitry mediating symptoms of psychiatric disorders. New optogenetics technology enables anatomical and functional dissection of mPFC circuitry with unprecedented spatial and temporal resolution. This provides important novel insights in the contribution of specific neuronal subpopulations and their connectivity to mPFC function in health and disease states. In this review, we present the current knowledge obtained with optogenetic methods concerning mPFC function and dysfunction and integrate this with findings from traditional intervention approaches used to investigate the mPFC circuitry in animal models of cognitive processing and psychiatric disorders.

Reliability of scoring arousals in normal children and children with obstructive sleep apnea syndrome.

PubMed

Wong, Tat Kong; Galster, Patricia; Lau, Tai Shing; Lutz, Janita M; Marcus, Carole L

2004-09-15

Scoring of arousals in children is based on an extension of adult criteria, as defined by the American Sleep Disorders Association (ASDA). By this, a minimum duration of 3 seconds is required. A few recent studies utilized modified criteria for the study of children, with durations as short as 1 second. However, the validity and reliability of scoring these shorter arousals have never been verified. Based on studies in adults, we hypothesized that interscorer agreement for scoring arousals shorter than 3 seconds was poor. Retrospective review of polysomnograms by 2 experienced sleep practitioners who independently scored arousals according to the ASDA 3-second criteria and modified duration criteria of 1 and 2 seconds. Academic hospital. 20 polysomnographic studies from children aged 3 to 8 years with mild to severe obstructive sleep apnea syndrome, and 16 polysomnographic studies from normal children. None. The intraclass correlation coefficient for scoring ASDA arousals was 0.90 (95% confidence interval: 0.81-0.95), indicating excellent interscorer agreement. The intraclass correlation coefficient for scoring modified 1-second and 2-second arousals were 0.35 (95% confidence interval: 0.02-0.61) and 0.42 (95% confidence interval: 0.12-0.65) respectively, indicating poor to fair interscorer agreement. Furthermore, modified 1-second and 2-second arousals accounted for less than 15% of all arousals scored. We conclude that there is much poorer interscorer agreement for scoring arousals shorter than 3 seconds, when compared to the standard ASDA criteria. We propose that scoring of arousals in children should follow the standard ASDA criteria.

Heart rate control in normal and aborted-SIDS infants.

PubMed

Pincus, S M; Cummins, T R; Haddad, G G

1993-03-01

Approximate entropy (ApEn), a mathematical formula quantifying regularity in data, was applied to heart rate data from normal and aborted-sudden infant death syndrome (SIDS) infants. We distinguished quiet from rapid-eye-movement (REM) sleep via the following three criteria, refining the notion of REM as more "variable": 1) REM sleep has greater overall variability (0.0374 +/- 0.0138 vs. 0.0205 +/- 0.0090 s, P < 0.005); 2) REM sleep is less stationary (StatAv = 0.742 +/- 0.110) than quiet sleep (StatAv = 0.599 +/- 0.159, P < 0.03); 3) after normalization to overall variability, REM sleep is more regular (ApEnsub = 1.224 +/- 0.092) than quiet sleep (ApEnsub = 1.448 +/- 0.071, P < 0.0001). Fifty percent of aborted-SIDS infants showed greater ApEn instability across quiet sleep than any normal infant exhibited, suggesting that autonomic regulation of heart rate occasionally becomes abnormal in a high-risk subject. There was an association between low ApEn values and aborted-SIDS events; 5 of 14 aborted-SIDS infants had at least one quiet sleep epoch with an ApEn value below the minimum of 45 normal-infant ApEn values.

Sleep and Development in Genetically Tractable Model Organisms.

PubMed

Kayser, Matthew S; Biron, David

2016-05-01

Sleep is widely recognized as essential, but without a clear singular function. Inadequate sleep impairs cognition, metabolism, immune function, and many other processes. Work in genetic model systems has greatly expanded our understanding of basic sleep neurobiology as well as introduced new concepts for why we sleep. Among these is an idea with its roots in human work nearly 50 years old: sleep in early life is crucial for normal brain maturation. Nearly all known species that sleep do so more while immature, and this increased sleep coincides with a period of exuberant synaptogenesis and massive neural circuit remodeling. Adequate sleep also appears critical for normal neurodevelopmental progression. This article describes recent findings regarding molecular and circuit mechanisms of sleep, with a focus on development and the insights garnered from models amenable to detailed genetic analyses. Copyright © 2016 by the Genetics Society of America.

Sleep architecture and sleep apnea in patients with Cushing's disease.

PubMed

Shipley, J E; Schteingart, D E; Tandon, R; Starkman, M N

1992-12-01

Patients with Cushing's syndrome (CS) frequently have sleep complaints. We evaluated sleep polysomnographically in 22 patients, including 17 with pituitary-ACTH-dependent Cushing's disease (CD) and five with CS from an adrenal tumor. Data were compared to healthy controls of comparable age. Seven patients (32%) demonstrated at least mild sleep apnea (> or = 9.4 events/hour), and four of 22 (18%) had > or = 17.5 events/hour. The apneic CD and CS patients had a trend for a greater complaint of excessive daytime sleepiness. Both apneic and nonapneic groups had considerable snoring and obesity. The electroencephalographic (EEG) sleep of nonapneic patients was compared to that of normal subjects. Nonapneic CD patients differed strikingly from healthy volunteers in sleep continuity and architecture, demonstrating lighter, fragmented sleep. Rapid eye movement (REM) sleep in CD patients bore many similarities to the sleep of patients with major depression, with REM latency being significantly shortened and REM density significantly increased. Continued examination of EEG sleep in CD patients may shed light on similarities in pathophysiology between CD and major depression, disorders which are characterized by both a dysfunction of the hypothalamic-pituitary-adrenal axis and alterations in mood.

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

NASA Technical Reports Server (NTRS)

Carskadon, Mary A.

1997-01-01

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

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

NASA Technical Reports Server (NTRS)

Carskadon, Mary A.

1997-01-01

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

Sleep in space as a new medical frontier: the challenge of preserving normal sleep in the abnormal environment of space missions

PubMed Central

Pandi-Perumal, Seithikurippu R.; Gonfalone, Alain A.

2016-01-01

Space agencies such as the National Aeronautics and Space Administration of the United States, the Russian Federal Space Agency, the European Space Agency, the China National Space Administration, the Japan Aerospace Exploration Agency, and Indian Space Research Organization, although differing in their local political agendas, have a common interest in promoting all applied sciences that may facilitate man’s adaptation to life beyond the earth. One of man’s most important adaptations has been the evolutionary development of sleep cycles in response to the 24 hour rotation of the earth. Less well understood has been man’s biological response to gravity. Before humans ventured into space, many questioned whether sleep was possible at all in microgravity environments. It is now known that, in fact, space travelers can sleep once they leave the pull of the earth’s gravity, but that the sleep they do get is not completely refreshing and that the associated sleep disturbances can be elaborate and variable. According to astronauts’ subjective reports, the duration of sleep is shorter than that on earth and there is an increased incidence of disturbed sleep. Objective sleep recordings carried out during various missions including the Skylab missions, space shuttle missions, and Mir missions all support the conclusion that, compared to sleep on earth, the duration in human sleep in space is shorter, averaging about six hours. In the new frontier of space exploration, one of the great practical problems to be solved relates to how man can preserve “normal” sleep in a very abnormal environment. The challenge of managing fatigue and sleep loss during space mission has critical importance for the mental efficiency and safety of the crew and ultimately for the success of the mission itself. Numerous "earthly" examples now show that crew fatigue on ships, trucks, and long-haul jetliners can lead to inadequate performance and sometimes fatal consequences, a reality

(Mis)perception of sleep in insomnia: a puzzle and a resolution.

PubMed

Harvey, Allison G; Tang, Nicole K Y

2012-01-01

Insomnia is prevalent, causing severe distress and impairment. This review focuses on illuminating the puzzling finding that many insomnia patients misperceive their sleep. They overestimate their sleep onset latency (SOL) and underestimate their total sleep time (TST), relative to objective measures. This tendency is ubiquitous (although not universal). Resolving this puzzle has clinical, theoretical, and public health importance. There are implications for assessment, definition, and treatment. Moreover, solving the puzzle creates an opportunity for real-world applications of theories from clinical, perceptual, and social psychology as well as neuroscience. Herein we evaluate 13 possible resolutions to the puzzle. Specifically, we consider the possible contribution, to misperception, of (1) features inherent to the context of sleep (e.g., darkness); (2) the definition of sleep onset, which may lack sensitivity for insomnia patients; (3) insomnia being an exaggerated sleep complaint; (4) psychological distress causing magnification; (5) a deficit in time estimation ability; (6) sleep being misperceived as wake; (7) worry and selective attention toward sleep-related threats; (8) a memory bias influenced by current symptoms and emotions, a confirmation bias/belief bias, or a recall bias linked to the intensity/recency of symptoms; (9) heightened physiological arousal; (10) elevated cortical arousal; (11) the presence of brief awakenings; (12) a fault in neuronal circuitry; and (13) there being 2 insomnia subtypes (one with and one without misperception). The best supported resolutions were misperception of sleep as wake, worry, and brief awakenings. A deficit in time estimation ability was not supported. We conclude by proposing several integrative solutions.

(Mis)Perception of Sleep in Insomnia: A puzzle and a resolution

PubMed Central

Harvey, Allison G.; Tang, Nicole

2011-01-01

Insomnia is prevalent, causing severe distress and impairment. This review focuses on illuminating the puzzling finding that many insomnia patients misperceive their sleep. They overestimate their sleep onset latency (SOL) and underestimate their total sleep time (TST), relative to objective measures. This tendency is ubiquitous (although not universal). Resolving this puzzle has clinical, theoretical, and public health importance. There are implications for assessment, definition, and treatment. Moreover, solving the puzzle creates an opportunity for "real world" applications of theories from clinical, perceptual, and social psychology as well as neuroscience. Herein we evaluate thirteen possible resolutions to the puzzle. Specifically, we consider the possible contribution, to misperception, of: (1) features inherent to the context of sleep (e.g., darkness); (2) the definition of sleep onset which may lack sensitivity for insomnia patients; (3) insomnia being an exaggerated sleep complaint; (4) psychological distress causing magnification; (5) a deficit in time estimation ability; (6) sleep being misperceived as wake; (7) worry and selective attention toward sleep-related threats; (8) a memory bias influenced by current symptoms and emotions, a confirmation bias/belief bias or a recall bias linked to the intensity/recency of symptoms; (9) heightened physiological arousal; (10) elevated cortical arousal; (11) the presence of brief awakenings; (12) a fault in neuronal circuitry; and (13) there being two insomnia subtypes (one with and one without misperception). The best supported resolutions were misperception of sleep as wake, worry, and brief awakenings. A deficit in time estimation ability was not supported. We conclude by proposing several integrative solutions. PMID:21967449

Narcolepsy: regional cerebral blood flow during sleep and wakefulness

DOE Office of Scientific and Technical Information (OSTI.GOV)

Sakai, F.; Meyer, J.S.; Karacan, I.

Serial measurements of regional cerebral blood flow were made by the 135Xe inhalation method during the early stages of sleep and wakefulness in eight normal volunteers and 12 patients with narcolepsy. Electroencephalogram, electro-oculogram, and submental electromyogram were recorded simultaneously. In normals, mean hemispheric gray matter blood flow (Fg) during stages I and II sleep was significantly less than waking values. Maximum regional blood flow decreases during sleep occurred in the brainstem-cerebellar, right inferior temporal, and bilateral frontal regions. In patients with narcolepsy, mean hemispheric Fg while awake was 80.5 +- 13 ml per 100 gm brain per minute. During REMmore » sleep, mean hemispheric Fg increased concurrently with large increases in brainstem-cerebellar region flow. During stages I and II sleep without REM, there were significant increases in mean hemispheric Fg and brainstem-cerebellar Fg, just the opposite of changes in normals. In narcolepsy, there appears to be a reversal of normal cerebral deactivation patterns, particularly involving the brainstem, during stages I and II sleep.« less

[Sleep disorders associated with essential tremor and Parkinson's disease].

PubMed

Chen, Juping; Yao, Jianxin; Chen, Li; Miao, Hong; Mao, Chengjie; Liu, Chunfeng

2015-01-20

To evaluate the sleep quality and explore the manifestations of sleep disorders for 62 essential tremor (ET) patients, 60 normal controls and 62 Parkinson's disease (PD) patients. A total of 62 ET patients, 60 normal controls and 62 PD patients from June 2009 to December 2013 were recruited. All of them were outpatients at Second Affiliated Hospital, Soochow University and Hospital of Changshu Hospital of Traditional Chinese Medicine. Sleep was assessed with Pittsburgh Sleep Quality Index (PSQI) and Epworth Sleepiness Scale (ESS). The global PSQI score was 4.7 ± 2.5 in controls, 6.0 ± 4.0 in ET cases and 7.4 ± 3. 7 in PD cases. PD cases had the highest PSQI score, followed by ET (intermediate) and lowest scores in controls (F = 9.022, P = 0.000). A poor quality of sleep was observed in normal controls (23/62, 38.3%) compared to ET cases (34/62, 54.8%) and PD cases (40/62, 64.5%) (χ² = 8.555, P = 0.014 when comparing all three groups and χ² = 1.206, P = 0.272 when ET vs PD). The ESS score increased from normal controls (4.4 ± 2.5) to ET cases (6.3 ± 4.8) and PD cases (8.2 ± 4.2). An ESS score ≥ 10 (an indicator of greater than normal levels of daytime sleepiness) was observed in 6 (10.0%) normal controls, compared to ET cases (16, 25.8%) and PD cases (20, 32.3%) (χ² = 9.047, P = 0.011 when comparing all three groups and χ² = 0.626, P = 0.429 when ET vs PD). For normal controls, ET and PD patients, the factor scores of subjective sleep were 0.6 ± 0.7, 0.8 ± 0.8 and 1.1 ± 0.7; the factor scores of quality sleep latency 0.6 ± 0.7, 0.9 ± 0.9 and 1.1 ± 1.0; the factor scores of sleep duration 0.6 ± 0.8, 0.7 ± 1.0 and 1.0 ± 0.9; the factor scores of sleep efficiency 0.6 ± 0.8, 0.9 ± 0.9 and 1.0 ± 1.0; the factor scores of sleep disturbances 1.2 ± 0.6, 1.2 ± 0.5 and 1.7 ± 0.7; the factor scores of daytime dysfunction 1.2 ± 1.0, 1.3 ± 1.0 and 2.0 ± 1.1 respectively. There were inter-group statistical differences in subjective sleep (F = 7

Neural circuitry coordinating male copulation

PubMed Central

Pavlou, Hania J; Lin, Andrew C; Neville, Megan C; Nojima, Tetsuya; Diao, Fengqiu; Chen, Brian E; White, Benjamin H; Goodwin, Stephen F

2016-01-01

Copulation is the goal of the courtship process, crucial to reproductive success and evolutionary fitness. Identifying the circuitry underlying copulation is a necessary step towards understanding universal principles of circuit operation, and how circuit elements are recruited into the production of ordered action sequences. Here, we identify key sex-specific neurons that mediate copulation in Drosophila, and define a sexually dimorphic motor circuit in the male abdominal ganglion that mediates the action sequence of initiating and terminating copulation. This sexually dimorphic circuit composed of three neuronal classes – motor neurons, interneurons and mechanosensory neurons – controls the mechanics of copulation. By correlating the connectivity, function and activity of these neurons we have determined the logic for how this circuitry is coordinated to generate this male-specific behavior, and sets the stage for a circuit-level dissection of active sensing and modulation of copulatory behavior. DOI: http://dx.doi.org/10.7554/eLife.20713.001 PMID:27855059

Optogenetic mapping of brain circuitry

NASA Astrophysics Data System (ADS)

Augustine, George J.; Berglund, Ken; Gill, Harin; Hoffmann, Carolin; Katarya, Malvika; Kim, Jinsook; Kudolo, John; Lee, Li M.; Lee, Molly; Lo, Daniel; Nakajima, Ryuichi; Park, Min Yoon; Tan, Gregory; Tang, Yanxia; Teo, Peggy; Tsuda, Sachiko; Wen, Lei; Yoon, Su-In

2012-10-01

Studies of the brain promise to be revolutionized by new experimental strategies that harness the combined power of optical techniques and genetics. We have mapped the circuitry of the mouse brain by using both optogenetic actuators that control neuronal activity and optogenetic sensors that detect neuronal activity. Using the light-activated cation channel, channelrhodopsin-2, to locally photostimulate neurons allows high-speed mapping of local and long-range circuitry. For example, with this approach we have mapped local circuits in the cerebral cortex, cerebellum and many other brain regions. Using the fluorescent sensor for chloride ions, Clomeleon, allows imaging of the spatial and temporal dimensions of inhibitory circuits in the brain. This approach allows imaging of both conventional "phasic" synaptic inhibition as well as unconventional "tonic" inhibition. The combined use of light to both control and monitor neural activity creates unprecedented opportunities to explore brain function, screen pharmaceutical agents, and potentially to use light to ameliorate psychiatric and neurological disorders.

Sleep and meal-time misalignment alters functional connectivity: a pilot resting-state study.

PubMed

Yoncheva, Y N; Castellanos, F X; Pizinger, T; Kovtun, K; St-Onge, M-P

2016-11-01

Delayed sleep and meal times promote metabolic dysregulation and obesity. Altered coordination of sleeping and eating times may impact food-reward valuation and interoception in the brain, yet the independent and collective contributions of sleep and meal times are unknown. This randomized, in-patient crossover study experimentally manipulates sleep and meal times while preserving sleep duration (7.05±0.44 h for 5 nights). Resting-state functional magnetic resonance imaging scans (2 × 5-minute runs) were obtained for four participants (three males; 25.3±4.6 years), each completing all study phases (normal sleep/normal meal; late sleep/normal meal; normal sleep/late meal; and late sleep/late meal). Normal mealtimes were 1, 5, 11 and 12.5 h after awakening; late mealtimes were 4.5, 8.5, 14.5 and 16 h after awakening. Seed-based resting-state functional connectivity (RSFC) was computed for a priori regions-of-interest (seeds) and contrasted across conditions. Statistically significant (P<0.05, whole-brain corrected) regionally specific effects were found for multiple seeds. The strongest effects were linked to the amygdala: increased RSFC for late versus normal mealtimes (equivalent to skipping breakfast). A main effect of sleep and interaction with meal time were also observed. Preliminary findings support the feasibility of examining the effects of sleep and meal-time misalignment, independent of sleep duration, on RSFC in regions relevant to food reward and interoception.

Sleep Characteristics of Self-Reported Long Sleepers

PubMed Central

Patel, Sanjay R.; Blackwell, Terri; Ancoli-Israel, Sonia; Stone, Katie L.

2012-01-01

Background: Self-reported long habitual sleep durations (≥ 9 h per night) consistently predict increased mortality. We compared objective sleep parameters of self-reported long versus normal duration sleepers to determine whether long sleepers truly sleep more or have an underlying sleep abnormality. Methods: Older men participating in the Osteoporotic Fractures in Men Study (MrOS) were recruited for a comprehensive sleep assessment, which included wrist actigraphy, overnight polysomnography (PSG), and a question about usual nocturnal sleep duration. Results: Of the 3134 participants (mean age 76.4 ± 5.6; 89.9% Caucasian), 1888 (60.2%) reported sleeping 7-8 h (normal sleepers) and 174 (5.6%) reported ≥ 9 h (long sleepers). On actigraphy, long sleepers spent on average 63.0 min more per night in bed (P < 0.001), slept 42.8 min longer (P < 0.001), and spent 6.8 min more per day napping (P = 0.01). Based on PSG, the apnea hypopnea index, periodic limb movement index, arousal index, and sleep stage distribution did not differ. After adjusting for differences in demographics, comorbidities, and medication usage, self-reported long sleepers continued to spend more time in bed and sleep more, based on both actigraphy and PSG. Each additional 30 min in bed or asleep as measured by actigraphy increased the odds of being a self-reported long-sleeper 1.74-fold and 1.33-fold, respectively (P < 0.001 for both). Conclusions: On objective assessment, self-reported long sleepers spend more time in bed and more time asleep than normal duration sleepers. This is not explained by differences in comorbidity or sleep disorders. Citation: Patel SR; Blackwell T; Ancoli-Israel S; Stone KL. Sleep characteristics of self-reported long sleepers. SLEEP 2012;35(5):641-648. PMID:22547890

Does objectively assessed sleep at five years predict sleep and psychological functioning at 14 years? - Hmm, yes and no!

PubMed

Brand, Serge; Hatzinger, Martin; Stadler, Christina; Bolten, Margarete; von Wyl, Agnes; Perren, Sonja; von Klitzing, Kai; Stadelmann, Stephanie; Holsboer-Trachsler, Edith

2015-01-01

We tested the hypothesis that objectively assessed sleep at kindergarten level predicts sleep and psychological functioning in adolescence. Thirty-seven adolescents aged 14 years (SD = 1.3), of 67 participants assessed as preschoolers, took part in a follow-up study nine years later. Participants completed a series of questionnaires related to sleep and psychological functioning. Sleep-EEG clusters of poor, normal and good sleepers assessed as children nine years earlier were used as predictors for subjective sleep and psychological functioning in adolescence. At the age of 14, those who were normal and good sleepers rather than poor sleepers at the age of five had more positive psychological functioning on dimensions including mental toughness, peer relationship, self-esteem, and perceived stress, but did not differ in current sleep patterns. Objectively assessed sleep patterns at the age of five are predictive of aspects of psychological functioning during adolescence. Copyright © 2014 Elsevier Ltd. All rights reserved.

Mapping the brain's metaphor circuitry: metaphorical thought in everyday reason

PubMed Central

Lakoff, George

2014-01-01

An overview of the basics of metaphorical thought and language from the perspective of Neurocognition, the integrated interdisciplinary study of how conceptual thought and language work in the brain. The paper outlines a theory of metaphor circuitry and discusses how everyday reason makes use of embodied metaphor circuitry. PMID:25566012

A Genetically Defined Circuit for Arousal from Sleep during Hypercapnia.

PubMed

Kaur, Satvinder; Wang, Joshua L; Ferrari, Loris; Thankachan, Stephen; Kroeger, Daniel; Venner, Anne; Lazarus, Michael; Wellman, Andrew; Arrigoni, Elda; Fuller, Patrick M; Saper, Clifford B

2017-12-06

The precise neural circuitry that mediates arousal during sleep apnea is not known. We previously found that glutamatergic neurons in the external lateral parabrachial nucleus (PBel) play a critical role in arousal to elevated CO2 or hypoxia. Because many of the PBel neurons that respond to CO2 express calcitonin gene-related peptide (CGRP), we hypothesized that CGRP may provide a molecular identifier of the CO2 arousal circuit. Here, we report that selective chemogenetic and optogenetic activation of PBel CGRP neurons caused wakefulness, whereas optogenetic inhibition of PBel CGRP neurons prevented arousal to CO2, but not to an acoustic tone or shaking. Optogenetic inhibition of PBel CGRP terminals identified a network of forebrain sites under the control of a PBel CGRP switch that is necessary to arouse animals from hypercapnia. Our findings define a novel cellular target for interventions that may prevent sleep fragmentation and the attendant cardiovascular and cognitive consequences seen in obstructive sleep apnea. VIDEO ABSTRACT. Copyright © 2017 Elsevier Inc. All rights reserved.

Precipitating factors of somnambulism: impact of sleep deprivation and forced arousals.

PubMed

Pilon, Mathieu; Montplaisir, Jacques; Zadra, Antonio

2008-06-10

Experimental attempts to induce sleepwalking with forced arousals during slow-wave sleep (SWS) have yielded mixed results in children and have not been investigated in adult patients. We hypothesized that the combination of sleep deprivation and external stimulation would increase the probability of inducing somnambulistic episodes in sleepwalkers recorded in the sleep laboratory. The main goal of this study was to assess the effects of forced arousals from auditory stimuli (AS) in adult sleepwalkers and control subjects during normal sleep and following post-sleep deprivation recovery sleep. Ten sleepwalkers and 10 controls were investigated. After a baseline night, participants were presented with AS at predetermined sleep stages either during normal sleep or recovery sleep following 25 hours of sleep deprivation. One week later, the conditions with AS were reversed. No somnambulistic episodes were induced in controls. When compared to the effects of AS during sleepwalkers' normal sleep, the presentation of AS during sleepwalkers' recovery sleep significantly increased their efficacy in experimentally inducing somnambulistic events and a significantly greater proportion of sleepwalkers (100%) experienced at least one induced episode during recovery SWS as compared to normal SWS (30%). There was no significant difference between the mean intensity of AS that induced episodes during sleepwalkers' SWS and the mean intensity of AS that awakened sleepwalkers and controls from SWS. Sleep deprivation and forced arousals during slow-wave sleep can induce somnambulistic episodes in predisposed adults. The results highlight the potential value of this protocol in establishing a video-polysomnographically based diagnosis for sleepwalking.

Sleep disorders in pregnancy

PubMed Central

Bourjeily, Ghada

2009-01-01

Sleep complaints are a common occurrence in pregnancy that are in part due to pregnancy-associated anatomic and physiological changes but may also be due to pathological causes. In the non-pregnant population, sleep deprivation has been associated with physical and cognitive issues; poor sleep may even be associated with adverse maternal outcomes. Maternal obesity, one of the most prevalent risk factors in obstetric practices, together with physiologic changes of pregnancy predispose to the development of sleep disordered breathing. Symptoms of sleep disordered breathing have also been associated with poor maternal outcomes. Management options of restless legs syndrome and narcolepsy pose a challenge in pregnancy; benefits of therapy need to be weighed against the potential harm to the fetus. This article briefly reviews the normal changes in pregnancy affecting sleep, gives an overview of certain sleep disorders occurring in pregnancy, and suggests management options specific for this population. PMID:27582822

Sleep Physiology, Abnormal States, and Therapeutic Interventions

PubMed Central

Wickboldt, Alvah T.; Bowen, Alex F.; Kaye, Aaron J.; Kaye, Adam M.; Rivera Bueno, Franklin; Kaye, Alan D.

2012-01-01

Sleep is essential. Unfortunately, a significant portion of the population experiences altered sleep states that often result in a multitude of health-related issues. The regulation of sleep and sleep-wake cycles is an area of intense research, and many options for treatment are available. The following review summarizes the current understanding of normal and abnormal sleep-related conditions and the available treatment options. All clinicians managing patients must recommend appropriate therapeutic interventions for abnormal sleep states. Clinicians' solid understanding of sleep physiology, abnormal sleep states, and treatments will greatly benefit patients regardless of their disease process. PMID:22778676

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.

Sleep Deprivation Disrupts Recall of Conditioned Fear Extinction.

PubMed

Straus, Laura D; Acheson, Dean T; Risbrough, Victoria B; Drummond, Sean P A

2017-03-01

Learned fear is crucial in the development and maintenance of posttraumatic stress disorder (PTSD) and other anxiety disorders, and extinction of learned fear is necessary for response to exposure-based treatments. In humans, research suggests disrupted sleep impairs consolidation of extinction, though no studies have examined this experimentally using total sleep deprivation. Seventy-one healthy controls underwent a paradigm to acquire conditioned fear to a visual cue. Twenty-four hours after fear conditioning, participants underwent extinction learning. Twenty-four hours after extinction learning, participants underwent extinction recall. Participants were randomized to three groups: 1) well-rested throughout testing ("normal sleep"; n = 21); 2) 36 hours total sleep deprivation before extinction learning ("pre-extinction deprivation"; n = 25); or 3) 36 hours total sleep deprivation after extinction learning and before extinction recall ("post-extinction deprivation"; n = 25). The groups were compared on blink EMG reactivity to the condition stimulus during extinction learning and recall. There were no differences among the three groups during extinction learning. During extinction recall, the pre-extinction deprivation group demonstrated significantly less extinction recall than the normal sleep group. There was no significant difference between the normal sleep and post-extinction deprivation group during extinction recall. Results indicated sleep deprivation prior to extinction training significantly disrupts extinction recall. These findings suggest that (1) sleep deprivation in the immediate aftermath of trauma could be a potential contributor to PTSD development and maintenance via interference with natural extinction processes and (2) management of sleep symptoms should be considered during extinction-based therapy.

Central Brain Circuitry for Color-Vision-Modulated Behaviors.

PubMed

Longden, Kit D

2016-10-24

Color is famous for not existing in the external world: our brains create the perception of color from the spatial and temporal patterns of the wavelength and intensity of light. For an intangible quality, we have detailed knowledge of its origins and consequences. Much is known about the organization and evolution of the first phases of color processing, the filtering of light in the eye and processing in the retina, and about the final phases, the roles of color in behavior and natural selection. To understand how color processing in the central brain has evolved, we need well-defined pathways or circuitry where we can gauge how color contributes to the computations involved in specific behaviors. Examples of such pathways or circuitry that are dedicated to processing color cues are rare, despite the separation of color and luminance pathways early in the visual system of many species, and despite the traditional definition of color as being independent of luminance. This minireview presents examples in which color vision contributes to behaviors dominated by other visual modalities, examples that are not part of the canon of color vision circuitry. The pathways and circuitry process a range of chromatic properties of objects and their illumination, and are taken from a variety of species. By considering how color processing complements luminance processing, rather than being independent of it, we gain an additional way to account for the diversity of color coding in the central brain, its consequences for specific behaviors and ultimately the evolution of color vision. Copyright © 2016 Elsevier Ltd. All rights reserved.

Cumulative Association of Obstructive Sleep Apnea Severity and Short Sleep Duration with the Risk for Hypertension

PubMed Central

Priou, Pascaline; Le Vaillant, Marc; Meslier, Nicole; Paris, Audrey; Pigeanne, Thierry; Nguyen, Xuan-Lan; Alizon, Claire; Bizieux-Thaminy, Acya; Leclair-Visonneau, Laurene; Humeau, Marie-Pierre; Gagnadoux, Frédéric

2014-01-01

Obstructive sleep apnea (OSA) and short sleep duration are individually associated with an increased risk for hypertension (HTN). The aim of this multicenter cross-sectional study was to test the hypothesis of a cumulative association of OSA severity and short sleep duration with the risk for prevalent HTN. Among 1,499 patients undergoing polysomnography for suspected OSA, 410 (27.3%) previously diagnosed as hypertensive and taking antihypertensive medication were considered as having HTN. Patients with total sleep time (TST) <6 h were considered to be short sleepers. Logistic regression procedures were performed to determine the independent association of HTN with OSA and sleep duration. Considering normal sleepers (TST ≥6 h) without OSA as the reference group, the odds ratio (OR) (95% confidence intervals) for having HTN was 2.51 (1.35–4.68) in normal sleepers with OSA and 4.37 (2.18–8.78) in short sleepers with OSA after adjustment for age, gender, obesity, diabetes, depression, current smoking, use of thyroid hormones, daytime sleepiness, poor sleep complaint, time in bed, sleep architecture and fragmentation, and study site. The risk for HTN appeared to present a cumulative association with OSA severity and short sleep duration (p<0.0001 for linear trend). The higher risk for HTN was observed in short sleepers with severe OSA (AHI ≥30) (OR, 4.29 [2.03–9.07]). In patients investigated for suspected OSA, sleep-disordered breathing severity and short sleep duration have a cumulative association with the risk for prevalent HTN. Further studies are required to determine whether interventions to optimize sleep may contribute to lower BP in patients with OSA. PMID:25531468

Sleep-related declarative memory consolidation and verbal replay during sleep talking in patients with REM sleep behavior disorder.

