Kavanau, J L
Some aspects of the evolution of mechanisms for enhancement and maintenance of synaptic efficacy are treated. After the origin of use-dependent synaptic plasticity, frequent synaptic activation (dynamic stabilization, DS) probably prolonged transient efficacy enhancements induced by single activations. In many "primitive" invertebrates inhabiting essentially unvarying aqueous environments, DS of synapses occurs primarily in the course of frequent functional use. In advanced locomoting ectotherms encountering highly varied environments, DS is thought to occur both through frequent functional use and by spontaneous "non-utilitarian" activations that occur primarily during rest. Non-utilitarian activations are induced by endogenous oscillatory neuronal activity, the need for which might have been one of the sources of selective pressure for the evolution of neurons with oscillatory firing capacities. As non-sleeping animals evolved increasingly complex brains, ever greater amounts of circuitry encoding inherited and experiential information (memories) required maintenance. The selective pressure for the evolution of sleep may have been the need to depress perception and processing of sensory inputs to minimize interference with DS of this circuitry. As the higher body temperatures and metabolic rates of endothermy evolved, mere skeletal muscle hypotonia evidently did not suffice to prevent sleep-disrupting skeletal muscle contractions during DS of motor circuitry. Selection against sleep disruption may have led to the evolution of further decreases in muscle tone, paralleling the increase in metabolic rate, and culminating in the postural atonia of REM (rapid eye movement) sleep. Phasic variations in heart and respiratory rates during REM sleep may result from superposition of activations accomplishing non-utilitarian DS of redundant and modulatory motor circuitry on the rhythmic autonomic control mechanisms. Accompanying non-utilitarian DS of circuitry during sleep
Targa, Adriano D S; Rodrigues, Lais S; Noseda, Ana Carolina D; Aurich, Mariana F; Andersen, Monica L; Tufik, Sergio; da Cunha, Cláudio; Lima, Marcelo M S
Sleep disturbances are among the most disabling non-motor symptoms in Parkinson's disease. The pedunculopontine tegmental nucleus and basal ganglia are likely involved in these dysfunctions, as they are affected by neurodegeneration in Parkinson's disease and have a role in sleep regulation. To investigate this, we promoted a lesion in the pedunculopontine tegmental nucleus or substantia nigra pars compacta of male rats, followed by 24 h of REM sleep deprivation. Then, we administrated a dopaminergic D2 receptor agonist, antagonist or vehicle directly in the striatum. After a period of 24 h of sleep-wake recording, we observed that the ibotenic acid infusion in the pedunculopontine tegmental nucleus blocked the so-called sleep rebound effect mediated by REM sleep deprivation, which was reversed by striatal D2 receptors activation. Rotenone infusion in the substantia nigra pars compacta also blocked the sleep rebound, however, striatal D2 receptors activation did not reverse it. In addition, rotenone administration decreased the time spent in NREM sleep, which was corroborated by positive correlations between dopamine levels in both substantia nigra pars compacta and striatum and the time spent in NREM sleep. These findings suggest a new circuitry for sleep regulation in Parkinson's disease, involving the triad composed by pedunculopontine nucleus, substantia nigra pars compacta and striatum, evidencing a potential therapeutic target for the sleep disturbances associated to this pathology.
Peever, John; Luppi, Pierre-Hervé; Montplaisir, Jacques
During rapid eye movement (REM) sleep, skeletal muscles are almost paralyzed. However, in REM sleep behavior disorder (RBD), which is a rare neurological condition, muscle atonia is lost, leaving afflicted individuals free to enact their dreams. Although this may sound innocuous, it is not, given that patients with RBD often injure themselves or their bed-partner. A major concern in RBD is that it precedes, in 80% of cases, development of synucleinopathies, such as Parkinson's disease (PD). This link suggests that neurodegenerative processes initially target the circuits controlling REM sleep. Clinical and basic neuroscience evidence indicates that RBD results from breakdown of the network underlying REM sleep atonia. This finding is important because it opens new avenues for treating RBD and understanding its link to neurodegenerative disorders.
Sleep in the elderly is characterized by a decrease in the ability to stay asleep resulting in a more fragmented sleep. Spindles are less frequent and less ample, shorter, without an increase during the night contrary young subjects. Delta activity in slow wave sleep is decreased in the 0.5-2 Hz frequency band only. REM sleep occurs earlier the first REM period duration increases. The REM sleep appearance is almost uniform during the night. REMs density does not increase toward the end of the sleeping period. The sleep-wake circadian rhythm is advanced (bedtime and morning awakening occur earlier). The temperature rhythm is also advanced. The rise in temperature after the nadir begins earlier for females and the initial ascent is more rapid. This explains why women wake up earlier and sleep for shorter durations than men. The nocturnal and diurnal mean plasmatic norepinephrine values increase. The rhythm of cortisol secretion is advanced. The GH and melatonin peaks of secretion are decreased. The acrophase of melatonin rhythm is occurring later in the elderly. These results suggest a weakening of circadian structure in the course of aging and an altered relationship between the pacemakers driving melatonin and cortisol circadian rhythms.
Potdar, Sheetal; Sheeba, Vasu
Sleep is a highly conserved behavior whose role is as yet unknown, although it is widely acknowledged as being important. Here we provide an overview of many vital questions regarding this behavior, that have been addressed in recent years using the genetically tractable model organism Drosophila melanogaster in several laboratories around the world. Rest in D. melanogaster has been compared to mammalian sleep and its homeostatic and circadian regulation have been shown to be controlled by intricate neuronal circuitry involving circadian clock neurons, mushroom bodies, and pars intercerebralis, although their exact roles are not entirely clear. We draw attention to the yet unanswered questions and contradictions regarding the nature of the interactions between the brain regions implicated in the control of sleep. Dopamine, octopamine, γ-aminobutyric acid (GABA), and serotonin are the chief neurotransmitters identified as functioning in different limbs of this circuit, either promoting arousal or sleep by modulating membrane excitability of underlying neurons. Some studies have suggested that certain brain areas may contribute towards both sleep and arousal depending on activation of specific subsets of neurons. Signaling pathways implicated in the sleep circuit include cyclic adenosine monophosphate (cAMP) and epidermal growth factor receptor-extracellular signal-regulated kinase (EGFR-ERK) signaling pathways that operate on different neural substrates. Thus, this field of research appears to be on the cusp of many new and exciting findings that may eventually help in understanding how this complex physiological phenomenon is modulated by various neuronal circuits in the brain. Finally, some efforts to approach the "Holy Grail" of why we sleep have been summarized.
Chamberlin, Nancy L.
Obstructive sleep apnea (OSA) is a disorder of repetitive sleep disruption caused by reduced or blocked respiratory airflow. Although an anatomically compromised airway accounts for the major predisposition to OSA, a patient's arousal threshold and factors related to the central control of breathing (ventilatory control stability) are also important. Arousal from sleep (defined by EEG desynchronization) may be the only mechanism that allows airway re-opening following an obstructive event. However, in many cases arousal is unnecessary and even worsens the severity of OSA. Mechanisms for arousal are poorly understood. However, accumulating data are elucidating the relevant neural pathways and neurotransmitters. For example, serotonin is critically required, but its site of action is unknown. Important neural substrates for arousal have been recently identified in the parabrachial complex (PB), a visceral sensory nucleus in the rostral pons. Moreover, glutamatergic signaling from the PB contributes to arousal caused by hypercapnia, one of the arousal-promoting stimuli in OSA. A major current focus of OSA research is to find means to maintain airway patency during sleep, without sleep interruption. PMID:23810448
Kayser, Matthew S; Yue, Zhifeng; Sehgal, Amita
Most animals sleep more early in life than in adulthood, but the function of early sleep is not known. Using Drosophila, we found that increased sleep in young flies was associated with an elevated arousal threshold and resistance to sleep deprivation. Excess sleep results from decreased inhibition of a sleep-promoting region by a specific dopaminergic circuit. Experimental hyperactivation of this circuit in young flies results in sleep loss and lasting deficits in adult courtship behaviors. These deficits are accompanied by impaired development of a single olfactory glomerulus, VA1v, which normally displays extensive sleep-dependent growth after eclosion. Our results demonstrate that sleep promotes normal brain development that gives rise to an adult behavior critical for species propagation and suggest that rapidly growing regions of the brain are most susceptible to sleep perturbations early in life.
McKenna, Dillon; Peever, John
During healthy rapid eye movement sleep, skeletal muscles are actively forced into a state of motor paralysis. However, in rapid eye movement sleep behavior disorder-a relatively common neurological disorder-this natural process is lost. A lack of motor paralysis (atonia) in rapid eye movement sleep behavior disorder allows individuals to actively move, which at times can be excessive and violent. At first glance this may sound harmless, but it is not because rapid eye movement sleep behavior disorder patients frequently injure themselves or the person they sleep with. It is hypothesized that the degeneration or dysfunction of the brain stem circuits that control rapid eye movement sleep paralysis is an underlying cause of rapid eye movement sleep behavior disorder. The link between brain stem degeneration and rapid eye movement sleep behavior disorder stems from the fact that rapid eye movement sleep behavior disorder precedes, in the majority (∼80%) of cases, the development of synucleinopathies such as Parkinson's disease, dementia with Lewy bodies, and multiple system atrophy, which are known to initially cause degeneration in the caudal brain stem structures where rapid eye movement sleep circuits are located. Furthermore, basic science and clinical evidence demonstrate that lesions within the rapid eye movement sleep circuits can induce rapid eye movement sleep-specific motor deficits that are virtually identical to those observed in rapid eye movement sleep behavior disorder. This review examines the evidence that rapid eye movement sleep behavior disorder is caused by synucleinopathic neurodegeneration of the core brain stem circuits that control healthy rapid eye movement sleep and concludes that rapid eye movement sleep behavior disorder is not a separate clinical entity from synucleinopathies but, rather, it is the earliest symptom of these disorders. © 2017 International Parkinson and Movement Disorder Society.
Vetrivelan, Ramalingam; Fuller, Patrick M; Tong, Qingchun; Lu, Jun
Considerable data support a role for glycinergic ventromedial medulla neurons in the mediation of the postsynaptic inhibition of spinal motoneurons necessary for the motor atonia of rapid-eye movement (REM) sleep in cats. These data are however difficult to reconcile with the fact that large lesions of the rostral ventral medulla do not result in loss of REM atonia in rats. In the present study, we sought to clarify which medullary networks in rodents are responsible for REM motor atonia by retrogradely tracing inputs to the spinal ventral horn from the medulla, ablating these medullary sources to determine their effects on REM atonia and using transgenic mice to identify the neurotransmitter(s) involved. Our results reveal a restricted region within the ventromedial medulla, termed here the ‘supraolivary medulla’ (SOM), which contains glutamatergic neurons that project to the spinal ventral horn. Cell-body specific lesions of the SOM resulted in an intermittent loss of muscle atonia, taking the form of exaggerated phasic muscle twitches, during REM sleep. A concomitant reduction in REM sleep time was observed in the SOM-lesioned animals. We next used mice with lox-P modified alleles of either the glutamate or GABA/glycine vesicular transporters to selectively eliminate glutamate or GABA/glycine neurotransmission from SOM neurons. Loss of SOM glutamate release, but not SOM GABA/glycine release, resulted in exaggerated muscle twitches during REM sleep that were similar to those observed following SOM lesions in rats. These findings, taken together, demonstrate that SOM glutamatergic neurons comprise key elements of the medullary circuitry mediating REM atonia. PMID:19625526
Gumenyuk, Valentina; Korzyukov, Oleg; Roth, Thomas; Bowyer, Susan M; Drake, Christopher L
Chronic sleep loss has been associated with increased daytime sleepiness, as well as impairments in memory and attentional processes. In the present study, we evaluated the neuronal changes of a pre-attentive process of wake auditory sensory gating, measured by brain event-related potential (ERP)--P50 in eight normal sleepers (NS) (habitual total sleep time (TST) 7 h 32 m) vs. eight chronic short sleeping individuals (SS) (habitual TST ≤6 h). To evaluate the effect of sleep extension on sensory gating, the extended sleep condition was performed in chronic short sleeping individuals. Thus, one week of time in bed (6 h 11 m) corresponding to habitual short sleep (hSS), and one week of extended time (∼ 8 h 25 m) in bed corresponding to extended sleep (eSS), were counterbalanced in the SS group. The gating ERP assessment was performed on the last day after each sleep condition week (normal sleep and habitual short and extended sleep), and was separated by one week with habitual total sleep time and monitored by a sleep diary. We found that amplitude of gating was lower in SS group compared to that in NS group (0.3 µV vs. 1.2 µV, at Cz electrode respectively). The results of the group × laterality interaction showed that the reduction of gating amplitude in the SS group was due to lower amplitude over the left hemisphere and central-midline sites relative to that in the NS group. After sleep extension the amplitude of gating increased in chronic short sleeping individuals relative to their habitual short sleep condition. The sleep condition × frontality interaction analysis confirmed that sleep extension significantly increased the amplitude of gating over frontal and central brain areas compared to parietal brain areas.
Meyer, J.S.; Ishikawa, Y.; Hata, T.; Karacan, I.
Measurements of regional or local cerebral blood flow (CBF) by the xenon-133 inhalation method and stable xenon computerized tomography CBF (CTCBF) method were made during relaxed wakefulness and different stages of REM and non-REM sleep in normal age-matched volunteers, narcoleptics, and sleep apneics. In the awake state, CBF values were reduced in both narcoleptics and sleep apneics in the brainstem and cerebellar regions. During sleep onset, whether REM or stage I-II, CBF values were paradoxically increased in narcoleptics but decreased severely in sleep apneics, while in normal volunteers they became diffusely but more moderately decreased. In REM sleep and dreaming CBF values greatly increased, particularly in right temporo-parietal regions in subjects experiencing both visual and auditory dreaming.