PubMed

Uguccioni, Ginevra; Pallanca, Olivier; Golmard, Jean-Louis; Dodet, Pauline; Herlin, Bastien; Leu-Semenescu, Smaranda; Arnulf, Isabelle

2013-01-01

To determine if sleep talkers with REM sleep behavior disorder (RBD) would utter during REM sleep sentences learned before sleep, and to evaluate their verbal memory consolidation during sleep. Eighteen patients with RBD and 10 controls performed two verbal memory tasks (16 words from the Free and Cued Selective Reminding Test and a 220-263 word long modified Story Recall Test) in the evening, followed by nocturnal video-polysomnography and morning recall (night-time consolidation). In 9 patients with RBD, daytime consolidation (morning learning/recall, evening recall) was also evaluated with the modified Story Recall Test in a cross-over order. Two RBD patients with dementia were studied separately. Sleep talking was recorded using video-polysomnography, and the utterances were compared to the studied texts by two external judges. Sleep-related verbal memory consolidation was maintained in patients with RBD (+24±36% words) as in controls (+9±18%, p=0.3). The two demented patients with RBD also exhibited excellent nighttime consolidation. The post-sleep performance was unrelated to the sleep measures (including continuity, stages, fragmentation and apnea-hypopnea index). Daytime consolidation (-9±19%) was worse than night-time consolidation (+29±45%, p=0.03) in the subgroup of 9 patients with RBD. Eleven patients with RBD spoke during REM sleep and pronounced a median of 20 words, which represented 0.0003% of sleep with spoken language. A single patient uttered a sentence that was judged to be semantically (but not literally) related to the text learned before sleep. Verbal declarative memory normally consolidates during sleep in patients with RBD. The incorporation of learned material within REM sleep-associated sleep talking in one patient (unbeknownst to himself) at the semantic level suggests a replay at a highly cognitive creative level.

Sleep-Related Declarative Memory Consolidation and Verbal Replay during Sleep Talking in Patients with REM Sleep Behavior Disorder

PubMed Central

Uguccioni, Ginevra; Pallanca, Olivier; Golmard, Jean-Louis; Dodet, Pauline; Herlin, Bastien; Leu-Semenescu, Smaranda; Arnulf, Isabelle

2013-01-01

Objective To determine if sleep talkers with REM sleep behavior disorder (RBD) would utter during REM sleep sentences learned before sleep, and to evaluate their verbal memory consolidation during sleep. Methods Eighteen patients with RBD and 10 controls performed two verbal memory tasks (16 words from the Free and Cued Selective Reminding Test and a 220-263 word long modified Story Recall Test) in the evening, followed by nocturnal video-polysomnography and morning recall (night-time consolidation). In 9 patients with RBD, daytime consolidation (morning learning/recall, evening recall) was also evaluated with the modified Story Recall Test in a cross-over order. Two RBD patients with dementia were studied separately. Sleep talking was recorded using video-polysomnography, and the utterances were compared to the studied texts by two external judges. Results Sleep-related verbal memory consolidation was maintained in patients with RBD (+24±36% words) as in controls (+9±18%, p=0.3). The two demented patients with RBD also exhibited excellent nighttime consolidation. The post-sleep performance was unrelated to the sleep measures (including continuity, stages, fragmentation and apnea-hypopnea index). Daytime consolidation (-9±19%) was worse than night-time consolidation (+29±45%, p=0.03) in the subgroup of 9 patients with RBD. Eleven patients with RBD spoke during REM sleep and pronounced a median of 20 words, which represented 0.0003% of sleep with spoken language. A single patient uttered a sentence that was judged to be semantically (but not literally) related to the text learned before sleep. Conclusion Verbal declarative memory normally consolidates during sleep in patients with RBD. The incorporation of learned material within REM sleep-associated sleep talking in one patient (unbeknownst to himself) at the semantic level suggests a replay at a highly cognitive creative level. PMID:24349492

[Sleep health education for elderly people].

PubMed

Miyazaki, Soichiro; Nishiyama, Akiko

2015-06-01

Successful aging is characterized by minimal age-associated loss of the physiological functions of sleep and circadian clock. Sleep health education is necessary to have normal, quality nighttime sleep and full daytime alertness. Elderly people show changes of sleep parameters, accompanied by increased napping. Many studies have reported that daytime sleepiness or napping in elderly people could have potentially serious effects such as dementia and life-style related diseases. The main topics of sleep health education for elderly people are as follows: Right knowledge of sleep mechanism, understanding the bad influence of excessive napping, the effects of light on the circadian rhythm and negative effects of caffeine, alcohol and television.

Determining resistivity of a geological formation using circuitry located within a borehole casing

DOEpatents

Vail III, William Banning

2006-01-17

Geological formation resistivity is determined. Circuitry is located within the borehole casing that is adjacent to the geological formation. The circuitry can measure one or more voltages across two or more voltage measurement electrodes associated with the borehole casing. The measured voltages are used by a processor to determine the resistivity of the geological formation. A common mode signal can also be reduced using the circuitry.

The Role of Sleep and Sleep Disorders in the Development, Diagnosis, and Management of Neurocognitive Disorders

PubMed Central

Miller, Michelle A.

2015-01-01

It is becoming increasingly apparent that sleep plays an important role in the maintenance, disease prevention, repair, and restoration of both mind and body. The sleep and wake cycles are controlled by the pacemaker activity of the superchiasmic nucleus in the hypothalamus but can be disrupted by diseases of the nervous system causing disordered sleep. A lack of sleep has been associated with an increase in all-cause mortality. Likewise, sleep disturbances and sleep disorders may disrupt neuronal pathways and have an impact on neurological diseases. Sleep deprivation studies in normal subjects demonstrate that a lack of sleep can cause attention and working memory impairment. Moreover, untreated sleep disturbances and sleep disorders such as obstructive sleep apnoe (OSA) can also lead to cognitive impairment. Poor sleep and sleep disorders may present a significant risk factor for the development of dementia. In this review, the underlying mechanisms and the role of sleep and sleep disorders in the development of neurocognitive disorders [dementia and mild cognitive impairment (MCI)] and how the presence of sleep disorders could direct the process of diagnosis and management of neurocognitive disorders will be discussed. PMID:26557104

A Subset of Cholinergic Mushroom Body Neurons Requires Go Signaling to Regulate Sleep in Drosophila

PubMed Central

Yi, Wei; Zhang, Yunpeng; Tian, Yinjun; Guo, Jing; Li, Yan; Guo, Aike

2013-01-01

Study Objectives: Identifying the neurochemistry and neural circuitry of sleep regulation is critical for understanding sleep and various sleep disorders. Fruit flies display sleep-like behavior, sharing essential features with sleep of vertebrate. In the fruit fly's central brain, the mushroom body (MB) has been highlighted as a sleep center; however, its neurochemical nature remains unclear, and whether it promotes sleep or wake is still a topic of controversy. Design: We used a video recording system to accurately monitor the locomotor activity and sleep status. Gene expression was temporally and regionally manipulated by heat induction and the Gal4/UAS system. Measurements and Results: We found that expressing pertussis toxin (PTX) in the MB by c309-Gal4 to block Go activity led to unique sleep defects as dramatic sleep increase in daytime and fragmented sleep in nighttime. We narrowed down the c309-Gal4 expressing brain regions to the MB α/β core neurons that are responsible for the Go-mediated sleep effects. Using genetic tools of neurotransmitter-specific Gal80 and RNA interference approach to suppress acetylcholine signal, we demonstrated that these MB α/β core neurons were cholinergic and sleep-promoting neurons, supporting that Go mediates an inhibitory signal. Interestingly, we found that adjacent MB α/β neurons were also cholinergic but wake-promoting neurons, in which Go signal was also required. Conclusion: Our findings in fruit flies characterized a group of sleep-promoting neurons surrounded by a group of wake-promoting neurons. The two groups of neurons are both cholinergic and use Go inhibitory signal to regulate sleep. Citation: Yi W; Zhang Y; Tian Y; Guo J; Li Y; Guo A. A subset of cholinergic mushroom body neurons requires go signaling to regulate sleep in Drosophila. SLEEP 2013;36(12):1809-1821. PMID:24293755

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 and Respiration in Microgravity

NASA Technical Reports Server (NTRS)

West, John B.; Elliott, Ann R.; Prisk, G. Kim; Paiva, Manuel

2003-01-01

Sleep is often reported to be of poor quality in microgravity, and studies on the ground have shown a strong relationship between sleep-disordered breathing and sleep disruption. During the 16-day Neurolab mission, we studied the influence of possible changes in respiratory function on sleep by performing comprehensive sleep recordings on the payload crew on four nights during the mission. In addition, we measured the changes in the ventilatory response to low oxygen and high carbon dioxide in the same subjects during the day, hypothesizing that changes in ventilatory control might affect respiration during sleep. Microgravity caused a large reduction in the ventilatory response to reduced oxygen. This is likely the result of an increase in blood pressure at the peripheral chemoreceptors in the neck that occurs when the normally present hydrostatic pressure gradient between the heart and upper body is abolished. This reduction was similar to that seen when the subjects were placed acutely in the supine position in one-G. In sharp contrast to low oxygen, the ventilatory response to elevated carbon dioxide was unaltered by microgravity or the supine position. Because of the similarities of the findings in microgravity and the supine position, it is unlikely that changes in ventilatory control alter respiration during sleep in microgravity. During sleep on the ground, there were a small number of apneas (cessation of breathing) and hypopneas (reduced breathing) in these normal subjects. During sleep in microgravity, there was a reduction in the number of apneas and hypopneas per hour compared to preflight. Obstructive apneas virtually disappeared in microgravity, suggesting that the removal of gravity prevents the collapse of upper airways during sleep. Arousals from sleep were reduced in microgravity compared to preflight, and virtually all of this reduction was as a result of a reduction in the number of arousals from apneas and hypopneas. We conclude that any sleep

Impaired sexual maturation associated with sleep apnea syndrome during puberty: a case study.

PubMed

Mosko, S S; Lewis, E; Sassin, J F

1980-01-01

A 20-year-old hypogonadal man was discovered to have had obstructive sleep apnea syndrome--secondary to hypertrophied tonsils, adenoids, and uvula--spanning the years of puberty. All-night polysomnographic recordings and 24 hr measurements of plasma luteinizing hormone (LH) concentrations (sampling at 20 min intervals) were performed before and after combined tonsillectomy, adenoidectomy, and uvulectomy. Two weeks preoperatively, nocturnal sleep was markedly disturbed by 407 apneic episodes, and the patient was found to be hypogonadotropic. Daytime LH concentrations were in the low-normal range for an adult male, and concentrations fell dramatically during nocturnal sleep. This contrasts with both the sleep-related elevation of LH normally seen in puberty and the adult pattern, where no difference is observed in mean concentrations during waking and sleep. Two week and 6 month postoperative evaluations revealed complete alleviation of the sleep apnea syndrome and normalization of the 24 hr pattern of plasma LH, although LH values remained in the low-normal range. Plasma testosterone concentrations were in the low to low-normal range both pre- and postoperatively. No evidence of continued sexual development, beyond that achieved preoperatively, was observed 20 months after surgery, despite continued relief from apnea. These data suggest that sleep apnea during puberty may impair sexual development by preventing the sleep-related elevation in LH secretion normally observed during a critical period spanning puberty.

Sleep duration and sleep quality in relation to 12-year cardiovascular disease incidence: the MORGEN study.

PubMed

Hoevenaar-Blom, Marieke P; Spijkerman, Annemieke M W; Kromhout, Daan; van den Berg, Julia F; Verschuren, W M Monique

2011-11-01

We studied sleep duration and sleep quality in relation to cardiovascular disease (CVD) incidence. Dutch population-based cohort study. 20,432 men and women aged 20-65 and with no history of CVD. N/A. Sleep duration and sleep quality were assessed by a self-administered questionnaire. Morbidity data, vital status, and causes of death were obtained through linkage with several national registries. Hazard ratios (HRs) and 95% confidence intervals (95% CIs) were calculated using Cox proportional hazards models. During 10-15 years of follow-up, 1,486 CVD and 1,148 coronary heart disease (CHD) events occurred. Short sleepers (≤ 6 h) had a 15% higher risk of total CVD (HR: 1.15; 95%CI: 1.00-1.32) and a 23% higher risk of CHD (HR: 1.23 [1.04-1.45]) compared to normal sleepers (7 h) after adjustment for all confounders. Additional adjustment for intermediate biological risk factors attenuated these relative risks to 1.11 (0.97-1.27) for total CVD and to 1.19 (1.00-1.40) for CHD. Short sleepers with poor sleep quality had a 63% higher risk of CVD (HR: 1.63 [1.21-2.19]) and a 79% higher risk of CHD incidence (HR: 1.79 [1.24-2.58]) compared to normal sleepers with good sleep quality, after adjustments for all confounders. We observed no associations between long sleep duration (≥ 9 h) and CVD or CHD incidence. Short sleepers, especially those with poor sleep quality, have an increased risk of total CVD and CHD incidence. Future investigations should not only focus on sleep duration, but should also take sleep quality into account.

Sleep in the intensive care unit

PubMed Central

Beltrami, Flávia Gabe; Nguyen, Xuân-Lan; Pichereau, Claire; Maury, Eric; Fleury, Bernard; Fagondes, Simone

2015-01-01

ABSTRACT Poor sleep quality is a consistently reported by patients in the ICU. In such a potentially hostile environment, sleep is extremely fragmented and sleep architecture is unconventional, with a predominance of superficial sleep stages and a limited amount of time spent in the restorative stages. Among the causes of sleep disruption in the ICU are factors intrinsic to the patients and the acute nature of their condition, as well as factors related to the ICU environment and the treatments administered, such as mechanical ventilation and drug therapy. Although the consequences of poor sleep quality for the recovery of ICU patients remain unknown, it seems to influence the immune, metabolic, cardiovascular, respiratory, and neurological systems. There is evidence that multifaceted interventions focused on minimizing nocturnal sleep disruptions improve sleep quality in ICU patients. In this article, we review the literature regarding normal sleep and sleep in the ICU. We also analyze sleep assessment methods; the causes of poor sleep quality and its potential implications for the recovery process of critically ill patients; and strategies for sleep promotion. PMID:26785964

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.

Menopause related sleep disorders.

PubMed

Eichling, Philip S; Sahni, Jyotsna

2005-07-15

Sleep difficulty is one of the hallmarks of menopause. Following recent studies showing no cardiac benefit and increased breast cancer, the question of indications for hormonal therapy has become even more pertinent. Three sets of sleep disorders are associated with menopause: insomnia/depression, sleep disordered breathing and fibromyalgia. The primary predictor of disturbed sleep architecture is the presence of vasomotor symptoms. This subset of women has lower sleep efficiency and more sleep complaints. The same group is at higher risk of insomnia and depression. The "domino theory" of sleep disruption leading to insomnia followed by depression has the most scientific support. Estrogen itself may also have an antidepressant as well as a direct sleep effect. Treatment of insomnia in responsive individuals may be a major remaining indication for hormone therapy. Sleep disordered breathing (SDB) increases markedly at menopause for reasons that include both weight gain and unclear hormonal mechanisms. Due to the general under-recognition of SDB, health care providers should not assume sleep complaints are due to vasomotor related insomnia/depression without considering SDB. Fibromyalgia has gender, age and probably hormonal associations. Sleep complaints are almost universal in FM. There are associated polysomnogram (PSG) findings. FM patients have increased central nervous system levels of the nociceptive neuropeptide substance P (SP) and lower serotonin levels resulting in a lower pain threshold to normal stimuli. High SP and low serotonin have significant potential to affect sleep and mood. Treatment of sleep itself seems to improve, if not resolve FM. Menopausal sleep disruption can exacerbate other pre-existing sleep disorders including RLS and circadian disorders.

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

PubMed Central

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

2017-01-01

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. PMID:28193862

Relationship of slow and rapid EEG components of CAP to ASDA arousals in normal sleep.

PubMed

Parrino, L; Smerieri, A; Rossi, M; Terzano, M G

2001-12-15

Besides arousals (according to the ASDA definition), sleep contains also K-complexes and delta bursts which, in spite of their sleep-like features, are endowed with activating effects on autonomic functions. The link between phasic delta activities and enhancement of vegetative functions indicates the possibility of physiological activation without sleep disruption (i.e., arousal without awakening). A functional connection seems to include slow (K-complexes and delta bursts) and rapid (arousals) EEG events within the comprehensive term of activating complexes. CAP (cyclic alternating pattern) is the spontaneous EEG rhythm that ties both slow and rapid activating complexes together during NREM sleep. The present study aims at exploring the relationship between arousals and CAP components in a selected sample of healthy sleepers. Polysomnographic analysis according to the scoring rules for sleep stages and arousals. CAP analysis included also tabulation of subtypes A1 (slow EEG activating complexes), A2 and A3 (activating complexes with fast EEG components). 40 sleep-lab accomplished recordings. Healthy subjects belonging to a wide age range (38 +/- 20 yrs.). N/A. Of all the arousals occurring in NREM sleep, 87% were inserted within CAP. Subtypes A2 and A3 of CAP corresponded strikingly with arousals (r=0.843; p<0.0001), while no statistical relationship emerged when arousals were matched with subtypes A1 of CAP. Subtypes A1 instead correlated positively with the percentages of deep sleep (r=0.366; p<0.02). The CAP subtype classification encompasses both the process of sleep maintenance (subtypes A1) and sleep fragmentation (subtypes A2 and A3), and provides a periodicity dimension to the activating events of NREM sleep.

Firefighter Shift Schedules Affect Sleep Quality.

PubMed

Billings, Joel; Focht, Will

2016-03-01

The aim of this study was to investigate the prevalence and severity of firefighter sleep quality across department shift schedules. Sleep quality was assessed using a Pittsburgh Sleep Quality Index in a sample of 109 male career firefighters from six fire departments in three Southwestern US states. The three shift schedules studied were 24on/48off, 48on/96off, and Kelly. Seventy-three percent of firefighters report poor sleep quality. The 24on/48off shift schedule is associated with the best sleep quality and Kelly is associated with the worst sleep quality. Firefighters working second jobs report significantly poorer sleep quality than those who do not. Shift schedules that disrupt normal circadian rhythms more result in poorer sleep quality, which can lead to less effective emergency response and increased risk to firefighter health and safety.

Extreme Violation of Sleep Hygiene: Sleeping Against the Biological Clock During a Multiday Relay Event.

PubMed

van Maanen, Annette; Roest, Bas; Moen, Maarten; Oort, Frans; Vergouwen, Peter; Paul, Ingrid; Groenenboom, Petra; Smits, Marcel

2015-12-01

Sleep hygiene is important for sleep quality and optimal performance during the day. However, it is not always possible to follow sleep hygiene requirements. In multiday relay events, athletes have to sleep immediately after physical exertion and sometimes against their biological clock. In this pilot study we investigated the effect of having to sleep at an abnormal circadian time on sleep duration. Eight runners and two cyclists performing a 500 km relay race were followed. They were divided into two groups that took turns in running and resting. Each group ran four times for approximately five hours while the other group slept. As a result, sleep times varied between normal and abnormal times. All athletes wore actigraphs to record the duration and onset of sleep. Linear mixed model analyses showed that athletes slept on average 43 minutes longer when they slept during usual (night) times than during abnormal (day) times. In general, sleep duration decreased during the race with on average 18 minutes per period. This pilot study shows that, even under extreme violation of sleep hygiene rules, there still is an apparent effect of circadian rhythm on sleep duration in relay race athletes.

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.

Narcolepsy with Long Sleep Time: A Specific Entity?

PubMed Central

Vernet, Cyrille; Arnulf, Isabelle

2009-01-01

Background: The classical narcolepsy patient reports intense feelings of sleepiness (with/out cataplexy), normal or disrupted nighttime sleep, and takes short and restorative naps. However, with long-term monitoring, we identified some narcoleptics resembling patients with idiopathic hypersomnia. Objective: To isolate and describe a new subtype of narcolepsy with long sleep time). Setting: University Hospital Design: Controlled, prospective cohort Participants: Out of 160 narcoleptics newly diagnosed within the past 3 years, 29 (18%) had a long sleep time (more than 11 h/24 h). We compared narcoleptics with (n = 23) and without (n = 29) long sleep time to 25 hypersomniacs with long sleep time and 20 healthy subjects. Intervention: Patients and controls underwent face-to face interviews, questionnaires, human leukocyte antigen (HLA) genotype, an overnight polysomnography, multiple sleep latency tests, and 24-h ad libitum sleep monitoring. Results: Narcoleptics with long sleep time had a similar disease course and similar frequencies of cataplexy, sleep paralysis, hallucinations, multiple sleep onset in REM periods, short mean sleep latencies, and HLA DQB1*0602 positivity as narcoleptics with normal sleep time did. However, they had longer sleep time during 24 h, and higher sleep efficiency, lower Epworth Sleepiness Scale scores, and reported their naps were more often unrefreshing. Only 3/23 had core narcolepsy (HLA and cataplexy positive). Conclusions: The subgroup of narcoleptics with a long sleep time comprises 18% of narcoleptics. Their symptoms combine the disabilities of both narcolepsy (severe sleepiness) and idiopathic hypersomnia (long sleep time and unrefreshing naps). Thus, they may constitute a group with multiple arousal system dysfunctions. Citation: Vernet C; Arnulf I. Narcolepsy with long sleep time: a specific entity? SLEEP 2009;32(9):1229-1235. PMID:19750928

Neuronal machinery of sleep homeostasis in Drosophila.

PubMed

Donlea, Jeffrey M; Pimentel, Diogo; Miesenböck, Gero

2014-02-19

Sleep is under homeostatic control, but the mechanisms that sense sleep need and correct sleep deficits remain unknown. Here, we report that sleep-promoting neurons with projections to the dorsal fan-shaped body (FB) form the output arm of Drosophila's sleep homeostat. Homeostatic sleep control requires the Rho-GTPase-activating protein encoded by the crossveinless-c (cv-c) gene in order to transduce sleep pressure into increased electrical excitability of dorsal FB neurons. cv-c mutants exhibit decreased sleep time, diminished sleep rebound, and memory deficits comparable to those after sleep loss. Targeted ablation and rescue of Cv-c in sleep-control neurons of the dorsal FB impair and restore, respectively, normal sleep patterns. Sleep deprivation increases the excitability of dorsal FB neurons, but this homeostatic adjustment is disrupted in short-sleeping cv-c mutants. Sleep pressure thus shifts the input-output function of sleep-promoting neurons toward heightened activity by modulating ion channel function in a mechanism dependent on Cv-c. Copyright © 2014 The Authors. Published by Elsevier Inc. All rights reserved.

Etiologies and evaluation of sleep disturbances in adolescence.

PubMed

Owens, Judith A

2010-12-01

The etiologies of sleep disturbances in adolescents are varied and include biological, environmental, and sociocultural factors. Health care practitioners need to have a basic understanding of normal sleep development in adolescents and the risk factors for inadequate sleep, as well as an appreciation for the myriad potential consequences of insufficient sleep (ie, mood dysregulation, academic failure, and obesity). This chapter provides a systematic approach to screening and evaluating adolescent sleep complaints in the clinical setting and provides suggestions for anticipatory guidance regarding healthy sleep, which should be part of standard adolescent health care.

Shorter sleep duration and better sleep quality are associated with greater tissue density in the brain.

PubMed

Takeuchi, Hikaru; Taki, Yasuyuki; Nouchi, Rui; Yokoyama, Ryoichi; Kotozaki, Yuka; Nakagawa, Seishu; Sekiguchi, Atsushi; Iizuka, Kunio; Yamamoto, Yuki; Hanawa, Sugiko; Araki, Tsuyoshi; Miyauchi, Carlos Makoto; Shinada, Takamitsu; Sakaki, Kohei; Nozawa, Takayuki; Ikeda, Shigeyuki; Yokota, Susumu; Daniele, Magistro; Sassa, Yuko; Kawashima, Ryuta

2018-04-11

Poor sleep quality is associated with unfavorable psychological measurements, whereas sleep duration has complex relationships with such measurements. The aim of this study was to identify the associations between microstructural properties of the brain and sleep duration/sleep quality in a young adult. The associations between mean diffusivity (MD), a measure of diffusion tensor imaging (DTI), and sleep duration/sleep quality were investigated in a study cohort of 1201 normal young adults. Positive correlations between sleep duration and MD of widespread areas of the brain, including the prefrontal cortex (PFC) and the dopaminergic systems, were identified. Negative correlations between sleep quality and MD of the widespread areas of the brain, including the PFC and the right hippocampus, were also detected. Lower MD has been previously associated with more neural tissues in the brain. Further, shorter sleep duration was associated with greater persistence and executive functioning (lower Stroop interference), whereas good sleep quality was associated with states and traits relevant to positive affects. These results suggest that bad sleep quality and longer sleep duration were associated with aberrant neurocognitive measurements in the brain in healthy young adults.

Electro-oculography-based detection of sleep-wake in sleep apnea patients.

PubMed

Virkkala, Jussi; Toppila, Jussi; Maasilta, Paula; Bachour, Adel

2015-09-01

Recently, we have developed a simple method that uses two electro-oculography (EOG) electrodes for the automatic scoring of sleep-wake in normal subjects. In this study, we investigated the usefulness of this method on 284 consecutive patients referred for a suspicion of sleep apnea who underwent a polysomnography (PSG). We applied the AASM 2007 scoring rules. A simple automatic sleep-wake classification algorithm based on 18-45 Hz beta power was applied to the calculated bipolar EOG channel and was compared to standard polysomnography. Epoch by epoch agreement was evaluated. Eighteen patients were excluded due to poor EOG quality. One hundred fifty-eight males and 108 females were studied, their mean age was 48 (range 17-89) years, apnea-hypopnea index 13 (range 0-96) /h, BMI 29 (range 17-52) kg/m(2), and sleep efficiency 78 (range 0-98) %. The mean agreement in sleep-wake states between EOG and PSG was 85% and the Cohen's kappa was 0.56. Overall epoch-by-epoch agreement was 85%, and the Cohen's kappa was 0.57 with positive predictive value of 91% and negative predictive value of 65%. The EOG method can be applied to patients referred for suspicion of sleep apnea to indicate the sleep-wake state.

Neural Circuitry of Impaired Emotion Regulation in Substance Use Disorders.

PubMed

Wilcox, Claire E; Pommy, Jessica M; Adinoff, Bryon

2016-04-01

Impaired emotion regulation contributes to the development and severity of substance use disorders (substance disorders). This review summarizes the literature on alterations in emotion regulation neural circuitry in substance disorders, particularly in relation to disorders of negative affect (without substance disorder), and it presents promising areas of future research. Emotion regulation paradigms during functional magnetic resonance imaging are conceptualized into four dimensions: affect intensity and reactivity, affective modulation, cognitive modulation, and behavioral control. The neural circuitry associated with impaired emotion regulation is compared in individuals with and without substance disorders, with a focus on amygdala, insula, and prefrontal cortex activation and their functional and structural connectivity. Hypoactivation of the rostral anterior cingulate cortex/ventromedial prefrontal cortex (rACC/vmPFC) is the most consistent finding across studies, dimensions, and clinical populations (individuals with and without substance disorders). The same pattern is evident for regions in the cognitive control network (anterior cingulate and dorsal and ventrolateral prefrontal cortices) during cognitive modulation and behavioral control. These congruent findings are possibly related to attenuated functional and/or structural connectivity between the amygdala and insula and between the rACC/vmPFC and cognitive control network. Although increased amygdala and insula activation is associated with impaired emotion regulation in individuals without substance disorders, it is not consistently observed in substance disorders. Emotion regulation disturbances in substance disorders may therefore stem from impairments in prefrontal functioning, rather than excessive reactivity to emotional stimuli. Treatments for emotion regulation in individuals without substance disorders that normalize prefrontal functioning may offer greater efficacy for substance disorders

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.

Adenosine, caffeine, and performance: from cognitive neuroscience of sleep to sleep pharmacogenetics.

PubMed

Urry, Emily; Landolt, Hans-Peter

2015-01-01

An intricate interplay between circadian and sleep-wake homeostatic processes regulate cognitive performance on specific tasks, and individual differences in circadian preference and sleep pressure may contribute to individual differences in distinct neurocognitive functions. Attentional performance appears to be particularly sensitive to time of day modulations and the effects of sleep deprivation. Consistent with the notion that the neuromodulator, adenosine , plays an important role in regulating sleep pressure, pharmacologic and genetic data in animals and humans demonstrate that differences in adenosinergic tone affect sleepiness, arousal and vigilant attention in rested and sleep-deprived states. Caffeine--the most often consumed stimulant in the world--blocks adenosine receptors and normally attenuates the consequences of sleep deprivation on arousal, vigilance, and attention. Nevertheless, caffeine cannot substitute for sleep, and is virtually ineffective in mitigating the impact of severe sleep loss on higher-order cognitive functions. Thus, the available evidence suggests that adenosinergic mechanisms, in particular adenosine A2A receptor-mediated signal transduction, contribute to waking-induced impairments of attentional processes, whereas additional mechanisms must be involved in higher-order cognitive consequences of sleep deprivation. Future investigations should further clarify the exact types of cognitive processes affected by inappropriate sleep. This research will aid in the quest to better understand the role of different brain systems (e.g., adenosine and adenosine receptors) in regulating sleep, and sleep-related subjective state, and cognitive processes. Furthermore, it will provide more detail on the underlying mechanisms of the detrimental effects of extended wakefulness, as well as lead to the development of effective, evidence-based countermeasures against the health consequences of circadian misalignment and chronic sleep restriction.

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.

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

Sleep restriction may lead to disruption in physiological attention and reaction time.

PubMed

Choudhary, Arbind Kumar; Kishanrao, Sadawarte Sahebrao; Dadarao Dhanvijay, Anup Kumar; Alam, Tanwir

2016-01-01

Sleepiness is the condition where for some reason fails to go into a sleep state and will have difficulty in remaining awake even while carrying out activities. Sleep restriction occurs when an individual fails to get enough sleep due to high work demands. The mechanism between sleep restriction and underlying brain physiology deficits is not well assumed. The objective of the present study was to investigate the mental attention (P300) and reaction time [visual (VRT) and auditory (ART)] among night watchmen, at subsequent; first (1st) day, fourth (4th) day and seventh (7th) day of restricted sleep period. After exclusion and inclusion criteria, the study was performed among 50 watchmen (age=18-35 years) (n=50) after providing written informed consent and divided into two group. Group I-(Normal sleep) (n=28) working in day time and used to have normal sleep in night (≥8 h); Group II-(Restricted sleep) (n=22) - working in night time and used to have less sleep in night (≤3 h). Statistical significance between the different groups was determined by the independent student ' t ' test and the significance level was fixed at p≤0.05. We observed that among all normal and restricted sleep watchmen there was not any significant variation in Karolinska Sleepiness Scale (KSS) score, VRT and ART, along with latency and amplitude of P300 on 1st day of restricted sleep. However at subsequent on 4th day and 7th day of restricted sleep, there was significant increase in (KSS)score, and prolongation of VRT and ART as well as alteration in latency and amplitude of P300 wave in restricted sleep watchmen when compare to normal sleep watchmen. The present finding concludes that loss of sleep has major impact in dynamic change in mental attention and reaction time among watchmen employed in night shift. Professional regulations and work schedules should integrate sleep schedules before and during the work period as an essential dimension for their healthy life.

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.

Metabolic consequences of sleep and circadian disorders.

PubMed

Depner, Christopher M; Stothard, Ellen R; Wright, Kenneth P

2014-07-01

Sleep and circadian rhythms modulate or control daily physiological patterns with importance for normal metabolic health. Sleep deficiencies associated with insufficient sleep schedules, insomnia with short-sleep duration, sleep apnea, narcolepsy, circadian misalignment, shift work, night eating syndrome, and sleep-related eating disorder may all contribute to metabolic dysregulation. Sleep deficiencies and circadian disruption associated with metabolic dysregulation may contribute to weight gain, obesity, and type 2 diabetes potentially by altering timing and amount of food intake, disrupting energy balance, inflammation, impairing glucose tolerance, and insulin sensitivity. Given the rapidly increasing prevalence of metabolic diseases, it is important to recognize the role of sleep and circadian disruption in the development, progression, and morbidity of metabolic disease. Some findings indicate sleep treatments and countermeasures improve metabolic health, but future clinical research investigating prevention and treatment of chronic metabolic disorders through treatment of sleep and circadian disruption is needed.

Metabolic consequences of sleep and circadian disorders

PubMed Central

Depner, Christopher M.; Stothard, Ellen R.; Wright, Kenneth P.

2014-01-01

Sleep and circadian rhythms modulate or control daily physiological patterns with importance for normal metabolic health. Sleep deficiencies associated with insufficient sleep schedules, insomnia with short-sleep duration, sleep apnea, narcolepsy, circadian misalignment, shift work, night eating syndrome and sleep-related eating disorder may all contribute to metabolic dysregulation. Sleep deficiencies and circadian disruption associated with metabolic dysregulation may contribute to weight gain, obesity, and type 2 diabetes potentially by altering timing and amount of food intake, disrupting energy balance, inflammation, impairing glucose tolerance and insulin sensitivity. Given the rapidly increasing prevalence of metabolic diseases, it is important to recognize the role of sleep and circadian disruption in the development, progression, and morbidity of metabolic disease. Some findings indicate sleep treatments and countermeasures improve metabolic health, but future clinical research investigating prevention and treatment of chronic metabolic disorders through treatment of sleep and circadian disruption is needed. PMID:24816752

Progress toward the maintenance and repair of degenerating retinal circuitry.

PubMed

Vugler, Anthony A

2010-01-01

Retinal diseases such as age-related macular degeneration and retinitis pigmentosa remain major causes of severe vision loss in humans. Clinical trials for treatment of retinal degenerations are underway and advancements in our understanding of retinal biology in health/disease have implications for novel therapies. A review of retinal biology is used to inform a discussion of current strategies to maintain/repair neural circuitry in age-related macular degeneration, retinitis pigmentosa, and Type 2 Leber congenital amaurosis. In age-related macular degeneration/retinitis pigmentosa, a progressive loss of rods/cones results in corruption of bipolar cell circuitry, although retinal output neurons/photoreceptive melanopsin cells survive. Visual function can be stabilized/enhanced after treatment in age-related macular degeneration, but in advanced degenerations, reorganization of retinal circuitry may preclude attempts to restore cone function. In Type 2 Leber congenital amaurosis, useful vision can be restored by gene therapy where central cones survive. Remarkable progress has been made in restoring vision to rodents using light-responsive ion channels inserted into bipolar cells/retinal ganglion cells. Advances in genetic, cellular, and prosthetic therapies show varying degrees of promise for treating retinal degenerations. While functional benefits can be obtained after early therapeutic interventions, efforts should be made to minimize circuitry changes as soon as possible after rod/cone loss. Advances in retinal anatomy/physiology and genetic technologies should allow refinement of future reparative strategies.

Extreme Violation of Sleep Hygiene: Sleeping Against the Biological Clock During a Multiday Relay Event

PubMed Central

van Maanen, Annette; Roest, Bas; Moen, Maarten; Oort, Frans; Vergouwen, Peter; Paul, Ingrid; Groenenboom, Petra; Smits, Marcel

2015-01-01

Background: Sleep hygiene is important for sleep quality and optimal performance during the day. However, it is not always possible to follow sleep hygiene requirements. In multiday relay events, athletes have to sleep immediately after physical exertion and sometimes against their biological clock. Objectives: In this pilot study we investigated the effect of having to sleep at an abnormal circadian time on sleep duration. Patients and Methods: Eight runners and two cyclists performing a 500 km relay race were followed. They were divided into two groups that took turns in running and resting. Each group ran four times for approximately five hours while the other group slept. As a result, sleep times varied between normal and abnormal times. All athletes wore actigraphs to record the duration and onset of sleep. Results: Linear mixed model analyses showed that athletes slept on average 43 minutes longer when they slept during usual (night) times than during abnormal (day) times. In general, sleep duration decreased during the race with on average 18 minutes per period. Conclusions: This pilot study shows that, even under extreme violation of sleep hygiene rules, there still is an apparent effect of circadian rhythm on sleep duration in relay race athletes. PMID:26715971

Intergenerational Neuroimaging of Human Brain Circuitry

PubMed Central

Ho, Tiffany C.; Sanders, Stephan J.; Gotlib, Ian H.; Hoeft, Fumiko

2016-01-01

Neuroscientists are increasingly using advanced neuroimaging methods to elucidate the intergenerational transmission of human brain circuitry. This new line of work promises to shed insight into the ontogeny of complex behavioral traits, including psychiatric disorders, and possible mechanisms of transmission. Here, we highlight recent intergenerational neuroimaging studies and provide recommendations for future work. PMID:27623194

Sleep in disorders of consciousness

PubMed Central

Cologan, Victor; Schabus, Manvel; Ledoux, Didier; Moonen, Gustave; Maquet, Pierre; Laureys, Steven

2010-01-01

SUMMARY From a behavioral as well as neurobiological point of view, sleep and consciousness are intimately connected. A better understanding of sleep cycles and sleep architecture of patients suffering from disorders of consciousness (DOC) might therefore improve the clinical care for these patients as well as our understanding of the neural correlations of consciousness. Defining sleep in severely brain-injured patients is however problematic as both their electrophysiological and sleep patterns differ in many ways from healthy individuals. This paper discusses the concepts involved in the study of sleep of patients suffering from DOC and critically assesses the applicability of standard sleep criteria in these patients. The available literature on comatose and vegetative states as well as that on locked-in and related states following traumatic or non-traumatic severe brain injury will be reviewed. A wide spectrum of sleep disturbances ranging from almost normal patterns to severe loss and architecture disorganization are reported in cases of DOC and some patterns correlate with diagnosis and prognosis. At the present time the interactions of sleep and consciousness in brain-injured patients are a little studied subject but, the authors suggest, a potentially very interesting field of research. PMID:19524464

Sleep staging with movement-related signals.

PubMed

Jansen, B H; Shankar, K

1993-05-01

Body movement related signals (i.e., activity due to postural changes and the ballistocardiac effort) were recorded from six normal volunteers using the static-charge-sensitive bed (SCSB). Visual sleep staging was performed on the basis of simultaneously recorded EEG, EMG and EOG signals. A statistical classification technique was used to determine if reliable sleep staging could be performed using only the SCSB signal. A classification rate of between 52% and 75% was obtained for sleep staging in the five conventional sleep stages and the awake state. These rates improved from 78% to 89% for classification between awake, REM and non-REM sleep and from 86% to 98% for awake versus asleep classification.

Sleep instability and cognitive status in drug-resistant epilepsies.

PubMed

Pereira, Alessandra Marques; Bruni, Oliviero; Ferri, Raffaele; Nunes, Magda Lahorgue

2012-05-01

The aims of this study were to evaluate the sleep habits of children with drug resistant epilepsy and to correlate sleep abnormalities with epilepsy and level of intelligence. Twenty five subjects with drug resistant epilepsy (14 males, age range 2-16.4 years) were recruited for this study. A control group was formed by 23 normal children. Two instruments to assess sleep habits were administered to the patients with epilepsy: a questionnaire on sleep habits (to preschool children) and a questionnaire on sleep behavior (for children aged more than seven years old); a cognitive test (Wechsler Intelligence Scale for Children-WISC) was also performed. Patients underwent a complete polysomnographic study and sleep parameters, including CAP, were analyzed and correlated according to cognitive-behavioral measures in children with epilepsy. Children with drug-resistant epilepsy and severe mental retardation showed sleep abnormalities such as low sleep efficiency, high percentage of wakefulness after sleep onset, reduced slow wave sleep, and reduced REM sleep. Sleep microstructure evaluated by means of CAP analysis showed a decrease in A1 index during N3 in patients with more severe cognitive impairment. Children with epilepsy and cognitive impairment (n=10) had higher Sleep Behavior Questionnaire for Children (SBQC) total scores (65.60 ± 18.56) compared to children with epilepsy and normal IQ (50.00 ± 10.40), p<0.05. Children with drug-resistant epilepsy have a greater incidence of sleep problems regarding qualitative aspects, macrostructure, and CAP. The decrease of CAP rate and of A1, mainly during slow wave sleep (associated to REM sleep reduction), might represent a sleep microstructural pattern of intellectual disability. Copyright © 2012 Elsevier B.V. All rights reserved.

[Non-epileptic paroxysmal sleep disorders].

PubMed

Malagón-Valdez, Jorge

2013-09-06

Non-epileptic paroxysmal disorders during sleep are a great challenge for the clinician. It is important to know the various clinical manifestations for appropriate differential diagnosis, since alterations in sleep, mostly motor, are part of these disorders. Our paper describes the normal sleep stages and electroencephalographic characteristics and polysomnography basic data. The confusions especially with nocturnal frontal lobe epilepsy are frequent and cause unnecessary drugs administered, the emotional burden of the parents or caretakers, which is the diagnosis of epilepsy. We discuss the possible causes of diagnostic errors.

DSM-5 Insomnia and Short Sleep: Comorbidity Landscape and Racial Disparities.

PubMed

Kalmbach, David A; Pillai, Vivek; Arnedt, J Todd; Drake, Christopher L

2016-12-01

We estimated rates of cardiometabolic disease, pain conditions, and psychiatric illness associated with Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) insomnia disorder (current and in remission) and habitual short sleep (fewer than 6 h), and examined the roles of insomnia and short sleep in racial disparities in disease burden between black and non-Hispanic white Americans. This epidemiological survey study was cross-sectional. The community-based sample consisted of 3,911 subjects (46.0 y ± 13.3; 65.4% female; 25.0% black) across six sleep groups based on DSM-5 insomnia classification ( never vs. remitted vs. current ) and self-reported habitual sleep duration ( normal vs. short ). Vascular events, cardiometabolic disease, pain conditions, and psychiatric symptoms were self-reported. Short sleeping insomniacs were at elevated risk for myocardial infarction, stroke, treated hypertension, diabetes, chronic pain, back pain, depression, and anxiety, independent of sex, age, and obesity. Morbidity profiles for insomniacs with normal sleep duration and former insomniacs, irrespective of sleep duration, were similar with elevations in treated hypertension, chronic pain, depression, and anxiety. Regarding racial disparities, cardiometabolic and psychiatric illness burden was greater for blacks, who were more likely to have short sleep and the short sleep insomnia phenotype. Evidence suggested that health disparities may be attributable in part to race-related differences in sleep. Insomnia disorder with short sleep is the most severe phenotype of insomnia and comorbid with many cardiometabolic and psychiatric illnesses, whereas morbidity profiles are highly similar between insomniacs with normal sleep duration and former insomniacs. Short sleep endemic to black Americans increases risk for the short sleep insomnia phenotype and likely contributes to racial disparities in cardiometabolic disease and psychiatric illness. © 2016 Associated

The Neuroprotective Aspects of Sleep.

PubMed

Eugene, Andy R; Masiak, Jolanta

2015-03-01

Sleep is an important component of human life, yet many people do not understand the relationship between the brain and the process of sleeping. Sleep has been proven to improve memory recall, regulate metabolism, and reduce mental fatigue. A minimum of 7 hours of daily sleep seems to be necessary for proper cognitive and behavioral function. The emotional and mental handicaps associated with chronic sleep loss as well as the highly hazardous situations which can be contributed to the lack of sleep is a serious concern that people need to be aware of. When one sleeps, the brain reorganizes and recharges itself, and removes toxic waste byproducts which have accumulated throughout the day. This evidence demonstrates that sleeping can clear the brain and help maintain its normal functioning. Multiple studies have been done to determine the effects of total sleep deprivation; more recently some have been conducted to show the effects of sleep restriction, which is a much more common occurrence, have the same effects as total sleep deprivation. Each phase of the sleep cycle restores and rejuvenates the brain for optimal function. When sleep is deprived, the active process of the glymphatic system does not have time to perform that function, so toxins can build up, and the effects will become apparent in cognitive abilities, behavior, and judgment. As a background for this paper we have reviewed literature and research of sleep phases, effects of sleep deprivation, and the glymphatic system of the brain and its restorative effect during the sleep cycle.

The Neuroprotective Aspects of Sleep

PubMed Central

Eugene, Andy R.; Masiak, Jolanta

2015-01-01

Sleep is an important component of human life, yet many people do not understand the relationship between the brain and the process of sleeping. Sleep has been proven to improve memory recall, regulate metabolism, and reduce mental fatigue. A minimum of 7 hours of daily sleep seems to be necessary for proper cognitive and behavioral function. The emotional and mental handicaps associated with chronic sleep loss as well as the highly hazardous situations which can be contributed to the lack of sleep is a serious concern that people need to be aware of. When one sleeps, the brain reorganizes and recharges itself, and removes toxic waste byproducts which have accumulated throughout the day. This evidence demonstrates that sleeping can clear the brain and help maintain its normal functioning. Multiple studies have been done to determine the effects of total sleep deprivation; more recently some have been conducted to show the effects of sleep restriction, which is a much more common occurrence, have the same effects as total sleep deprivation. Each phase of the sleep cycle restores and rejuvenates the brain for optimal function. When sleep is deprived, the active process of the glymphatic system does not have time to perform that function, so toxins can build up, and the effects will become apparent in cognitive abilities, behavior, and judgment. As a background for this paper we have reviewed literature and research of sleep phases, effects of sleep deprivation, and the glymphatic system of the brain and its restorative effect during the sleep cycle. PMID:26594659

Sleep and Premenstrual Syndrome

PubMed Central

Jehan, Shazia; Auguste, Evan; Hussain, Mahjabeen; Pandi-Perumal, Seithikurippu R.; Brzezinski, Amon; Gupta, Ravi; Attarian, Hrayr; Jean-Louis, Giradin; McFarlane, Samy I.

2016-01-01

The etiology of premenstrual syndrome (PMS) is unknown; it may be due to the normal effect of hormones during the menstrual cycle as it occurs in the late luteal phase of the menstrual cycle.PMS affects women of childbearing age and remits with the onset of menstruation. The menstrual phase is known to influence stage 2 and REM sleep in women, irrespective of premenstrual dysphoric disorder (PMDD). Women with PMDD showed a decreased response to melatonin in their luteal phase as compared to the follicular phase of the menstrual cycle. However, melatonin duration or timing of offset in the morning has not been reported to correlate with the mood. Rather, improvement in mood-related symptoms of PMDD has been found to be influenced by sleep deprivation, be it sleep restrictions in early or late night. Sleep disturbance and decreased melatonin secretions due to hormonal fluctuations during the luteal phase of the menstrual cycle could explain the sleep complaints of PMDD. PMID:28239684

Sleep, its subjective perception, and daytime performance in insomniacs with a pattern of alpha sleep.

PubMed

Schneider-Helmert, D; Kumar, A

1995-01-15

Intrusion of alpha activity, an electroencephalographic (EEG) pattern typical for wakefulness, into sleep stages has repeatedly been described and investigated in various populations. Some studies suggested that it is a less deep and restorative sleep, but others did not support this interpretation. The present study was carried out to collect ample data on neurophysiology and subjective experience of sleep and on daytime cognitive performance to clarify this point. A sample of 128 primary insomniacs was investigated with polysomnography (PSG) that was submitted to a computerized, automatic analysis of alpha activity during sleep. It yielded two groups of 64 Ss each with a normal, that is, nonalpha sleep EEG and with alpha-sleep, respectively. Contrasting the two groups for PSG showed that alpha sleep Ss had significantly more stage 4 and a (nonsignificant) tendency for more awakenings. Subjectively, they largely underestimated intermittent wake time and consequently overestimated sleep duration by 50 min. The performance test battery showed a difference in one test only, that is, a better short-term memory function by alpha sleep Ss. In conclusion, there was no result supporting the assumption that alpha sleep is less restorative, but a significant lack of perception of intermittent awakenings during night sleep by alpha sleep Ss was found. The authors propose an explanation and point to the implications this misperception might have for the clinician.

Altered Sleep Patterns and Physiologic Characteristics in Spontaneous Dwarf Rats

PubMed Central

Andersen, Monica L; Lee, Kil S; Guindalini, Camila; Leite, Waldemarks A; Bignotto, Magda; Tufik, Sergio

2009-01-01

Spontaneous dwarf rats are a useful experimental model for studying various biologic events associated with pituitary dwarfism. Dwarf rats occurred serendipitously in our colony of Wistar rats during experimental breeding. This study aimed to describe the sleep pattern and physiologic characteristics of these rats compared with normal-sized adult rats. Because growth hormone can attenuate the upregulation of ceruloplasmin expression caused by acute inflammation, we also assessed the basal levels of serum ceruloplasmin in these animals. At 90 d of age, body weight and length were significantly lower in dwarf rats relative to normal rats. Dwarves had lower concentrations of serum testosterone and growth hormone, but progesterone was unchanged. Corticosterone levels did not differ between groups. During the light period, the percentage of sleep time recorded and duration of slow-wave sleep did not differ between groups. However, compared with controls, dwarf rats had marked fragmentation of sleep and less paradoxical sleep. During the dark phase, sleep patterns in dwarf rats were within the normal range. Immunoblotting data showed that the levels of ceruloplasmin in serum were lower in dwarf rats. Our findings provide insight into pathologic processes related to growth hormone deficiency. PMID:19712574

BDNF in sleep, insomnia, and sleep deprivation.

PubMed

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

2016-01-01

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

Apparatus, system and method for providing cryptographic key information with physically unclonable function circuitry

DOEpatents

Areno, Matthew

2015-12-08

Techniques and mechanisms for providing a value from physically unclonable function (PUF) circuitry for a cryptographic operation of a security module. In an embodiment, a cryptographic engine receives a value from PUF circuitry and based on the value, outputs a result of a cryptographic operation to a bus of the security module. The bus couples the cryptographic engine to control logic or interface logic of the security module. In another embodiment, the value is provided to the cryptographic engine from the PUF circuitry via a signal line which is distinct from the bus, where any exchange of the value by either of the cryptographic engine and the PUF circuitry is for communication of the first value independent of the bus.

Short- and Long-Term Sleep Stability in Insomniacs and Healthy Controls.

PubMed

Gaines, Jordan; Vgontzas, Alexandros N; Fernandez-Mendoza, Julio; Basta, Maria; Pejovic, Slobodanka; He, Fan; Bixler, Edward O

2015-11-01

Assess the short- and long-term stability of sleep duration in patients with insomnia and normal-sleeping controls. Observational short-term and prospective studies. Sleep laboratory. Patients with insomnia (n = 150) and controls (n = 151) were recruited from the local community or sleep disorders clinic. A subsample of 95 men from the Penn State Adult Cohort (PSAC) were followed up 2.6 y after their initial visit. Participants underwent a physical examination and 8-h polysomnography (PSG) recording for 3 consecutive nights (controls and insomniacs), or 2 single nights separated by several years (PSAC). Intraclass correlation coefficients (ICCs) assessed the stability of the variables total sleep time (TST), sleep onset latency (SOL), and wake after sleep onset (WASO). We also examined persistence of the first-night classification of "short" versus "normal" sleep duration on subsequent nights. Stability of TST, SOL, and WASO based on 1 night were slight to moderate in both patients with insomnia (ICC = 0.37-0.57) and controls (ICC = 0.39-0.59), and became substantial to almost perfect when based on the average of 3 nights (ICC = 0.64-0.81). We observed similar degrees of stability for TST and WASO in the longitudinal sample, with moderate stability based on a single night and substantial stability based on both nights. In examining the persistence of "short" and "normal" sleep duration, 71.4% (controls), 74.7% (patients with insomnia), and 72.6% (longitudinal sample) of participants retained their first-night classifications over subsequent nights. Sleep duration variables, particularly total sleep time based on 3 consecutive nights in both patients with insomnia and controls or two single-night recordings separated by several years, are stable and reflect a person's habitual sleep. Furthermore, a single night in the laboratory may be useful for reliably classifying one's sleep duration. © 2015 Associated Professional Sleep Societies, LLC.

Effects of Antidepressants on Sleep.

PubMed

Wichniak, Adam; Wierzbicka, Aleksandra; Walęcka, Małgorzata; Jernajczyk, Wojciech

2017-08-09

The aim of this review article was to summarize recent publications on effects of antidepressants on sleep and to show that these effects not only depend on the kind of antidepressant drugs but are also related to the dose, the time of drug administration, and the duration of the treatment. Complaints of disrupted sleep are very common in patients suffering from depression, and they are listed among diagnostic criteria for this disorder. Moreover, midnocturnal insomnia is the most frequent residual symptom of depression. Thus, all antidepressants should normalize sleep. However, at least in short-term treatment, many antidepressants with so-called activating effects (e.g. fluoxetine, venlafaxine) may disrupt sleep, while others with sedative properties (e.g., doxepin, mirtazapine, trazodone) rapidly improve sleep, but may cause problems in long-term treatment due to oversedation.For sleep-promoting action, the best effects can frequently be achieved with a very low dose, administered early enough before bedtime and importantly, always as a part of more complex interventions based on the cognitive-behavioral protocol to treat insomnia (CBT-I). For successful treatment of depression, it is necessary to understand the effects of antidepressants on sleep. Each physician should also be aware that some antidepressants may worsen or induce primary sleep disorders like restless legs syndrome, sleep bruxism, REM sleep behavior disorder, nightmares, and sleep apnea, which may result from an antidepressant-induced weight gain.

Sleep and bodily functions: the physiological interplay between body homeostasis and sleep homeostasis.

PubMed

Amici, R; Bastianini, S; Berteotti, C; Cerri, M; Del Vecchio, F; Lo Martire, V; Luppi, M; Perez, E; Silvani, A; Zamboni, G; Zoccoli, G

2014-01-01

Body homeostasis and sleep homeostasis may both rely on the complex integrative activity carried out by the hypothalamus. Thus, the three main wake-sleep (WS) states (i.e. wakefulness, NREM sleep, and REM sleep) may be better understood if the different cardio-respiratory and metabolic parameters, which are under the integrated control of the autonomic and the endocrine systems, are studied during sleep monitoring. According to this view, many physiological events can be considered as an expression of the activity that physiological regulations should perform in order to cope with the need to fulfill body and sleep homeostasis. This review is aimed at making an assessment of data showing the existence of a physiological interplay between body homeostasis and sleep homeostasis, starting from the spontaneous changes observed in the somatic and autonomic activity during sleep, through evidence showing the deep changes occurring in the central integration of bodily functions during the different WS states, to the changes in the WS states observed when body homeostasis is challenged by the external environment and when the return to normal ambient conditions allows sleep homeo- stasis to run without apparent physiological restrictions. The data summarized in this review suggest that an approach to the dichotomy between NREM and REM sleep based on physiological regulations may offer a framework within which observations that a traditional behavioral approach may overlook can be interpreted. The study of the interplay between body and sleep homeostasis appears, therefore, to be a way to understand the function of complex organisms beyond that of the specific regulations.

Obstructive sleep apnea and sedation in the endoscopy suite.

PubMed

Moos, Daniel D

2006-01-01

Patients with obstructive sleep apnea are at risk of mortality and morbidity related to the administration of sedatives, anesthetics, and opioids. Commonly employed sedatives and analgesics promote pharyngeal collapse and alter normal respiratory responses to obstruction and apnea. Literature concerning patients with obstructive sleep apnea undergoing moderate and deep sedation in the endoscopy suite is lacking. The purpose of this article is to provide the reader with a review of normal airway patency, the effects of obstructive sleep apnea on airway patency, and the impact that analgesics and sedatives may impart on the airway of patients with obstructive sleep apnea. The goal of this article is to increase awareness, stimulate discussions within the gastroenterological community, and encourage research regarding sedation in this at-risk population.

A neural circuitry that emphasizes spinal feedback generates diverse behaviours of human locomotion

PubMed Central

Song, Seungmoon; Geyer, Hartmut

2015-01-01

Neural networks along the spinal cord contribute substantially to generating locomotion behaviours in humans and other legged animals. However, the neural circuitry involved in this spinal control remains unclear. We here propose a specific circuitry that emphasizes feedback integration over central pattern generation. The circuitry is based on neurophysiologically plausible muscle-reflex pathways that are organized in 10 spinal modules realizing limb functions essential to legged systems in stance and swing. These modules are combined with a supraspinal control layer that adjusts the desired foot placements and selects the leg that is to transition into swing control during double support. Using physics-based simulation, we test the proposed circuitry in a neuromuscular human model that includes neural transmission delays, musculotendon dynamics and compliant foot–ground contacts. We find that the control network is sufficient to compose steady and transitional 3-D locomotion behaviours including walking and running, acceleration and deceleration, slope and stair negotiation, turning, and deliberate obstacle avoidance. The results suggest feedback integration to be functionally more important than central pattern generation in human locomotion across behaviours. In addition, the proposed control architecture may serve as a guide in the search for the neurophysiological origin and circuitry of spinal control in humans. PMID:25920414

Auditory input modulates sleep: an intra-cochlear-implanted human model.

PubMed

Velluti, Ricardo A; Pedemonte, Marisa; Suárez, Hámlet; Bentancor, Claudia; Rodríguez-Servetti, Zulma

2010-12-01

To properly demonstrate the effect of auditory input on sleep of intra-cochlear-implanted patients, the following approach was developed. Four implanted deaf patients were recorded during four nights: two nights with the implant OFF, with no auditory input, and two nights with the implant ON, that is, with normal auditory input, being only the common night sounds present, without any additional auditory stimuli delivered. The sleep patterns of another five deaf people were used as controls, exhibiting normal sleep organization. Moreover, the four experimental patients with intra-cochlear devices and the implant OFF also showed normal sleep patterns. On comparison of the night recordings with the implant ON and OFF, a new sleep organization was observed for the recordings with the implant ON, suggesting that brain plasticity may produce changes in the sleep stage percentages while maintaining the ultradian rhythm. During sleep with the implant ON, the analysis of the electroencephalographic delta, theta and alpha bands in the frequency domain, using the Fast Fourier Transform, revealed a diversity of changes in the power originated in the contralateral cortical temporal region. Different power shifts were observed, perhaps related to the exact position of the implant inside the cochlea and the scalp electrode location. In conclusion, this pilot study shows that the auditory input in humans can introduce changes in central nervous system activity leading to shifts in sleep characteristics, as previously demonstrated in guinea pigs. We are postulating that an intra-cochlear-implanted deaf patient may have a better recovery if the implant is maintained ON during the night, that is, during sleep. © 2010 European Sleep Research Society.

Neural Circuitry of Impaired Emotion Regulation in Substance Use Disorders

PubMed Central

Wilcox, Claire E.; Pommy, Jessica M.; Adinoff, Bryon

2016-01-01

Impaired emotion regulation contributes to the development and severity of substance use disorders (substance disorders). This review summarizes the literature on alterations in emotion regulation neural circuitry in substance disorders, particularly in relation to disorders of negative affect (without substance disorder), and it presents promising areas of future research. Emotion regulation paradigms during functional magnetic resonance imaging are conceptualized into four dimensions: affect intensity and reactivity, affective modulation, cognitive modulation, and behavioral control. The neural circuitry associated with impaired emotion regulation is compared in individuals with and without substance disorders, with a focus on amygdala, insula, and prefrontal cortex activation and their functional and structural connectivity. Hypoactivation of the rostral anterior cingulate cortex/ventromedial prefrontal cortex (rACC/vmPFC) is the most consistent finding across studies, dimensions, and clinical populations (individuals with and without substance disorders). The same pattern is evident for regions in the cognitive control network (anterior cingulate and dorsal and ventrolateral prefrontal cortices) during cognitive modulation and behavioral control. These congruent findings are possibly related to attenuated functional and/or structural connectivity between the amygdala and insula and between the rACC/vmPFC and cognitive control network. Although increased amygdala and insula activation is associated with impaired emotion regulation in individuals without substance disorders, it is not consistently observed in substance disorders. Emotion regulation disturbances in substance disorders may therefore stem from impairments in prefrontal functioning, rather than excessive reactivity to emotional stimuli. Treatments for emotion regulation in individuals without substance disorders that normalize prefrontal functioning may offer greater efficacy for substance disorders

Associations between insomnia, sleep duration and poor work ability.

PubMed

Lian, Yulong; Xiao, Jing; Liu, Yan; Ning, Li; Guan, Suzhen; Ge, Hua; Li, Fuye; Liu, Jiwen

2015-01-01

The aim of this study was to examine the independent and joint effect of insomnia and objective sleep duration on poor work ability. In this cross-sectional study, a total of 2820 Chinese manufacturing workers were categorized as insomnia patients and individuals with normal sleeping pattern by interview according to DSM-IV criteria. Sleep duration was classified into four categories: ≥7h, 6-7h, 5-6h, and <5h according to objective sleep duration of Watch-PAT-200 test. Work ability was assessed using the Chinese Work Ability Index (WAI) questionnaire. Regression analysis examined the independent and joint association of sleep duration and insomnia with poor work ability, after adjusting for various confounding factors. Insomnia and objective short sleep duration were both independently associated with poor work ability. Compared with the normal sleeping and ≥7h sleep duration group, the highest risk of poor work ability was in the insomnia patients with <5h sleep duration [odds ratio (OR) 3.43, 95% confidence interval (CI) 1.87-5.23], followed by the individuals with insomnia who slept 5-6h (OR 2.03, 95% CI 1.42-2.67). Insomnia and sleep duration in workers are both separately and together associated with increased risk of poor work ability. Objective sleep duration should be taken into consideration when assessing the work ability of people with insomnia. Copyright © 2014 Elsevier Inc. All rights reserved.

Direct Activation of Sleep-Promoting VLPO Neurons by Volatile Anesthetics Contributes to Anesthetic Hypnosis

PubMed Central

Moore, Jason T; Chen, Jingqiu; Han, Bo; Meng, Qing Cheng; Veasey, Sigrid C; Beck, Sheryl G; Kelz, Max B

2013-01-01

Summary Background Despite seventeen decades of continuous clinical use, the neuronal mechanisms through which volatile anesthetics act to produce unconsciousness remain obscure. One emerging possibility is that anesthetics exert their hypnotic effects by hijacking endogenous arousal circuits. A key sleep-promoting component of this circuitry is the ventrolateral preoptic nucleus (VLPO), a hypothalamic region containing both state-independent neurons and neurons that preferentially fire during natural sleep. Results Using c-Fos immunohistochemistry as a biomarker for antecedent neuronal activity, we show that isoflurane and halothane increase the number of active neurons in the VLPO, but only when mice are sedated or unconscious. Destroying VLPO neurons produces an acute resistance to isoflurane-induced hypnosis. Electrophysiological studies prove that the neurons depolarized by isoflurane belong to the subpopulation of VLPO neurons responsible for promoting natural sleep, while neighboring non-sleep-active VLPO neurons are unaffected by isoflurane. Finally, we show that this anesthetic-induced depolarization is not solely due to a presynaptic inhibition of wake-active neurons as previously hypothesized, but rather is due to a direct postsynaptic effect on VLPO neurons themselves arising from the closing of a background potassium conductance. Conclusions Cumulatively, this work demonstrates that anesthetics are capable of directly activating endogenous sleep-promoting networks and that such actions contribute to their hypnotic properties. PMID:23103189

Direct activation of sleep-promoting VLPO neurons by volatile anesthetics contributes to anesthetic hypnosis.

PubMed

Moore, Jason T; Chen, Jingqiu; Han, Bo; Meng, Qing Cheng; Veasey, Sigrid C; Beck, Sheryl G; Kelz, Max B

2012-11-06

Despite seventeen decades of continuous clinical use, the neuronal mechanisms through which volatile anesthetics act to produce unconsciousness remain obscure. One emerging possibility is that anesthetics exert their hypnotic effects by hijacking endogenous arousal circuits. A key sleep-promoting component of this circuitry is the ventrolateral preoptic nucleus (VLPO), a hypothalamic region containing both state-independent neurons and neurons that preferentially fire during natural sleep. Using c-Fos immunohistochemistry as a biomarker for antecedent neuronal activity, we show that isoflurane and halothane increase the number of active neurons in the VLPO, but only when mice are sedated or unconscious. Destroying VLPO neurons produces an acute resistance to isoflurane-induced hypnosis. Electrophysiological studies prove that the neurons depolarized by isoflurane belong to the subpopulation of VLPO neurons responsible for promoting natural sleep, whereas neighboring non-sleep-active VLPO neurons are unaffected by isoflurane. Finally, we show that this anesthetic-induced depolarization is not solely due to a presynaptic inhibition of wake-active neurons as previously hypothesized but rather is due to a direct postsynaptic effect on VLPO neurons themselves arising from the closing of a background potassium conductance. Cumulatively, this work demonstrates that anesthetics are capable of directly activating endogenous sleep-promoting networks and that such actions contribute to their hypnotic properties. Copyright © 2012 Elsevier Ltd. All rights reserved.