The main purpose of the present study was to develop an automatic hybrid system and evaluate its performance in the differentiation of normal and disturbed sleep. The study was carried out in roughly the following steps: At the beginning the quantity of five EEG waveforms, delta, theta, alpha, sigma and beta were examined with respect to sleep stages and their temporal distributions and inter-relationships throughout the nights in young 20-22 year-old, healthy individuals. These data were used as a basis for the choice of parameters for a sleep stage scoring program. Secondly, the sleep stage scoring software was developed using as test material three subject groups: about 10 years older controls, anonymous alcoholics and chronic alcoholics in the withdrawal phase. The last group was examined on two occasions, first in the initial withdrawal and then after two weeks' abstinence between the recordings. The sleep stage scoring program was evaluated in comparison with a visual sleep stage determination and its performance was also tested on the young normals. Attention was paid to three main points: First, how well does an automatic system imitate the visual classification of a human subject, when both the human and the computer classifications are compared side by side at a 20 s epoch level? Second, even if this comparison did not show a satisfactory agreement, could the computer classification still replace the visual sleep stage scoring when the objective is to describe the neurophysiological characteristics of the human whole-night sleep process or differentiate between normal and disturbed sleep. For this purpose it was examined, whether the values for the sleep stage parameters obtained by visual classification corresponded to those obtained by computer scoring and whether the differences found between the groups by manual methods could also be obtained by computer classification. The third goal was to see whether other measures than parameters received by sleep
Penzel, Thomas; Wessel, Niels; Riedl, Maik; Kantelhardt, Jan W.; Rostig, Sven; Glos, Martin; Suhrbier, Alexander; Malberg, Hagen; Fietze, Ingo
Sleep is an active and regulated process with restorative functions for physical and mental conditions. Based on recordings of brain waves and the analysis of characteristic patterns and waveforms it is possible to distinguish wakefulness and five sleep stages. Sleep and the sleep stages modulate autonomous nervous system functions such as body temperature, respiration, blood pressure, and heart rate. These functions consist of a sympathetic tone usually related to activation and to parasympathetic (or vagal) tone usually related to inhibition. Methods of statistical physics are used to analyze heart rate and respiration to detect changes of the autonomous nervous system during sleep. Detrended fluctuation analysis and synchronization analysis and their applications to heart rate and respiration during sleep in healthy subjects and patients with sleep disorders are presented. The observed changes can be used to distinguish sleep stages in healthy subjects as well as to differentiate normal and disturbed sleep on the basis of heart rate and respiration recordings without direct recording of brain waves. Of special interest are the cardiovascular consequences of disturbed sleep because they present a risk factor for cardiovascular disorders such as arterial hypertension, cardiac ischemia, sudden cardiac death, and stroke. New derived variables can help to find indicators for these health risks.
Gol'bin, A Ts; Guzeva, V I; Shepoval'nikov, A N
The present article is an attempt to perform a conceptual clinical and physiological analysis of a large spec- trum of sleep-related phenomena called parasomnias in children, based on data from three independent in- stitutions. Parasonmias appear in the process of falling asleep, at the time of sleep stage changes, and upon awakening. They are common for both healthy children and those with neurological and psychiatric disorders. Brief descriptions of clinical pictures of several groups of parasomnias and their polysomnographic characteristics are presented. Instances of stereotyped rhythmic movements (e.g. head rocking), paroxysmal somatic and behavioral episodes (night terrors and nightmares), "static" phenomena (sleep with open eyes, strange body positions), as well as somnambulism are specifically described. Common features of parasomnias as a group have been identified (the "Parasomnia syndrome"). It was found that sleep architecture frequently normalizes after a parasomnia episode, whereas parasomnias are self-liquidated after sleep matures (self-cure). The significance of gender differences in parasomnias have been reviewed. Possible compensatory physiological functions of parasomnias acting as "switches" or "stabilizers" of sleep stages to "off-set" deviated or immature sleep-wake mechanisms were discussed.
Drakatos, Panagis; Leschziner, Guy
Patients with narcolepsy usually develop excessive daytime sleepiness (EDS) before or coincide with the occurrence of cataplexy, with the latter most commonly associated with low cerebrospinal fluid (CSF) hypocretin-1 levels. Cataplexy preceding the development of other features of narcolepsy is a rare phenomenon. We describe a case of isolated cataplexy in the context of two non-diagnostic multiple sleep latency tests and normal CSF-hypocretin-1 levels (217 pg/mL) who gradually developed EDS and low CSF-hypocretin-1 (< 110 pg/mL). Citation: Drakatos P, Leschziner G. Cataplexy with normal sleep studies and normal csf hypocretin: an explanation? J Clin Sleep Med 2016;12(3):449–450. PMID:26564387
Saunamäki, Tiia; Huupponen, Eero; Loponen, Juho
Objective. Obstructive sleep apnea (OSA) decreases sleep spindle density and frequency. We evaluated the effects of continuous positive airway pressure (CPAP) treatment on different features of sleep spindles. Methods. Twenty OSA patients underwent two night polysomnographies in a diagnostic phase and one night polysomnography after 6 months of CPAP treatment. The control group comprised 20 healthy controls. Sleep spindles were analyzed by a previously developed automated method. Unilateral and bilateral spindles were identified in central and frontopolar brain locations. Spindle density and frequency were determined for the first and last half of the NREM time. Results. The density of bilateral central spindles, which did not change in the untreated OSA patients, increased towards the morning hours during CPAP treatment and in the controls. Central spindles did not become faster with sleep in OSA patients and the central spindles remained slow in the left hemisphere even with CPAP. Conclusion. CPAP treatment normalized spindle features only partially. The changes may be associated with deficits in thalamocortical spindle generating loops. Significance. This study shows that some sleep spindle changes persist after CPAP treatment in OSA patients. The association of these changes to daytime symptoms in OSA patients needs to be further evaluated. PMID:28261503
Jensen, Peter S; Sorensen, Helge B D; Leonthin, Helle L; Jennum, Poul
The aim of this study was to develop a fully automatic sleep scoring algorithm on the basis of a reproduction of new international sleep scoring criteria from the American Academy of Sleep Medicine. A biomedical signal processing algorithm was developed, allowing for automatic sleep depth quantification of routine polysomnographic recordings through feature extraction, supervised probabilistic Bayesian classification, and heuristic rule-based smoothing. The performance of the algorithm was tested using 28 manually classified day-night polysomnograms from 18 normal subjects and 10 patients with Parkinson disease or multiple system atrophy. This led to quantification of automatic versus manual epoch-by-epoch agreement rates for both normals and abnormals. Resulting average agreement rates were 87.7% (Cohen's Kappa: 0.79) and 68.2% (Cohen's Kappa: 0.26) in the normal and abnormal group, respectively. Based on an observed reliability of the manual scorer of 92.5% (Cohen's Kappa: 0.87) in the normal group and 85.3% (Cohen's Kappa: 0.73) in the abnormal group, this study concluded that although the developed algorithm was capable of scoring normal sleep with an accuracy around the manual interscorer reliability, it failed in accurately scoring abnormal sleep as encountered for the Parkinson disease/multiple system atrophy patients.
... is REM sleep? What is the effect of sleep deprivation? What are sleep myths? What are sleep disorders? ... is REM sleep? What is the effect of sleep deprivation? What are sleep myths? What are sleep disorders? ...
Spruyt, Karen; O'Brien, Louise M; Cluydts, Raymond; Verleye, Gino Benjamin; Ferri, Raffaele
The objectives of the study were to describe the prevalence, odds, and predictors of 36 paediatric sleep behaviours and describe their coexistence in a school-age normal population. The design was community-based questionnaire survey of sleep-wake patterns, sleep environment, and 36 sleep behaviours indicative of six sleep disorder-subscales using the Health-Behaviour Questionnaire. A caregivers' report of 3045 children aged 6-13 years in Belgium constituted the participants. Prevalence of each sleep behaviour was calculated. Log-linear modelling within and between the sleep disorder-subscales was used to screen for coexistence. The effect size of selected night-time parameters to the likelihood of sleep behaviours and disorder-subscale was expressed as odds ratios via logit regression analysis. Significant differences in sleep-wake patterns were found between weekday and weekend. Ranking by odds showed that: (1) sleep problems such as 'tired when waking up', 'repetitive limb movements', 'going to bed reluctantly', and 'sleep paralysis' and; (2) the disorder-subscale 'excessive somnolence' are common in children. Coexistences within and between disorder-subscales of sleep problems are evident in a school-age, normal population. These results suggest that disorders of excessive somnolence (DES) are highly prevalent in a non-clinical sample of school-age children. Furthermore, sleep-onset latency and a noisy, not well-darkened room are predictive towards the odds for exhibiting sleep problems and disorders. It is advocated that more information on the importance of good sleep-wake hygiene should reach parents and children.
Tobaldini, Eleonora; Nobili, Lino; Strada, Silvia; Casali, Karina R.; Braghiroli, Alberto; Montano, Nicola
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. PMID:24137133
Markov, Dimitri; Goldman, Marina
Sleep is a vital, highly organized process regulated by complex systems of neuronal networks and neurotransmitters. Sleep plays an important role in the regulation of central nervous system and body physiologic functions. Sleep architecture changes with age and is easily susceptible to external and internal disruption. Reduction or disruption of sleep can affect numerous functions varying from thermoregulation to learning and memory during the waking state.
Mahowald, Mark W.; Schenck, Carlos H.; O'Connor, Kevin A.
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.
Boselli, M; Parrino, L; Smerieri, A; Terzano, M G
EEG arousals were quantified in 40 nocturnal polysomnographic recordings belonging to four age groups (teenagers: 10 to 19 years; young adults: 20 to 39 years; middle-aged: 40 to 59 years; elderly: > or = 60 years). Ten subjects (five males and five females) participated in each group. The subjects were healthy and sound sleepers. All sleep recordings were preceded by an adaptation night which aimed at excluding the presence of sleep-related disorders. The recordings were carried out in a partially soundproof recording chamber and in a standard laboratory setting. Arousal indices (AI), defined as the number of arousals per hour of sleep, were calculated for total sleep time (AI/TST) and for all the sleep stages. AI/TST increased linearly with age (r = 0.852; p < 0.00001): teenagers (13.8), young adults (14.7), middle-aged (17.8), elderly (27.1). An age-related positive linear correlation was found also for the arousal indices referred to NREM sleep (r = 0.811; p < 0.00001) and to stages 1 and 2 (r = 0.712; p < 0.00001), while in stages 3 and 4 and in REM sleep, arousal indices showed stable values across the ages. Overall, arousals lasted 14.9 +/- 2.3 seconds, with arousal duration stable across the ages (range of means: 13.3-16.6 seconds) and no relevant differences between NREM sleep (14.6 +/- 2.5 seconds) and REM sleep (16.2 +/- 5 seconds). The paper discusses the impact of age on arousals, the similarities between arousals and the phases d'activation transitoire, and the consideration that arousals are physiological components of sleep.
Bruni, Oliviero; Baumgartner, Emma; Sette, Stefania; Ancona, Mario; Caso, Gianni; Di Cosimo, Maria Elisabetta; Mannini, Andrea; Ometto, Mariangela; Pasquini, Anna; Ulliana, Antonella; Ferri, Raffaele
Study Objectives: To longitudinally examine sleep patterns, habits, and parent-reported sleep problems during the first year of life. Methods: Seven hundred four parent/child pairs participated in a longitudinal cohort study. Structured interview recording general demographic data, feeding habits, intercurrent diseases, family history, sleep habits, and parental evaluation of the infant's sleep carried out at 1, 3, 6, 9, and 12 months Results: Nocturnal, daytime, and total sleep duration showed a high inter-individual variability in the first year of life associated with changes in the first 6 months and stability from 6 to 12 months. Bedtime was at around 22:00 and remained stable at 6, 9, and 12 months of age. Approximately 20% of the infants had more than 2 awakenings and slept more often in the parent bed. Nearly 10% of the infants were considered as having a problematic sleep by parents and this significantly correlated with nocturnal awakenings and difficulties falling asleep. Conclusions: Sleep patterns change during the first year of life but most sleep variables (i.e., sleep latency and duration) show little variation from 6 to 12 months. Our data provide a context for clinicians to discuss sleep issues with parents and suggest that prevention efforts should focus to the first 3-6 months, since sleep patterns show stability from that time point to 12 months. Citation: Bruni O, Baumgartner E, Sette S, Ancona M, Caso G, Di Cosimo ME, Mannini A, Ometto M, Pasquini A, Ulliana A, Ferri R. Longitudinal study of sleep behavior in normal infants during the first year of life. J Clin Sleep Med 2014;10(10):1119-1127. PMID:25317093
Spira, Adam P.; Gonzalez, Christopher E.; Venkatraman, Vijay K.; Wu, Mark N.; Pacheco, Jennifer; Simonsick, Eleanor M.; Ferrucci, Luigi; Resnick, Susan M.
Study Objectives: To determine the association between self-reported sleep duration and cortical thinning among older adults. Methods: We studied 122 cognitively normal participants in the Baltimore Longitudinal Study of Aging with a mean age = 66.6 y (range, 51–84) at baseline sleep assessment and 69.5 y (range, 56–86) at initial magnetic resonance imaging (MRI) scan. Participants reported average sleep duration and completed a mean of 7.6 1.5-T MRI scans (range, 3–11), with mean follow-up from initial scan of 8.0 y (range, 2.0–11.8). Results: In analyses adjusted for age, sex, education, race, and interval between sleep assessment and initial MRI scan, participants reporting > 7 h sleep at baseline had thinner cortex in the inferior occipital gyrus and sulcus of the left hemisphere at initial MRI scan than those reporting 7 h (cluster P < 0.05). In adjusted longitudinal analyses, compared to those reporting 7 h of sleep, participants reporting < 7 h exhibited higher rates of subsequent thinning in the superior temporal sulcus and gyrus, inferior and middle frontal gyrus, and superior frontal sulcus of the left hemisphere, and in the superior frontal gyrus of the right hemisphere; those reporting > 7 h of sleep had higher rates of thinning in the superior frontal and middle frontal gyrus of the left hemisphere (cluster P < 0.05 for all). In sensitivity analyses, adjustment for apolipoprotein E (APOE) e4 genotype reduced or eliminated some effects but revealed others. When reports of < 7 h of sleep were compared to reports of 7 or 8 h combined, there were no significant associations with cortical thinning. Conclusions: Among cognitively normal older adults, sleep durations of < 7 h and > 7 h may increase the rate of subsequent frontotemporal gray matter atrophy. Additional studies, including those that use objective sleep measures and investigate mechanisms linking sleep duration to gray matter loss, are needed. Citation: Spira AP, Gonzalez CE, Venkatraman
De Cock, Valérie Cochen; Vidailhet, Marie; Leu, Smaranda; Texeira, Antonio; Apartis, Emmanuelle; Elbaz, Alexis; Roze, Emmanuel; Willer, Jean Claude; Derenne, Jean Philippe; Agid, Yves; Arnulf, Isabelle
Although normal subjects do not move during REM sleep, patients with Parkinson's disease may experience REM sleep behaviour disorder (RBD). The characteristics of the abnormal REM sleep movements in RBD have, however, not been studied. We interviewed one hundred consecutive non-demented patients with Parkinson's disease and their bed partners using a structured questionnaire assessing the presence of RBD. They rated the quality of movements, voice and facial expression during RBD as being better, equal or worse than in awake ON levodopa condition. Night-time sleep and movements were video-monitored during polysomnography in 51 patients to evaluate the presence of bradykinesia, tremor and hypophonia during REM sleep. Fifty-nine patients had clinical RBD with 53/59 bed partners able to evaluate them. All 53 (100%) reported an improvement of at least one component of motor control during RBD. By history, movements were improved in 87% patients (faster, 87%; stronger, 87%; smoother, 51%), speech was better in 77% patients (more intelligible, 77%; louder, 38%; better articulated, 57%) and facial expression was normalized in 47% patients. Thirty-eight per cent of bed partners reported that movements were 'much better', even in the most disabled patients. The video-monitored purposeful movements in REM sleep were also surprisingly fast, ample, coordinated and symmetrical, without obvious sign of parkinsonism. The movements were, however, jerky, violent and often repetitive. While all patients had asymmetrical parkinsonism when awake, most of the time they used the more disabled arm, hand and leg during the RBD (P = 0.04). Movements involved six times as often the upper limbs and the face as the lower limbs (OR: 5.9, P = 0.004). The percentage of time containing tremor EMG activity decreased with sleep stages from 34.9 +/- 15.5% during wakefulness, to 3.6 +/- 5.7% during non-REM sleep stages 1-2, 1.4 +/- 3.0% during non-REM sleep stages 3-4, and 0.06 +/- 0.2% during REM
Cassoff, J; Bhatti, J A; Gruber, R
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.
Chouvarda, Ioanna; Mendez, Martin Oswaldo; Rosso, V; Bianchi, Anna M; Parrino, Liborio; Grassi, Andrea; Terzano, Mario Giovanni; Cerutti, Sergio; Maglaveras, Nicos
This work aims to investigate new markers for the quantitative characterization of insomnia, in the context of sleep microstructure, as expressed by cyclic alternating pattern (CAP) sleep. The study group includes 11 subjects with normal sleep and 10 subjects with diagnosed primary insomnia. Differences between normal sleepers and insomniacs are investigated, in terms of dynamics and content of CAP events. The overall rate of CAP and of different phases is considered. The dynamic in the structure and alternation of CAP events is further studied in different scales by use of wavelet analysis, and calculation of energy/entropy features. The content of CAP events is studied in terms of electroencephalography (EEG) complexity analysis for the different types of events. Statistically significant differences are highlighted, both in structure and content. Besides confirming the increase in CAP rate, main findings regarding the microstructure difference in insomnia include: 1) as regards the deep sleep building phases, more irregular activation-deactivation patterns, with bigger deactivation time, i.e., distance between consecutive activation events, and appearing with higher EEG complexity in deactivation, and 2) a bigger duration of desynchronisation phases, with increased EEG complexity and more irregular patterns. This analysis extends previous findings on the relation between CAPrate increase and sleep instability mechanisms, proposing specific features of CAP that seem to play a role in insomnia (as consistently presented via classification analysis). This opens new perspectives for the understanding of the role of CAP in the quantitative characterization of sleep and its disorders.
Saletu, B; Gruber, G; Saletu, M; Brandstätter, N; Hauer, C; Prause, W; Ritter, K; Saletu-Zyhlarz, G
Although the restless legs syndrome (RLS) is a disorder with a relatively high prevalence rate (8% in Austria) and leads to insomnia and excessive daytime tiredness, there is a paucity of sleep laboratory data concerning objective and subjective sleep and awakening quality. Thus, the aim of this study was to investigate 12 untreated RLS patients as compared with 12 normal controls and subsequently measure the acute effects of 0.5 mg ropinirole (Requip((R))) - a nonergoline dopamine agonist - as compared with placebo. In 3 nights (adaptation, placebo, ropinirole night) sleep induction, maintenance and architecture were measured objectively by polysomnography, subjective sleep and awakening quality were assessed by self-rating scales and visual-analog scales, and objective awakening quality was evaluated by a psychometric test battery. In polysomnography, RLS patients demonstrated, as compared with normal controls, a decreased total sleep time (TST) and sleep efficacy, increased wakefulness during the total sleep period and frequency of nocturnal awakenings, increased sleep stage S1, decreased S2 and increased stage shifts. Subjective sleep quality tended to decrease, and morning well-being, mood, affectivity and wakefulness were deteriorated. In the noopsyche, fine motor activity and reaction time performance were deteriorated. Ropinirole 0.5 mg induced, as compared with placebo, an increase in TST, sleep efficacy, S2 sleep and stage shifts. In the morning, somatic complaints increased slightly, while fine motor activity and reaction time performance improved. Our findings suggest a key-lock principle in the diagnosis/treatment of RLS and a dopaminergic mechanism in its pathogenesis, which is supported by the data on periodic leg movements during sleep and arousals of the subsequent paper.
Pandi-Perumal, Seithikurippu R; Gonfalone, Alain A
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
Beattie, Louise; Espie, Colin A; Kyle, Simon D; Biello, Stephany M
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.
Couturier, Jennifer L.; Speechley, Kathy N.; Steele, Margaret; Norman, Ross; Stringer, Bernadette; Nicolson, Rob
Objective: This study compares parents' perceptions of the prevalence, severity, and pattern of sleep problems in children of normal intelligence with pervasive developmental disorders (PDDs) with a normative comparison group of children. Method: A survey including the Children's Sleep Habits Questionnaire was mailed to a sample of parents of…
Gimeno, F; Peset, R
Changes in oxygen saturation and heart frequency were measured during sleep in a group of 21 normal subjects (9 women and 12 men) aged 19-25. At the time of the investigation all were non-smokers, they had no respiratory complaints, and indices of lung function (lung volumes, volume-pressure diagram, and diffusing capacity for carbon monoxide) were within normal limits. In contrast to published data, there were no major changes in oxygen saturation and no differences between men and women. PMID:6474401
Lauridsen, Mette Munk; Frøjk, Jesper; de Muckadell, Ove B Schaffalitzky; Vilstrup, Hendrik
The continuous reaction times (CRT) method describes arousal functions. Reaction time instability in a patient with liver disease indicates covert hepatic encephalopathy (cHE). The effects of sleep deprivation are unknown although cirrhosis patients frequently suffer from sleep disorders. The aim of this study was to determine if sleep deprivation influences the CRT test. Eighteen cirrhosis patients and 27 healthy persons were tested when rested and after one night's sleep deprivation. The patients filled out validated sleep quality questionnaires. Seven patients (38%) had unstable reaction times (a CRTindex < 1.9) compatible with cHE. In these patients, the wakefulness improved or normalized their reaction speed and CRTindex (p = 0.01). There was no change in the other patients' reaction speed or stability. Seven patients (38%) reported poor sleep that was not related to their CRT tests before or after the sleep deprivation. In the healthy participants, the sleep deprivation slowed their reaction times by 11% (p < 0.0001) and in 7 persons (25%) destabilized them. The acute sleep deprivation normalized or improved the reaction time stability of the patients with a CRTindex below 1.9 and had no effect in the patients with a CRTindex above 1.9. There was no relation between reported sleep quality and reaction time results. Thus, in cirrhosis patients, sleep disturbances do not lead to 'falsely' slowed and unstable reaction times. In contrast, the acute sleep deprivation slowed and destabilized the reaction times of the healthy participants. This may have negative consequences for decision-making.
Chi, Luqi; Comyn, Francois-Louis; Keenan, Brendan T.; Cater, Jacqueline; Maislin, Greg; Pack, Allan I.; Schwab, Richard J.
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
Taillard, Jacques; Moore, Nicholas; Claustrat, Bruno; Coste, Olivier; Bioulac, Bernard; Philip, Pierre
In our 24-h society, nocturnal sleep-related accidents are common. Because all individuals are not equal in their responses to sleep loss, it is very important to identify predictors of vulnerability to sleep deprivation in normal subjects. We investigated the performance of a cognitive test of sustained attention, electroencephalogram theta/alpha power, subjective sleepiness, and two circadian markers (core temperature and melatonin) in 18 healthy men (nine morning types and nine evening types, 21.4 +/- 1.9 years) during a 36-h sleep deprivation in a constant routine protocol. Sleep need (self-reported) and baseline sleep structure were also investigated. Nighttime performance impairment was defined as the difference between the mean nocturnal number of lapses (00:00-07:30 [corrected] hours) and the mean diurnal number of lapses (07:30-20:30 hours) expressed as a percentage. Feeling fully alert in the morning just after awakening and/or sleepy in early afternoon were the only two factors (Multiple R > 0.80, > 60% of explained variance) which better predicted the decrease in performances of nocturnal operational tasks requiring sustained attention.
Scullin, Michael K; Bliwise, Donald L
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 across seven diverse correlational and experimental domains that historically have had little crosstalk. Broadly speaking, sleep and cognitive functions are often related in advancing age, though the prevalence of null effects in healthy older adults (including correlations in the unexpected, negative direction) 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.
Scullin, Michael K.; Bliwise, Donald L.
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
Lal, S; Thavundayil, J X; Krishnan, B; Nair, N P; Schwartz, G; Kiely, M E; Guyda, H
One night's sleep deprivation (SD) increased the growth hormone (GH) response to clonidine (20 ug/kg i.v.) in 11 normal men ( p < 0.005). This finding may indicate that SD enhances alpha-2 adrenergic receptor function or that the GH response to GH releasing factor in increased by SD.
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.
van der Kloet, Dalena; Giesbrecht, Timo; Lynn, Steven Jay; Merckelbach, Harald; de Zutter, André
We conducted a longitudinal study to investigate the relation between sleep experiences and dissociative symptoms in a mixed inpatient sample at a private clinic evaluated on arrival and at discharge 6 to 8 weeks later. Using hierarchical regression analyses and structural equation modeling, we found a link between sleep experiences and dissociative symptoms and determined that specifically decreases in narcoleptic experiences rather than insomnia accompany a reduction in dissociative symptoms. Although sleep improvements were associated with a general reduction in psychopathology, this reduction could not fully account for the substantial and specific effect that we found for dissociation. Our findings are consistent with Watson's (2001) hypothesis that disruptions in the sleep-wake cycle lead to intrusions of sleep phenomena into waking consciousness, resulting in dissociative experiences. Accordingly, sleep hygiene may contribute to the treatment or prevention of dissociative symptoms.
Boyle, P J; Scott, J C; Krentz, A J; Nagy, R J; Comstock, E; Hoffman, C
Systemic glucose utilization declines during sleep in man. We tested the hypothesis that this decline in utilization is largely accounted for by reduced brain glucose metabolism. 10 normal subjects underwent internal jugular and radial artery cannulation to determine cerebral blood flow by N2O equilibrium technique and to quantitate cross-brain glucose and oxygen differences before and every 3 h during sleep. Sleep stage was graded by continuous electroencephalogram, and systemic glucose turnover was estimated by isotope dilution. Brain glucose metabolism fell from 33.6 +/- 2.2 mumol/100 g per min (mean +/- SE) before sleep (2300 h) to a mean nadir of 24.3 +/- 1.1 mumol/100 g per min at 0300 h during sleep (P = 0.001). Corresponding rates of systemic glucose utilization fell from 13.2 +/- 0.8 to 11.0 +/- 0.5 mumol/kg per min (P = 0.003). Diminished brain glucose metabolism was the product of a reduced arteriovenous glucose difference, 0.643 +/- 0.024 to 0.546 +/- 0.020 mmol/liter (P = 0.002), and cerebral blood flow, 50.3 +/- 2.8 to 44.6 +/- 1.4 cc/100 g per min (P = 0.021). Brain oxygen metabolism fell commensurately from 153.4 +/- 11.8 to 128.0 +/- 8.4 mumol/100 g per min (P = 0.045). The observed reduction in brain metabolism occurred independent of stage of central nervous system electrical activity (electroencephalographic data), and was more closely linked to duration of sleep. We conclude that a decline in brain glucose metabolism is a significant determinant of falling rates of systemic glucose utilization during sleep. Images PMID:8113391
Charnay, Yves; Leger, Lucienne
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
Auer, Thomas O; Benton, Richard
The sexual behavior of Drosophila melanogaster is an outstanding paradigm to understand the molecular and neuronal basis of sophisticated animal actions. We discuss recent advances in our knowledge of the genetic hardwiring of the underlying neuronal circuitry, and how pertinent sensory cues are differentially detected and integrated in the male and female brain. We also consider how experience influences these circuits over short timescales, and the evolution of these pathways over longer timescales to endow species-specific sexual displays and responses.