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.

The Social Patterning of Sleep in African Americans: Associations of Socioeconomic Position and Neighborhood Characteristics with Sleep in the Jackson Heart Study.

PubMed

Johnson, Dayna A; Lisabeth, Lynda; Hickson, DeMarc; Johnson-Lawrence, Vicki; Samdarshi, Tandaw; Taylor, Herman; Diez Roux, Ana V

2016-09-01

We investigated cross-sectional associations of individual-level socioeconomic position (SEP) and neighborhood characteristics (social cohesion, violence, problems, disadvantage) with sleep duration and sleep quality in 5,301 African Americans in the Jackson Heart Study. All measures were self-reported. Sleep duration was assessed as hours of sleep; sleep quality was reported as poor (1) to excellent (5). SEP was measured by categorized years of education and income. Multinomial logistic and linear regression models were fit to examine the associations of SEP and neighborhood characteristics (modeled dichotomously and tertiles) with sleep duration (short vs. normal, long vs. normal) and continuous sleep duration and quality after adjustment for demographics and risk factors. The mean sleep duration was 6.4 ± 1.5 hours, 54% had a short (≤ 6 h) sleep duration, 5% reported long (≥ 9 h) sleep duration, and 24% reported fair to poor sleep quality. Lower education was associated with greater odds of long sleep (odds ratio [OR] = 2.19, 95% confidence interval [CI] = 1.42, 3.38) and poorer sleep quality (β = -0.17, 95% CI = -0.27, -0.07) compared to higher education after adjustment for demographics and risk factors. Findings were similar for income. High neighborhood violence was associated with shorter sleep duration (-9.82 minutes, 95% CI = -16.98, -2.66) and poorer sleep quality (β = -0.11, 95% CI = -0.20, 0.00) after adjustment for demographics and risk factors. Results were similar for neighborhood problems. In secondary analyses adjusted for depressive symptoms in a subset of participants, most associations were attenuated and only associations of low SEP with higher odds of long sleep and higher neighborhood violence with poorer sleep quality remained statistically significant. Social and environmental characteristics are associated with sleep duration and quality in African Americans. Depressive symptoms may explain at least part of this association. �

A new view of “dream enactment” in REM sleep behavior disorder

PubMed Central

Blumberg, Mark S.; Plumeau, Alan M.

2015-01-01

SUMMARY REM sleep behavior disorder (RBD) is a disorder in which patients exhibit increased muscle tone and exaggerated myoclonic twitching during REM sleep. In addition, violent movements of the limbs, and complex behaviors that can sometimes appear to involve the enactment of dreams, are associated with RBD. These behaviors are widely thought to result from a dysfunction involving atonia-producing neural circuitry in the brainstem, thereby unmasking cortically generated dreams. Here we scrutinize the assumptions that led to this interpretation of RBD. In particular, we challenge the assumption that motor cortex produces twitches during REM sleep, thus calling into question the related assumption that motor cortex is primarily responsible for all of the pathological movements of RBD. Moreover, motor cortex is not even necessary to produce complex behavior; for example, stimulation of some brainstem structures can produce defensive and aggressive behaviors in rats and monkeys that are striking similar to those reported in human patients with RBD. Accordingly, we suggest an interpretation of RBD that focuses increased attention on the brainstem as a source of the pathological movements and that considers sensory feedback from moving limbs as an important influence on the content of dream mentation. PMID:26802823

DSM-5 Insomnia and Short Sleep: Comorbidity Landscape and Racial Disparities

PubMed Central

Kalmbach, David A.; Pillai, Vivek; Arnedt, J. Todd; Drake, Christopher L.

2016-01-01

Study Objectives: We estimated rates of cardiometabolic disease, pain conditions, and psychiatric illness associated with Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) insomnia disorder (current and in remission) and habitual short sleep (fewer than 6 h), and examined the roles of insomnia and short sleep in racial disparities in disease burden between black and non-Hispanic white Americans. Methods: This epidemiological survey study was cross-sectional. The community-based sample consisted of 3,911 subjects (46.0 y ± 13.3; 65.4% female; 25.0% black) across six sleep groups based on DSM-5 insomnia classification (never vs. remitted vs. current) and self-reported habitual sleep duration (normal vs. short). Vascular events, cardiometabolic disease, pain conditions, and psychiatric symptoms were self-reported. Results: Short sleeping insomniacs were at elevated risk for myocardial infarction, stroke, treated hypertension, diabetes, chronic pain, back pain, depression, and anxiety, independent of sex, age, and obesity. Morbidity profiles for insomniacs with normal sleep duration and former insomniacs, irrespective of sleep duration, were similar with elevations in treated hypertension, chronic pain, depression, and anxiety. Regarding racial disparities, cardiometabolic and psychiatric illness burden was greater for blacks, who were more likely to have short sleep and the short sleep insomnia phenotype. Evidence suggested that health disparities may be attributable in part to race-related differences in sleep. Conclusions: Insomnia disorder with short sleep is the most severe phenotype of insomnia and comorbid with many cardiometabolic and psychiatric illnesses, whereas morbidity profiles are highly similar between insomniacs with normal sleep duration and former insomniacs. Short sleep endemic to black Americans increases risk for the short sleep insomnia phenotype and likely contributes to racial disparities in cardiometabolic disease

The relationship between complaints of night-time heartburn and sleep-related gastroesophageal reflux.

PubMed

Orr, W C; Goodrich, S; Estep, M E; Shepherd, K

2014-01-01

This study investigated whether the complaint of night-time heartburn (NHB) as opposed to daytime heartburn (DHB) is a reliable reflection of actual sleep-related reflux events. Three groups of individuals were studied: individuals with complaints of NHB at least twice per week (n = 24), individuals with complaints of DHB (n = 23), and normal participants without any complaints of regular heartburn during the day or night (n = 25). All three groups were studied on one occasion with combined pH monitoring and polysomnography, and subjective questionnaires about sleep disturbance and sleep quality were given to all participants. The NHB group had significantly more sleep-related reflux events compared with both DHB and control groups (P < 0.01). DHB subjects had significantly (P < 0.05) more sleep-related reflux events than normal controls. Total acid contact time (ACT) was significantly (P < 0.05) elevated in the NHB group compared with both the DHB and control group. Sleep-related ACT was also significantly (P < 0.05) elevated in the NHB group compared with the other two groups, while upright (daytime) ACT was not significantly different. The NHB group was significantly (P < 0.05) worse regarding measures of both objective and subjective sleep quality. Subjects with exclusively DHB do have sleep-related reflux that is greater than normal controls. Subjects with NHB have significantly more sleep-related reflux, and both objective and subjective sleep abnormalities compared with normal controls. Complaints of NHB reflect sleep-related reflux events and may be indicative of a more clinically significant condition. © 2013 Wiley Periodicals, Inc. and the International Society for Diseases of the Esophagus.

Abnormal sleep/wake dynamics in orexin knockout mice.

PubMed

Diniz Behn, Cecilia G; Klerman, Elizabeth B; Mochizuki, Takatoshi; Lin, Shih-Chieh; Scammell, Thomas E

2010-03-01

Narcolepsy with cataplexy is caused by a loss of orexin (hypocretin) signaling, but the physiologic mechanisms that result in poor maintenance of wakefulness and fragmented sleep remain unknown. Conventional scoring of sleep cannot reveal much about the process of transitioning between states or the variations within states. We developed an EEG spectral analysis technique to determine whether the state instability in a mouse model of narcolepsy reflects abnormal sleep or wake states, faster movements between states, or abnormal transitions between states. We analyzed sleep recordings in orexin knockout (OXKO) mice and wild type (WT) littermates using a state space analysis technique. This non-categorical approach allows quantitative and unbiased examination of sleep/wake states and state transitions. OXKO mice spent less time in deep, delta-rich NREM sleep and in active, theta-rich wake and instead spent more time near the transition zones between states. In addition, while in the midst of what should be stable wake, OXKO mice initiated rapid changes into NREM sleep with high velocities normally seen only in transition regions. Consequently, state transitions were much more frequent and rapid even though the EEG progressions during state transitions were normal. State space analysis enables visualization of the boundaries between sleep and wake and shows that narcoleptic mice have less distinct and more labile states of sleep and wakefulness. These observations provide new perspectives on the abnormal state dynamics resulting from disrupted orexin signaling and highlight the usefulness of state space analysis in understanding narcolepsy and other sleep disorders.

Vestibular vertigo is associated with abnormal sleep duration.

PubMed

Albathi, Monirah; Agrawal, Yuri

2017-01-01

Several small studies in animals and humans have suggested a relationship between vestibular function and sleep. In this study, we evaluate the association between vestibular vertigo and sleep duration in a large, representative sample of US adults. We used data from the National Health Interview Survey, which administered a Balance Supplement in 2008 in a sample of 20,950 adult respondents. We evaluated the cross-sectional association between vestibular vertigo (based on a well-validated definition) and sleep duration (defined as short <6 hours, normal 6-8 hours, and long >8 hours). We performed multiple and multinomial logistic regression analyses to estimate the odds ratio and relative risk ratio (RRR) of impaired sleep duration compared to normal sleep duration associated with vestibular vertigo. Analyses were adjusted for demographic, lifestyle and health behavior characteristics as well as relevant comorbid conditions. Thirty percent of individuals with vestibular vertigo reported abnormal sleep duration (15.5% short duration and 14.8% long duration). In adjusted analyses, individuals with vestibular vertigo had a 1.75 (95% CI 1.45-2.11) RRR of having short sleep duration compared to individuals without vestibular vertigo, and a 1.55 (95% CI 1.26-1.91) RRR of having long sleep duration compared to individuals without vestibular vertigo. This study presents epidemiologic evidence to support the association between vestibular function and sleep duration. Individuals with vestibular vertigo had a higher RRR for abnormally short or long sleep duration. Further work is needed to evaluate the causal direction(s) of this association.

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.

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

PubMed

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

2012-01-01

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

CONTROL OF SLEEP AND WAKEFULNESS

PubMed Central

Brown, Ritchie E.; Basheer, Radhika; McKenna, James T.; Strecker, Robert E.; McCarley, Robert W.

2013-01-01

This review summarizes the brain mechanisms controlling sleep and wakefulness. Wakefulness promoting systems cause low-voltage, fast activity in the electroencephalogram (EEG). Multiple interacting neurotransmitter systems in the brain stem, hypothalamus, and basal forebrain converge onto common effector systems in the thalamus and cortex. Sleep results from the inhibition of wake-promoting systems by homeostatic sleep factors such as adenosine and nitric oxide and GABAergic neurons in the preoptic area of the hypothalamus, resulting in large-amplitude, slow EEG oscillations. Local, activity-dependent factors modulate the amplitude and frequency of cortical slow oscillations. Non-rapid-eye-movement (NREM) sleep results in conservation of brain energy and facilitates memory consolidation through the modulation of synaptic weights. Rapid-eye-movement (REM) sleep results from the interaction of brain stem cholinergic, aminergic, and GABAergic neurons which control the activity of glutamatergic reticular formation neurons leading to REM sleep phenomena such as muscle atonia, REMs, dreaming, and cortical activation. Strong activation of limbic regions during REM sleep suggests a role in regulation of emotion. Genetic studies suggest that brain mechanisms controlling waking and NREM sleep are strongly conserved throughout evolution, underscoring their enormous importance for brain function. Sleep disruption interferes with the normal restorative functions of NREM and REM sleep, resulting in disruptions of breathing and cardiovascular function, changes in emotional reactivity, and cognitive impairments in attention, memory, and decision making. PMID:22811426

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

Future Directions in Sleep and Developmental Psychopathology.

PubMed

Meltzer, Lisa J

2017-01-01

It is critical for psychologists to gain a better understanding about the intersection between sleep and developmental psychopathology. However, while many strive to answer the question of whether sleep causes developmental psychopathology, or vice versa, ultimately the relationship between sleep and developmental psychopathology is complex and dynamic. This article considers future directions in the field of clinical child and adolescent psychology that go beyond this mechanistic question, highlighting areas important to address for clinicians and researchers who strive to better understand how best to serve children and adolescents with developmental psychopathology. Questions are presented about what is normal in terms of sleep across development, the role of individual variability in terms of sleep needs and vulnerability to sleep loss, and how sleep may serve as a risk or resilience factor for developmental psychopathology, concluding with considerations for interventions.

Restricted sleep and negative affective states in commercial pilots during short haul operations.

PubMed

Drury, D Arthur; Ferguson, Sally A; Thomas, Matthew J W

2012-03-01

This study aims to investigate (1) the relationship between restricted sleep and Heightened Emotional Activity (HEA) during normal flight operations, and (2) whether sleep patterns influence the strength of the HEA as a response to threats. Accident investigation reports continue to highlight the relationship between restricted sleep and poor safety outcomes. However, to date we have a limited understanding of how sleep and HEA interact. A total of 302 sectors of normal airline flight operations were observed by trained observers, and instances of heightened emotional activity were recorded. During the cruise phase of each of these sectors, crew members were asked to calculate the amount of sleep they had obtained in previous 24 and 48 h. In the 302 sectors of normal flight operations, 535 instances of HEA were observed. Descriptive analyses of instances of HEA and sleep in the prior 24 and 48 h showed a significant relationship between the occurrence of HEA and recent sleep. The relationship between restricted sleep and HEA suggests that there may well be further implications with respect to operational safety. Copyright © 2011 Elsevier Ltd. All rights reserved.

Long-term oscillations in the sleep/wake cycle of infants

NASA Astrophysics Data System (ADS)

Diambra, L.; Malta, C. P.; Capurro, A.

2009-11-01

The development of circadian sleep-wakefulness rhythm was investigated by a longitudinal study of six normal infants. We propose an entropy based measure for the sleep/wake cycle fragmentation. Our results confirm that the sleep/wake cycle fragmentation and the sleep/wake ratio decrease, while the circadian power increases during the maturation process of infants. In addition to these expected linear trends in the variables devised to quantify sleep consolidation, circadian power and sleep/wake ratio, we found that they present infradian rhythms in the monthly range.

Sleep quality and arousal in migraine and tension-type headache: the headache-sleep study.

PubMed

Engstrøm, M; Hagen, K; Bjørk, M H; Stovner, L J; Sand, T

2014-01-01

The present paper summarizes and compares data from our studies on subjective and objective sleep quality and pain thresholds in tension-type headache (TTH), migraine, and controls. In a blinded controlled explorative study, we recorded polysomnography (PSG) and pressure, heat, and cold pain thresholds in 34 controls, 20 TTH, and 53 migraine patients. Sleep quality was assessed by questionnaires, sleep diaries, and PSG. Migraineurs who had their recordings more than 2 days from an attack were classified as interictal while the rest were classified as either preictal or postictal. Interictal migraineurs (n=33) were also divided into two groups if their headache onsets mainly were during sleep and awakening (sleep migraine, SM), or during daytime and no regular onset pattern (non-sleep migraine, NSM). TTH patients were divided into a chronic or episodic group according to headache days per month. Compared to controls, all headache groups reported more anxiety and sleep-related symptoms. TTH and NSM patients reported more daytime tiredness and tended to have lower pain thresholds. Despite normal sleep times in diary, TTH and NSM had increased slow-wave sleep as seen after sleep deprivation. Migraineurs in the preictal phase had shorter latency to sleep onset than controls. Except for a slight but significantly increased awakening index SM, patients differed little from controls in objective measurements. We hypothesize that TTH and NSM patients on the average need more sleep than healthy controls. SM patients seem more susceptible to sleep disturbances. Inadequate rest might be an attack-precipitating- and hyperalgesia-inducing factor. © 2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.

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

Sleep-Dependent Consolidation of Procedural Motor Memories in Children and Adults: The Pre-Sleep Level of Performance Matters

ERIC Educational Resources Information Center

Wilhelm, Ines; Metzkow-Meszaros, Maila; Knapp, Susanne; Born, Jan

2012-01-01

In striking contrast to adults, in children sleep following training a motor task did not induce the expected (offline) gain in motor skill performance in previous studies. Children normally perform at distinctly lower levels than adults. Moreover, evidence in adults suggests that sleep dependent offline gains in skill essentially depend on the…

Abnormal Sleep/Wake Dynamics in Orexin Knockout Mice

PubMed Central

Diniz Behn, Cecilia G.; Klerman, Elizabeth B.; Mochizuki, Takatoshi; Lin, Shih-Chieh; Scammell, Thomas E.

2010-01-01

Study Objectives: Narcolepsy with cataplexy is caused by a loss of orexin (hypocretin) signaling, but the physiologic mechanisms that result in poor maintenance of wakefulness and fragmented sleep remain unknown. Conventional scoring of sleep cannot reveal much about the process of transitioning between states or the variations within states. We developed an EEG spectral analysis technique to determine whether the state instability in a mouse model of narcolepsy reflects abnormal sleep or wake states, faster movements between states, or abnormal transitions between states. Design: We analyzed sleep recordings in orexin knockout (OXKO) mice and wild type (WT) littermates using a state space analysis technique. This non-categorical approach allows quantitative and unbiased examination of sleep/wake states and state transitions. Measurements and Results: OXKO mice spent less time in deep, delta-rich NREM sleep and in active, theta-rich wake and instead spent more time near the transition zones between states. In addition, while in the midst of what should be stable wake, OXKO mice initiated rapid changes into NREM sleep with high velocities normally seen only in transition regions. Consequently, state transitions were much more frequent and rapid even though the EEG progressions during state transitions were normal. Conclusions: State space analysis enables visualization of the boundaries between sleep and wake and shows that narcoleptic mice have less distinct and more labile states of sleep and wakefulness. These observations provide new perspectives on the abnormal state dynamics resulting from disrupted orexin signaling and highlight the usefulness of state space analysis in understanding narcolepsy and other sleep disorders. Citation: Diniz Behn CG; Klerman EB; Mochizuki T; Lin S; Scammell TE. Abnormal sleep/wake dynamics in orexin knockout mice. SLEEP 2010;33(3):297-306. PMID:20337187

Association of sleep impairments and gastrointestinal disorders in the context of the visceral theory of sleep.

PubMed

Pigarev, Ivan N; Pigareva, Marina L

2017-01-01

It was noticed long ago that sleep disorders or interruptions to the normal sleep pattern were associated with various gastrointestinal disorders. We review the studies which established the causal link between these disorders and sleep impairment. However, the mechanism of interactions between the quality of sleep and gastrointestinal pathophysiology remained unclear. Recently, the visceral theory of sleep was formulated. This theory proposes that the same brain structures, and particularly the same cortical sensory areas, which in wakefulness are involved in processing of the exteroceptive information, switch during sleep to the processing of information coming from various visceral systems. We review the studies which demonstrated that neurons of the various cortical areas (occipital, parietal, frontal) during sleep began to fire in response to activation coming from the stomach and small intestine. These data demonstrate that, during sleep, the computational power of the central nervous system, including all cortical areas, is engaged in restoration of visceral systems. Thus, the general mechanism of the interaction between quality of sleep and health became clear.

Biotelemetry and computer analysis of sleep processes on earth and in space.

NASA Technical Reports Server (NTRS)

Adey, W. R.

1972-01-01

Developments in biomedical engineering now permit study of states of sleep, wakefulness, and focused attention in man exposed to rigorous environments, including aerospace flight. These new sensing devices, data acquisition systems, and computational methods have also been extensively applied to clinical problems of disordered sleep. A 'library' of EEG data has been prepared for sleep in normal man, and characterized for its group features by computational analysis. Sleep in an astronaut in space flight has been examined for the first and second 'nights' of space flight. Normal 90-min cycles were detected during the second night. Sleep patterns in quadriplegic patients deprived of all sensory inputs below the neck have indicated major deviations.

DNA decorated carbon nanotube sensors on CMOS circuitry for environmental monitoring

NASA Astrophysics Data System (ADS)

Liu, Yu; Chen, Chia-Ling; Agarwal, V.; Li, Xinghui; Sonkusale, S.; Dokmeci, Mehmet R.; Wang, Ming L.

2010-04-01

Single-walled carbon nanotubes (SWNTs) with their large surface area, high aspect ratio are one of the novel materials which have numerous attractive features amenable for high sensitivity sensors. Several nanotube based sensors including, gas, chemical and biosensors have been demonstrated. Moreover, most of these sensors require off chip components to detect the variations in the signals making them complicated and hard to commercialize. Here we present a novel complementary metal oxide semiconductor (CMOS) integrated carbon nanotube sensors for portable high sensitivity chemical sensing applications. Multiple zincation steps have been developed to ascertain proper electrical connectivity between the carbon nanotubes and the foundry made CMOS circuitry. The SWNTs have been integrated onto (CMOS) circuitry as the feedback resistor of a Miller compensated operational amplifier utilizing low temperature Dielectrophoretic (DEP) assembly process which has been tailored to be compatible with the post-CMOS integration at the die level. Building nanotube sensors directly on commercial CMOS circuitry allows single chip solutions eliminating the need for long parasitic lines and numerous wire bonds. The carbon nanotube sensors realized on CMOS circuitry show strong response to various vapors including Dimethyl methylphosphonate and Dinitrotoluene. The remarkable set of attributes of the SWNTs realized on CMOS electronic chips provides an attractive platform for high sensitivity portable nanotube based bio and chemical sensors.

The Social Patterning of Sleep in African Americans: Associations of Socioeconomic Position and Neighborhood Characteristics with Sleep in the Jackson Heart Study

PubMed Central

Johnson, Dayna A.; Lisabeth, Lynda; Hickson, DeMarc; Johnson-Lawrence, Vicki; Samdarshi, Tandaw; Taylor, Herman; Diez Roux, Ana V.

2016-01-01

Study Objectives: We investigated cross-sectional associations of individual-level socioeconomic position (SEP) and neighborhood characteristics (social cohesion, violence, problems, disadvantage) with sleep duration and sleep quality in 5,301 African Americans in the Jackson Heart Study. Methods: All measures were self-reported. Sleep duration was assessed as hours of sleep; sleep quality was reported as poor (1) to excellent (5). SEP was measured by categorized years of education and income. Multinomial logistic and linear regression models were fit to examine the associations of SEP and neighborhood characteristics (modeled dichotomously and tertiles) with sleep duration (short vs. normal, long vs. normal) and continuous sleep duration and quality after adjustment for demographics and risk factors. Results: The mean sleep duration was 6.4 ± 1.5 hours, 54% had a short (≤ 6 h) sleep duration, 5% reported long (≥ 9 h) sleep duration, and 24% reported fair to poor sleep quality. Lower education was associated with greater odds of long sleep (odds ratio [OR] = 2.19, 95% confidence interval [CI] = 1.42, 3.38) and poorer sleep quality (β = −0.17, 95% CI = −0.27, −0.07) compared to higher education after adjustment for demographics and risk factors. Findings were similar for income. High neighborhood violence was associated with shorter sleep duration (−9.82 minutes, 95% CI = −16.98, −2.66) and poorer sleep quality (β = −0.11, 95% CI = −0.20, 0.00) after adjustment for demographics and risk factors. Results were similar for neighborhood problems. In secondary analyses adjusted for depressive symptoms in a subset of participants, most associations were attenuated and only associations of low SEP with higher odds of long sleep and higher neighborhood violence with poorer sleep quality remained statistically significant. Conclusions: Social and environmental characteristics are associated with sleep duration and quality in African Americans

The role of sleep on cognition and functional connectivity in patients with multiple sclerosis.

PubMed

van Geest, Quinten; Westerik, B; van der Werf, Y D; Geurts, J J G; Hulst, H E

2017-01-01

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.

Irregular sleep-wake syndrome

MedlinePlus

... loses its normal circadian cycle. People with changing work shifts and travelers who often change time zones may ... These people have a different condition, such as shift work sleep disorder or jet lag syndrome .

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

Automatic quadrature control and measuring system. [using optical coupling circuitry

NASA Technical Reports Server (NTRS)

Hamlet, J. F. (Inventor)

1974-01-01

A quadrature component cancellation and measuring system comprising a detection system for detecting the quadrature component from a primary signal, including reference circuitry to define the phase of the quadrature component for detection is described. A Raysistor optical coupling control device connects an output from the detection system to a circuit driven by a signal based upon the primary signal. Combining circuitry connects the primary signal and the circuit controlled by the Raysistor device to subtract quadrature components. A known current through the optically sensitive element produces a signal defining the magnitude of the quadrature component.

Mandible behaviour interpretation during wakefulness, sleep and sleep-disordered breathing.

PubMed

Maury, Gisèle; Senny, Frédéric; Cambron, Laurent; Albert, Adelin; Seidel, Laurence; Poirrier, Robert

2014-12-01

The mandible movement (MM) signal provides information on mandible activity. It can be read visually to assess sleep-wake state and respiratory events. This study aimed to assess (1) the training of independent scorers to recognize the signal specificities; (2) intrascorer reproducibility and (3) interscorer variability. MM was collected in the mid-sagittal plane of the face of 40 patients. The typical MM was extracted and classified into seven distinct pattern classes: active wakefulness (AW), quiet wakefulness or quiet sleep (QW/S), sleep snoring (SS), sleep obstructive events (OAH), sleep mixed apnea (MA), respiratory related arousal (RERA) and sleep central events (CAH). Four scorers were trained; their diagnostic capacities were assessed on two reading sessions. The intra- and interscorer agreements were assessed using Cohen's κ. Intrascorer reproducibility for the two sessions ranged from 0.68 [95% confidence interval (CI): 0.59-0.77] to 0.88 (95% CI: 0.82-0.94), while the between-scorer agreement amounted to 0.68 (95% CI: 0.65-0.71) and 0.74 (95% CI: 0.72-0.77), respectively. The overall accuracy of the scorers was 75.2% (range: 72.4-80.7%). CAH MMs were the most difficult to discern (overall accuracy 65.6%). For the two sessions, the recognition rate of abnormal respiratory events (OAH, CAH, MA and RERA) was excellent: the interscorer mean agreement was 90.7% (Cohen's κ: 0.83; 95% CI: 0.79-0.88). The discrimination of OAH, CAH, MA characteristics was good, with an interscorer agreement of 80.8% (Cohen's κ: 0.65; 95% CI: 0.62-0.68). Visual analysis of isolated MMs can successfully diagnose sleep-wake state, normal and abnormal respiration and recognize the presence of respiratory effort. © 2014 European Sleep Research Society.

Sleep spindle density in narcolepsy.

PubMed

Christensen, Julie Anja Engelhard; Nikolic, Miki; Hvidtfelt, Mathias; Kornum, Birgitte Rahbek; Jennum, Poul

2017-06-01

Patients with narcolepsy type 1 (NT1) show alterations in sleep stage transitions, rapid-eye-movement (REM) and non-REM sleep due to the loss of hypocretinergic signaling. However, the sleep microstructure has not yet been evaluated in these patients. We aimed to evaluate whether the sleep spindle (SS) density is altered in patients with NT1 compared to controls and patients with narcolepsy type 2 (NT2). All-night polysomnographic recordings from 28 NT1 patients, 19 NT2 patients, 20 controls (C) with narcolepsy-like symptoms, but with normal cerebrospinal fluid hypocretin levels and multiple sleep latency tests, and 18 healthy controls (HC) were included. Unspecified, slow, and fast SS were automatically detected, and SS densities were defined as number per minute and were computed across sleep stages and sleep cycles. The between-cycle trends of SS densities in N2 and NREM sleep were evaluated within and between groups. Between-group comparisons in sleep stages revealed no significant differences in any type of SS. Within-group analyses of the SS trends revealed significant decreasing trends for NT1, HC, and C between first and last sleep cycle. Between-group analyses of SS trends between first and last sleep cycle revealed that NT2 differ from NT1 patients in the unspecified SS density in NREM sleep, and from HC in the slow SS density in N2 sleep. SS activity is preserved in NT1, suggesting that the ascending neurons to thalamic activation of SS are not significantly affected by the hypocretinergic system. NT2 patients show an abnormal pattern of SS distribution. Copyright © 2017 Elsevier B.V. All rights reserved.

Memory Before and After Sleep in Patients with Moderate Obstructive Sleep Apnea

PubMed Central

Kloepfer, Corinna; Riemann, Dieter; Nofzinger, Eric A.; Feige, Bernd; Unterrainer, Josef; O'Hara, Ruth; Sorichter, Stephan; Nissen, Christoph

2009-01-01

Objective: The aim of this study was to investigate the effects of obstructive sleep apnea (OSA) on procedural and declarative memory encoding in the evening prior to sleep, on memory consolidation during subsequent sleep, and on retrieval in the morning after sleep. Methods: Memory performance (procedural mirror-tracing task, declarative visual and verbal memory task) and general neuropsychological performance were assessed before and after one night of polysomnographic monitoring in 15 patients with moderate OSA and 20 age-, sex-, and IQ-matched healthy subjects. Results: Encoding levels prior to sleep were similar across groups for all tasks. Conventional analyses of averaged mirror tracing performance suggested a significantly reduced overnight improvement in OSA patients. Single trial analyses, however, revealed that this effect was due to significantly flattened learning curves in the evening and morning session in OSA patients. OSA patients showed a significantly lower verbal retention rate and a non-significantly reduced visual retention rate after sleep compared to healthy subjects. Polysomnography revealed a significantly reduced REM density, increased frequency of micro-arousals, elevated apnea-hypopnea index, and subjectively disturbed sleep quality in OSA patients compared to healthy subjects. Conclusions: The results suggest that moderate OSA is associated with a significant impairment of procedural and verbal declarative memory. Future work is needed to further determine the contribution of structural or functional alterations in brain circuits relevant for memory, and to test whether OSA treatment improves or normalizes the observed deficits in learning. Citation: Kloepfer C; Riemann D; Nofzinger EA; Feige B; Unterrainer J; O'Hara R; Sorichter S; Nissen C. Memory before and after sleep in patients with moderate obstructive sleep apnea. J Clin Sleep Med 2009;5(6):540-548. PMID:20465021

Sleep abnormalities in children with Dravet syndrome.

PubMed

Dhamija, Radhika; Erickson, Maia K; St Louis, Erik K; Wirrell, Elaine; Kotagal, Suresh

2014-05-01

Mutations in the voltage-gated sodium channel SCN1A gene are responsible for the majority of Dravet syndrome cases. There is evidence that the Nav1.1 channel coded by the SCN1A gene is involved in sleep regulation. We evaluated sleep abnormalities in children with Dravet syndrome using nocturnal polysomnography. We identified six children at our institution with genetically confirmed Dravet syndrome who had also undergone formal sleep consultation with nocturnal polysomnography. Indications for polysomnography were parental concern of daytime fatigue or sleepiness, hyperactivity, inattention, disruptive behavior, nighttime awakenings, or nocturnal seizures. Sleep studies were scored according to guidelines of the American Academy of Sleep Medicine and non-rapid eye movement cyclic alternating pattern was visually identified and scored according to established methods. The mean age of the subjects at the time of polysomnography was 6 years. Standard polysomnography did not show any consistent abnormalities in the obstructive or central apnea index, arousal index, sleep efficiency, or architecture. Cyclic alternating pattern analysis on five patients showed an increased mean rate of 50.3% (vs 31% to 34% in neurological normal children) with a mild increase in A1 subtype of 89.4% (vs 84.5%). A2/A3 subtype (5.3% vs 7.3%) and B phase duration (22.4 vs 24.7 seconds) were similar to previously reported findings in neurologically normal children. Despite parental concerns for sleep disturbance in patients with Dravet syndrome, we could not identify abnormalities in sleep macroarchitecture. Non-rapid eye movement sleep microarchitecture was, however, abnormal, with increased A1 subtype, somewhat resembling a tracé alternant pattern of neonates and possibly suggestive of cortical synaptic immaturity in Dravet syndrome. Larger studies are needed to replicate these results. Copyright © 2014 Elsevier Inc. All rights reserved.