Gibbs, H. M.; Gibson, U.; Peyghambarian, N.; Sarid, D.; Stegeman, G.
An Optical Circuitry Cooperative (OCC) has been formed as an NSF cooperative research center in which six or more companies contribute financial support; NSF provides support which declines to zero in five years. Companies benefit from a center by early access to research results, leverage for their research dollars, participation in research selection, and improved relations with faculty and students. The university receives support for a major research program that increases its research capability, provides reasonably stable funding, and opens more opportunities for graduate students. The potential of optical circuitry has been discussed for many years, but the excitement is growing rapidly on the strength of the success of optical fibers for optical transmission, the generation of subpicosecond opitcal pulses, and the development of promising optical logic elements, such as optical bistable devices. And yet, much research remains to be done to discover the best nonlinear optical materials and fabrication techniques. OCC will perform research to provide a data base to allow the development of optical circuitry devices. The areas encompassed by OCC include all-optical logic, picosecond decision-making, guided-wave preprocessors, opti-cal interconnects within computers (both fiber and whole-array imaging), optical storage, and optical computer architecture and devices.
Fantalova, V L
Polygraphic study of day sleep was carried out in 30 nurslings with consideration to the EEG, oculogram, muscle tone indices, variations in skin resistance, respiration, ECG, rheoencephalogram and rheogram of the calf. Nurslings with cerebral affections of perinatal genesis were examined by the same method. It was possible to distinguish the main stages of slow sleep and stages of rapid sleep in young nurslings, although the electroencephalographic expression of the stages in children had its specific features. Age dynamics of the polygraphic picture of sleep showed electroencephalographic, vegetative and motor components of sleep to distinctly coordinate by stages and, at the same time, to possess marked autonomicity; this was also confirmed by analysis of cerebral pathology.
Mann, K; Röschke, J; Benkert, O; Aldenhoff, J; Nink, M; Beyer, J; Lehnert, H
Corticotropin-releasing hormone (CRH) is well-known to be a centrally acting respiratory stimulant after systemic application both in healthy subjects and in patients suffering from respiratory failure. In order to study the effects of CRH on sleep EEG and respiratory parameters during sleep, 14 healthy male volunteers were investigated in a single-blind placebo controlled design. After an adaptation night, polysomnography was performed during two successive nights between 23.00 hrs. and 7.00 hrs. During one night placebo was applied, on the other 50 micrograms ovine CRH was administered intravenously as a bolus every hour from 0.00 hrs. to 6.00 hrs. For the assessment of respiration, blood oxygen saturation and thoracic wall movements were measured, as well as nasal and oral airflow using the thermistor method. Sleep efficiency parameters and subjective perception of sleep quality were not affected following CRH. The following alterations were found regarding sleep architecture: REM sleep as well as slow wave sleep showed a tendency to decrease under CRH, whereas light sleep tended to increase. After an injection of CRH a stimulation of respiration could be observed, with an increase of tidal volume over a time interval of a few minutes. Blood oxygen saturation was only slightly increased. Cortisol and ACTH concentrations were found to be constantly elevated. These results indicate that respiration during sleep is clearly affected by CRH with only slight alterations of global sleep parameters. No association was found between stimulation of ventilation and the occurrence of arousals; the respiratory analeptic effect of CRH thus appears to be specific.(ABSTRACT TRUNCATED AT 250 WORDS)
Walia, Harneet K.; Chung, Mina K.; Ibrahim, Sally; Mehra, Reena
Accumulating data implicate obstructive sleep apnea (OSA) as a predisposing factor to the development of atrial fibrillation (AF), the latter representing the most common sustained cardiac arrhythmia. The postulated mechanisms leading to atrial arrhythmogenesis in OSA include alterations in intrathoracic pressures, intermittent hypoxemia, and autonomic nervous system fluctuations. Although these OSA-related pathophysiologic pathways may result in atrial structural and electrical remodeling, thereby predisposing to AF, there are data to suggest that the immediate influences of respiratory events may trigger arrhythmic events. This case demonstrates an immediate reversal of AF to normal sinus rhythm with optimal continuous positive airway pressure (CPAP) therapy in the background of severe OSA. These findings of immediate benefit of reversal of OSA pathophysiology on cardiac arrhythmia suggest OSA may have acute influences on cardiac electrophysiology. Citation: Walia HK, Chung MK, Ibrahim S, Mehra R. Positive airway pressure-induced conversion of atrial fibrillation to normal sinus rhythm in severe obstructive sleep apnea. J Clin Sleep Med 2016;12(9):1301–1303. PMID:27166298
Mendez, Martin Oswaldo; Chouvarda, Ioanna; Alba, Alfonso; Bianchi, Anna Maria; Grassi, Andrea; Arce-Santana, Edgar; Milioli, Guilia; Terzano, Mario Giovanni; Parrino, Liborio
An analysis of the EEG signal during the B-phase and A-phases transitions of the cyclic alternating pattern (CAP) during sleep is presented. CAP is a sleep phenomenon composed by consecutive sequences of A-phases (each A-phase could belong to a possible group A1, A2 or A3) observed during the non-REM sleep. Each A-phase is separated by a B-phase which has the basal frequency of the EEG during a specific sleep stage. The patterns formed by these sequences reflect the sleep instability and consequently help to understand the sleep process. Ten recordings from healthy good sleepers were included in this study. The current study investigates complexity, statistical and frequency signal properties of electroencephalography (EEG) recordings at the transitions: B-phase--A-phase. In addition, classification between the onset-offset of the A-phases and B-phase was carried out with a kNN classifier. The results showed that EEG signal presents significant differences (p < 0.05) between A-phases and B-phase for the standard deviation, energy, sample entropy, Tsallis entropy and frequency band indices. The A-phase onset showed values of energy three times higher than B-phase at all the sleep stages. The statistical analysis of variance shows that more than 80% of the A-phase onset and offset is significantly different from the B-phase. The classification performance between onset or offset of A-phases and background showed classification values over 80% for specificity and accuracy and 70% for sensitivity. Only during the A3-phase, the classification was lower. The results suggest that neural assembles that generate the basal EEG oscillations during sleep present an over-imposed coordination for a few seconds due to the A-phases. The main characteristics for automatic separation between the onset-offset A-phase and the B-phase are the energy at the different frequency bands.
Pavlov, Valentin A.; Tracey, Kevin J.
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
Pavlov, Valentin A; Tracey, Kevin J
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 neuro-immune 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 define the emerging field of Bioelectronic Medicine.
Neurological sleep disorders are common in the general population and may have a strong impact on quality of life. General practitioners play a key role in recognizing and managing sleep disorders in the general population. They should therefore be familiar with the most important neurological sleep disorders. This review provides a comprehensive overview of the most prevalent and important neurological sleep disorders, including Restless legs syndrome (with and without periodic limb movements in sleep), narcolepsy, NREM- and REM-sleep parasomnias and the complex relationship between sleep and epilepsies. Although narcolepsy is considered as a rare disease, recent discoveries in narcolepsy research provided insight in the function of brain circuitries involved in sleep wake regulation. REM sleep behavioral parasomnia (RBD) is increasingly recognized to represent an early manifestation of neurodegenerative disorders, in particular evolving synucleinopathies. Early diagnosis may thus open new perspectives for developing novel treatment options by targeting neuroprotective substances.
Meerlo, Peter; Mistlberger, Ralph E.; Jacobs, Barry L.; Heller, H. Craig; McGinty, Dennis
Research over the last few decades has firmly established that new neurons are generated in selected areas of the adult mammalian brain, particularly the dentate gyrus of the hippocampal formation and the subventricular zone of the lateral ventricles. The function of adult-born neurons is still a matter of debate. In the case of the hippocampus, integration of new cells in to the existing neuronal circuitry may be involved in memory processes and the regulation of emotionality. In recent years, various studies have examined how the production of new cells and their development into neurons is affected by sleep and sleep loss. While disruption of sleep for a period shorter than one day appears to have little effect on the basal rate of cell proliferation, prolonged restriction or disruption of sleep may have cumulative effects leading to a major decrease in hippocampal cell proliferation, cell survival and neurogenesis. Importantly, while short sleep deprivation may not affect the basal rate of cell proliferation, one study in rats shows that even mild sleep restriction may interfere with the increase in neurogenesis that normally occurs with hippocampus-dependent learning. Since sleep deprivation also disturbs memory formation, these data suggest that promoting survival, maturation and integration of new cells may be an unexplored mechanism by which sleep supports learning and memory processes. Most methods of sleep deprivation that have been employed affect both non-rapid eye movement (NREM) and rapid eye movement (REM) sleep. Available data favor the hypothesis that decreases in cell proliferation are related to a reduction in REM sleep, whereas decreases in the number of cells that subsequently develop into adult neurons may be related to reductions in both NREM and REM sleep. The mechanisms by which sleep loss affects different aspects of adult neurogenesis are unknown. It has been proposed that adverse effects of sleep disruption may be mediated by stress and
Fukuda, K; Ogilvie, R D; Takeuchi, T
There were no differences between Canada and Japan in the prevalence and symptoms of sleep paralysis (SP), but many more Canadians considered SP to be a dream. The difference was considered to be derived from the fact that there is a common expression for SP in Japan but there is not one in Canada. Then, we investigated why there are individuals who consider SP to be a dream and others who do not, and found that many Japanese who regarded it as a dream did not report the symptom of 'unable to move', while in Canada, self-evaluation of spirituality was different between the two groups.
Pandi-Perumal, Seithikurippu R.; Gonfalone, Alain A.
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
Vinod Saladi, Srinivas; Marathe, Himangi; de la Serna, Ivana L
Melanoma is an aggressive malignancy that is resistant to current therapy, and the most lethal of all human skin cancers. It is characterized by several genetic alterations that lead to changes in gene expression and tumorigenesis by triggering alterations in the normal transcriptional circuitry. Transformation and tumor progression are thought to be promoted by a complex interplay between the accumulation of genetic alterations and epigenetic changes. In this review, we discuss recent studies that have implicated SWI/SNF chromatin remodeling enzymes as epigenetic regulators of a transcriptional circuit that operates within the context the genetic alterations that frequently occur in melanoma.
Cohen, Ruben; Looney, Stephen; Kalathingal, Sajitha; De Rossi, Scott
Purpose To evaluate the upper airway dimensions of obstructive sleep apnea (OSA) and control subjects using a cone-beam computed tomography (CBCT) unit commonly applied in clinical practice in order to assess airway dimensions in the same fashion as that routinely employed in a clinical setting. Materials and Methods This was a retrospective analysis utilizing existing CBCT scans to evaluate the dimensions of the upper airway in OSA and control subjects. The CBCT data of sixteen OSA and sixteen control subjects were compared. The average area, average volume, total volume, and total length of the upper airway were computed. Width and anterior-posterior (AP) measurements were obtained on the smallest axial slice. Results OSA subjects had a significantly smaller average airway area, average airway volume, total airway volume, and mean airway width. OSA subjects had a significantly larger airway length measurement. The mean A-P distance was not significantly different between groups. Conclusion OSA subjects have a smaller upper airway compared to controls with the exception of airway length. The lack of a significant difference in the mean A-P distance may indicate that patient position during imaging (upright vs. supine) can affect this measurement. Comparison of this study with a future prospective study design will allow for validation of these results. PMID:27051634
Lahm, Ryan; Iaizzo, Paul A
This study explores the hypothesis that a high degree of sustained muscle activity associated with a sub-optimal spinal orientation may compromise an individual's ability to relax or initiate sleep. Data from 22 participants who were considered to be part of a normal, back-pain-free population were used in these studies. Participants laid down on a mattress in a foetal position (i.e. on their sides) at three varying bed pressures while EMG activities, heart rates, blood pressures, subjective comfort levels and spinal alignment data were recorded. Minor effects of mattress inflation pressures were associated with changes in EMG activity, heart rate, blood pressure and/or subjective comfort. In contrast, spinal alignment assessment revealed significant differences between the three different inflation pressures studied (827.4, 2413.2 and 3999.0 Pa). It was concluded that in a population of normal participants, although mattress inflation pressure induced significant changes in spinal alignment, these changes were of little physiological consequence. Nevertheless, this data provides baseline information needed to assess similar correlations in a symptomatic population (e.g. those with either acute or chronic neck or back pain).
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
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.
Schittecatte, Michel; Dumont, Françoise; Machowski, Robert; Fontaine, Eric; Cornil, Catherine; Mendlewicz, Julien; Wilmotte, Jean
To determine whether alpha(2)-adrenergic receptor (alpha2AR) subsensitivity is a state or a trait marker of depression, we consecutively challenged 32 drug-free depressed patients with a clonidine REM suppression test (CREST). We then treated the patients with fluvoxamine, a selective serotonin reuptake inhibitor, or mirtazapine, a selective alpha(2)-adrenergic receptor antagonist. The first 10 patients from each treatment group who recovered were given a second challenge test. The CREST values of the two treatment groups at each time point were compared, and also compared with the CREST values of a group of 10 normal subjects. Before treatment, the REM sleep response to clonidine in the two groups of patients was significantly blunted compared with the REM sleep response in the healthy subjects. After treatment, there was still an abnormal REM sleep response to clonidine in the fluvoxamine-treated patients, despite clinical recovery, but there was a normalized REM sleep response in the mirtazapine-treated patients. These results are compatible with the hypothesis that alpha2AR subsensitivity is a trait marker of depression and suggest that the effects of these two antidepressants on alpha2AR sensitivity may not be linked to the alleviation of depression.
of single crystalline nanomaterials. Highly ordered and parallel arrays of optically active CdSe nanowires and high mobility Ge/Si nanowires are...for enabling the fabrication of the all- nanowire sensor circuitry. First, highly aligned CdSe and Ge/Si NW arrays were assembled at pre-defined...FETs (Tl and T2) amplifying the photoresponse of a CdSe nanosensor. (B) Schematic of the all- nanowire optical sensor circuit based on ordered
Seicean, Sinziana; Strohl, Kingman P; Seicean, Andreea; Gibby, Conrad; Marwick, Thomas H
Sleep disordered breathing (SDB) is associated with type 2 diabetes mellitus (T2DM) and cardiovascular disease; however, the contribution of SDB to incident heart failure (HF), coronary artery disease (CAD), and atrial fibrillation (AF) in patients with T2DM is unknown. We followed up 834 consecutive asymptomatic patients with T2DM (age 56 ± 11 years, 369 women) with normal exercise echocardiographic findings for ≤8 years using electronic health records. The demographics, cardiac risk factors, symptoms, diagnoses, and medications were collected at the echocardiography and validated from the electronic health records. SDB was confirmed by a comprehensive sleep evaluation and/or polysomnography before echocardiography. SDB was diagnosed in 188 patients (21%) at baseline; 116 were untreated. During a median follow-up of 4.9 years (interquartile range 3.9 to 6.1), 22 congestive HF, 72 CAD, and 40 AF incident events were observed. In the Cox proportional hazards models, SDB was associated with incident CAD (hazard ratio 1.8, 95% confidence interval 1.1 to 3.0, p = 0.01; adjusted hazard ratio 1.9, 95% confidence interval 1.2 to 3.2, p <0.01) and AF (hazard ratio 2.6, 95% confidence interval 1.4 to 4.7, p = 0.01; adjusted hazard ratio 2.9, 95% confidence interval 1.5 to 5.9, p <0.01). Limiting SDB to only those patients diagnosed using polysomnography (n = 132), SDB was associated with incident CAD (hazard ratio 1.9, 95% confidence interval 1.1 to 3.3, p = 0.03; adjusted hazard ratio 2.2, 95% confidence interval 1.2 to 3.9, p = 0.01) and HF (hazard ratio 2.7, 95% confidence interval 1.1 to 7.0, p = 0.03; adjusted hazard ratio 3.5, 95% confidence interval 1.4 to 9.0, p <0.01). Female gender, age, elevated blood pressure, and left ventricular mass were additional correlates of CAD in those with asymptomatic T2DM. In conclusion, the association of SDB with incident CAD, AF, and HF in patients with T2DM justifies more liberal screening for SDB in patients with T2DM
Rogers, N. L.; Szuba, M. P.; Staab, J. P.; Evans, D. L.; Dinges, D. F.
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.
Fernandez, Hubert H; Okun, Michael S; Rodriguez, Ramon L; Malaty, Irene A; Romrell, Janet; Sun, Anqi; Wu, Samuel S; Pillarisetty, Sandeep; Nyathappa, Anand; Eisenschenk, Stephan
Polysomnographic studies of Parkinson's disease (PD) patients with visual hallucinations (VH) usually reveal short, fragmented rapid eye movement (REM) sleep, with lower sleep efficiency and reduced total REM sleep. Quetiapine has been demonstrated in open-label trials to be effective for the treatment of insomnia and VH in PD. To confirm quetiapine's efficacy in improving VH, and to determine whether the mechanism was due to its effect on REM sleep architecture, we performed a pilot, double-blind, placebo-controlled study. Sixteen PD patients experiencing VH were recruited. Eight patients were randomized to quetiapine and eight patients to placebo. Patients underwent pre- and post-treatment polysomnography. The Clinical Global Impression Scale (CGIS), Brief Psychiatric Rating Scale (BPRS), and Unified Parkinson Disease Rating Scale (UPDRS) motor subscale were obtained. There were no differences in baseline characteristics between the treatment arms except that the placebo group had more sleep in stage REM (74.7 min vs. 40.1 min; p < .001). Data were imputed for all patients who prematurely discontinued (four quetiapine and one placebo) in an intention-to-treat analysis. The average quetiapine dose was 58.3 mg/day. While there was no significant difference in the change in REM duration pre- vs. post-treatment in either arm, patients randomized to quetiapine improved on the CGIS (p = .03) and the hallucination item of the BPRS (p = .02). No difference was noted in the UPDRS motor scores. Despite the small sample, this is the first double-blind trial to show quetiapine's efficacy over placebo in controlling VH in the PD population. However, normalization of sleep architecture was not supported as the mechanism.
Daily cycles of wakefulness and sleep are regulated by coordinated interactions between wakefulness- and sleep-regulating neural circuitry. Wakefulness is associated with neuronal activity in cholinergic neurons in the brainstem and basal forebrain, monoaminergic neurons in the brainstem and posterior hypothalamus, and hypocretin (orexin) neurons in the lateral hypothalamus that act in a coordinated manner to stimulate cortical activation on the one hand and behavioral arousal on the other hand. Each of these neuronal groups subserves distinct aspects of wakefulness-related functions of the brain. Normal transitions from wakefulness to sleep involve sleep-related inhibition and/or disfacilitation of the multiple arousal systems. The cell groups that shut off the network of arousal systems, at sleep onset, occur with high density in the ventral lateral preoptic area (VLPO) and the median preoptic nucleus (MnPN) of the hypothalamus. Preoptic neurons are activated during sleep and exhibit sleep-wake state-dependent discharge patterns that are reciprocal of that observed in several arousal systems. Neurons in the VLPO contain the inhibitory neuromodulator, galanin, and the inhibitory neurotransmitter, gamma-aminobutyric acid (GABA). The majority of MnPN sleep-active neurons synthesize GABA. VLPO and MnPN neurons are sources of projections to arousal-regulatory systems in the posterior and lateral hypothalamus and the rostral brainstem. Mechanisms of sleep induction by these nuclei are hypothesized to involve GABA-mediated inhibition of multiple arousal systems. Normal cycling between discrete behavioral states is mediated by the combined influence of a sleep need that increases with continued wakefulness and an intrinsic circadian oscillation. This chapter will review anatomical and functional properties of populations of sleep-/wake-regulating neurons, focusing on recent findings supporting functional significance of the VLPO and MnPN in the regulation of sleep
Boudreau, Eilis A; Johnson, Kyle P; Jackman, Angela R; Blancato, Jan; Huizing, Marjan; Bendavid, Claude; Jones, Marypat; Chandrasekharappa, Settara C; Lewy, Alfred J; Smith, Ann C M; Magenis, R Ellen
Smith-Magenis syndrome (SMS) is a disorder characterized by multiple congenital anomalies and behavior problems, including abnormal sleep patterns. It is most commonly due to a 3.5 Mb interstitial deletion of chromosome 17 band p11.2. Secretion of melatonin, a hormone produced by the pineal gland, is the body's signal for nighttime darkness. Published reports of 24-hr melatonin secretion patterns in two independent SMS cohorts (US and France) document an inverted endogenous melatonin pattern in virtually all cases (96%), suggesting that this finding is pathognomic for the syndrome. We report on a woman with SMS due to an atypical large proximal deletion ( approximately 6Mb; cen<->TNFRSFproteinB) of chromosome band (17)(p11.2p11.2) who presents with typical sleep disturbances but a normal pattern of melatonin secretion. We further describe a melatonin light suppression test in this patient. This is the second reported patient with a normal endogenous melatonin rhythm in SMS associated with an atypical large deletion. These two patients are significant because they suggest that the sleep disturbances in SMS cannot be solely attributed to the abnormal diurnal melatonin secretion versus the normal nocturnal pattern.
Nurses are accustomed to helping others with their sleep problems and dealing with issues such as pain that may delay or interrupt sleep. However, they may be less familiar with what constitutes a healthy night's sleep. This article examines what is known about the process and purpose of sleep, and examines the ways in which factors that promote wakefulness and sleep combine to help establish a normal circadian rhythm. Theories relating to the function of sleep are discussed and research is considered that suggests that sleep deficit may lead to metabolic risks, including heart disease, obesity, type 2 diabetes mellitus and several types of cancer.
de la Iglesia, Horacio O; Moreno, Claudia; Lowden, Arne; Louzada, Fernando; Marqueze, Elaine; Levandovski, Rosa; Pilz, Luisa K; Valeggia, Claudia; Fernandez-Duque, Eduardo; Golombek, Diego A; Czeisler, Charles A; Skene, Debra J; Duffy, Jeanne F; Roenneberg, Till
While we do not yet understand all the functions of sleep, its critical role for normal physiology and behaviour is evident. Its amount and temporal pattern depend on species and condition. Humans sleep about a third of the day with the longest, consolidated episode during the night. The change in lifestyle from hunter-gatherers via agricultural communities to densely populated industrialized centres has certainly affected sleep, and a major concern in the medical community is the impact of insufficient sleep on health [1,2]. One of the causal mechanisms leading to insufficient sleep is altered exposure to the natural light-dark cycle. This includes the wide availability of electric light, attenuated exposure to daylight within buildings, and evening use of light-emitting devices, all of which decrease the strength of natural light-dark signals that entrain circadian systems .
Pavlou, Hania J; Lin, Andrew C; Neville, Megan C; Nojima, Tetsuya; Diao, Fengqiu; Chen, Brian E; White, Benjamin H; Goodwin, Stephen F
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
Chouvarda, I; Mendez, M O; Alba, A; Bianchi, A M; Grassi, A; Arce-Santana, E; Rosso, V; Terzano, M G; Parrino, L
This study analyzes the nonlinear properties of the EEG at transition points of the sequences that build the Cyclic Alternating Pattern (CAP). CAP is a sleep phenomenon built up by consecutive sequences of activations and non-activations observed during the sleep time. The sleep condition can be evaluated from the patterns formed by these sequences. Eleven recordings from healthy and good sleepers were included in this study. We investigated the complexity properties of the signal at the onset and offset of the activations. The results show that EEG signals present significant differences (p<0.05) between activations and non-activations in the Sample Entropy and Tsallis Entropy indices. These indices could be useful in the development of automatic methods for detecting the onset and offset of the activations, leading to significant savings of the physician's time by simplifying the manual inspection task.
... 5 Sleep Problems in Asthma and COPD NORMAL AIRWAY Good quality sleep is important for everyone. People ... COPD can take to improve their sleep. OBSTRUCTED AIRWAY What kind of night disturbances can I get ...
Educational aims The reader will be able to: Understand normal sleep patterns in infancyAppreciate disorders of breathing in infancyAppreciate disorders of respiratory control Normal sleep in infancy is a time of change with alterations in sleep architecture, sleep duration, sleep patterns and respiratory control as an infant grows older. Interactions between sleep and respiration are key to the mechanisms by which infants are vulnerable to sleep disordered breathing. This review discusses normal sleep in infancy, as well as normal sleep breathing in infancy. Sleep disordered breathing (obstructive and central) as well as disorders of ventilatory control and infant causes of hypoventilation are all reviewed in detail. PMID:27064478
Neitz, J; Neitz, M
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.
Mander, Bryce A; Winer, Joseph R; Walker, Matthew P
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?
... sleep cycle has stages, from light drowsiness to deep sleep. During the stage called rapid eye movement ( ... REM sleep. Sleepwalking (somnambulism) most often occurs during deep, non-REM sleep (called N3 sleep) early in ...
Takeuchi, T; Miyasita, A; Sasaki, Y; Inugami, M; Fukuda, K
We elicited isolated sleep paralysis (ISP) from normal subjects by a nocturnal sleep interruption schedule. On four experimental nights, 16 subjects had their sleep interrupted for 60 minutes by forced awakening at the time when 40 minutes of nonrapid eye movement (NREM) sleep had elapsed from the termination of rapid eye movement (REM) sleep in the first or third sleep cycle. This schedule produced a sleep onset REM period (SOREMP) after the interruption at a high rate of 71.9%. We succeeded in eliciting six episodes of ISP in the sleep interruptions performed (9.4%). All episodes of ISP except one occurred from SOREMP, indicating a close correlation between ISP and SOREMP. We recorded verbal reports about ISP experiences and recorded the polysomnogram (PSG) during ISP. All of the subjects with ISP experienced inability to move and were simultaneously aware of lying in the laboratory. All but one reported auditory/visual hallucinations and unpleasant emotions. PSG recordings during ISP were characterized by a REM/W stage dissociated state, i.e. abundant alpha electroencephalographs and persistence of muscle atonia shown by the tonic electromyogram. Judging from the PSG recordings, ISP differs from other dissociated states such as lucid dreaming, nocturnal panic attacks and REM sleep behavior disorders. We compare some of the sleep variables between ISP and non-ISP nights. We also discuss the similarities and differences between ISP and sleep paralysis in narcolepsy.
Osorio, Ricardo S.; Ayappa, Indu; Mantua, Janna; Gumb, Tyler; Varga, Andrew; Mooney, Anne M.; Burschtin, Omar E.; Taxin, Zachary; During, Emmanuel; Spector, Nicole; Biagioni, Milton; Pirraglia, Elizabeth; Lau, Hiuyan; Zetterberg, Henrik; Blennow, Kaj; Lu, Shou-En; Mosconi, Lisa; Glodzik, Lidia; Rapoport, David M.; de Leon, Mony J.