Sensitive Periods of Emotion Regulation: Influences of Parental Care on Frontoamygdala Circuitry and Plasticity

ERIC Educational Resources Information Center

Gee, Dylan G.

2016-01-01

Early caregiving experiences play a central role in shaping emotional development, stress physiology, and refinement of limbic circuitry. Converging evidence across species delineates a sensitive period of heightened neuroplasticity when frontoamygdala circuitry is especially amenable to caregiver inputs early in life. During this period, parental…

Cues of Fatigue: Effects of Sleep Deprivation on Facial Appearance

PubMed Central

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

2013-01-01

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

Circadian Rhythms, Sleep, and Disorders of Aging.

PubMed

Mattis, Joanna; Sehgal, Amita

2016-04-01

Sleep-wake cycles are known to be disrupted in people with neurodegenerative disorders. These findings are now supported by data from animal models for some of these disorders, raising the question of whether the disrupted sleep/circadian regulation contributes to the loss of neural function. As circadian rhythms and sleep consolidation also break down with normal aging, changes in these may be part of what makes aging a risk factor for disorders like Alzheimer's disease (AD). Mechanisms underlying the connection between circadian/sleep dysregulation and neurodegeneration remain unclear, but several recent studies provide interesting possibilities. While mechanistic analysis is under way, it is worth considering treatment of circadian/sleep disruption as a means to alleviate symptoms of neurodegenerative disorders. Copyright © 2016 Elsevier Ltd. All rights reserved.

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

PubMed

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

2013-09-01

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

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

PubMed Central

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

2012-01-01

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

Habitual short sleep impacts frontal switch mechanism in attention to novelty.

PubMed

Gumenyuk, Valentina; Roth, Thomas; Korzyukov, Oleg; Jefferson, Catherine; Bowyer, Susan; Drake, Christopher L

2011-12-01

Reduced time in bed relative to biological sleep need is common. The impact of habitual short sleep on auditory attention has not been studied to date. In the current study, we utilized novelty oddball tasks to evaluate the effect of habitual short sleep on brain function underlying attention control processes measured by the mismatch negativity (MMN, index of pre-attentive stage), P3a (attention-dependent), and P3b (memory-dependent) event related brain potentials (ERPs). An extended time in bed in a separate study was used to evaluate the possible reversal of the impairments of these processes in habitual short sleepers. Ten self-defined short sleepers (total sleep time [TST] ≤ 6 h) and 9 normal-sleeping subjects with TST 7-8 h, participated. ERPs were recorded via a 64-channel EEG system. Two test conditions: "ignore" and "attend" were implemented. The ERPs were analyzed and compared between groups on the 2 task conditions and frontal/central/parietal electrodes by 3-factor ANOVA. Sleep diary data were compared between groups by t-test. Sleep was recorded by the Zeo sleep monitoring system for a week in both habitual and extended sleep conditions at home. The main findings of the present study show that short sleeping individuals had deficiency in activity of the MMN and P3a brain responses over frontal areas compared to normal-sleeping subjects. The P3b amplitude was increased over frontal areas and decreased over parietal with respect to the control group. Extension of time in bed for one week increased TST (from 5.7 h to 7.4 h), and concomitantly MMN amplitude increased from -0.1 μV up to -1.25 μV over frontal areas. Reduced time in bed is associated with deficiency of the neuronal process associated with change detection, which may recover after one week of sleep extension, whereas attention-dependent neural processes do not normalize after this period of time in habitually short sleeping individuals and may require longer recovery periods.

Association between sleep duration and sarcopenia among community-dwelling older adults

PubMed Central

Hu, Xiaoyi; Jiang, Jiaojiao; Wang, Haozhong; Zhang, Lei; Dong, Birong; Yang, Ming

2017-01-01

Abstract Both sleep disorders and sarcopenia are common among older adults. However, little is known about the relationship between these 2 conditions. This study aimed to investigate the possible association between sleep duration and sarcopenia in a population of Chinese community-dwelling older adults. Community-dwelling older adults aged 60 years or older were recruited. Self-reported sleep duration, anthropometric data, gait speed, and handgrip strength were collected by face-to-face interviews. Sarcopenia was defined according to the recommended algorithm of the Asian Working Group for Sarcopenia (AWGS). We included 607 participants aged 70.6 ± 6.6 years (range, 60–90 years) in the analyses. The prevalence of sarcopenia in the whole study population was 18.5%. In women, the prevalence of sarcopenia was significantly higher in the short sleep duration group (< 6 hours) and long sleep duration group (>8 hours) compared with women in the normal sleep duration group (6–8 hours; 27.5%, 22.2% and 13.9%, respectively; P = .014). Similar results were found in men; however, the differences between groups were not statistically significant (18.5%, 20.6%, and 13.0%, respectively; P = .356). After adjustments for the potential confounding factors, older women having short sleep duration (OR: 4.34; 95% CI: 1.74–10.85) or having long sleep duration (OR: 2.50; 95% CI: 1.05–6.99) had greater risk of sarcopenia compared with women having normal sleep duration. With comparison to men with normal sleep duration, the adjusted OR for sarcopenia was 2.12 (0.96–8.39) in the short sleep duration group and 2.25 (0.88–6.87) in the long sleep duration group, respectively. A U-shape relationship between self-reported sleep duration and sarcopenia was identified in a population of Chinese community-dwelling older adults, especially in women. PMID:28272238

Abnormalities of neural circuitry in Alzheimer's disease: hippocampus and cortical cholinergic innervation.

PubMed

Geula, C

1998-07-01

Severe pathology in Alzheimer's disease (AD) results in marked disruption of cortical circuitry. Formation of neurofibrillary tangles, neuronal loss, decrease in dendritic extent, and synaptic depletion combine to halt communication among various cortical areas, resulting in anatomic isolation and fragmentation of many cortical zones. The clinical manifestation of this disruption is severe and debilitating cognitive dysfunction, often accompanied by psychiatric and behavioral disturbances and a diminished ability to perform activities of daily living. However, different cortical circuits are not equally vulnerable to AD pathology. In particular, two cortical systems that appear to be involved in the neural processing of memory are selectively vulnerable to degeneration in AD. One consists of connections between the hippocampus and its neighboring cortical structures within the temporal lobe. The second is the cortical cholinergic system that originates in neurons within the basal forebrain and innervates the entire cortical mantle. The circuitry in these systems shows early and severe degenerative changes in the course of AD. The selective vulnerability of these circuits is the probable reason for the early and marked loss of memory observed in these patients. This review presents current knowledge of the general pattern of cortical circuitry, followed by a summary of abnormalities of this circuitry in AD. The cortical circuits that exhibit selective pathology in AD are described in greater detail. Therapeutic implications of the abnormal circuitry in AD are also discussed. For therapies to be effective, early diagnosis of AD is necessary. Future efforts at AD therapy must be combined with an equally intense effort to develop tools capable of early diagnosis of AD, preferably at a preclinical stage before the onset of cognitive symptoms.

Removal of unwanted variation reveals novel patterns of gene expression linked to sleep homeostasis in murine cortex.

PubMed

Gerstner, Jason R; Koberstein, John N; Watson, Adam J; Zapero, Nikolai; Risso, Davide; Speed, Terence P; Frank, Marcos G; Peixoto, Lucia

2016-10-25

Why we sleep is still one of the most perplexing mysteries in biology. Strong evidence indicates that sleep is necessary for normal brain function and that sleep need is a tightly regulated process. Surprisingly, molecular mechanisms that determine sleep need are incompletely described. Moreover, very little is known about transcriptional changes that specifically accompany the accumulation and discharge of sleep need. Several studies have characterized differential gene expression changes following sleep deprivation. Much less is known, however, about changes in gene expression during the compensatory response to sleep deprivation (i.e. recovery sleep). In this study we present a comprehensive analysis of the effects of sleep deprivation and subsequent recovery sleep on gene expression in the mouse cortex. We used a non-traditional analytical method for normalization of genome-wide gene expression data, Removal of Unwanted Variation (RUV). RUV improves detection of differential gene expression following sleep deprivation. We also show that RUV normalization is crucial to the discovery of differentially expressed genes associated with recovery sleep. Our analysis indicates that the majority of transcripts upregulated by sleep deprivation require 6 h of recovery sleep to return to baseline levels, while the majority of downregulated transcripts return to baseline levels within 1-3 h. We also find that transcripts that change rapidly during recovery (i.e. within 3 h) do so on average with a time constant that is similar to the time constant for the discharge of sleep need. We demonstrate that proper data normalization is essential to identify changes in gene expression that are specifically linked to sleep deprivation and recovery sleep. Our results provide the first evidence that recovery sleep is comprised of two waves of transcriptional regulation that occur at different times and affect functionally distinct classes of genes.

Bedtime and sleep timing but not sleep duration are associated with eating habits in primary school children.

PubMed

Thivel, David; Isacco, Laurie; Aucouturier, Julien; Pereira, Bruno; Lazaar, Nordine; Ratel, Sébastien; Doré, Eric; Duché, Pascale

2015-04-01

In the context of childhood obesity progression, sleep patterns have been associated with unhealthy eating habits and energy intake. The association between several eating habits and sleep patterns in children has been recently studied. The aim of this study was to explore the association between sleep patterns, eating habits, and physical fitness in primary school children. A total of 236 children of 6 to 10 years old were recruited. Anthropometric characteristics and body composition were measured, and cardiorespiratory (20-m shuttle run test) and musculoskeletal (squat jump and cycling peak power) fitness tests were performed. Parents were asked to fill out an eating habits questionnaire, and children were classified into 4 categories as a function of the number of eating risk factors they presented. Parents completed a questionnaire about their child's bedtime and waking hours during weekdays and weekends. Weight (p < .01), waist circumference, and fat mass (p < .05) were significantly higher in late sleepers (27.6 ± 6.3 kg; 60.1 ± 7.6 cm; 19.52 ± 7.44) compared with normal sleepers (25.4 ± 3.7 kg; 58.2 ± 4.9 cm; 17.44% ± 6.23%). None of the physical fitness parameters were associated with sleep duration, bedtime, wake-up time, nor were they significantly different between late and normal sleepers. Bedtime was significantly earlier in children consuming breakfast everyday (08:30 vs. 09:00 PM, p < .01); later in children snacking (09:15 vs. 09:30 PM, p < .05) or watching TV at lunch (10:00 vs 09:30 PM, p < .05). There is an association between the proportion of normal and late sleepers and the accumulation of healthy eating habits (p < .001). Bedtime and sleep timings (normal or late sleepers) are associated with eating habits in primary school children. It seems necessary to consider the number of unhealthy eating habits adopted by children when studying these associations.

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

New modules are added to vibrissal premotor circuitry with the emergence of exploratory whisking

PubMed Central

Takatoh, Jun; Nelson, Anders; Zhou, Xiang; Bolton, M. McLean; Ehlers, Michael D.; Arenkiel, Benjamin R.; Mooney, Richard; Wang, Fan

2012-01-01

SUMMARY Rodents begin to use bilaterally coordinated, rhythmic sweeping of their vibrissae (“whisking”) for environmental exploration around two weeks after birth. Whether and how vibrissal control circuitry changes after birth is unknown, and relevant premotor circuitry remains poorly characterized. Using a modified rabies virus transsynaptic tracing strategy, we labeled neurons synapsing directly onto vibrissa facial motor neurons (vFMNs). Sources of potential excitatory, inhibitory, and modulatory vFMN premotor neurons, and differences between the premotor circuitry for vFMNs innervating intrinsic versus extrinsic vibrissal muscles, were systematically characterized. The emergence of whisking is accompanied by the addition of “new” sets of bilateral excitatory inputs to vFMNs from neurons in the lateral paragigantocellularis (LPGi). Furthermore, descending axons from the motor cortex directly innervate LPGi premotor neurons. Thus, neural modules well suited to facilitate the bilateral coordination and cortical control of whisking are added to premotor circuitry in parallel with the emergence of this exploratory behavior. PMID:23352170

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.

Working hours and sleep duration in midlife as determinants of health-related quality of life among older businessmen.

PubMed

von Bonsdorff, Mikaela Birgitta; Strandberg, Arto; von Bonsdorff, Monika; Törmäkangas, Timo; Pitkälä, Kaisu H; Strandberg, Timo E

2017-01-25

Long working hours and short sleep duration are associated with a range of adverse health consequences. However, the combined effect of these two exposures on health-related quality of life (HRQoL) has not been investigated. We studied white men born between 1919 and 1934 in the Helsinki Businessmen Study (HBS, initial n = 3,490). Data on clinical variables, self-rated health (SRH), working hours and sleep duration in 1974, and RAND-36 (SF-36) HRQoL survey in the year 2000 were available for 1,527 men. Follow-up time was 26 years. By combining working hours and sleep duration, four categories were formed: (i) normal work (≤50 hours/week) and normal sleep (>47 hours/week); (ii) long work (>50 hours/week) and normal sleep; (iii) normal work and short sleep (≤47 hours/week); and (iv) long work and short sleep. The association with RAND-36 domains was examined using multiple linear regression models adjusted for age, smoking and SRH. Compared to those with normal work and sleep in midlife, men with long work and short sleep had poorer RAND-36 scores for physical functioning, vitality and general health, and those with long work and normal sleep had poorer scores for physical functioning in old age. Adjustment for midlife smoking and SRH attenuated the associations, but the one for long work and short sleep and physical functioning remained significant (difference in mean physical functioning score −4.58, 95% confidence interval −9.00 to −0.15). Businessmen who had long working hours coupled with short sleep duration in midlife had poorer physical health in old age. © The Author 2016. Published by Oxford University Press on behalf of the British Geriatrics Society. All rights reserved. For Permissions, please email: journals.permissions@oup.com

Interface Electronic Circuitry for an Electronic Tongue

NASA Technical Reports Server (NTRS)

Keymeulen, Didier; Buehler, Martin

2007-01-01

Electronic circuitry has been developed to serve as an interface between an electronic tongue and digital input/output boards in a laptop computer that is used to control the tongue and process its readings. Electronic tongues can be used for a variety of purposes, including evaluating water quality, analyzing biochemicals, analyzing biofilms, and measuring electrical conductivities of soils.

Blood-gene expression reveals reduced circadian rhythmicity in individuals resistant to sleep deprivation.

PubMed

Arnardottir, Erna S; Nikonova, Elena V; Shockley, Keith R; Podtelezhnikov, Alexei A; Anafi, Ron C; Tanis, Keith Q; Maislin, Greg; Stone, David J; Renger, John J; Winrow, Christopher J; Pack, Allan I

2014-10-01

To address whether changes in gene expression in blood cells with sleep loss are different in individuals resistant and sensitive to sleep deprivation. Blood draws every 4 h during a 3-day study: 24-h normal baseline, 38 h of continuous wakefulness and subsequent recovery sleep, for a total of 19 time-points per subject, with every 2-h psychomotor vigilance task (PVT) assessment when awake. Sleep laboratory. Fourteen subjects who were previously identified as behaviorally resistant (n = 7) or sensitive (n = 7) to sleep deprivation by PVT. Thirty-eight hours of continuous wakefulness. We found 4,481 unique genes with a significant 24-h diurnal rhythm during a normal sleep-wake cycle in blood (false discovery rate [FDR] < 5%). Biological pathways were enriched for biosynthetic processes during sleep. After accounting for circadian effects, two genes (SREBF1 and CPT1A, both involved in lipid metabolism) exhibited small, but significant, linear changes in expression with the duration of sleep deprivation (FDR < 5%). The main change with sleep deprivation was a reduction in the amplitude of the diurnal rhythm of expression of normally cycling probe sets. This reduction was noticeably higher in behaviorally resistant subjects than sensitive subjects, at any given P value. Furthermore, blood cell type enrichment analysis showed that the expression pattern difference between sensitive and resistant subjects is mainly found in cells of myeloid origin, such as monocytes. Individual differences in behavioral effects of sleep deprivation are associated with differences in diurnal amplitude of gene expression for genes that show circadian rhythmicity. © 2014 Associated Professional Sleep Societies, LLC.

How (and why) the immune system makes us sleep.

PubMed

Imeri, Luca; Opp, Mark R

2009-03-01

Good sleep is necessary for physical and mental health. For example, sleep loss impairs immune function, and sleep is altered during infection. Immune signalling molecules are present in the healthy brain, where they interact with neurochemical systems to contribute to the regulation of normal sleep. Animal studies have shown that interactions between immune signalling molecules (such as the cytokine interleukin 1) and brain neurochemical systems (such as the serotonin system) are amplified during infection, indicating that these interactions might underlie the changes in sleep that occur during infection. Why should the immune system cause us to sleep differently when we are sick? We propose that the alterations in sleep architecture during infection are exquisitely tailored to support the generation of fever, which in turn imparts survival value.

The association of sleep duration and sleep quality with non-alcoholic fatty liver disease in a Taiwanese population.

PubMed

Chou, Yu-Tsung; Cheng, Hsiang-Ju; Wu, Jin-Shang; Yang, Yi-Ching; Chou, Chieh-Ying; Chang, Chih-Jen; Lu, Feng-Hwa

2018-06-18

The association of sleep duration/quality with nonalcoholic fatty liver disease (NAFLD) is inconclusive. Several important covariates were not adjusted concomitantly in some studies, and the severity of NAFLD was not considered. Furthermore, the gender impact of sleep duration or sleep quality on NAFLD remains unclear. We thus aimed to examine the association of sleep duration and quality with NAFLD by gender in a Taiwanese population. A total of 6663 subjects aged 18 years or more were enrolled. The severity of NAFLD was divided into mild, moderate, and severe degrees based on ultrasound findings. The sleep duration was classified into three groups: short (<6h), normal (6-8h), and long (>8h). Pittsburgh Sleep Quality Index (PSQI) was used to evaluate sleep quality, and poor sleep quality was defined as a global PSQI score greater than 5. After adjustment for potential confounders, multinomial logistic regression showed that poor sleep quality was negatively associated with both mild and moderate-to-severe NAFLD in males, but sleep duration was not independently related to NAFLD. In females, sleep condition was not related to NAFLD. Poor sleep quality but not sleep duration was associated with a lower risk of not only moderate to severe but also mild NAFLD in males. In females, the association of sleep quality and duration with the risk of NAFLD was insignificant. Copyright © 2018 Asia Oceania Association for the Study of Obesity. Published by Elsevier Ltd. All rights reserved.

Common Features of Neural Activity during Singing and Sleep Periods in a Basal Ganglia Nucleus Critical for Vocal Learning in a Juvenile Songbird

PubMed Central

Yanagihara, Shin; Hessler, Neal A.

2011-01-01

Reactivations of waking experiences during sleep have been considered fundamental neural processes for memory consolidation. In songbirds, evidence suggests the importance of sleep-related neuronal activity in song system motor pathway nuclei for both juvenile vocal learning and maintenance of adult song. Like those in singing motor nuclei, neurons in the basal ganglia nucleus Area X, part of the basal ganglia-thalamocortical circuit essential for vocal plasticity, exhibit singing-related activity. It is unclear, however, whether Area X neurons show any distinctive spiking activity during sleep similar to that during singing. Here we demonstrate that, during sleep, Area X pallidal neurons exhibit phasic spiking activity, which shares some firing properties with activity during singing. Shorter interspike intervals that almost exclusively occurred during singing in awake periods were also observed during sleep. The level of firing variability was consistently higher during singing and sleep than during awake non-singing states. Moreover, deceleration of firing rate, which is considered to be an important firing property for transmitting signals from Area X to the thalamic nucleus DLM, was observed mainly during sleep as well as during singing. These results suggest that songbird basal ganglia circuitry may be involved in the off-line processing potentially critical for vocal learning during sensorimotor learning phase. PMID:21991379

Distinct associations between energy balance and the sleep characteristics slow wave sleep and rapid eye movement sleep.

PubMed

Rutters, F; Gonnissen, H K; Hursel, R; Lemmens, S G; Martens, E A; Westerterp-Plantenga, M S

2012-10-01

Epidemiologically, an inverse relationship between body mass index (BMI) and sleep duration is observed. Intra-individual variance in the amount of slow wave sleep (SWS) or rapid eye movement (REM) sleep has been related to variance of metabolic and endocrine parameters, which are risk factors for the disturbance of energy balance (EB). To investigate inter-individual relationships between EB (EB= energy intake-energy expenditure∣, MJ/24 h), SWS or REM sleep, and relevant parameters in normal-weight men during two 48 h stays in the controlled environment of a respiration chamber. A total of 16 men (age 23±3.7 years, BMI 23.9±1.9 kg m(-2)) stayed in the respiration chamber twice for 48 h to assure EB. Electroencephalography was used to monitor sleep (2330-0730 hrs). Hunger and fullness were scored by visual analog scales; mood was determined by State Trait Anxiety Index-state and food reward by liking and wanting. Baseline blood and salivary samples were collected before breakfast. Subjects were fed in EB, except for the last dinner, when energy intake was ad libitum. The subjects slept on average 441.8±49 min per night, and showed high within-subject reliability for the amount of SWS and REM sleep. Linear regression analyses showed that EB was inversely related to the amount of SWS (r=-0.43, P<0.03), and positively related to the amount of REM sleep (r=0.40, P<0.05). Relevant parameters such as hunger, reward, stress and orexigenic hormone concentrations were related to overeating, as well as to the amount of SWS and REM sleep, however, after inclusion of these parameters in a multiple regression, the amount of SWS and REM sleep did not add to the explained variance of EB, which suggests that due to their individual associations, these EB parameters are mediator variables. A positive EB due to overeating, was explained by a smaller amount of SWS and higher amount of REM sleep, mediated by hunger, fullness, State Trait Anxiety Index-state scores, glucose

Female impulsive aggression: a sleep research perspective.

PubMed

Lindberg, Nina; Tani, Pekka; Putkonen, Hanna; Sailas, Eila; Takala, Pirjo; Eronen, Markku; Virkkunen, Matti

2009-01-01

The rate of violent crimes among girls and women appears to be increasing. One in every five female prisoners has been reported to have antisocial personality disorder. However, it has been quite unclear whether the impulsive, aggressive behaviour among women is affected by the same biological mechanisms as among men. Psychiatric sleep research has attempted to identify diagnostically sensitive and specific sleep patterns associated with particular disorders. Most psychiatric disorders are typically characterized by a severe sleep disturbance associated with decreased amounts of slow wave sleep (SWS), the physiologically significant, refreshing part of sleep. Among men with antisocial behaviour with severe aggression, on the contrary, increased SWS has been reported, reflecting either specific brain pathology or a delay in the normal development of human sleep patterns. In our preliminary study among medication-free, detoxified female homicidal offenders with antisocial personality disorder, the same profound abnormality in sleep architecture was found. From the perspective of sleep research, the biological correlates of severe impulsive aggression seem to share similar features in both sexes.

A proposed mathematical model for sleep patterning.

PubMed

Lawder, R E

1984-01-01

The simple model of a ramp, intersecting a triangular waveform, yields results which conform with seven generalized observations of sleep patterning; including the progressive lengthening of 'rapid-eye-movement' (REM) sleep periods within near-constant REM/nonREM cycle periods. Predicted values of REM sleep time, and of Stage 3/4 nonREM sleep time, can be computed using the observed values of other parameters. The distributions of the actual REM and Stage 3/4 times relative to the predicted values were closer to normal than the distributions relative to simple 'best line' fits. It was found that sleep onset tends to occur at a particular moment in the individual subject's '90-min cycle' (the use of a solar time-scale masks this effect), which could account for a subject with a naturally short sleep/wake cycle synchronizing to a 24-h rhythm. A combined 'sleep control system' model offers quantitative simulation of the sleep patterning of endogenous depressives and, with a different perturbation, qualitative simulation of the symptoms of narcolepsy.

Sleep and circadian rhythm disturbance in bipolar disorder.

PubMed

Bradley, A J; Webb-Mitchell, R; Hazu, A; Slater, N; Middleton, B; Gallagher, P; McAllister-Williams, H; Anderson, K N

2017-07-01

Subjective reports of insomnia and hypersomnia are common in bipolar disorder (BD). It is unclear to what extent these relate to underlying circadian rhythm disturbance (CRD). In this study we aimed to objectively assess sleep and circadian rhythm in a cohort of patients with BD compared to matched controls. Forty-six patients with BD and 42 controls had comprehensive sleep/circadian rhythm assessment with respiratory sleep studies, prolonged accelerometry over 3 weeks, sleep questionnaires and diaries, melatonin levels, alongside mood, psychosocial functioning and quality of life (QoL) questionnaires. Twenty-three (50%) patients with BD had abnormal sleep, of whom 12 (52%) had CRD and 29% had obstructive sleep apnoea. Patients with abnormal sleep had lower 24-h melatonin secretion compared to controls and patients with normal sleep. Abnormal sleep/CRD in BD was associated with impaired functioning and worse QoL. BD is associated with high rates of abnormal sleep and CRD. The association between these disorders, mood and functioning, and the direction of causality, warrants further investigation.

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.

Insomnia Patients With Objective Short Sleep Duration Have a Blunted Response to Cognitive Behavioral Therapy for Insomnia.

PubMed

Bathgate, Christina J; Edinger, Jack D; Krystal, Andrew D

2017-01-01

This study examined whether individuals with insomnia and objective short sleep duration <6 h, a subgroup with greater risks of adverse health outcomes, differ in their response to cognitive-behavioral therapy for insomnia (CBT-I) when compared to individuals with insomnia and normal sleep duration ≥6 h. Secondary analyses of a randomized, clinical trial with 60 adult participants (n = 31 women) from a single academic medical center. Outpatient treatment lasted 8 weeks, with a final follow-up conducted at 6 months. Mixed-effects models controlling for age, sex, CBT-I treatment group assignment, and treatment provider examined sleep parameters gathered via actigraphy, sleep diaries, and an Insomnia Symptom Questionnaire (ISQ) across the treatment and follow-up period. Six months post-CBT-I treatment, individuals with insomnia and normal sleep duration ≥6 h fared significantly better on clinical improvement milestones than did those with insomnia and short sleep duration <6 h. Specifically, individuals with insomnia and normal sleep duration had significantly higher insomnia remission (ISQ < 36.5; χ2[1, N = 60] = 44.72, p < .0001), more normative sleep efficiency (SE) on actigraphy (SE > 80%; χ2[1, N = 60] = 21, p < .0001), normal levels of middle of the night wake after sleep onset (MWASO) <31 minutes (χ2[1, N = 60] = 37.85, p < .0001), and a >50% decline in MWASO (χ2[1, N = 60] = 60, p < .0001) compared to individuals with insomnia and short sleep duration. Additionally, those with insomnia and normal sleep duration had more success decreasing their total wake time (TWT) at the 6-month follow-up compared to those with insomnia and short sleep duration (χ2[2, N = 60] = 44.1, p < .0001). Receiver-operating characteristic curve analysis found that using a 6-h cutoff with actigraphy provided a 95.7% sensitivity and 91.9% specificity for determining insomnia remission, with the area under the curve = 0.986. Findings suggest that individuals with insomnia and

Sleep Misperception in Chronic Insomnia Patients with Obstructive Sleep Apnea Syndrome: Implications for Clinical Assessment.

PubMed

Choi, Su Jung; Suh, Sooyeon; Ong, Jason; Joo, Eun Yeon

2016-11-15

To investigate whether sleep perception (SP), defined by the ratio of subjective and objective total sleep time, and habitual sleep time in various sleep disorders may be based on comorbid insomnia status. We enrolled 420 patients (age 20-79 y) who underwent polysomnography (PSG). They were divided into three groups based on chief complaints: chronic insomnia (CI, n = 69), patients with both obstructive sleep apnea and insomnia (OSA-I, n = 49) or OSA only (OSA, n = 149). Healthy volunteers were also recruited (normal controls [NC], n = 80). We compared differences in PSG parameters and habitual sleep duration and investigated the discrepancy between objective and subjective total sleep time (TST) and sleep latency among four groups. Subjective TST was defined as sleep time perceived by participants the next morning of PSG. SP for TST was highest in the OSA group (median 92.9%), and lowest in the CI group (80.3%). SP of the NC group (91.4%) was higher than the CI, but there was no difference between OSA-I and OSA groups. OSA-I had higher depressive mood compared to the OSA group (p < 0.001). SP was positively associated with the presence of OSA and habitual sleep duration and negatively related to the presence of insomnia and arousal index of PSG. Insomnia patients with (OSA-I) or without OSA (CI) reported the smallest discrepancy between habitual sleep duration and objective TST. Patients with OSA with or without insomnia have different PSG profiles, which suggests that objective measures of sleep are an important consideration for differentiating subtypes of insomnia and tailoring proper treatment. A commentary on this articles appears in this issue on page 1437. © 2016 American Academy of Sleep Medicine

Persistent insomnia: the role of objective short sleep duration and mental health.

PubMed

Vgontzas, Alexandros N; Fernandez-Mendoza, Julio; Bixler, Edward O; Singareddy, Ravi; Shaffer, Michele L; Calhoun, Susan L; Liao, Duanping; Basta, Maria; Chrousos, George P

2012-01-01

Few population-based, longitudinal studies have examined risk factors for persistent insomnia, and the results are inconsistent. Furthermore, none of these studies have examined the role of polysomnographic (PSG) variables such as sleep duration or sleep apnea on the persistence of insomnia. Representative longitudinal study. Sleep laboratory. From a random, general population sample of 1741 individuals of the adult Penn State Cohort, 1395 were followed-up after 7.5 years. Individuals underwent one-night PSG and full medical evaluation at baseline and a telephone interview at follow-up. PSG sleep duration was analyzed as a continuous variable and as a categorical variable: < 6 h sleep (short sleep duration) and ≥ 6 h sleep (longer sleep duration). The rates of insomnia persistence, partial remission, and full remission were 44.0%, 30.0%, and 26.0%, respectively. Objective short sleep duration significantly increased the odds of persistent insomnia as compared to normal sleep (OR = 3.19) and to fully remitted insomnia (OR = 4.92). Mental health problems at baseline were strongly associated with persistent insomnia as compared to normal sleep (OR = 9.67) and to a lesser degree compared to fully remitted insomnia (OR = 3.68). Smoking, caffeine, and alcohol consumption and sleep apnea did not predict persistent insomnia. Objective short sleep duration and mental health problems are the strongest predictors of persistent insomnia. These data further support the validity and clinical utility of objective short sleep duration as a novel marker of the biological severity of insomnia.

Heightened sexual interest and sleep disturbance

NASA Technical Reports Server (NTRS)

Zarcone, V.; De La Pena, A.; Dement, W. C.

1974-01-01

The study demonstrates a behavioral effect of selective sleep disturbance in normal human subjects. Ten male subjects were selectively REM-deprived for two nights by awakening them at the onset of REM sleep. In addition, there were baseline and non-REM awakening conditions. Heightened sexual interest was defined by the number of film frames (using a Mackworth camera) in which subjects fixated on parts of the female figure in photographs. The largest mean difference in sexual interest was found between baseline and REM-deprivation. Both the non-REM awakenings and REM-sleep deprivation enhanced sexual interest. The failure to demonstrate a significant difference between REM-deprivation and non-REM awakenings may be due to the fact that subjects were REM-sleep-deprived in both conditions. It is suggested that REM-sleep loss may lead to increased selective attention and preoccupation with any cues which are usually interesting.

Cardio-respiratory control during sleep in infancy.