Background Previous studies have suggested a link between Sleep Disordered Breathing (SDB) and dementia risk. In the present study, we analyzed the relationship between SDB severity, cerebrospinal fluid (CSF) Alzheimer's disease (AD) biomarkers, and the ApoE alleles. Methods 95 cognitively normal elderly participants were analyzed for SDB severity, CSF measures of phosphorylated-tau (P-Tau), total-tau (T-Tau), and amyloid beta 42 (Aβ42), as well as ApoE allele status. Findings In ApoE3+ subjects, significant differences were found between sleep groups for P-Tau (F[df2]=4.3, p=0.017), and T-Tau (F[df2]=3.3, p=0.043). Additionally, among ApoE3+ subjects, the apnea/hypopnea with 4% O2-desaturation index (AHI4%) was positively correlated with P-Tau (r=0.30, p=0.023), T-Tau (r=0.31, p=0.021), and Aβ42 (r=0.31, p=0.021). In ApoE2+ subjects, AHI4% was correlated with lower levels of CSF Aβ42 (r=−0.71, p=0.004), similarly to ApoE4+ subjects where there was also a trend towards lower CSF Aβ42 levels Interpretation Our observations suggest that there is an association between SDB and CSF AD- biomarkers in cognitively normal elderly. Existing therapies for SDB such as CPAP could delay the onset to mild cognitive impairment or dementia in normal elderly. PMID:24439479
Osorio, Ricardo S; Ayappa, Indu; Mantua, Janna; Gumb, Tyler; Varga, Andrew; Mooney, Anne M; Burschtin, Omar E; Taxin, Zachary; During, Emmanuel; Spector, Nicole; Biagioni, Milton; Pirraglia, Elizabeth; Lau, Hiuyan; Zetterberg, Henrik; Blennow, Kaj; Lu, Shou-En; Mosconi, Lisa; Glodzik, Lidia; Rapoport, David M; de Leon, Mony J
Previous studies have suggested a link between sleep disordered breathing (SDB) and dementia risk. In the present study, we analyzed the relationship between SDB severity, cerebrospinal fluid (CSF) Alzheimer's disease-biomarkers, and the ApoE alleles. A total of 95 cognitively normal elderly participants were analyzed for SDB severity, CSF measures of phosphorylated-tau (p-tau), total-tau (t-tau), and amyloid beta 42 (Aβ-42), as well as ApoE allele status. In ApoE3+ subjects, significant differences were found between sleep groups for p-tau (F[df2] = 4.3, p = 0.017), and t-tau (F[df2] = 3.3, p = 0.043). Additionally, among ApoE3+ subjects, the apnea and/or hypopnea with 4% O2-desaturation index was positively correlated with p-tau (r = 0.30, p = 0.023), t-tau (r = 0.31, p = 0.021), and Aβ-42 (r = 0.31, p = 0.021). In ApoE2+ subjects, the apnea and/or hypopnea with 4% O2-desaturation index was correlated with lower levels of CSF Aβ-42 (r = -0.71, p = 0.004), similarly to ApoE4+ subjects where there was also a trend toward lower CSF Aβ-42 levels. Our observations suggest that there is an association between SDB and CSF Alzheimer's disease-biomarkers in cognitively normal elderly individuals. Existing therapies for SDB such as continuous positive airway pressure could delay the onset to mild cognitive impairment or dementia in normal elderly individuals.
Enciso, Reyes; Shigeta, Yuko; Nguyen, Manuel; Clark, Glenn T.
Objective To compare the incidental radiographic findings in the maxillofacial structures and the pharyngeal airway between moderate/severe Obstructive Sleep Apnea (OSA) subjects and mild OSA/normal subjects using Cone-Beam Computed Tomography (CBCT) scans. Study Design 53 moderate/severe OSA subjects (with a Respiratory Disturbance Index [RDI]≥15 events/hr) and 33 mild OSA/normal subjects, (RDI<15) based on ambulatory somnographic assessment were recruited. Supine CBCT’s were taken and sent for radiological report. The incidental findings were compared between the two groups. Results Moderate/severe subjects had larger prevalence of conchae bullosa, hypertrophic turbinates, hypertrophic tonsils, elongated or posteriorly placed soft palate, narrower airway, enlarged tongue, and focal calcifications, though no significant differences were found. Conclusions CBCT is useful in identifying maxillofacial and airway anomalies that could interfere with normal breathing. However, no significant difference was found in prevalence of incidental findings between moderate/severe OSA and mild/normal subjects. Further studies are necessary to generalize our results. PMID:22862979
Sleep disturbance is a common problem in general adult population. Recent evidence suggests the link between the occurrence of cardiovascular events and several sleep disturbances including sleep apnea syndrome, insomnia and periodic limb movements during sleep. Sleep duration may affect the cardiovascular outcome. Shift work also may increase the risk of ischemic heart disease. Normalization of sleep rhythm has a potential to be a therapeutic target of ischemic heart diseases, although further study is required to evaluate the preventive effect on cardiovascular events. Here we describe the current understandings regarding the roles of sleep disorders during the pathogenesis of cardiovascular events.
Voges, Caroline; Helmchen, Christoph; Heide, Wolfgang; Sprenger, Andreas
Adaptation of saccade amplitude in response to intra-saccadic target displacement is a type of implicit motor learning which is required to compensate for physiological changes in saccade performance. Once established trials without intra-saccadic target displacement lead to de-adaptation or extinction, which has been attributed either to extra-retinal mechanisms of spatial constancy or to the influence of the stable visual surroundings. Therefore we investigated whether visual deprivation (“Ganzfeld”-stimulation or sleep) can partially maintain this motor learning compared to free viewing of the natural surroundings. Thirty-five healthy volunteers performed two adaptation blocks of 100 inward adaptation trials – interspersed by an extinction block – which were followed by a two-hour break with or without visual deprivation (VD). Using additional adaptation and extinction blocks short and long (4 weeks) term memory of this implicit motor learning were tested. In the short term, motor memory tested immediately after free viewing was superior to adaptation performance after VD. In the long run, however, effects were opposite: motor memory and relearning of adaptation was superior in the VD conditions. This could imply independent mechanisms that underlie the short-term ability of retrieving learned saccadic gain and its long term consolidation. We suggest that subjects mainly rely on visual cues (i.e., retinal error) in the free viewing condition which makes them prone to changes of the visual stimulus in the extinction block. This indicates the role of a stable visual array for resetting adapted saccade amplitudes. In contrast, visual deprivation (GS and sleep), might train subjects to rely on extra-retinal cues, e.g., efference copy or prediction to remap their internal representations of saccade targets, thus leading to better consolidation of saccadic adaptation. PMID:25867186
Schwartz, Michael D.; Kilduff, Thomas S.
SYNOPSIS Since the discovery of Rapid Eye Movement (REM) sleep in the late 1950s, identification of the neural circuitry underlying wakefulness, sleep onset and the alternation between REM and non-REM (NREM) sleep has been an active area of investigation. Synchronization and desynchronization of cortical activity as detected in the electroencephalogram (EEG) is due to a corticothalamocortical loop, intrinsic cortical oscillators, monoaminergic and cholinergic afferent input to the thalamus, and the basal forebrain cholinergic input directly to the cortex. The monoaminergic and cholinergic systems are largely wake-promoting; the brainstem cholinergic nuclei are also involved in REM sleep regulation. These wake-promoting systems receive excitatory input from the hypothalamic hypocretin/orexin system. Sleep-promoting nuclei are GABAergic in nature and found in the preoptic area, brainstem and lateral hypothalamus. Although the pons is critical for the expression of REM sleep, recent research has suggested that melanin-concentrating hormone/GABAergic cells in the lateral hypothalamus "gate" REM sleep. The temporal distribution of sleep and wakefulness is due to interaction between the circadian system and the sleep homeostatic system. Although the hypothalamic suprachiasmatic nuclei contain the circadian pacemaker, the neural circuitry underlying the sleep homeostat is less clear. Prolonged wakefulness results in the accumulation of extracellular adenosine, possibly from glial sources, which is an important feedback molecule for the sleep homeostatic system. Cortical neuronal nitric oxide (nNOS) neurons may also play a role in propagating slow waves through the cortex in NREM sleep. Several neuropeptides and other neurochemicals likely play important roles in sleep/wake control. Although the control of sleep and wakefulness seemingly involves multiple redundant systems, each of these systems provides a vulnerability that can result in sleep/wake dysfunction that may
Askenasy, J J M
The present article is meant to suggest an approach to the guidelines for the therapy of sleep disturbances in Parkinson's Disease (PD) patients.The factors affecting the quality of life in PD patients are depression, sleep disturbances and dependence. A large review of the literature on sleep disturbances in PD patients, provided the basis for the following classification of the sleep-arousal disturbances in PD patients. We suggest a model based on 3 steps in the treatment of sleep disturbances in PD patients. This model allowing the patient, the spouse or the caregiver a quiet sleep at night, may postpone the retirement and the institutionalization of the PD patient. I. Correct diagnosis of sleep disorders based on detailed anamnesis of the patient and of the spouse or of the caregiver. One week recording on a symptom diary (log) by the patient or the caregiver. Correct diagnosis of sleep disorders co morbidities. Selection of the most appropriate sleep test among: polysomnography (PSG), multiple sleep latency test (MSLT), multiple wake latency test (MWLT), Epworth Sleepiness Scale, actigraphy or video-PSG. II. The nonspecific therapeutic approach consists in: a) Checking the sleep effect on motor performance, is it beneficial, worse or neutral. b) Psycho-physical assistance. c) Dopaminergic adjustment is necessary owing to the progression of the nigrostriatal degeneration and the increased sensitivity of the terminals, which alter the normal modulator mechanisms of the motor centers in PD patients. Among the many neurotransmitters of the nigro-striatal pathway one can distinguish two with a major influence on REM and NonREM sleep. REM sleep corresponds to an increased cholinergic receptor activity and a decreased dopaminergic activity. This is the reason why REM sleep deprivation by suppressing cholinergic receptor activity ameliorates PD motor symptoms. L-Dopa and its agonists by suppressing cholinergic receptors suppress REM sleep. The permanent adjustment
Larsen, Cory A.
This report details the current progress in the design, implementation, and validation of the signal conditioning circuitry used in a measurement instrumentation system. The purpose of this text is to document the current progress of a particular design in signal conditioning circuitry in an instrumentation system. The input of the signal conditioning circuitry comes from a piezoresistive transducer and the output will be fed to a 250 ksps, 12-bit analog-to-digital converter (ADC) with an input range of 0-5 V. It is assumed that the maximum differential voltage amplitude input from the sensor is 20 mV with an unknown, but presumably high, sensor bandwidth. This text focuses on a specific design; however, the theory is presented in such a way that this text can be used as a basis for future designs.
Mancuso, James J; Kim, Jinsook; Lee, Soojung; Tsuda, Sachiko; Chow, Nicholas B H; Augustine, George J
Recently developed optogenetic technologies offer the promise of high-speed mapping of brain circuitry. Genetically targeted light-gated channels and pumps, such as channelrhodopsins and halorhodopsin, allow optical control of neuronal activity with high spatial and temporal resolution. Optogenetic probes of neuronal activity, such as Clomeleon and Mermaid, allow light to be used to monitor the activity of a genetically defined population of neurons. Combining these two complementary sets of optogenetic probes will make it possible to perform all-optical circuit mapping. Owing to the improved efficiency and higher speed of data acquisition, this hybrid approach should enable high-throughput mapping of brain circuitry.
Eugene, Andy R; Masiak, Jolanta
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.
Eugene, Andy R.; Masiak, Jolanta
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
Ray, Laura B.; Sockeel, Stéphane; Soon, Melissa; Bore, Arnaud; Myhr, Ayako; Stojanoski, Bobby; Cusack, Rhodri; Owen, Adrian M.; Doyon, Julien; Fogel, Stuart M.
A spindle detection method was developed that: (1) extracts the signal of interest (i.e., spindle-related phasic changes in sigma) relative to ongoing “background” sigma activity using complex demodulation, (2) accounts for variations of spindle characteristics across the night, scalp derivations and between individuals, and (3) employs a minimum number of sometimes arbitrary, user-defined parameters. Complex demodulation was used to extract instantaneous power in the spindle band. To account for intra- and inter-individual differences, the signal was z-score transformed using a 60 s sliding window, per channel, over the course of the recording. Spindle events were detected with a z-score threshold corresponding to a low probability (e.g., 99th percentile). Spindle characteristics, such as amplitude, duration and oscillatory frequency, were derived for each individual spindle following detection, which permits spindles to be subsequently and flexibly categorized as slow or fast spindles from a single detection pass. Spindles were automatically detected in 15 young healthy subjects. Two experts manually identified spindles from C3 during Stage 2 sleep, from each recording; one employing conventional guidelines, and the other, identifying spindles with the aid of a sigma (11–16 Hz) filtered channel. These spindles were then compared between raters and to the automated detection to identify the presence of true positives, true negatives, false positives and false negatives. This method of automated spindle detection resolves or avoids many of the limitations that complicate automated spindle detection, and performs well compared to a group of non-experts, and importantly, has good external validity with respect to the extant literature in terms of the characteristics of automatically detected spindles. PMID:26441604
... For Consumers Consumer Information by Audience For Women Sleep Problems Share Tweet Linkedin Pin it More sharing ... PDF 474KB) En Español Medicines to Help You Sleep Tips for Better Sleep Basic Facts about Sleep ...
... the day, even if you have had enough sleep? You might have a sleep disorder. The most common kinds are Insomnia - a hard time falling or staying asleep Sleep apnea - breathing interruptions during sleep Restless legs syndrome - ...
Ho, Tiffany C; Sanders, Stephan J; Gotlib, Ian H; Hoeft, Fumiko
Neuroscientists are increasingly using advanced neuroimaging methods to elucidate the intergenerational transmission of human brain circuitry. This new line of work promises to shed light on 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.
Keymeulen, Didier; Buehler, Martin
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.
Bubser, Michael; Byun, Nellie; Wood, Michael R; Jones, Carrie K
The muscarinic cholinergic system constitutes an important part of the neuronal circuitry that modulates normal cognition. Muscarinic receptor antagonists are well known to produce or exacerbate impairments in attention, learning, and memory. Conversely, both direct-acting muscarinic receptor agonists and indirect-acting muscarinic cholinergic agonists, such as acetylcholinesterase inhibitors, have shown cognition-enhancing properties, including improvements in normal cognitive function, reversal of cognitive deficits induced by muscarinic receptor antagonists, and attenuation of cognitive deficits in psychiatric and neurological disorders, such as Alzheimer's disease and schizophrenia. However, until recently, the lack of small molecule ligands that antagonize or activate specific muscarinic acetylcholine receptor (mAChR) subtypes with high selectivity has been a major obstacle in defining the relative contributions of individual mAChRs to different aspects of cognitive function and for the development of novel therapeutic agents. These limitations may be potentially overcome by the recent discovery of novel mAChR subtype-selective compounds, notably allosteric agonists and positive allosteric modulators, which exhibit greater selectivity for individual mAChR subtypes than previous mAChR orthosteric agonists. In preclinical studies, these novel ligands have shown promising efficacy in several models for the enhancement of cognition. In this chapter, we will review the muscarinic cholinergic circuitry and pharmacology of mAChR agonists and antagonists relevant to the modulation of different aspects of cognition in animals and clinical populations.
Plante, Gérard E
It is not surprising that cardiovascular diseases such as congestive heart failure and coronary insufficiency can give rise to varying degrees of sleep impairment; it is less readily appreciated that certain physiologic events occurring during sleep-as well as long-term unsatisfactory sleep-may cause or increase the risk of cardiovascular conditions such as hypertension, atherosclerosis, stroke, and cardiac arrythmias. Heart rate abnormalities during sleep in normotensive subjects predict later cardiovascular disease, and their early identification alerts the physician to undertake preventive measures. Maneuvers, such as induction of hypoxia, can elicit abnormal blood pressure responses during sleep, and such responses have been used to identify impending cardiovascular problems that could become therapeutic targets. The spontaneously hypertensive rat has been used to examine the effect of sympathetic nervous system (SNS) activity on the heart under a variety of experimental conditions, including quiet and paradoxical sleep. The results have disclosed significant differences between the responses of spontaneously hypertensive rats and normal rats to SNS stimulation. Exploration of other pathophysiologic pathways affected by exposure to light and dark, including those responsive to the cyclic production of melatonin, will improve our understanding of the effect of disruptions of the circadian cycle on cardiovascular function. There is growing evidence that melatonin can influence important processes such as fluid, nitrogen, and acid-base balance. Human subjects whose nocturnal arterial blood pressure fails to show the "normal" decrement during sleep ("nondippers") are also prone to sleep poorly, exhibit increased SNS activity during sleep, and have an increased risk of total and cardiovascular disease mortality. Chronic sleep deficit is now known to be a risk factor for obesity and may contribute to the visceral form of obesity that underlies the metabolic syndrome
Roky, Rachida; Herrera, Christopher Paul; Ahmed, Qanta
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.
Penn, N E; Kripke, D F; Scharff, J
Sleep paralysis is a sensation of an inability to speak or move other muscles when falling asleep or awakening. Sleep paralysis by itself has been reported as occurring infrequently and many clinicians are uncertain of its significance. In contrast, sleep paralysis in conjunction with sleep attacks has been reported as a concomitant of narcolepsy. To further examine the incidence of sleep paralysis, the responses of 80 first-year medical students, 16.25% had experienced predormital, postdormital, or both types of sleep paralysis. These episodes occurred infrequently--only once or twice for most of these students. Reports of sleep paralysis were not associated with sleep attacks or cataplexy. These results support two previous studies which found that sleep paralysis alone occurs frequently among normals.
Wickboldt, Alvah T.; Bowen, Alex F.; Kaye, Aaron J.; Kaye, Adam M.; Rivera Bueno, Franklin; Kaye, Alan D.
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
Mays, L E; Gamlin, P D
Experiments in primates have contributed greatly to our understanding of the neural mechanisms involved in the eye movements required to view objects at different distances. Early work focused on the circuitry for generating horizontal vergence eye movements alone. However, vergence eye movements are associated with lens accommodation and are usually accompanied by saccadic eye movements, so more recent work has been directed at understanding the interactions between vergence and accommodation, and between vergence and saccades. A new model explains the neural basis for interactions between vergence and accommodation by a neural network in which pre-motor elements are shared by these two systems. The effects of saccades on vergence eye movements appear to be the result of shared pre-motor circuits as well. Current evidence suggests that pontine omnipause neurons, known to be crucial for the generation of saccades, play an important role in the vergence pre-motor circuitry.
Smythe, Robert; Palmer, Dean; Gursel, Yekta; Reder, Leonard; Savedra, Raymond
Modules of additional drive circuitry have been developed to enhance the functionality of a family of commercially available positioning motors (Picomotor . or equivalent) that provide linear motion controllable, in principle, to within increments .30 nm. A motor of this type includes a piezoelectric actuator that turns a screw. Unlike traditional piezoelectrically actuated mechanisms, a motor of this type does not rely on the piezoelectric transducer to hold position: the screw does not turn except when the drive signal is applied to the actuator.
Larson, William E.; Ihlefeld, Curtis M.; Medelius, Pedro J.; Delgado, H. (Technical Monitor)
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.
Riga, Danai; Matos, Mariana R.; Glas, Annet; Smit, August B.; Spijker, Sabine; Van den Oever, Michel C.
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
Paterson, Louise M; Nutt, David J; Wilson, Sue J
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.
Jun, Jonathan C; Chopra, Swati; Schwartz, Alan R
Sleep apnoea is a disorder characterised by repetitive pauses in breathing during sleep caused by airway occlusion (obstructive sleep apnoea) or altered control of breathing (central sleep apnoea). In this Clinical Year in Review, we summarise high-impact research from the past year pertaining to management, diagnosis and cardio-metabolic consequences of sleep apnoea.
Montague, S.; Smith, J.H.; Sniegowski, J.J.; McWhorter, P.J.
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.
Montague, Stephen; Smith, James H.; Sniegowski, Jeffry J.; McWhorter, Paul J.
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.
Keene, Alex C.; Duboué, Erik R.; McDonald, Daniel M.; Dus, Monica; Suh, Greg S.B.; Waddell, Scott; Blau, Justin
Summary Neural systems controlling the vital functions of sleep and feeding in mammals are tightly inter-connected: sleep deprivation promotes feeding, while starvation suppresses sleep. Here we show that starvation in Drosophila potently suppresses sleep suggesting that these two homeostatically regulated behaviors are also integrated in flies. The sleep suppressing effect of starvation is independent of the mushroom bodies, a previously identified sleep locus in the fly brain, and therefore is regulated by distinct neural circuitry. The circadian clock genes Clock (Clk) and cycle (cyc) are critical for proper sleep suppression during starvation. However, the sleep suppression is independent of light cues and of circadian rhythms because starved period mutants sleep like wild type flies. By selectively targeting subpopulations of Clk-expressing neurons we localize the observed sleep phenotype to the dorsally located circadian neurons. These findings show that Clk and cyc act during starvation to modulate the conflict of whether flies sleep or search for food. PMID:20541409
Keene, Alex C; Duboué, Erik R; McDonald, Daniel M; Dus, Monica; Suh, Greg S B; Waddell, Scott; Blau, Justin
Neural systems controlling the vital functions of sleep and feeding in mammals are tightly interconnected: sleep deprivation promotes feeding, whereas starvation suppresses sleep. Here we show that starvation in Drosophila potently suppresses sleep, suggesting that these two homeostatically regulated behaviors are also integrated in flies. The sleep-suppressing effect of starvation is independent of the mushroom bodies, a previously identified sleep locus in the fly brain, and therefore is regulated by distinct neural circuitry. The circadian clock genes Clock (Clk) and cycle (cyc) are critical for proper sleep suppression during starvation. However, the sleep suppression is independent of light cues and of circadian rhythms as shown by the fact that starved period mutants sleep like wild-type flies. By selectively targeting subpopulations of Clk-expressing neurons, we localize the observed sleep phenotype to the dorsally located circadian neurons. These findings show that Clk and cyc act during starvation to modulate the conflict of whether flies sleep or search for food.
Xia, Dunzhu; Yu, Cheng; Kong, Lun
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.
Xia, Dunzhu; Yu, Cheng; Kong, Lun
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
Chouvarda, I; Grassi, A; Mendez, M O; Bianchi, A M; Parrino, L; Milioli, G; Terzano, M; Maglaveras, N; Cerutti, S
This work aims to investigate sleep microstructure as expressed by Cyclic Alternating Pattern (CAP), and its possible alterations in pathological sleep. Three groups, of 10 subjects each, are considered: a) normal sleep, b) psychophysiological insomnia, and c) sleep misperception. One night sleep PSG and sleep macro- micro structure annotations were available per subject. The statistical properties and the dynamics of CAP events are in focus. Multiscale and non-linear methods are presented for the analysis of the microstructure event time series, applied for each type of CAP events, and their combination. The results suggest that a) both types of insomnia present CAP differences from normal sleep related to hyperarousal, b) sleep misperception presents more extensive differences from normal, potentially reflecting multiple sleep mechanisms, c) there are differences between the two types of insomnia as regard to the intertwining of events of different subtypes. The analysis constitutes a contribution towards new markers for the quantitative characterization of insomnia, and its subtypes.
Holman, R B; Elliott, G R; Barchas, J D
Information which has emerged thus far relates to the overall transmitter mechanisms of sleep. The data, while conflicting, point to the involvement of many neuroregulators at numerous integrative levels of the process. However the long term question still remain: what triggers and maintain sleep, what stops sleep, what occurs to the body and brain during sleep--in essence, why sleep? These questions are now problems for behavioral neurochemists, whereas in a previous era, they were problems for philosophers. Unfortunately, our answers to date, while in another idiom, have hardly been more complete or satisfying. To answer these questions, it will be necessary to understand, in detail, the manner in which neurobiochemical processes relate to the functional physiology of sleep. Although existing studies have given invaluable insight into the neurochemical anatomy of sleep, we have only recently acquired the technical and biochemical expertise necessary to investigate sleep as it occurs normally. Future research must focus on the dynamic changes associated with the regulatory mechanisms of neurotransmitters. Many questions can be asked. With sleep transitions, what changes occur in transmitter content, synthesis, or release? Are there changes in metabolic pathways, reflecting a shift from intra- to interneuronal metabolism? What changes occur in pre- and postsynaptic neurotransmitter receptors to affect sensitivity? What constraints do genetic (245) and environmental (246) factors impose upon these mechanisms? Knowledge of such parameters will allow us to construct more complete models of the neuroregulatory basis of sleep and waking. However, as we acquire this knowledge, we must avoid the temptation of assuming causation when the evidence merely shows correlation. Neuroregulation are involved in the control of number different behaviors; and, at present, we have few, if any, methods of establishing causative links between a specific neuroregulator and a specific
Westerlund, Anna; Lagerros, Ylva Trolle; Kecklund, Göran; Axelsson, John; Åkerstedt, Torbjörn
This study aimed to examine the association between polysomnographic sleep and subjective habitual sleep quality and restoration from sleep. Thirty-one normal sleepers completed the Karolinska Sleep Questionnaire and multiple home polysomnography recordings (n = 2-5). Using linear regression, sleep quality and restoration were separately analyzed as functions of standard polysomnography parameters: sleep efficiency, total sleep time, sleep latency, stage 1 and 2 sleep, slow-wave sleep, rapid eye movement sleep, wake time after sleep onset, and awakenings (n), averaged across recordings. Stage 2 and slow-wave sleep predicted worse and better sleep quality, respectively. Also, slow-wave sleep predicted less subjective restoration, although adjustment for age attenuated this relation. Our findings lend some physiological validity to ratings of habitual sleep quality in normal sleepers. Data were less supportive of a physiological correlate of ratings of restoration from sleep.
Arns, Martijn; Kenemans, J Leon
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.
Holland, Samuel D. (Inventor); Delaune, Paul B. (Inventor); Turner, Kathryn M. (Inventor)
Processing circuitry is provided for a high voltage operated radiation detector. An event detector utilizes a comparator configured to produce an event signal based on a leading edge threshold value. A preferred event detector does not produce another event signal until a trailing edge threshold value is satisfied. The event signal can be utilized for counting the number of particle hits and also for controlling data collection operation for a peak detect circuit and timer. The leading edge threshold value is programmable such that it can be reprogrammed by a remote computer. A digital high voltage control is preferably operable to monitor and adjust high voltage for the detector.
Katz, Richard B.; Wang, J. J.
This report summarizes the use of SX series devices and their JTAG 1149.1 circuitry. 'JTAG' circuitry was originally designed to standardize testing of boards via a simple control port interface electrically without having to use devices such as a bed of nails tester. JTAG is also used for other functions such as executing built-in-test sequences, identifying devices, or, through custom instructions, other functions designed in by the chip designer. The JTAG circuitry is designed for test only; it has no functional use in the integrated circuit during normal operations. The JTAG circuitry and the mode of the device is controlled by a circuit block known as the 'TAP controller,' which is a sixteen-state state machine along with various registers. The controller is normally in an operational state known as TEST-LOGIC-RESET. In this state, the device is held in a fully functional, operational mode. However, a Single Event Upset (SEU) may remove the TAP controller from this state, causing a loss of control of the integrated circuit, unless certain precautions are taken, such as grounding the optional JTAG TRST signal.