PubMed

Horne, Rosemary S C

2014-06-01

During the first year of life and particularly the first 6 months autonomic control of the cardio-respiratory system is still undergoing maturation and infants are at risk of cardio-respiratory instability. These instabilities are most marked during sleep, which is important as infants spend the majority of each 24 hours in sleep. Sleep state has a marked effect on the cardio-respiratory system with instabilities being more common in active sleep compared to quiet sleep. Responses to hypoxia are also immature during infancy and may make young infants more vulnerable to cardio-respiratory instability. It has been proposed that an inability to respond appropriately to a life threatening event underpins the Sudden Infant Death Syndrome (SIDS). The major risk factors for SIDS, prone sleeping and maternal smoking, both impair cardio-respiratory control in normal healthy term infants. Crown Copyright © 2013. Published by Elsevier Ltd. All rights reserved.

Free Recall of Word Lists under Total Sleep Deprivation and after Recovery Sleep

PubMed Central

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

2012-01-01

Study Objectives: One task that has been used to assess memory effects of prior total sleep deprivation (TSD) is the immediate free recall of word lists; however, results have been mixed. A possible explanation for this is task impurity, since recall of words from different serial positions reflects use of distinct types of memory (last words: short-term memory; first and intermediate words: episodic memory). Here we studied the effects of 2 nights of TSD on immediate free recall of semantically unrelated word lists considering the serial position curve. Design: Random allocation to a 2-night TSD protocol followed by one night of recovery sleep or to a control group. Setting: Study conducted under continuous behavioral monitoring. Participants: 24 young, healthy male volunteers. Intervention: 2 nights of total sleep deprivation (TSD) and one night of recovery sleep. Measurements and Results: Participants were shown five 15 unrelated word-lists at baseline, after one and 2 nights of TSD, and after one night of recovery sleep. We also investigated the development of recall strategies (learning) and susceptibility to interference from previous lists. No free recall impairment occurred during TSD, irrespective of serial position. Interference was unchanged. Both groups developed recall strategies, but task learning occurred earlier in controls and was evident in the TSD group only after sleep recovery. Conclusion: Prior TSD spared episodic memory, short-term phonological memory, and interference, allowed the development of recall strategies, but may have decreased the advantage of using these strategies, which returned to normal after recovery sleep. Citation: Zanini GAV; Tufik S; Andersen ML; da Silva RCM; Bueno OFA; Rodrigues CC; Pompéia S. Free recall of word lists under total sleep deprivation and after recovery sleep. SLEEP 2012;35(2):223-230. PMID:22294812

SLEEP COMPLAINTS IN COMMUNITY-LIVING OLDER PERSONS: A MULTIFACTORIAL GERIATRIC SYNDROME

PubMed Central

Vaz Fragoso, Carlos A.; Gill, Thomas M.

2009-01-01

Among older persons, sleep complaints in the form of insomnia and daytime drowsiness are highly prevalent and associated with adverse outcomes. The underlying mechanisms are linked to age-related declines in physiology, i.e., normal aging, and age-related increases in disease prevalence, i.e., usual aging. In this monograph, we describe how normal aging leads to less restorative sleep, characterized by reductions in homeostatic and circadian sleep, and to phase advancement of the sleep-wake cycle, characterized by older persons being more alert in the early morning but drowsier in the early evening. We also describe how usual aging leads to sleep complaints through reductions in health status, loss of physical function, and primary sleep disorders. Psychosocial influences are likewise described and their relevance to sleep complaints is discussed. We subsequently incorporate these aging-related changes into a conceptual model that describes sleep complaints as a consequence of multiple and interdependent predisposing, precipitating, and perpetuating factors, akin to a geriatric syndrome. We conclude our discussion by applying our conceptual model to the sleep-related care of an older person with insomnia and daytime drowsiness, and suggest that the diagnostic assessment consider, in addition to primary sleep disorders, multiple domains including medical, physical, cognitive, psychological, and social issues with the intent of developing an overall therapeutic plan and establishing long-term follow-up. PMID:17916123

Characterization of sleep patterns and problems in healthcare workers in a tertiary care hospital.

PubMed

Buscemi, Dolores; Anvari, Rezza; Raj, Rishi; Nugent, Kenneth

2014-01-01

Restrictions in sleep can have important adverse effects on health and job performance. We collected information about sleep from US healthcare workers to determine whether they had sleep difficulties. We used an Internet-based survey to collect information on sleep patterns and sleep quality in healthcare workers at a tertiary care hospital. We classified these workers into short sleepers (<7 hours), normal sleepers (7-8 hours), and long sleepers (≥9 hours). We compared these three groups using simple descriptive statistics. We used logistic regression to identify factors associated with short sleep times. Of 3012 questionnaires distributed, 376 healthcare workers (12.5%) replied to this survey. The median age was 38 years, the median body mass index was 28 kg/m, and 76% were women. The median sleep duration on weekdays was 7 hours. Sixty-nine respondents (18.4%) were short sleepers, 269 of the respondents (71.5%) were normal sleepers, and 38 respondents (10.1%) were long sleepers. A total of 113 (30.1%) had sleep difficulties more than 50% of the time and 140 respondents (37.3%) were bothered by lack of energy from poor sleep. Short sleepers were less likely than other types of sleepers to have normal bedtimes and regular mealtimes. Eighty-four respondents (22.3%) went to bed between 2 AM and 2 PM. These workers were younger; slept less on the weekdays and weekends; and reported more difficulty with sleeping, feeling depressed, overconsumption of alcoholic beverages, and personal stressors. Most healthcare workers have healthy sleep patterns; however, many workers have poor sleep quality. Workers with "odd" bedtimes have abnormal sleep patterns and abnormal sleep quality; these workers need additional evaluation to understand the causes and consequences of their sleep patterns.

Obstructive sleep apnea: the sleeping giant of the childhood obesity epidemic.

PubMed

Mofid, Marcie

2014-10-01

Obstructive sleep apnea (OSA) is more common among obese children than in those of normal weight and can have serious consequences for neurocognitive function, behavior, and school performance. This article reviews OSA and steps for identifying the condition early and taking a multidisciplinary approach to long-term treatment.

Total Sleep Deprivation and Recovery Sleep Affect the Diurnal Variation of Agility Performance: The Gender Differences.

PubMed

Romdhani, Mohamed; Hammouda, Omar; Smari, Khawla; Chaabouni, Yassine; Mahdouani, Kacem; Driss, Tarak; Souissi, Nizar

2018-05-30

Romdhani, M, Hammouda, O, Smari, K, Chaabouni, Y, Mahdouani, K, Driss, T, and Souissi, N. Total sleep deprivation and recovery sleep affect the diurnal variation of agility performance: The gender differences. J Strength Cond Res XX(X): 000-000, 2018-This study aimed to investigate the effects of time-of-day, 24 and 36 hours of total sleep deprivation (TSD), and recovery sleep (RS) on repeated-agility performances. Twenty-two physical education students (11 male and 11 female students) completed 5 repeated modified agility T-test (RMAT) sessions (i.e., 2 after normal sleep night [NSN] [at 07:00 and 17:00 hours], 2 after TSD [at 07:00 hours, i.e., 24-hour TSD and at 17:00 hours, i.e., 36-hour TSD], and 1 after RS at 17:00 hours). The RMAT index decreased from the morning to the afternoon after NSN (p < 0.05, d = 1.05; p < 0.01, d = 0.73) and after TSD (p < 0.001, d = 0.92; d = 1.08), respectively, for total time (TT) and peak time (PT). This finding indicates a diurnal variation in repeated agility, which persisted after TSD. However, the diurnal increase in PT was less marked in the female group after NSN (2.98 vs. 6.24%). Moreover, TT and PT increased, respectively, after 24-hour TSD (p < 0.001; d = 0.84, d = 0.87) and 36-hour TSD (p < 0.001, d = 1.12; p < 0.01, d = 0.65). Female participants' PT was less affected by 24-hour TSD (1.76 vs. 6.81%) compared with male participants' PT. After 36-hour TSD, the amount of decrease was not different between groups, which increased the diurnal amplitude of PT only for male participants. Total sleep deprivation suppressed the diurnal increase of PT and increased the diurnal amplitude of oral temperature only in women. Nevertheless, RS normalized the sleep-loss-induced performance disruption. Conclusively, sleep loss and RS differently affect repeated-agility performance of men and women during the day. Sleep extension postdeprivation could have potent restorative effect on repeated-agility performances, and female

Descending projections of the hamster intergeniculate leaflet: relationship to the sleep/arousal and visuomotor systems

NASA Technical Reports Server (NTRS)

Morin, Lawrence P.; Blanchard, Jane H.

2005-01-01

The intergeniculate leaflet (IGL), homolog of the primate pregeniculate nucleus, modulates circadian rhythms. However, its extensive anatomical connections suggest that it may regulate other systems, particularly those for visuomotor function and sleep/arousal. Here, descending IGL-efferent pathways are identified with the anterograde tracer, Phaseolus vulgaris leucoagglutinin, with projections to over 50 brain stem nuclei. Projections of the ventral lateral geniculate are similar, but more limited. Many of the nuclei with IGL afferents contribute to circuitry governing visuomotor function. These include the oculomotor, trochlear, anterior pretectal, Edinger-Westphal, and the terminal nuclei; all layers of the superior colliculus, interstitial nucleus of the medial longitudinal fasciculus, supraoculomotor periaqueductal gray, nucleus of the optic tract, the inferior olive, and raphe interpositus. Other target nuclei are known to be involved in the regulation of sleep, including the lateral dorsal and pedunculopontine tegmentum. The dorsal raphe also receives projections from the IGL and may contribute to both sleep/arousal and visuomotor function. However, the locus coeruleus and medial vestibular nucleus, which contribute to sleep and eye movement regulation and which send projections to the IGL, do not receive reciprocal projections from it. The potential involvement of the IGL with the sleep/arousal system is further buttressed by existing evidence showing IGL-efferent projections to the ventrolateral preoptic area, dorsomedial, and medial tuberal hypothalamus. In addition, the great majority of all regions receiving IGL projections also receive input from the orexin/hypocretin system, suggesting that this system contributes not only to the regulation of sleep, but to eye movement control as well.

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.

How (and why) the immune system makes us sleep

PubMed Central

Imeri, Luca; Opp, Mark R.

2010-01-01

Good sleep is necessary for physical and mental health. For example, sleep loss impairs immune function, and sleep is altered during infection. Immune signalling molecules are present in the healthy brain, where they interact with neurochemical systems to contribute to the regulation of normal sleep. Animal studies have shown that interactions between immune signalling molecules (such as the cytokine interleukin 1) and brain neurochemical systems (such as the serotonin system) are amplified during infection, indicating that these interactions might underlie the changes in sleep that occur during infection. Why should the immune system cause us to sleep differently when we are sick? We propose that the alterations in sleep architecture during infection are exquisitely tailored to support the generation of fever, which in turn imparts survival value. PMID:19209176

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

PubMed

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

2012-02-01

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

Nonlinear aspects of the EEG during sleep in children

NASA Astrophysics Data System (ADS)

Berryman, Matthew J.; Coussens, Scott W.; Pamula, Yvonne; Kennedy, Declan; Lushington, Kurt; Shalizi, Cosma; Allison, Andrew; Martin, A. James; Saint, David; Abbott, Derek

2005-05-01

Electroencephalograph (EEG) analysis enables the dynamic behavior of the brain to be examined. If the behavior is nonlinear then nonlinear tools can be used to glean information on brain behavior, and aid in the diagnosis of sleep abnormalities such as obstructive sleep apnea syndrome (OSAS). In this paper the sleep EEGs of a set of normal children and children with mild OSAS are evaluated for nonlinear brain behaviour. We found that there were differences in the nonlinearity of the brain behaviour between different sleep stages, and between the two groups of children.

A Physiologically Based Model of Orexinergic Stabilization of Sleep and Wake

PubMed Central

Fulcher, Ben D.; Phillips, Andrew J. K.; Postnova, Svetlana; Robinson, Peter A.

2014-01-01

The orexinergic neurons of the lateral hypothalamus (Orx) are essential for regulating sleep-wake dynamics, and their loss causes narcolepsy, a disorder characterized by severe instability of sleep and wake states. However, the mechanisms through which Orx stabilize sleep and wake are not well understood. In this work, an explanation of the stabilizing effects of Orx is presented using a quantitative model of important physiological connections between Orx and the sleep-wake switch. In addition to Orx and the sleep-wake switch, which is composed of mutually inhibitory wake-active monoaminergic neurons in brainstem and hypothalamus (MA) and the sleep-active ventrolateral preoptic neurons of the hypothalamus (VLPO), the model also includes the circadian and homeostatic sleep drives. It is shown that Orx stabilizes prolonged waking episodes via its excitatory input to MA and by relaying a circadian input to MA, thus sustaining MA firing activity during the circadian day. During sleep, both Orx and MA are inhibited by the VLPO, and the subsequent reduction in Orx input to the MA indirectly stabilizes sustained sleep episodes. Simulating a loss of Orx, the model produces dynamics resembling narcolepsy, including frequent transitions between states, reduced waking arousal levels, and a normal daily amount of total sleep. The model predicts a change in sleep timing with differences in orexin levels, with higher orexin levels delaying the normal sleep episode, suggesting that individual differences in Orx signaling may contribute to chronotype. Dynamics resembling sleep inertia also emerge from the model as a gradual sleep-to-wake transition on a timescale that varies with that of Orx dynamics. The quantitative, physiologically based model developed in this work thus provides a new explanation of how Orx stabilizes prolonged episodes of sleep and wake, and makes a range of experimentally testable predictions, including a role for Orx in chronotype and sleep inertia. PMID

Upper Airway Collapsibility During REM Sleep in Children with the Obstructive Sleep Apnea Syndrome

PubMed Central

Huang, Jingtao; Karamessinis, Laurie R.; Pepe, Michelle E.; Glinka, Stephen M.; Samuel, John M.; Gallagher, Paul R.; Marcus, Carole L.

2009-01-01

Study Objectives: In children, most obstructive events occur during rapid eye movement (REM) sleep. We hypothesized that children with the obstructive sleep apnea syndrome (OSAS), in contrast to age-matched control subjects, would not maintain airflow in the face of an upper airway inspiratory pressure drop during REM sleep. Design: During slow wave sleep (SWS) and REM sleep, we measured airflow, inspiratory time, inspiratory time/total respiratory cycle time, respiratory rate, tidal volume, and minute ventilation at a holding pressure at which flow limitation occurred and at 5 cm H2O below the holding pressure in children with OSAS and in control subjects. Setting: Sleep laboratory. Participants: Fourteen children with OSAS and 23 normal control subjects. Results: In both sleep states, control subjects were able to maintain airflow, whereas subjects with OSAS preserved airflow in SWS but had a significant decrease in airflow during REM sleep (change in airflow of 18.58 ± 12.41 mL/s for control subjects vs −44.33 ± 14.09 mL/s for children with OSAS, P = 0.002). Although tidal volume decreased, patients with OSAS were able to maintain minute ventilation by increasing the respiratory rate and also had an increase in inspiratory time and inspiratory time per total respiratory cycle time Conclusion: Children with OSAS do not maintain airflow in the face of upper-airway inspiratory-pressure drops during REM sleep, indicating a more collapsible upper airway, compared with that of control subjects during REM sleep. However, compensatory mechanisms exist to maintain minute ventilation. Local reflexes, central control mechanisms, or both reflexes and control mechanisms need to be further explored to better understand the pathophysiology of this abnormality and the compensation mechanism. Citation: Huang J; Karamessinis LR; Pepe ME; Glinka SM; Samuel JM; Gallagher PR; Marcus CL. Upper airway collapsibility during REM sleep in children with the obstructive sleep apnea

Establishing normal values for pediatric nighttime sleep measured by actigraphy: a systematic review and meta-analysis.

PubMed

Galland, Barbara C; Short, Michelle A; Terrill, Philip; Rigney, Gabrielle; Haszard, Jillian J; Coussens, Scott; Foster-Owens, Mistral; Biggs, Sarah N

2018-04-01

Despite the widespread use of actigraphy in pediatric sleep studies, there are currently no age-related normative data. To systematically review the literature, calculate pooled mean estimates of actigraphy-derived pediatric nighttime sleep variables and to examine the magnitude of change with age. A systematic search was performed across eight databases of studies that included at least one actigraphy sleep variable from healthy children aged 0-18 years. Data suitable for meta-analysis were confined to ages 3-18 years with seven actigraphy variables analyzed using random effects meta-analysis and meta-regression performed using age as a covariate. In total, 1334 articles did not meet inclusion criteria; 87 had data suitable for review and 79 were suitable for meta-analysis. Pooled mean estimates for overnight sleep duration declined from 9.68 hours (3-5 years age band) to 8.98, 8.85, 8.05, and 7.4 for age bands 6-8, 9-11, 12-14, and 15-18 years, respectively. For continuous data, the best-fit (R2 = 0.74) equation for hours over the 0-18 years age range was 9.02 - 1.04 × [(age/10)^2 - 0.83]. There was a significant curvilinear association between both sleep onset and offset with age (p < .001). Sleep latency was stable at 19.4 min per night. There were significant differences among the older age groups between weekday and weekend/nonschool days (18 studies). Total sleep time in 15-18 years old was 56 min longer, and sleep onset and offset almost 1 and 2 hours later, respectively, on weekend or nonschool days. These normative values have potential application to assist the interpretation of actigraphy measures from nighttime recordings across the pediatric age range, and aid future research.

Autonomic consequences of arousal from sleep: mechanisms and implications.

PubMed

Horner, R L

1996-12-01

Normal spontaneous arousals from sleep are associated with transient increases in blood pressure, heart rate, and ventilation caused by large transient changes in autonomic output. These autonomic changes are out of proportion to obvious physiological need and are in excess of those observed in later periods of quiet wakefulness. This paper discusses some of the mechanisms underlying the cardio-respiratory consequences of arousal from sleep, and discusses why the normal onset of wakefulness may be associated with such large changes in autonomic output.

Apnea-induced rapid eye movement sleep disruption impairs human spatial navigational memory.

PubMed

Varga, Andrew W; Kishi, Akifumi; Mantua, Janna; Lim, Jason; Koushyk, Viachaslau; Leibert, David P; Osorio, Ricardo S; Rapoport, David M; Ayappa, Indu

2014-10-29

Hippocampal electrophysiology and behavioral evidence support a role for sleep in spatial navigational memory, but the role of particular sleep stages is less clear. Although rodent models suggest the importance of rapid eye movement (REM) sleep in spatial navigational memory, a similar role for REM sleep has never been examined in humans. We recruited subjects with severe obstructive sleep apnea (OSA) who were well treated and adherent with continuous positive airway pressure (CPAP). Restricting CPAP withdrawal to REM through real-time monitoring of the polysomnogram provides a novel way of addressing the role of REM sleep in spatial navigational memory with a physiologically relevant stimulus. Individuals spent two different nights in the laboratory, during which subjects performed timed trials before and after sleep on one of two unique 3D spatial mazes. One night of sleep was normally consolidated with use of therapeutic CPAP throughout, whereas on the other night, CPAP was reduced only in REM sleep, allowing REM OSA to recur. REM disruption via this method caused REM sleep reduction and significantly fragmented any remaining REM sleep without affecting total sleep time, sleep efficiency, or slow-wave sleep. We observed improvements in maze performance after a night of normal sleep that were significantly attenuated after a night of REM disruption without changes in psychomotor vigilance. Furthermore, the improvement in maze completion time significantly positively correlated with the mean REM run duration across both sleep conditions. In conclusion, we demonstrate a novel role for REM sleep in human memory formation and highlight a significant cognitive consequence of OSA. Copyright © 2014 the authors 0270-6474/14/3414571-07$15.00/0.

Sleep disturbance and neurocognitive function during the recovery from a sport-related concussion in adolescents.

PubMed

Kostyun, Regina O; Milewski, Matthew D; Hafeez, Imran

2015-03-01

Sleep disturbances are a hallmark sign after a sport-related concussion (SRC). Poor sleep has been shown to adversely affect baseline neurocognitive test scores, but it is not comprehensively understood how neurocognitive function is affected by disrupted sleep during recovery from a concussion. To identify the correlation between adolescent athletes' neurocognitive function and their self-reported sleep quantity and sleep disturbance symptoms during recovery from SRC. Cross-sectional study; Level of evidence, 3. Immediate Post-Concussion Assessment and Cognition Testing (ImPACT) data were retrospectively collected for 545 adolescent athletes treated for SRC at a sports medicine concussion clinic. Patients were stratified into groups based on 2 criteria: self-reported sleep duration and self-reported sleep disturbance symptoms during postinjury ImPACT testing. Sleep duration was classified as short (<7 hours), intermediate (7-9 hours), and long (>9 hours). Sleep disturbance symptoms were self-reported as part of the Post-Concussion Symptom Scale (PCSS) as either sleeping less than normal, sleeping more than normal, or having trouble falling asleep. One-way analyses of variance were conducted to examine the effects that sleep duration as well as self-reported sleep disturbance symptoms had on composite scores. A total of 1067 ImPACT tests were analyzed: test 1, 545; test 2, 380; and test 3, 142. Sleeping fewer than 7 hours the night before testing correlated with higher PCSS scores (P < .001), whereas sleeping longer than 9 hours correlated with worse visual memory (P = .01), visual motor speed (P <.001), and reaction time (P = .04) composite scores. With regard to self-reported sleep disturbance symptoms, patients demonstrated worse composite scores during ImPACT testing when they self-reported sleeping more than normal (ImPACT test 1: verbal memory, P < .001; visual motor speed, P = .05; reaction time, P = .01; ImPACT test 2: verbal memory, P < .001; visual memory

Hypersynchronous delta waves and somnambulism: brain topography and effect of sleep deprivation.

PubMed

Pilon, Mathieu; Zadra, Antonio; Joncas, Steve; Montplaisir, Jacques

2006-01-01

Hypersynchronous delta activity (HSD) is usually described as several continuous high-voltage delta waves (> or = 150 microV) in the sleep electroencephalogram of somnambulistic patients. However, studies have yielded varied and contradictory results. The goal of the present study was to evaluate HSD over different electroencephalographic derivations during the non-rapid eye movement (NREM) sleep of somnambulistic patients and controls during normal sleep and following 38 hours of sleep deprivation, as well as prior to sleepwalking episodes. N/A. Sleep disorders clinic. Ten adult sleepwalkers and 10 sex- and age-matched control subjects were investigated polysomnographically during a baseline night and following 38 hours of sleep deprivation. N/A. During normal sleep, sleepwalkers had a significantly higher ratio of HSD over the time spent in stage 2, 3 and 4 on frontal and central derivations when compared with controls. Sleep deprivation resulted in a significant increase in the ratio of the time in HSD over the time in stage 4 on the frontal lead in both groups and on the central lead in controls. There was no evidence for a temporal accumulation of HSD prior to the episodes. HSD shows a clear frontocentral gradient across all subjects during both baseline and recovery sleep and has relatively low specificity for the diagnosis of NREM parasomnias. Increases in HSD after sleep deprivation may reflect an enhancement of the homeostatic process underlying sleep regulation.

Blood-Gene Expression Reveals Reduced Circadian Rhythmicity in Individuals Resistant to Sleep Deprivation

PubMed Central

Arnardottir, Erna S.; Nikonova, Elena V.; Shockley, Keith R.; Podtelezhnikov, Alexei A.; Anafi, Ron C.; Tanis, Keith Q.; Maislin, Greg; Stone, David J.; Renger, John J.; Winrow, Christopher J.; Pack, Allan I.

2014-01-01

Study Objectives: To address whether changes in gene expression in blood cells with sleep loss are different in individuals resistant and sensitive to sleep deprivation. Design: Blood draws every 4 h during a 3-day study: 24-h normal baseline, 38 h of continuous wakefulness and subsequent recovery sleep, for a total of 19 time-points per subject, with every 2-h psychomotor vigilance task (PVT) assessment when awake. Setting: Sleep laboratory. Participants: Fourteen subjects who were previously identified as behaviorally resistant (n = 7) or sensitive (n = 7) to sleep deprivation by PVT. Intervention: Thirty-eight hours of continuous wakefulness. Measurements and Results: We found 4,481 unique genes with a significant 24-h diurnal rhythm during a normal sleep-wake cycle in blood (false discovery rate [FDR] < 5%). Biological pathways were enriched for biosynthetic processes during sleep. After accounting for circadian effects, two genes (SREBF1 and CPT1A, both involved in lipid metabolism) exhibited small, but significant, linear changes in expression with the duration of sleep deprivation (FDR < 5%). The main change with sleep deprivation was a reduction in the amplitude of the diurnal rhythm of expression of normally cycling probe sets. This reduction was noticeably higher in behaviorally resistant subjects than sensitive subjects, at any given P value. Furthermore, blood cell type enrichment analysis showed that the expression pattern difference between sensitive and resistant subjects is mainly found in cells of myeloid origin, such as monocytes. Conclusion: Individual differences in behavioral effects of sleep deprivation are associated with differences in diurnal amplitude of gene expression for genes that show circadian rhythmicity. Citation: Arnardottir ES, Nikonova EV, Shockley KR, Podtelezhnikov AA, Anafi RC, Tanis KQ, Maislin G, Stone DJ, Renger JJ, Winrow CJ, Pack AI. Blood-gene expression reveals reduced circadian rhythmicity in individuals resistant to

Sex differences in paradoxical sleep: influences of estrus cycle and ovariectomy.

PubMed

Fang, J; Fishbein, W

1996-09-23

Previously, we reported that paradoxical sleep (PS) is sexually dimorphic in mice and rats. Since some early studies indicate that PS is suppressed during proestrus night, it is important to know whether the estrus cycle and accompanying circulating ovarian hormones could explain the sexual dimorphism of PS. To examine this, sleep patterns of male rats were compared with those of normal cycling female rats and ovariectomized females in a 12:12 h light/dark cycle. Slow wave sleep and total sleep time are indistinguishable between the males, cycling females and ovariectomized females. However, normal males display significantly more PS than cycling females during both daytime and nighttime (average of all estrus stages). On the other hand, while ovariectomy has no visible effect on daytime sleep--the sexual dimorphism of PS is unchanged by ovariectomy--during nighttime, ovariectomy produces a selective increase of PS, eliminating the sex difference during the night. In sum, normal cycling females show no change in daytime sleep patterns across the estrus cycle, but have significantly less PS during proestrus nights than during metestrus and diestrus nights. The results indicate that the sex difference in nighttime PS is due to the suppression of PS by ovarian hormones during proestrus and, to a less extent, estrus nights. The sex difference in daytime PS, on the other hand, appears to be independent of circulating ovarian hormones.

Functional conservation of MBD proteins: MeCP2 and Drosophila MBD proteins alter sleep.

PubMed

Gupta, T; Morgan, H R; Bailey, J A; Certel, S J

2016-11-01

Proteins containing a methyl-CpG-binding domain (MBD) bind 5mC and convert the methylation pattern information into appropriate functional cellular states. The correct readout of epigenetic marks is of particular importance in the nervous system where abnormal expression or compromised MBD protein function, can lead to disease and developmental disorders. Recent evidence indicates that the genome of Drosophila melanogaster is methylated and two MBD proteins, dMBD2/3 and dMBD-R2, are present. Are Drosophila MBD proteins required for neuronal function, and as MBD-containing proteins have diverged and evolved, does the MBD domain retain the molecular properties required for conserved cellular function across species? To address these questions, we expressed the human MBD-containing protein, hMeCP2, in distinct amine neurons and quantified functional changes in sleep circuitry output using a high throughput assay in Drosophila. hMeCP2 expression resulted in phase-specific sleep loss and sleep fragmentation with the hMeCP2-mediated sleep deficits requiring an intact MBD domain. Reducing endogenous dMBD2/3 and dMBD-R2 levels also generated sleep fragmentation, with an increase in sleep occurring upon dMBD-R2 reduction. To examine if hMeCP2 and dMBD-R2 are targeting common neuronal functions, we reduced dMBD-R2 levels in combination with hMeCP2 expression and observed a complete rescue of sleep deficits. Furthermore, chromosomal binding experiments indicate MBD-R2 and MeCP2 associate on shared genomic loci. Our results provide the first demonstration that Drosophila MBD-containing family members are required for neuronal function and suggest that the MBD domain retains considerable functional conservation at the whole organism level across species. © 2016 John Wiley & Sons Ltd and International Behavioural and Neural Genetics Society.

Impaired Sleep Predicts Cognitive Decline in Old People: Findings from the Prospective KORA Age Study.

PubMed

Johar, Hamimatunnisa; Kawan, Rasmila; Emeny, Rebecca Thwing; Ladwig, Karl-Heinz

2016-01-01

To investigate the association between sleep-related characteristics and cognitive change over 3 years of follow up in an aged population. Sleep characteristics and covariates were assessed at baseline in a standardized interview and clinical examination of the population-based KORA Age Study (n = 740, mean age = 75 years). Cognitive score (determined by telephone interview for cognitive status, TICS-m) was recorded at baseline and 3 years later. At baseline, 82.83% (n = 613) of participants had normal cognitive status, 13.51% (n = 100) were classified with mild cognitive impairment (MCI), and 3.64% (n = 27) with probable dementia. The effect of three distinct patterns of poor sleep (difficulties initiating [DIS] or maintaining sleep [DMS], daytime sleepiness [DS] or sleep duration) were considered on a change in cognitive score with adjustments for potential confounders in generalized linear regression models. Cognitive decline was more pronounced in individuals with DMS compared to those with no DMS (β = 1.33, 95% CI = 0.41-2.24, P < 0.001). However, the predictive power of DMS was only significant in individuals with normal cognition and not impaired subjects at baseline. Prolonged sleep duration increased the risk for cognitive decline in cognitively impaired elderly (β = 1.86, 95% CI = 0.15-3.57, P = 0.03). Other sleep characteristics (DIS and DS) were not significantly associated with cognitive decline. DMS and long sleep duration were associated with cognitive decline in normal and cognitively impaired elderly, respectively. The identification of impaired sleep quality may offer intervention strategies to deter cognitive decline in the elderly with normal cognitive function. © 2016 Associated Professional Sleep Societies, LLC.

A review of current sleep screening applications for smartphones.

PubMed

Behar, Joachim; Roebuck, Aoife; Domingos, João S; Gederi, Elnaz; Clifford, Gari D

2013-07-01

Sleep disorders are a common problem and contribute to a wide range of healthcare issues. The societal and financial costs of sleep disorders are enormous. Sleep-related disorders are often diagnosed with an overnight sleep test called a polysomnogram, or sleep study involving the measurement of brain activity through the electroencephalogram. Other parameters monitored include oxygen saturation, respiratory effort, cardiac activity (through the electrocardiogram), as well as video recording, sound and movement activity. Monitoring can be costly and removes the patients from their normal sleeping environment, preventing repeated unbiased studies. The recent increase in adoption of smartphones, with high quality on-board sensors has led to the proliferation of many sleep screening applications running on the phone. However, with the exception of simple questionnaires, no existing sleep-related application available for smartphones is based on scientific evidence. This paper reviews the existing smartphone applications landscape used in the field of sleep disorders and proposes possible advances to improve screening approaches.

Sleep Disturbance in Female Flight Attendants and Teachers.

PubMed

Grajewski, Barbara; Whelan, Elizabeth A; Nguyen, Mimi M; Kwan, Lorna; Cole, Roger J

2016-07-01

Flight attendants (FAs) may experience circadian disruption due to travel during normal sleep hours and through multiple time zones. This study investigated whether FAs are at higher risk for sleep disturbance compared to teachers, as assessed by questionnaire, diary, and activity monitors. Sleep/wake cycles of 45 FAs and 25 teachers were studied. For one menstrual cycle, participants wore an activity monitor and kept a daily diary. Sleep metrics included total sleep in the main sleep period (MSP), sleep efficiency (proportion of MSP spent sleeping), and nocturnal sleep fraction (proportion of sleep between 10 p.m. to 8 a.m. home time). Relationships between sleep metrics and occupation were analyzed with mixed and generalized linear models. Both actigraph and diary data suggest that FAs sleep longer than teachers. However, several actigraph indices of sleep disturbance indicated that FAs incurred significant impairment of sleep compared to teachers. FAs were more likely than teachers to have poor sleep efficiency [adjusted odds ratio (OR) for lowest quartile of sleep efficiency = 1.9, 95% Confidence Interval (CI) 1.2 - 3.0] and to have a smaller proportion of their sleep between 10 p.m. and 8 a.m. home time (adjusted OR for lowest quartile of nocturnal sleep fraction = 3.1, CI 1.1 -9.0). Study FAs experienced increased sleep disturbance compared to teachers, which may indicate circadian disruption. Grajewski B, Whelan EA, Nguyen MM, Kwan L, Cole RJ. Sleep disturbance in female flight attendants and teachers. Aerosp Med Hum Perform. 2016; 87(7)638-645.

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.

Cholinergic Oculomotor Nucleus Activity Is Induced by REM Sleep Deprivation Negatively Impacting on Cognition.

PubMed

Santos, Patrícia Dos; Targa, Adriano D S; Noseda, Ana Carolina D; Rodrigues, Lais S; Fagotti, Juliane; Lima, Marcelo M S

2017-09-01

Several efforts have been made to understand the involvement of rapid eye movement (REM) sleep for cognitive processes. Consolidation or retention of recognition memories is severely disrupted by REM sleep deprivation (REMSD). In this regard, pedunculopontine tegmental nucleus (PPT) and other brainstem nuclei, such as pontine nucleus (Pn) and oculomotor nucleus (OCM), appear to be candidates to take part in this REM sleep circuitry with potential involvement in cognition. Therefore, the objective of this study was to investigate a possible association between the performance of Wistar rats in a declarative memory and PPT, Pn, and OCM activities after different periods of REMSD. We examined c-Fos and choline acetyltransferase (ChaT) expressions as indicators of neuronal activity as well as a familiarity-based memory test. The animals were distributed in groups: control, REMSD, and sleep rebound (REB). At the end of the different REMSD (24, 48, 72, and 96 h) and REB (24 h) time points, the rats were immediately tested in the object recognition test and then the brains were collected. Results indicated that OCM neurons presented an increased activity, due to ChaT-labeling associated with REMSD that negatively correlated (r = -0.32) with the cognitive performance. This suggests the existence of a cholinergic compensatory mechanism within the OCM during REMSD. We also showed that 24 h of REMSD impacted similarly in memory, compared to longer periods of REMSD. These data extend the notion that REM sleep is influenced by areas other than PPT, i.e., Pn and OCM, which could be key players in both sleep processes and cognition.

The emotional brain and sleep: an intimate relationship.

PubMed

Vandekerckhove, Marie; Cluydts, Raymond

2010-08-01

Research findings confirm our own experiences in life where daytime events and especially emotionally stressful events have an impact on sleep quality and well-being. Obviously, daytime emotional stress may have a differentiated effect on sleep by influencing sleep physiology and dream patterns, dream content and the emotion within a dream, although its exact role is still unclear. Other effects that have been found are the exaggerated startle response, decreased dream recall and elevated awakening thresholds from rapid eye movement (REM)-sleep, increased or decreased latency to REM-sleep, increased REM-density, REM-sleep duration and the occurrence of arousals in sleep as a marker of sleep disruption. However, not only do daytime events affect sleep, also the quality and amount of sleep influences the way we react to these events and may be an important determinant in general well-being. Sleep seems restorative in daily functioning, whereas deprivation of sleep makes us more sensitive to emotional and stressful stimuli and events in particular. The way sleep impacts next day mood/emotion is thought to be affected particularly via REM-sleep, where we observe a hyperlimbic and hypoactive dorsolateral prefrontal functioning in combination with a normal functioning of the medial prefrontal cortex, probably adaptive in coping with the continuous stream of emotional events we experience. (c) 2010 Elsevier Ltd. All rights reserved.

Association between maternal symptoms of sleep disordered breathing and fetal telomere length.

PubMed

Salihu, Hamisu M; King, Lindsey; Patel, Priyanshi; Paothong, Arnut; Pradhan, Anupam; Louis, Judette; Naik, Eknath; Marty, Phillip J; Whiteman, Valerie

2015-04-01

Our investigation aims to assess the impact of symptoms of maternal sleep-disordered breathing, specifically sleep apnea risk and daytime sleepiness, on fetal leukocyte telomere length. Pregnant women were recruited upon hospital delivery admission. Sleep exposure outcomes were measured using the Berlin Questionnaire to quantify sleep apnea and the Epworth Sleepiness Scale to measure daytime sleepiness. Participants were classified as "High Risk" or "Low Risk" for sleep apnea based on responses to the Berlin, while "Normal" or "Abnormal" daytime sleepiness was determined based on responses to the Epworth. Neonatal umbilical cord blood samples (N = 67) were collected and genomic DNA was isolated from cord blood leukocytes using Quantitative PCR. A ratio of relative telomere length was derived by telomere repeat copy number and single copy gene copy number (T/S ratio) and used to compare telomere lengths. Bootstrap and ANOVA statistical procedures were employed. On the Berlin, 68.7% of participants were classified as Low Risk while 31.3% were classified as High Risk for sleep apnea. According to the Epworth scale, 80.6% were determined to have Normal daytime sleepiness, and 19.4% were found to have Abnormal daytime sleepiness. The T/S ratio among pregnant women at High Risk for sleep apnea was significantly shorter than for those at Low Risk (P value < 0.05), and the T/S ratio among habitual snorers was significantly shorter than among non-habitual snorers (P value < 0.05). Although those with Normal Sleepiness had a longer T/S ratio than those with Abnormal Sleepiness, the difference was not statistically significant. Our results provide the first evidence demonstrating shortened telomere length among fetuses exposed to maternal symptoms of sleep disordered breathing during pregnancy, and suggest sleep disordered breathing as a possible mechanism of accelerated chromosomal aging. © 2015 Associated Professional Sleep Societies, LLC.

Habitual Short Sleep Impacts Frontal Switch Mechanism in Attention to Novelty

PubMed Central

Gumenyuk, Valentina; Roth, Thomas; Korzyukov, Oleg; Jefferson, Catherine; Bowyer, Susan; Drake, Christopher L.

2011-01-01

Study Objectives: Reduced time in bed relative to biological sleep need is common. The impact of habitual short sleep on auditory attention has not been studied to date. In the current study, we utilized novelty oddball tasks to evaluate the effect of habitual short sleep on brain function underlying attention control processes measured by the mismatch negativity (MMN, index of pre-attentive stage), P3a (attention-dependent), and P3b (memory-dependent) event related brain potentials (ERPs). An extended time in bed in a separate study was used to evaluate the possible reversal of the impairments of these processes in habitual short sleepers. Methods: Ten self-defined short sleepers (total sleep time [TST] ≤ 6h) and 9 normal-sleeping subjects with TST 7-8 h, participated. ERPs were recorded via a 64-channel EEG system. Two test conditions: “ignore” and “attend” were implemented. The ERPs were analyzed and compared between groups on the 2 task conditions and frontal/central/parietal electrodes by 3-factor ANOVA. Sleep diary data were compared between groups by t-test. Sleep was recorded by the Zeo sleep monitoring system for a week in both habitual and extended sleep conditions at home. Results: The main findings of the present study show that short sleeping individuals had deficiency in activity of the MMN and P3a brain responses over frontal areas compared to normal-sleeping subjects. The P3b amplitude was increased over frontal areas and decreased over parietal with respect to the control group. Extension of time in bed for one week increased TST (from 5.7 h to 7.4 h), and concomitantly MMN amplitude increased from −0.1μV up to −1.25 μV over frontal areas. Conclusions: Reduced time in bed is associated with deficiency of the neuronal process associated with change detection, which may recover after one week of sleep extension, whereas attention-dependent neural processes do not normalize after this period of time in habitually short sleeping

Sleep and circadian rhythm disruption in schizophrenia†

PubMed Central

Wulff, Katharina; Dijk, Derk-Jan; Middleton, Benita; Foster, Russell G.; Joyce, Eileen M.

2012-01-01

Background Sleep disturbances comparable with insomnia occur in up to 80% of people with schizophrenia, but very little is known about the contribution of circadian coordination to these prevalent disruptions. Aims A systematic exploration of circadian time patterns in individuals with schizophrenia with recurrent sleep disruption. Method We examined the relationship between sleep-wake activity, recorded actigraphically over 6 weeks, along with ambient light exposure and simultaneous circadian clock timing, by collecting weekly 48 h profiles of a urinary metabolite of melatonin in 20 out-patients with schizophrenia and 21 healthy control individuals matched for age, gender and being unemployed. Results Significant sleep/circadian disruption occurred in all the participants with schizophrenia. Half these individuals showed severe circadian misalignment ranging from phase-advance/delay to non-24 h periods in sleep-wake and melatonin cycles, and the other half showed patterns from excessive sleep to highly irregular and fragmented sleep epochs but with normally timed melatonin production. Conclusions Severe circadian sleep/wake disruptions exist despite stability in mood, mental state and newer antipsychotic treatment. They cannot be explained by the individuals' level of everyday function. PMID:22194182

Sleep Duration in Rough Sea Conditions.

PubMed

Matsangas, Panagiotis; Shattuck, Nita L; McCauley, Michael E

2015-10-01

Environmental motion can affect shipboard sleep of crewmembers. Slamming and similar harsh motion may interfere with sleep, whereas mild motion and sopite syndrome may enhance sleep. If sleep needs vary by sea condition, this factor should be considered when assessing human performance at sea. The goal of this study was to assess sleep duration in different sea conditions. Crewmembers (N = 52) from a U.S. Navy vessel participated in the study while performing their normal daily schedule of duties. Sleep was assessed with wrist-worn actigraphy. Motion sickness and sopite syndrome were assessed using standardized questionnaires. In rough sea conditions, crewmembers experienced increased severity of motion sickness and sopite syndrome compared to their ratings during calmer sea conditions. Crewmembers slept significantly longer during sea state 5-6 compared to sleep on days with sea state 4 (25% increase) and sea state 3-4 (30% increase). Specifically, daily sleep increased from 6.97 ± 1.24 h in sea state 3-4, to 7.23 ± 1.65 h in sea state 4, to 9.04 ± 2.90 h in sea state 5-6. Although the duration of sleep in rough seas increased significantly compared to calmer sea conditions, causal factors are inconclusive. Accumulated sleep debt, motion-induced fatigue, and sopite syndrome all may have contributed, but results suggest that motion sickness and sopite syndrome were the predominant stressors. If sleep needs increase in severe motion environments, this factor should be taken into account when developing daily activity schedules or when modeling manning requirements on modern ships.

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.

Sleep, chronic pain, and opioid risk for apnea.

PubMed

Marshansky, Serguei; Mayer, Pierre; Rizzo, Dorrie; Baltzan, Marc; Denis, Ronald; Lavigne, Gilles J

2017-07-19

Pain is an unwelcome sleep partner. Pain tends to erode sleep quality and alter the sleep restorative process in vulnerable patients. It can contribute to next-day sleepiness and fatigue, affecting cognitive function. Chronic pain and the use of opioid medications can also complicate the management of sleep disorders such as insomnia (difficulty falling and/or staying asleep) and sleep-disordered breathing (sleep apnea). Sleep problems can be related to various types of pain, including sleep headache (hypnic headache, cluster headache, migraine) and morning headache (transient tension type secondary to sleep apnea or to sleep bruxism or tooth grinding) as well as periodic limb movements (leg and arm dysesthesia with pain). Pain and sleep management strategies should be personalized to reflect the patient's history and ongoing complaints. Understanding the pain-sleep interaction requires assessments of: i) sleep quality, ii) potential contributions to fatigue, mood, and/or wake time functioning; iii) potential concomitant sleep-disordered breathing (SDB); and more importantly; iv) opioid use, as central apnea may occur in at-risk patients. Treatments include sleep hygiene advice, cognitive behavioral therapy, physical therapy, breathing devices (continuous positive airway pressure - CPAP, or oral appliance) and medications (sleep facilitators, e.g., zolpidem; or antidepressants, e.g., trazodone, duloxetine, or neuroleptics, e.g., pregabalin). In the presence of opioid-exacerbated SDB, if the dose cannot be reduced and normal breathing restored, servo-ventilation is a promising avenue that nevertheless requires close medical supervision. Copyright © 2017 Elsevier Inc. All rights reserved.

Method, apparatus and system to compensate for drift by physically unclonable function circuitry

DOEpatents

Hamlet, Jason

2016-11-22

Techniques and mechanisms to detect and compensate for drift by a physically uncloneable function (PUF) circuit. In an embodiment, first state information is registered as reference information to be made available for subsequent evaluation of whether drift by PUF circuitry has occurred. The first state information is associated with a first error correction strength. The first state information is generated based on a first PUF value output by the PUF circuitry. In another embodiment, second state information is determined based on a second PUF value that is output by the PUF circuitry. An evaluation of whether drift has occurred is performed based on the first state information and the second state information, the evaluation including determining whether a threshold error correction strength is exceeded concurrent with a magnitude of error being less than the first error correction strength.

Disruption of hierarchical predictive coding during sleep

PubMed Central

Strauss, Melanie; Sitt, Jacobo D.; King, Jean-Remi; Elbaz, Maxime; Azizi, Leila; Buiatti, Marco; Naccache, Lionel; van Wassenhove, Virginie; Dehaene, Stanislas

2015-01-01

When presented with an auditory sequence, the brain acts as a predictive-coding device that extracts regularities in the transition probabilities between sounds and detects unexpected deviations from these regularities. Does such prediction require conscious vigilance, or does it continue to unfold automatically in the sleeping brain? The mismatch negativity and P300 components of the auditory event-related potential, reflecting two steps of auditory novelty detection, have been inconsistently observed in the various sleep stages. To clarify whether these steps remain during sleep, we recorded simultaneous electroencephalographic and magnetoencephalographic signals during wakefulness and during sleep in normal subjects listening to a hierarchical auditory paradigm including short-term (local) and long-term (global) regularities. The global response, reflected in the P300, vanished during sleep, in line with the hypothesis that it is a correlate of high-level conscious error detection. The local mismatch response remained across all sleep stages (N1, N2, and REM sleep), but with an incomplete structure; compared with wakefulness, a specific peak reflecting prediction error vanished during sleep. Those results indicate that sleep leaves initial auditory processing and passive sensory response adaptation intact, but specifically disrupts both short-term and long-term auditory predictive coding. PMID:25737555

Ventilatory response to induced auditory arousals during NREM sleep.

PubMed

Badr, M S; Morgan, B J; Finn, L; Toiber, F S; Crabtree, D C; Puleo, D S; Skatrud, J B

1997-09-01

Sleep state instability is a potential mechanism of central apnea/hypopnea during non-rapid eye movement (NREM) sleep. To investigate this postulate, we induced brief arousals by delivering transient (0.5 second) auditory stimuli during stable NREM sleep in eight normal subjects. Arousal was determined according to American Sleep Disorders Association (ASDA) criteria. A total of 96 trials were conducted; 59 resulted in cortical arousal and 37 did not result in arousal. In trials associated with arousal, minute ventilation (VE) increased from 5.1 +/- 1.24 minutes to 7.5 +/- 2.24 minutes on the first posttone breath (p = 0.001). However, no subsequent hypopnea or apnea occurred as VE decreased gradually to 4.8 +/- 1.5 l/minute (p > 0.05) on the fifth posttone breath. Trials without arousal did not result in hyperpnea on the first breath nor subsequent hypopnea. We conclude that 1) auditory stimulation resulted in transient hyperpnea only if associated with cortical arousal; 2) hypopnea or apnea did not occur following arousal-induced hyperpnea in normal subjects; 3) interaction with fluctuating chemical stimuli or upper airway resistance may be required for arousals to cause sleep-disordered breathing.

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.

Partial sleep deprivation does not alter processes involved in semantic word priming: event-related potential evidence.

PubMed

Tavakoli, Paniz; Muller-Gass, Alexandra; Campbell, Kenneth

2015-03-01

Sleep deprivation has generally been observed to have a detrimental effect on tasks that require sustained attention for successful performance. It might however be possible to counter these effects by altering cognitive strategies. A recent semantic word priming study indicated that subjects used an effortful predictive-expectancy search of semantic memory following normal sleep, but changed to an automatic, effortless strategy following total sleep deprivation. Partial sleep deprivation occurs much more frequently than total sleep deprivation. The present study therefore employed a similar priming task following either 4h of sleep or following normal sleep. The purpose of the study was to determine whether partial sleep deprivation would also lead to a shift in cognitive strategy to compensate for an inability to sustain attention and effortful processing necessary for using the predicative expectancy strategy. Sixteen subjects were presented with word pairs, a prime and a target that were either strongly semantically associated (cat...dog), weakly associated (cow...barn) or not associated (apple...road). The subject's task was to determine if the target word was semantically associated to the prime. A strong priming effect was observed in both conditions. RTs were slower, accuracy lower, and N400 larger to unassociated targets, independent of the amount of sleep. The overall N400 did not differ as a function of sleep. The scalp distribution of the N400 was also similar following both normal sleep and sleep loss. There was thus little evidence of a difference in the processing of the target stimulus as a function of the amount sleep. Similarly, ERPs in the period between the onset of the prime and the subsequent target also did not differ between the normal sleep and sleep loss conditions. In contrast to total sleep deprivation, subjects therefore appeared to use a common predictive expectancy strategy in both conditions. This strategy does however require an

Effects of Macrophage Depletion on Sleep in Mice

PubMed Central

Ames, Conner; Boland, Erin; Szentirmai, Éva

2016-01-01

The reciprocal interaction between the immune system and sleep regulation has been widely acknowledged but the cellular mechanisms that underpin this interaction are not completely understood. In the present study, we investigated the role of macrophages in sleep loss- and cold exposure-induced sleep and body temperature responses. Macrophage apoptosis was induced in mice by systemic injection of clodronate-containing liposomes (CCL). We report that CCL treatment induced an immediate and transient increase in non-rapid-eye movement sleep (NREMS) and fever accompanied by decrease in rapid-eye movement sleep, motor activity and NREMS delta power. Chronically macrophage-depleted mice had attenuated NREMS rebound after sleep deprivation compared to normal mice. Cold-induced increase in wakefulness and decrease in NREMS, rapid-eye movement sleep and body temperature were significantly enhanced in macrophage-depleted mice indicating increased cold sensitivity. These findings provide further evidence for the reciprocal interaction among the immune system, sleep and metabolism, and identify macrophages as one of the key cellular elements in this interplay. PMID:27442442

Reversible obstructive sleep apnea caused by occupational exposure to guar gum dust.

PubMed

Leznoff, A; Haight, J S; Hoffstein, V

1986-05-01

This report describes a case of reversible obstructive sleep apnea caused by occupational exposure to an inhaled allergen, guar gum powder. The patient, a pet food plant employee, also experienced severe cough, rhinitis, and conjunctivitis. Skin tests confirmed the specific guar allergy. Pharyngeal cross-sectional area was smaller than normal. Pulmonary function studies, histamine challenge tests, nasal air-flow resistance measurements, and nocturnal polysomnography were performed on 3 separate occasions: while the patient was working at his usual occupation, at the end of a 3-wk holiday, and after a guar dust challenge in an inhalation chamber. Pulmonary function and histamine challenge tests were consistently normal. At the time of the initial tests, nasal resistance was elevated, and nocturnal polysomnography revealed obstructive sleep apnea. After absence from work, obstructive sleep apnea resolved, and the nasal resistance returned to normal. After challenge with guar gum dust, the patient developed increased resistance to nasal air flow, and obstructive sleep apnea reappeared. This case demonstrates that allergy can cause reversible obstructive sleep apnea and that occupational exposure should be considered in the assessment of patients with this disease.

Spaceflight induces changes in the synaptic circuitry of the postnatal developing neocortex

NASA Technical Reports Server (NTRS)

DeFelipe, J.; Arellano, J. I.; Merchan-Perez, A.; Gonzalez-Albo, M. C.; Walton, K.; Llinas, R.

2002-01-01

The establishment of the adult pattern of neocortical circuitry depends on various intrinsic and extrinsic factors, whose modification during development can lead to alterations in cortical organization and function. We report the effect of 16 days of spaceflight [Neurolab mission; from postnatal day 14 (P14) to P30] on the neocortical representation of the hindlimb synaptic circuitry in rats. As a result, we show, for the first time, that development in microgravity leads to changes in the number and morphology of cortical synapses in a laminar-specific manner. In the layers II/III and Va, the synaptic cross-sectional lengths were significantly larger in flight animals than in ground control animals. Flight animals also showed significantly lower synaptic densities in layers II/III, IV and Va. The greatest difference was found in layer II/III, where there was a difference of 344 million synapses per mm(3) (15.6% decrease). Furthermore, after a 4 month period of re-adaptation to terrestrial gravity, some changes disappeared (i.e. the alterations were transient), while conversely, some new differences also appeared. For example, significant differences in synaptic density in layers II/III and Va after re-adaptation were no longer observed, whereas in layer IV the density of synapses increased notably in flight animals (a difference of 185 million synapses per mm(3) or 13.4%). In addition, all the changes observed only affected asymmetrical synapses, which are known to be excitatory. These results indicates that terrestrial gravity is a necessary environmental parameter for normal cortical synaptogenesis. These findings are fundamental in planning future long-term spaceflights.

Perceptual impairment in face identification with poor sleep

PubMed Central

Beattie, Louise; Walsh, Darragh; McLaren, Jessica; Biello, Stephany M.

2016-01-01

Previous studies have shown impaired memory for faces following restricted sleep. However, it is not known whether lack of sleep impairs performance on face identification tasks that do not rely on recognition memory, despite these tasks being more prevalent in security and forensic professions—for example, in photo-ID checks at national borders. Here we tested whether poor sleep affects accuracy on a standard test of face-matching ability that does not place demands on memory: the Glasgow Face-Matching Task (GFMT). In Experiment 1, participants who reported sleep disturbance consistent with insomnia disorder show impaired accuracy on the GFMT when compared with participants reporting normal sleep behaviour. In Experiment 2, we then used a sleep diary method to compare GFMT accuracy in a control group to participants reporting poor sleep on three consecutive nights—and again found lower accuracy scores in the short sleep group. In both experiments, reduced face-matching accuracy in those with poorer sleep was not associated with lower confidence in their decisions, carrying implications for occupational settings where identification errors made with high confidence can have serious outcomes. These results suggest that sleep-related impairments in face memory reflect difficulties in perceptual encoding of identity, and point towards metacognitive impairment in face matching following poor sleep. PMID:27853547

Stitching Codeable Circuits: High School Students' Learning about Circuitry and Coding with Electronic Textiles

ERIC Educational Resources Information Center

Litts, Breanne K.; Kafai, Yasmin B.; Lui, Debora A.; Walker, Justice T.; Widman, Sari A.

2017-01-01

Learning about circuitry by connecting a battery, light bulb, and wires is a common activity in many science classrooms. In this paper, we expand students' learning about circuitry with electronic textiles, which use conductive thread instead of wires and sewable LEDs instead of lightbulbs, by integrating programming sensor inputs and light…

Adenosine A2A receptors in ventral striatum, hypothalamus and nociceptive circuitry. Implications for drug addiction, sleep and pain

PubMed Central

Ferré, S.; Diamond, I.; Goldberg, S.R.; Yao, L.; Hourani, S.M.O.; Huang, Z.L.; Urade, Y.; Kitchen, I.

2007-01-01

Adenosine A2A receptors localized in the dorsal striatum are considered as a new target for the development of antiparkinsonian drugs. Co-administration of A2A receptor antagonists has shown a significant improvement of the effects of L-DOPA. The present review emphasizes the possible application of A2A receptor antagonists in pathological conditions other than parkinsonism, including drug addiction, sleep disorders and pain. In addition to the dorsal striatum, the ventral striatum (nucleus accumbens) contains a high density of A2A receptors, which presynaptically and postsynaptically regulate glutamatergic transmission in the cortical glutamatergic projections to the nucleus accumbens. It is currently believed that molecular adaptations of the cortico-accumbens glutamatergic synapses are involved in compulsive drug seeking and relapse. Here we review recent experimental evidence suggesting that A2A antagonists could become new therapeutic agents for drug addiction. Morphological and functional studies have identified lower levels of A2A receptors in brain areas other than the striatum, such as the ventrolateral preoptic area of the hypothalamus, where adenosine plays an important role in sleep regulation. Although initially believed to be mostly dependent on A1 receptors, here we review recent studies that demonstrate that the somnogenic effects of adenosine are largely mediated by hypothalamic A2A receptors. A2A receptor antagonists could therefore be considered as a possible treatment for narcolepsy and other sleep-related disorders. Finally, nociception is another adenosine-regulated neural function previously thought to mostly involve A1 receptors. Although there is some conflicting literature on the effects of agonists and antagonists, which may partly be due to the lack of selectivity of available drugs, the studies in A2A receptor knockout mice suggest that A2A receptor antagonists might have some therapeutic potential in pain states, in particular where

Delayed Sleep Phase Disorder In Temporal Isolation

PubMed Central

Campbell, Scott S.; Murphy, Patricia J.

2007-01-01

Study Objectives: This study sought to characterize sleep and the circadian rhythm of body core temperature of an individual with delayed sleep phase disorder (DSPD) in the absence of temporal cues and social entrainment and to compare those measures to age-matched normal control subjects studied under identical conditions. Design: Polysomnography and body temperature were recorded continuously for 4 days in entrained conditions, followed immediately by 17 days in a “free-running” environment. Setting: Temporal isolation facility in the Laboratory of Human Chronobiology, Weill Cornell Medical College. Participants: One individual who met criteria for delayed sleep phase disorder according to the International Classification of Sleep Disorders Diagnostic and Coding Manual (ICSD-2) and 3 age-matched control subjects. Interventions: None. Measurements and Results: The DSPD subject had a spontaneous period length (tau) of 25.38 hours compared to an average tau of 24.44 hours for the healthy controls. The DSPD subject also showed an altered phase relationship between sleep/wake and body temperature rhythms, as well as longer sleep latency, poorer sleep efficiency, and altered distribution of slow wave sleep (SWS) within sleep episodes, compared to control subjects. Conclusions: Delayed sleep phase disorder may be the reflection of an abnormal circadian timing system characterized not only by a long tau, but also by an altered internal phase relationship between the sleep/wake system and the circadian rhythm of body temperature. The latter results in significantly disturbed sleep, even when DSPD patients are permitted to sleep and wake at their preferred times. Citation: Campbell SS; Murphy PJ. Delayed sleep phase disorder in temporal isolation. SLEEP 2007;30(9):1225-1228. PMID:17910395

Insufficient sleep in adolescents: causes and consequences.

PubMed

Owens, Judith A; Weiss, Miriam R

2017-08-01

Insufficient sleep poses an important and complicated set of health risks in the adolescent population. Not only is deficient sleep (defined as both sleep duration inadequate to meet sleep needs and sleep timing misaligned with the body's circadian rhythms) at epidemic levels in this population, but the contributing factors are both complex and numerous and there are a myriad of negative physical and mental health, safety and performance consequences. Causes of inadequate sleep identified in this population include internal biological processes such as the normal shift (delay) in circadian rhythm that occurs in association with puberty and a developmentally-based slowing of the "sleep drive", and external factors including extracurricular activities, excessive homework load, evening use of electronic media, caffeine intake and early school start times. Consequences range from inattentiveness, reduction in executive functioning and poor academic performance to increased risk of obesity and cardio-metabolic dysfunction, mood disturbances which include increased suicidal ideation, a higher risk of engaging in health risk behaviors such as alcohol and substance use, and increased rates of car crashes, occupational injuries and sports-related injuries. In response to these concerns, a number of promising measures have been proposed to reduce the burden of adolescent sleep loss, including healthy sleep education for students and families, and later school start times to allow adolescents to obtain sufficient and appropriately-timed sleep.

Catecholaminergic connectivity to the inner ear, central auditory and vocal motor circuitry in the plainfin midshipman fish, Porichthys notatus

PubMed Central

Forlano, Paul M.; Kim, Spencer D.; Krzyminska, Zuzanna M.; Sisneros, Joseph A.

2014-01-01

Although the neuroanatomical distribution of catecholaminergic (CA) neurons has been well documented across all vertebrate classes, few studies have examined CA connectivity to physiologically and anatomically identified neural circuitry that controls behavior. The goal of this study was to characterize CA distribution in the brain and inner ear of the plainfin midshipman fish (Porichthys notatus) with particular emphasis on their relationship with anatomically labeled circuitry that both produces and encodes social acoustic signals in this species. Neurobiotin labeling of the main auditory endorgan, the saccule, combined with tyrosine hydroxylase immunofluorescence (TH-ir) revealed a strong CA innervation of both the peripheral and central auditory system. Diencephalic TH-ir neurons in the periventricular posterior tuberculum, known to be dopaminergic, send ascending projections to the ventral telencephalon and prominent descending projections to vocal-acoustic integration sites, notably the hindbrain octavolateralis efferent nucleus, as well as onto the base of hair cells in the saccule via nerve VIII. Neurobiotin backfills of the vocal nerve in combination with TH-ir revealed CA terminals on all components of the vocal pattern generator which appears to largely originate from local TH-ir neurons but may include diencephalic projections as well. This study provides strong evidence for catecholamines as important neuromodulators of both auditory and vocal circuitry and acoustic-driven social behavior in midshipman fish. This first demonstration of TH-ir terminals in the main endorgan of hearing in a non-mammalian vertebrate suggests a conserved and important anatomical and functional role for dopamine in normal audition. PMID:24715479

Consumer sleep tracking devices: a review of mechanisms, validity and utility.

PubMed

Kolla, Bhanu Prakash; Mansukhani, Subir; Mansukhani, Meghna P

2016-05-01

Consumer sleep tracking devices such as fitness trackers and smartphone apps have become increasingly popular. These devices claim to measure the sleep duration of their users and in some cases purport to measure sleep quality and awaken users from light sleep, potentially improving overall sleep. Most of these devices appear to utilize data generated from in-built accelerometers to determine sleep parameters but the exact mechanisms and algorithms are proprietary. The growing literature comparing these devices against polysomnography/actigraphy shows that they tend to underestimate sleep disruptions and overestimate total sleep times and sleep efficiency in normal subjects. In this review, we evaluate the current literature comparing the accuracy of consumer sleep tracking devices against more conventional methods used to measure sleep duration and quality. We discuss the current technology that these devices utilize as well as summarize the value of these devices in clinical evaluations and their potential limitations.

Methscopolamine Inhibition of Sleep-Related Growth Hormone Secretion

PubMed Central

Mendelson, Wallace B.; Sitaram, Natarajan; Wyatt, Richard Jed; Gillin, J. Christian; Jacobs, Laurence S.

1978-01-01

We have examined the effects of cholinergic blockade with 0.5 mg methscopolamine bromide, intramuscularly, on sleep-related and insulin-induced growth hormone (GH) secretion. 17 normal young men were studied; 8 had sleep studies, and 12 (including 3 who also had sleep studies) had insulin tolerance tests (ITT) with 0.1 U/kg of regular insulin. After an adjustment night in the sleep laboratory, saline control night and methscopolamine night studies were done in random sequence; study procedures included electroencephalographic, electromyographic, and electrooculographic recordings, and blood sampling every 20 min for hormone radioimmunoassays. Prolactin levels were also measured during sleep. For methscopolamine night studies, the mean overall control GH level of 2.89±0.44 ng/ml and the mean peak control GH level of 11.09±3.11 ng/ml were dramatically reduced to 0.75±0.01 and 1.04±0.25 ng/ml, respectively (P<0.0001 and <0.001). Despite virtual absence of GH secretion during the night in every study subject, no measured sleep characteristic was affected by methscopolamine, including total slow-wave sleep (12.1±2.6% control vs. 10.3±2.5% drug, P>0.2). Sleep prolactin levels were not changed by methscopolamine. In contrast to the abolition of sleep-related GH secretion, administration of methscopolamine had only a marginal effect on the GH response to insulin hypoglycemia. None of nine time points differed significantly, as was also the case with peak levels, mean increments, and areas under the curves (P>0.2). Analysis of variance did, however, indicate that the lower GH concentrations achieved during ITT after methscopolamine (average 31.7% below control) were significantly different than control concentrations. We conclude that the burst of GH secretion which normally occurs after sleep onset is primed by a cholinergic mechanism which does not influence slow-wave sleep. Cholinergic mechanisms do not appear to play an important role in sleep-related prolactin

Rest-activity rhythm and sleep characteristics associated with depression symptom severity in strained dementia caregivers.

PubMed

Smagula, Stephen F; Krafty, Robert T; Taylor, Briana J; Martire, Lynn M; Schulz, Richard; Hall, Martica H

2017-12-01

Depression is associated with disturbances to sleep and the 24-h sleep-wake pattern (known as the rest-activity rhythm: RAR). However, there remains a need to identify the specific sleep/RAR correlates of depression symptom severity in population subgroups, such as strained dementia caregivers, who are at elevated risk for major depressive disorder. We assessed the cross-sectional associations of sleep/RARs with non-sleep depression symptom severity among 57 (mean age: 74 years, standard deviation: 7.4) strained dementia caregivers who were currently without clinical depression. We derived sleep measures from polysomnography and actigraphy, modelled RARs using a sigmoidally transformed cosine curve and measured non-sleep depression symptom severity using the Hamilton Depression Rating Scale (HRDS) with sleep items removed. The following sleep-wake measures were associated with greater depression symptom severity (absolute Spearman's correlations ranged from 0.23 to 0.32): more time awake after sleep onset (WASO), higher RAR middle level (mesor), relatively shorter active periods (alpha), earlier evening settling time (down-mesor) and less steep RARs (beta). In multivariable analysis, high WASO and low RAR beta were associated independently with depression symptom severity. Predicted non-sleep HDRS means (95% confidence intervals) in caregivers with and without these characteristics were: normal WASO/beta = 3.7 (2.3-5.0), high WASO/normal beta = 5.5 (3.5-7.6), normal WASO/low beta = 6.3 (3.6-8.9) and high WASO/low beta = 8.1 (5.3-10.9). Thus, in our sample of strained caregivers, greater sleep fragmentation (WASO) and less sustained/sharply segregated resting and active periods (low RAR beta) correlate uniquely with depression symptom severity. Longitudinal studies are needed to establish whether these independent sleep-wake correlates of depression symptoms explain heightened depression risk in dementia caregivers. © 2017 European Sleep Research Society.

Neural circuitry and immunity

PubMed Central

Pavlov, Valentin A.; Tracey, Kevin J.

2015-01-01

Research during the last decade has significantly advanced our understanding of the molecular mechanisms at the interface between the nervous system and the immune system. Insight into bidirectional neuroimmune communication has characterized the nervous system as an important partner of the immune system in the regulation of inflammation. Neuronal pathways, including the vagus nerve-based inflammatory reflex are physiological regulators of immune function and inflammation. In parallel, neuronal function is altered in conditions characterized by immune dysregulation and inflammation. Here, we review these regulatory mechanisms and describe the neural circuitry modulating immunity. Understanding these mechanisms reveals possibilities to use targeted neuromodulation as a therapeutic approach for inflammatory and autoimmune disorders. These findings and current clinical exploration of neuromodulation in the treatment of inflammatory diseases defines the emerging field of Bioelectronic Medicine. PMID:26512000

Functional Anatomy of Non-REM Sleep

PubMed Central

de Andrés, Isabel; Garzón, Miguel; Reinoso-Suárez, Fernando

2011-01-01

The state of non-REM sleep (NREM), or slow wave sleep, is associated with a synchronized EEG pattern in which sleep spindles and/or K complexes and high-voltage slow wave activity (SWA) can be recorded over the entire cortical surface. In humans, NREM is subdivided into stages 2 and 3–4 (presently named N3) depending on the proportions of each of these polygraphic events. NREM is necessary for normal physical and intellectual performance and behavior. An overview of the brain structures involved in NREM generation shows that the thalamus and the cerebral cortex are absolutely necessary for the most significant bioelectric and behavioral events of NREM to be expressed; other structures like the basal forebrain, anterior hypothalamus, cerebellum, caudal brain stem, spinal cord and peripheral nerves contribute to NREM regulation and modulation. In NREM stage 2, sustained hyperpolarized membrane potential levels resulting from interaction between thalamic reticular and projection neurons gives rise to spindle oscillations in the membrane potential; the initiation and termination of individual spindle sequences depends on corticothalamic activities. Cortical and thalamic mechanisms are also involved in the generation of EEG delta SWA that appears in deep stage 3–4 (N3) NREM; the cortex has classically been considered to be the structure that generates this activity, but delta oscillations can also be generated in thalamocortical neurons. NREM is probably necessary to normalize synapses to a sustainable basal condition that can ensure cellular homeostasis. Sleep homeostasis depends not only on the duration of prior wakefulness but also on its intensity, and sleep need increases when wakefulness is associated with learning. NREM seems to ensure cell homeostasis by reducing the number of synaptic connections to a basic level; based on simple energy demands, cerebral energy economizing during NREM sleep is one of the prevalent hypotheses to explain NREM homeostasis

Activation of Corticostriatal Circuitry Relieves Chronic Neuropathic Pain

PubMed Central

Lee, Michelle; Manders, Toby R.; Eberle, Sarah E.; Su, Chen; D'amour, James; Yang, Runtao; Lin, Hau Yueh; Deisseroth, Karl; Froemke, Robert C.

2015-01-01

Neural circuits that determine the perception and modulation of pain remain poorly understood. The prefrontal cortex (PFC) provides top-down control of sensory and affective processes. While animal and human imaging studies have shown that the PFC is involved in pain regulation, its exact role in pain states remains incompletely understood. A key output target for the PFC is the nucleus accumbens (NAc), an important component of the reward circuitry. Interestingly, recent human imaging studies suggest that the projection from the PFC to the NAc is altered in chronic pain. The function of this corticostriatal projection in pain states, however, is not known. Here we show that optogenetic activation of the PFC produces strong antinociceptive effects in a rat model (spared nerve injury model) of persistent neuropathic pain. PFC activation also reduces the affective symptoms of pain. Furthermore, we show that this pain-relieving function of the PFC is likely mediated by projections to the NAc. Thus, our results support a novel role for corticostriatal circuitry in pain regulation. PMID:25834050

DNA-based random number generation in security circuitry.

PubMed

Gearheart, Christy M; Arazi, Benjamin; Rouchka, Eric C

2010-06-01

DNA-based circuit design is an area of research in which traditional silicon-based technologies are replaced by naturally occurring phenomena taken from biochemistry and molecular biology. This research focuses on further developing DNA-based methodologies to mimic digital data manipulation. While exhibiting fundamental principles, this work was done in conjunction with the vision that DNA-based circuitry, when the technology matures, will form the basis for a tamper-proof security module, revolutionizing the meaning and concept of tamper-proofing and possibly preventing it altogether based on accurate scientific observations. A paramount part of such a solution would be self-generation of random numbers. A novel prototype schema employs solid phase synthesis of oligonucleotides for random construction of DNA sequences; temporary storage and retrieval is achieved through plasmid vectors. A discussion of how to evaluate sequence randomness is included, as well as how these techniques are applied to a simulation of the random number generation circuitry. Simulation results show generated sequences successfully pass three selected NIST random number generation tests specified for security applications.

Sleep Architecture Linked to Airway Obstruction and Intracranial Hypertension in Children with Syndromic Craniosynostosis.

PubMed

Spruijt, Bart; Mathijssen, Irene M J; Bredero-Boelhouwer, Hansje H; Cherian, Perumpillichira J; Corel, Linda J A; van Veelen, Marie-Lise; Hayward, Richard D; Tasker, Robert C; Joosten, Koen F M

2016-12-01

Children with syndromic craniosynostosis often have obstructive sleep apnea and intracranial hypertension. The authors aimed to evaluate (1) sleep architecture, and determine whether this is influenced by the presence of obstructive sleep apnea and/or intracranial hypertension; and (2) the effect of treatment on sleep architecture. This study included patients with syndromic craniosynostosis treated at a national referral center, undergoing screening for obstructive sleep apnea and intracranial hypertension. Obstructive sleep apnea was identified by polysomnography, and categorized into no, mild, moderate, or severe. Intracranial hypertension was identified by the presence of papilledema on funduscopy, supplemented by optical coherence tomography and/or intracranial pressure monitoring. Regarding sleep architecture, sleep was divided into rapid eye movement or non-rapid eye movement sleep; respiratory effort-related arousals and sleep efficiency were scored. The authors included 39 patients (median age, 5.9 years): 19 with neither obstructive sleep apnea nor intracranial hypertension, 11 with obstructive sleep apnea (four moderate/severe), six with intracranial hypertension, and three with obstructive sleep apnea and intracranial hypertension. Patients with syndromic craniosynostosis, independent of the presence of mild obstructive sleep apnea and/or intracranial hypertension, have normal sleep architecture compared with age-matched controls. Patients with moderate/severe obstructive sleep apnea have a higher respiratory effort-related arousal index (p < 0.01), lower sleep efficiency (p = 0.01), and less rapid eye movement sleep (p = 0.04). An improvement in sleep architecture was observed following monobloc surgery (n = 5; rapid eye movement sleep, 5.3 percent; p = 0.04). Children with syndromic craniosynostosis have in principle normal sleep architecture. However, moderate/severe obstructive sleep apnea does lead to disturbed sleep architecture, which fits within

Honeybees consolidate navigation memory during sleep.

PubMed

Beyaert, Lisa; Greggers, Uwe; Menzel, Randolf

2012-11-15

Sleep is known to support memory consolidation in animals, including humans. Here we ask whether consolidation of novel navigation memory in honeybees depends on sleep. Foragers were exposed to a forced navigation task in which they learned to home more efficiently from an unexpected release site by acquiring navigational memory during the successful homing flight. This task was quantified using harmonic radar tracking and applied to bees that were equipped with a radio frequency identification device (RFID). The RFID was used to record their outbound and inbound flights and continuously monitor their behavior inside the colony, including their rest during the day and sleep at night. Bees marked with the RFID behaved normally inside and outside the hive. Bees slept longer during the night following forced navigation tasks, but foraging flights of different lengths did not lead to different rest times during the day or total sleep time during the night. Sleep deprivation before the forced navigation task did not alter learning and memory acquired during the task. However, sleep deprivation during the night after forced navigation learning reduced the probability of returning successfully to the hive from the same release site. It is concluded that consolidation of novel navigation memory is facilitated by night sleep in bees.

Persistent Insomnia: the Role of Objective Short Sleep Duration and Mental Health

PubMed Central

Vgontzas, Alexandros N.; Fernandez-Mendoza, Julio; Bixler, Edward O.; Singareddy, Ravi; Shaffer, Michele L.; Calhoun, Susan L.; Liao, Duanping; Basta, Maria; Chrousos, George P.

2012-01-01

Study Objectives: Few population-based, longitudinal studies have examined risk factors for persistent insomnia, and the results are inconsistent. Furthermore, none of these studies have examined the role of polysomnographic (PSG) variables such as sleep duration or sleep apnea on the persistence of insomnia. Design: Representative longitudinal study. Setting: Sleep laboratory. Participants: From a random, general population sample of 1741 individuals of the adult Penn State Cohort, 1395 were followed-up after 7.5 years. Measurements: Individuals underwent one-night PSG and full medical evaluation at baseline and a telephone interview at follow-up. PSG sleep duration was analyzed as a continuous variable and as a categorical variable: < 6 h sleep (short sleep duration) and ≥ 6 h sleep (longer sleep duration). Results: The rates of insomnia persistence, partial remission, and full remission were 44.0%, 30.0%, and 26.0%, respectively. Objective short sleep duration significantly increased the odds of persistent insomnia as compared to normal sleep (OR = 3.19) and to fully remitted insomnia (OR = 4.92). Mental health problems at baseline were strongly associated with persistent insomnia as compared to normal sleep (OR = 9.67) and to a lesser degree compared to fully remitted insomnia (OR = 3.68). Smoking, caffeine, and alcohol consumption and sleep apnea did not predict persistent insomnia. Conclusions: Objective short sleep duration and mental health problems are the strongest predictors of persistent insomnia. These data further support the validity and clinical utility of objective short sleep duration as a novel marker of the biological severity of insomnia. Citation: Vgontzas AN; Fernandez-Mendoza J; Bixler EO; Singareddy R; Shaffer ML; Calhoun SL; Liao D; Basta M; Chrousos GP. Persistent insomnia: the role of objective short sleep duration and mental health. SLEEP 2012;35(1):61-68. PMID:22215919

Sleep Position Trainer versus Tennis Ball Technique in Positional Obstructive Sleep Apnea Syndrome

PubMed Central

Eijsvogel, Michiel M.; Ubbink, Rinse; Dekker, Janita; Oppersma, Eline; de Jongh, Frans H.; van der Palen, Job; Brusse-Keizer, Marjolein G.

2015-01-01

Study Objective: Positional therapy (PT) is an effective therapy in positional obstructive sleep apnea syndrome (POSAS) when used, but the compliance of PT is low. The objective of this study was to investigate whether a new kind of PT is effective and can improve compliance. Methods: 29 patients were treated with the sleep position trainer (SPT), 26 patients with the tennis ball technique (TBT). At baseline and 1 month polysomnography, Epworth Sleepiness Scale (ESS) and the Quebec Sleep Questionnaire (QSQ) were taken. Daily compliance was objectively measured in both groups. Results: Both therapies prevent supine sleep position to a median of 0% (min-max: SPT 0.0% to 67%, TBT 0.0% to 38.9%), resulting in a treatment success (AHI < 5) in 68.0% of the SPT and 42.9% of the TBT patients. The ESS at baseline was < 10 in both groups. Sleep quality parameters, such as wake after sleep onset (WASO; p = 0.001) and awakenings (p = 0.006), improved more in the SPT group. Total QSQ scores (0.4 ± 0.2, p = 0.03), the QSQ domains nocturnal symptoms (0.7 ± 0.2, p = 0.01), and social interactions (0.8 ± 0.3, p = 0.02) changed in favor of the SPT group. Effective compliance (≥ 4 h/night + ≥ 5 days/week) was 75.9% for the SPT and 42.3% for the TBT users (p = 0.01). Conclusion: In mild POSAS with normal EES the new SPT device and the standard TBT are equally effective in reducing respiratory indices. However, compared to the TBT, sleep quality, quality of life, and compliance improved significantly more in the SPT group. Citation: Eijsvogel MM, Ubbink R, Dekker J, Oppersma E, de Jongh FH, van der Palen J, Brusse-Keizer MG. Sleep position trainer versus tennis ball technique in positional obstructive sleep apnea syndrome. J Clin Sleep Med 2015;11(2):139–147. PMID:25515276

The effect of sleep deprivation on BOLD activity elicited by a divided attention task.

PubMed

Jackson, Melinda L; Hughes, Matthew E; Croft, Rodney J; Howard, Mark E; Crewther, David; Kennedy, Gerard A; Owens, Katherine; Pierce, Rob J; O'Donoghue, Fergal J; Johnston, Patrick

2011-06-01

Sleep loss, widespread in today's society and associated with a number of clinical conditions, has a detrimental effect on a variety of cognitive domains including attention. This study examined the sequelae of sleep deprivation upon BOLD fMRI activation during divided attention. Twelve healthy males completed two randomized sessions; one after 27 h of sleep deprivation and one after a normal night of sleep. During each session, BOLD fMRI was measured while subjects completed a cross-modal divided attention task (visual and auditory). After normal sleep, increased BOLD activation was observed bilaterally in the superior frontal gyrus and the inferior parietal lobe during divided attention performance. Subjects reported feeling significantly more sleepy in the sleep deprivation session, and there was a trend towards poorer divided attention task performance. Sleep deprivation led to a down regulation of activation in the left superior frontal gyrus, possibly reflecting an attenuation of top-down control mechanisms on the attentional system. These findings have implications for understanding the neural correlates of divided attention and the neurofunctional changes that occur in individuals who are sleep deprived.

Insufficient sleep is associated with impaired nitric oxide-mediated endothelium-dependent vasodilation.

PubMed

Bain, Anthony R; Weil, Brian R; Diehl, Kyle J; Greiner, Jared J; Stauffer, Brian L; DeSouza, Christopher A

2017-10-01

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. 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. 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. 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. Copyright © 2017 Elsevier B.V. All rights reserved.

Total sleep deprivation decreases flow experience and mood status

PubMed Central

Kaida, Kosuke; Niki, Kazuhisa

2014-01-01

Background The purpose of this study was to examine the effect of sleep deprivation on flow experience. Methods Sixteen healthy male volunteers of mean age 21.4±1.59 (21–24) years participated in two experimental conditions, ie, sleep-deprivation and normal sleep. In the sleep-deprived condition, participants stayed awake at home for 36 hours (from 8 am until 10 pm the next day) beginning on the day prior to an experimental day. In both conditions, participants carried out a simple reaction time (psychomotor vigilance) task and responded to a questionnaire measuring flow experience and mood status. Results Flow experience was reduced after one night of total sleep deprivation. Sleep loss also decreased positive mood, increased negative mood, and decreased psychomotor performance. Conclusion Sleep deprivation has a strong impact on mental and behavioral states associated with the maintenance of flow, namely subjective well-being. PMID:24376356

Does Sleep Improve Memory Organization?

PubMed Central

Takeuchi, Masashi; Furuta, Hisakazu; Sumiyoshi, Tomiki; Suzuki, Michio; Ochiai, Yoko; Hosokawa, Munehito; Matsui, Mie; Kurachi, Masayoshi

2014-01-01

Sleep can integrate information into existing memory networks, look for common patterns and distil overarching rules, or simply stabilize and strengthen the memory exactly as it was learned. Recent research has shown that sleep facilitates abstraction of gist information as well as integration across multiple memories, insight into hidden solutions, and even the ability to make creative connections between distantly related ideas and concepts. To investigate the effect of sleep on memory organization, 35 normal volunteers were randomly assigned either to the sleep (n = 17) or wake group (n = 18). The sleep subjects performed the Japanese Verbal Learning Test (JVLT), a measure of learning and memory, three times in the evening, and slept. On the following morning (9 h later), they were asked to recall the words on the list. The wake subjects took the same test in the morning, and were asked to recall the words in the same time interval as in the sleep group. The semantic clustering ratio (SCR), divided by the total number of words recalled, was used as an index of memory organization. Our main interest was whether the sleep subjects elicit a greater increase in this measure from the third to the fourth assessments. Time × Group interaction effect on SCR was not significant between the sleep group and wake group as a whole. Meanwhile, the change in the SCR between the third and fourth trials was negatively correlated with duration of nocturnal waking in the sleep group, but not other sleep indices. Based on this observation, further analysis was conducted for subjects in the sleep group who awoke nocturnally for <60 min for comparison with the wake group. A significant Time × Group interaction was noted; these “good-sleepers” showed a significantly greater improvement in the memory index compared with the wake subjects. These results provide the first suggestion that sleep may enhance memory organization, which requires further study. PMID

Neurological, psychological and polygraphic findings in sleep drunkenness.

PubMed

Roth, B; Nevsímalová, S; Ságová, V; Paroubková, D; Horáková, A

1981-01-01

Eight patients suffering from idiopathic hypersomnia with sleep drunkenness were given neurological, psychological and polygraphic investigations, and that after 4, 8 and 12 hours of nocturnal sleep. Also examined and tested were 8 controls - after 4, 8 and 0 hours of sleep during the preceding night. The patients and the controls were awakened and tested in the afternoon hours 30-45 minutes after they had fallen asleep. Under those circumstances the state of sleep drunkenness was observed in the patients in 19 instances, but only once in the controls. While experiencing sleep drunkenness the subjects were found to have prominent cerebellar signs, proprioceptive hypo- or even areflexia, signs of vestibular and, rarely, pyramidal tract involvement. Psychological tests scores and scores for the fine and gross motricity tests were substantially worse in sleep drunkenness than in wakefulness. Sleep drunkenness manifested itself in the polygraphic recordings by signs of microsleep. Pathological predisposition to the development of sleep drunkenness in hypersomniacs was found to be the most significant factor responsible for the occurrence of this state. Attention is drawn to the analogy between states of sleep drunkenness and automatic behaviour in narcoleptics and hypersomniacs as a common feature of both states. The authors believe that sleep drunkenness in idiopathic hypersomnia develops as a result of chronic relative sleep deprivation in those patients whose sleep requirements are greater than conditions of normal life can permit.

Stress-free automatic sleep deprivation using air puffs

PubMed Central

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

2015-01-01

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

Stress-free automatic sleep deprivation using air puffs.

PubMed

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

2015-08-15

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

Functional Maps of Neocortical Local Circuitry

PubMed Central

Thomson, Alex M.; Lamy, Christophe

2007-01-01

This review aims to summarize data obtained with different techniques to provide a functional map of the local circuit connections made by neocortical neurones, a reference for those interested in cortical circuitry and the numerical information required by those wishing to model the circuit. A brief description of the main techniques used to study circuitry is followed by outline descriptions of the major classes of neocortical excitatory and inhibitory neurones and the connections that each layer makes with other cortical and subcortical regions. Maps summarizing the projection patterns of each class of neurone within the local circuit and tables of the properties of these local circuit connections are provided. This review relies primarily on anatomical studies that have identified the classes of neurones and their local and long distance connections and on paired intracellular and whole-cell recordings which have documented the properties of the connections between them. A large number of different types of synaptic connections have been described, but for some there are only a few published examples and for others the details that can only be obtained with paired recordings and dye-filling are lacking. A further complication is provided by the range of species, technical approaches and age groups used in these studies. Wherever possible the range of available data are summarised and compared. To fill some of the more obvious gaps for the less well-documented cases, data obtained with other methods are also summarized. PMID:18982117

Sleep disorders associated with primary mitochondrial diseases.

PubMed

Ramezani, Ryan J; Stacpoole, Peter W

2014-11-15

Primary mitochondrial diseases are caused by heritable or spontaneous mutations in nuclear DNA or mitochondrial DNA. Such pathological mutations are relatively common in humans and may lead to neurological and neuromuscular complication that could compromise normal sleep behavior. To gain insight into the potential impact of primary mitochondrial disease and sleep pathology, we reviewed the relevant English language literature in which abnormal sleep was reported in association with a mitochondrial disease. We examined publication reported in Web of Science and PubMed from February 1976 through January 2014, and identified 54 patients with a proven or suspected primary mitochondrial disorder who were evaluated for sleep disturbances. Both nuclear DNA and mitochondrial DNA mutations were associated with abnormal sleep patterns. Most subjects who underwent polysomnography had central sleep apnea, and only 5 patients had obstructive sleep apnea. Twenty-four patients showed decreased ventilatory drive in response to hypoxia and/ or hyperapnea that was not considered due to weakness of the intrinsic muscles of respiration. Sleep pathology may be an underreported complication of primary mitochondrial diseases. The probable underlying mechanism is cellular energy failure causing both central neurological and peripheral neuromuscular degenerative changes that commonly present as central sleep apnea and poor ventilatory response to hyperapnea. Increased recognition of the genetics and clinical manifestations of mitochondrial diseases by sleep researchers and clinicians is important in the evaluation and treatment of all patients with sleep disturbances. Prospective population-based studies are required to determine the true prevalence of mitochondrial energy failure in subjects with sleep disorders, and conversely, of individuals with primary mitochondrial diseases and sleep pathology. © 2014 American Academy of Sleep Medicine.

Integration of human sleep-wake regulation and circadian rhythmicity

NASA Technical Reports Server (NTRS)

Dijk, Derk-Jan; Lockley, Steven W.

2002-01-01

The human sleep-wake cycle is generated by a circadian process, originating from the suprachiasmatic nuclei, in interaction with a separate oscillatory process: the sleep homeostat. The sleep-wake cycle is normally timed to occur at a specific phase relative to the external cycle of light-dark exposure. It is also timed at a specific phase relative to internal circadian rhythms, such as the pineal melatonin rhythm, the circadian sleep-wake propensity rhythm, and the rhythm of responsiveness of the circadian pacemaker to light. Variations in these internal and external phase relationships, such as those that occur in blindness, aging, morning and evening, and advanced and delayed sleep-phase syndrome, lead to sleep disruptions and complaints. Changes in ocular circadian photoreception, interindividual variation in the near-24-h intrinsic period of the circadian pacemaker, and sleep homeostasis can contribute to variations in external and internal phase. Recent findings on the physiological and molecular-genetic correlates of circadian sleep disorders suggest that the timing of the sleep-wake cycle and circadian rhythms is closely integrated but is, in part, regulated differentially.

Evaluation of neuromuscular activity in patients with obstructive sleep apnea using chin surface electromyography of polysomnography.

PubMed

Yin, Guo-ping; Ye, Jing-ying; Han, De-min; Wang, Xiao-yi; Zhang, Yu-huan; Li, Yan-ru

2013-01-01

It is believed that defects in upper airway neuromuscular control play a role in sleep apnea pathogenesis. Currently, there is no simple and non-invasive method for evaluating neuromuscular activity for the purpose of screening in patients with obstructive sleep apnea. This study was designed to assess the validity of chin surface electromyography of routine polysomnography in evaluating the neuromuscular activity of obstructive sleep apnea subjects and probe the neuromuscular contribution in the pathogenesis of the condition. The chin surface electromyography of routine polysomnography during normal breathing and obstructive apnea were quantified in 36 male patients with obstructive sleep apnea. The change of chin surface electromyography from normal breathing to obstructive apnea was expressed as the percent compensated electromyography value, where the percent compensated electromyography value = (normal breath surface electromyography - apnea surface electromyography)/normal breath surface electromyography, and the percent compensated electromyography values among subjects were compared. The relationship between sleep apnea related parameters and the percent compensated electromyography value was examined. The percent compensated electromyography value of the subjects varied from 1% to 90% and had a significant positive correlation with apnea hypopnea index (R(2) = 0.382, P < 0.001). Recording and analyzing chin surface electromyography by routine polysomnography is a valid way of screening the neuromuscular activity in patients with obstructive sleep apnea. The neuromuscular contribution is different among subjects with obstructive sleep apnea.

Sleep habits in middle-aged, non-hospitalized men and women with schizophrenia: a comparison with healthy controls.

PubMed

Poulin, Julie; Chouinard, Sylvie; Pampoulova, Tania; Lecomte, Yves; Stip, Emmanuel; Godbout, Roger

2010-10-30

Patients with schizophrenia may have sleep disorders even when clinically stable under antipsychotic treatments. To better understand this issue, we measured sleep characteristics between 1999 and 2003 in 150 outpatients diagnosed with Diagnostic and Statistical Manual of Mental Disorders, fourth edition (DSM-IV) schizophrenia or schizoaffective disorder and 80 healthy controls using a sleep habits questionnaire. Comparisons between both groups were performed and multiple comparisons were Bonferroni corrected. Compared to healthy controls, patients with schizophrenia reported significantly increased sleep latency, time in bed, total sleep time and frequency of naps during weekdays and weekends along with normal sleep efficiency, sleep satisfaction, and feeling of restfulness in the morning. In conclusion, sleep-onset insomnia is a major, enduring disorder in middle-aged, non-hospitalized patients with schizophrenia that are otherwise clinically stable under antipsychotic and adjuvant medications. Noteworthy, these patients do not complain of sleep-maintenance insomnia but report increased sleep propensity and normal sleep satisfaction. These results may reflect circadian disturbances in schizophrenia, but objective laboratory investigations are needed to confirm subjective sleep reports. Copyright © 2009 Elsevier Ltd. All rights reserved.

Statistical physics approaches to quantifying sleep-stage transitions

NASA Astrophysics Data System (ADS)

Lo, Chung-Chuan

Sleep can be viewed as a sequence of transitions in a very complex neuronal system. Traditionally, studies of the dynamics of sleep control have focused on the circadian rhythm of sleep-wake transitions or on the ultradian rhythm of the sleep cycle. However, very little is known about the mechanisms responsible for the time structure or even the statistics of the rapid sleep-stage transitions that appear without periodicity. I study the time dynamics of sleep-wake transitions for different species, including humans, rats, and mice, and find that the wake and sleep episodes exhibit completely different behaviors: the durations of wake episodes are characterized by a scale-free power-law distribution, while the durations of sleep episodes have an exponential distribution with a characteristic time scale. The functional forms of the distributions of the sleep and wake durations hold for human subjects of different ages and for subjects with sleep apnea. They also hold for all the species I investigate. Surprisingly, all species have the same power-law exponent for the distribution of wake durations, but the exponential characteristic time of the distribution of sleep durations changes across species. I develop a stochastic model which accurately reproduces our empirical findings. The model suggests that the difference between the dynamics of the sleep and wake states arises from the constraints on the number of microstates in the sleep-wake system. I develop a measure of asymmetry in sleep-stage transitions using a transition probability matrix. I find that both normal and sleep apnea subjects are characterized by two types of asymmetric sleep-stage transition paths, and that the sleep apnea group exhibits less asymmetry in the sleep-stage transitions.

Sleep education in pediatric residency programs: a cross-cultural look.

PubMed

Mindell, Jodi A; Bartle, Alex; Ahn, Youngmin; Ramamurthy, Mahesh Babu; Huong, Huynh Thi Duy; Kohyama, Jun; Li, Albert M; Ruangdaraganon, Nichara; Sekartini, Rini; Teng, Arthur; Goh, Daniel Y T

2013-04-03

The objective of this study was to assess the prevalence of education about sleep and sleep disorders in pediatric residency programs and to identify barriers to providing such education. Surveys were completed by directors of 152 pediatric residency programs across 10 countries (Hong Kong, India, Indonesia, Japan, Singapore, South Korea, Thailand, United States-Canada, and Vietnam). Overall, the average amount of time spent on sleep education is 4.4 hours (median = 2.0 hours), with 23% responding that their pediatric residency program provides no sleep education. Almost all programs (94.8%) offer less than 10 hours of instruction. The predominant topics covered include sleep-related development, as well as normal sleep, sleep-related breathing disorders, parasomnias, and behavioral insomnia of childhood. These results indicate that there is still a need for more efforts to include sleep-related education in all pediatric residency programs, as well as coverage of the breadth of sleep-related topics. Such education would be consistent with the increased recognition of the importance of sleep and under-diagnosis of sleep disorders in children and adolescents.

Companionable sleep: Social regulation of sleep and co-sleeping in Egyptian families

PubMed Central

Worthman, Carol M.; Brown, Ryan A.

2013-01-01

This exploratory study examines family sleep patterns and quality in a setting of normative napping and co-sleeping. Participants comprised 78 members of 16 families from two locales in Egypt, Cairo and village. Each family member provided a history of sleeping arrangements, one week of continuous activity records, and details of each sleep event. Sleep records documented late-onset and dispersed sleep patterns with extensive co-sleeping. Of recorded sleep events, 69% involved co-sleeping, 24% included more than one co-sleeper, and only 21% were solitary. Mid-late afternoon napping occurred on 31% of days and night sleep onsets averaged after midnight. Age and gender structured sleep arrangements and together with locale, extensively explained sleep behavior (onset, duration, total) and quality. Co-sleepers had fewer night arousals, shorter and less variable night sleep duration, and less total sleep. Increased solitary sleep in adolescents and young adults was associated with increased sleep dysregulation, including exaggerated phase shifts in males and more nighttime arousals in females. Where normative, co-sleeping may provide psychosensory stimuli that moderate arousal and stabilize sleep. Such moderating features may address important self-regulatory developmental needs during adolescence. PMID:17371117

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