Katz, Richard B.; Wang, J. J.
This report summarizes the use of SX series devices and their JTAG 1149.1 circuitry. 'JTAG' circuitry was originally designed to standardize testing of boards via a simple control port interface electrically without having to use devices such as a bed of nails tester. JTAG is also used for other functions such as executing built-in-test sequences, identifying devices, or, through custom instructions, other functions designed in by the chip designer. The JTAG circuitry is designed for test only; it has no functional use in the integrated circuit during normal operations. The JTAG circuitry and the mode of the device is controlled by a circuit block known as the 'TAP controller,' which is a sixteen-state state machine along with various registers. The controller is normally in an operational state known as TEST-LOGIC-RESET. In this state, the device is held in a fully functional, operating mode. However, a Single Event Upset (SEU) may remove the TAP controller from this state, causing a loss of control of the integrated circuit, unless certain precautions are taken, such as grounding the optional JTAG TRST signal.
Simpson, Norah S.; Meier-Ewert, Hans K.; Haack, Monika
Controlled, experimental studies on the effects of acute sleep loss in humans have shown that mediators of inflammation are altered by sleep loss. Elevations in these mediators have been found to occur in healthy, rigorously screened individuals undergoing experimental vigils of more than 24 hours, and have also been seen in response to various durations of sleep restricted to between 25 and 50% of a normal 8 hour sleep amount. While these altered profiles represent small changes, such sub-clinical shifts in basal inflammatory cytokines are known to be associated with the future development of metabolic syndrome disease in healthy, asymptomatic individuals. Although the mechanism of this altered inflammatory status in humans undergoing experimental sleep loss is unknown, it is likely that autonomic activation and metabolic changes play key roles. PMID:21112025
Felder, Jennifer N.; Green, Steven R.; Rittenberg, Alison M.; Sasson, Noah J.; Bodfish, James W.
Social interaction deficits and restricted repetitive behaviors and interests that characterize autism spectrum disorders (ASDs) may both reflect aberrant functioning of brain reward circuits. However, no neuroimaging study to date has investigated the integrity of reward circuits using an incentive delay paradigm in individuals with ASDs. In the present study, we used functional magnetic resonance imaging to assess blood-oxygen level-dependent activation during reward anticipation and outcomes in 15 participants with an ASD and 16 matched control participants. Brain activation was assessed during anticipation of and in response to monetary incentives and object image incentives previously shown to be visually salient for individuals with ASDs (e.g. trains, electronics). Participants with ASDs showed decreased nucleus accumbens activation during monetary anticipation and outcomes, but not during object anticipation or outcomes. Group × reward-type-interaction tests revealed robust interaction effects in bilateral nucleus accumbens during reward anticipation and in ventromedial prefrontal cortex during reward outcomes, indicating differential responses contingent on reward type in these regions. Results suggest that ASDs are characterized by reward-circuitry hypoactivation in response to monetary incentives but not in response to autism-relevant object images. The clinical implications of the double dissociation of reward type and temporal phase in reward circuitry function in ASD are discussed. PMID:21148176
Depner, Christopher M.; Stothard, Ellen R.; Wright, Kenneth P.
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
The link between habitual short sleep and obesity is critically examined from a sleep perspective. Sleep estimates are confounded by 'time in bed', naps; the normal distribution of sleep duration. Wide categorizations of 'short sleep', with claims that <7 h sleep is associated with obesity and morbidity, stem from generalizations from 5 h sleepers (<8% of adults) and acute restriction studies involving unendurable sleepiness. Statistically significant epidemiological findings are of questionable clinical concern, even for 5 h sleepers, as any weight gains accumulate slowly over years; easily redressed by e.g. short exercise exposures, contrasting with huge accumulations of 'lost' sleep. Little evidence supports 'more sleep', alone, as an effective treatment for obesity. Impaired sleep quality and quantity are surrogates for many physical and psychological disorders, as can be obesity. Advocating more sleep, in these respects, could invoke unwarranted use of sleep aids including hypnotics. Inadequate sleep in obese children is usually symptomatic of problems not overcome by increasing sleep alone. Interestingly, neuropeptides regulating interactions between sleep, locomotion and energy balance in normal weight individuals, are an avenue for investigation in some obese short sleepers. The real danger of inadequate sleep lies with excessive daytime sleepiness, not obesity.
Wilcox, Claire E.; Pommy, Jessica M.; Adinoff, Bryon
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
The study of genetics is providing new and exciting insights into the pathogenesis, diagnosis, and treatment of disease. Both normal sleep and several types of sleep disturbances have been found to have significant genetic influences, as have traits of normal sleep, such as those evident in EEG patterns and the circadian sleep-wake cycle. The circadian sleep-wake cycle is based on a complex feedback loop of genetic transcription over a 24-h cycle. Restless legs syndrome (RLS) and periodic limb movements in sleep (PLMS) have familial aggregation, and several genes have a strong association with them. Recent genome-wide association studies have identified single nucleotide polymorphisms linked to RLS/PLMS, although none has a definite functional correlation. Narcolepsy/cataplexy are associated with HLA DQB1*0602 and a T-cell receptor α locus, although functional correlations have not been evident. Obstructive sleep apnea is a complex disorder involving multiple traits, such as anatomy of the oropharynx, ventilatory control, and traits associated with obesity. Although there is clear evidence of familial aggregation in the obstructive sleep apnea syndrome, no specific gene or locus has been identified for it. Angiotensin-converting enzyme has been proposed as a risk variant, but evidence is weak. Fatal familial insomnia and advanced sleep phase syndrome are sleep disorders with a definite genetic basis. PMID:23648914
Holland, Samuel D. (Inventor); Delaune, Paul B. (Inventor); Turner, Kathryn M. (Inventor)
Input circuitry is provided for a high voltage operated radiation detector to receive pulses from the detector having a rise time in the range of from about one nanosecond to about ten nanoseconds. An integrator circuit, which utilizes current feedback, receives the incoming charge from the radiation detector and creates voltage by integrating across a small capacitor. The integrator utilizes an amplifier which closely follows the voltage across the capacitor to produce an integrator output pulse with a peak value which may be used to determine the energy which produced the pulse. The pulse width of the output is stretched to approximately 50 to 300 nanoseconds for use by subsequent circuits which may then use amplifiers with lower slew rates.
Russo, Scott J.; Nestler, Eric J.
Mood disorders are common and debilitating conditions characterized in part by profound deficits in reward-related behavioral domains. A recent literature has identified important structural and functional alterations within the brain’s reward circuitry —particularly in the ventral tegmental area to nucleus accumbens pathway — that are associated with symptoms such as anhedonia and aberrant reward-associated perception and memory. This review synthesizes recent data from human and rodent studies from which emerges a circuit-level framework for understanding reward deficits in depression. We also discuss some of the molecular and cellular underpinnings of this framework, ranging from adaptations in glutamatergic synapses and neurotrophic factors to transcriptional and epigenetic mechanisms. PMID:23942470
Kingham, D J
A general theory of neural circuitry is proposed wherein neural impulses travel in a continuous circuit from the brain to the extremities and back to the brain. At the extremities the impulse may be modified by the environment there. At the spinal column the return signal is compared with the outgoing signal and the appropriate motoneuronal 'reflex' signal is generated if the difference is sufficiently large. In the thalamus the return signal is again compared with the outgoing signal and the difference between the two generates a sensory impulse which is sent to the cortical regions of the brain for comparison with stored patterns from similar signals of past experience. This theory allows for an explanation of feelings of pain and pleasure, pain remote from an area of trauma, phantom limb pain and the relationship between sensory impulses and motor impulses. New approaches to reducing pain are suggested by this theory.
Mazzoccoli, Gianluigi; Vinciguerra, Manlio; Papa, Gennaro; Piepoli, Ada
Colorectal cancer is the most prevalent among digestive system cancers. Carcinogenesis relies on disrupted control of cellular processes, such as metabolism, proliferation, DNA damage recognition and repair, and apoptosis. Cell, tissue, organ and body physiology is characterized by periodic fluctuations driven by biological clocks operating through the clock gene machinery. Dysfunction of molecular clockworks and cellular oscillators is involved in tumorigenesis, and altered expression of clock genes has been found in cancer patients. Epidemiological studies have shown that circadian disruption, that is, alteration of bodily temporal organization, is a cancer risk factor, and an increased incidence of colorectal neoplastic disease is reported in shift workers. In this review we describe the involvement of the circadian clock circuitry in colorectal carcinogenesis and the therapeutic strategies addressing temporal deregulation in colorectal cancer. PMID:24764658
Mazzoccoli, Gianluigi; Vinciguerra, Manlio; Papa, Gennaro; Piepoli, Ada
Colorectal cancer is the most prevalent among digestive system cancers. Carcinogenesis relies on disrupted control of cellular processes, such as metabolism, proliferation, DNA damage recognition and repair, and apoptosis. Cell, tissue, organ and body physiology is characterized by periodic fluctuations driven by biological clocks operating through the clock gene machinery. Dysfunction of molecular clockworks and cellular oscillators is involved in tumorigenesis, and altered expression of clock genes has been found in cancer patients. Epidemiological studies have shown that circadian disruption, that is, alteration of bodily temporal organization, is a cancer risk factor, and an increased incidence of colorectal neoplastic disease is reported in shift workers. In this review we describe the involvement of the circadian clock circuitry in colorectal carcinogenesis and the therapeutic strategies addressing temporal deregulation in colorectal cancer.
Chiba, Shigeru; Tamura, Yoshiyuki
There are three major neurophysiological mechanisms underlying the sleep-waking cycle: the sleep system, the waking system, and the system that determines sleep-waking timing. Sleep dlisorders of older adults seem to be caused by functional or organic changes in one or more of the three systems, and are roughly classified into two categories: (i) normal age-related, and (ii) pathological. The former includes decreased amplitude and advanced phase of circadian rhythms (body temperature, melatonin secretion, and sleep-waking), as well as reduced sleep duration, sleep fragmentation, and a decrease of slow-wave sleep in sleep architecture. Pathological sleep disorders include medical and psychiatric diseases (e.g., lifestyle-related diseases, dementia, delirium, and depression) and primary age-related sleep disorders (e.g., REM sleep behavior disorder and periodic limb move- ment disorders). This mini-review delineates the clinical features of sleep disorders in older adults.
Gutierrez, Guillermo; Williams, Jeffrey; Alrehaili, Ghadah A; McLean, Anna; Pirouz, Ramin; Amdur, Richard; Jain, Vivek; Ahari, Jalil; Bawa, Amandeep; Kimbro, Shawn
Characterizing respiratory rate variability (RRV) in humans during sleep is challenging, since it requires the analysis of respiratory signals over a period of several hours. These signals are easily distorted by movement and volitional inputs. We applied the method of spectral analysis to the nasal pressure transducer signal in 38 adults with no obstructive sleep apnea, defined by an apnea-hypopnea index <5, who underwent all-night polysomnography (PSG). Our aim was to detect and quantitate RRV during the various sleep stages, including wakefulness. The nasal pressure transducer signal was acquired at 100 Hz and consecutive frequency spectra were generated for the length of the PSG with the Fast Fourier Transform. For each spectrum, we computed the amplitude ratio of the first harmonic peak to the zero frequency peak (H1/DC), and defined as RRV as (100 - H1/DC) %. RRV was greater during wakefulness compared to any sleep stage, including rapid-eye-movement. Furthermore, RRV correlated with the depth of sleep, being lowest during N3. Patients spent most their sleep time supine, but we found no correlation between RRV and body position. There was a correlation between respiratory rate and sleep stage, being greater in wakefulness than in any sleep stage. We conclude that RRV varies according to sleep stage. Moreover, spectral analysis of nasal pressure signal appears to provide a valid measure of RRV during sleep. It remains to be seen if the method can differentiate normal from pathological sleep patterns.
Maddah, Mohsen; Rashidi, Arash; Mohammadpour, Behnoush; Vafa, Reza; Karandish, Majid
Objective: To investigate the relationship of snacking during school hours, sleep time, and breakfast consumption by weight status of Iranian high school girls in urban and rural areas in Guilan Province, Iran. Design: Data were collected by self-administered questionnaire and measure of body weight and height. Setting: High schools in urban and…
Allen, B. C.
Oscilloscope, with specially developed test circuitry, quickly checks semiconductors without removing them from the circuitry. For transistors, approximate gain and linearity, as well as PNP or NPN determinations are made. When testing diodes, open or short circuits, and reverse polarity show up plainly.
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
This report results from a contract tasking University of Erlangen-Nuremberg as follows: The contractor will investigate the use of Rapid Single Flux Quantum (RSFQ) logic circuitry to read qubits in 3-micron wide Josephson transmission line (JTL). He will construct semiconductor chips as necessary to test his theories on RSFQ circuitry and document his findings in a final report.
Krueger, J M; Takahashi, S; Kapás, L; Bredow, S; Roky, R; Fang, J; Floyd, R; Renegar, K B; Guha-Thakurta, N; Novitsky, S
The central thesis of this essay is that the cytokine network in brain is a key element in the humoral regulation of sleep responses to infection and in the physiological regulation of sleep. We hypothesize that many cytokines, their cellular receptors, soluble receptors, and endogenous antagonists are involved in physiological sleep regulation. The expressions of some cytokines are greatly amplified by microbial challenge. This excess cytokine production during infection induces sleep responses. The excessive sleep and wakefulness that occur at different times during the course of the infectious process results from dynamic changes in various cytokines that occur during the host's response to infectious challenge. Removal of any one somnogenic cytokine inhibits normal sleep, alters the cytokine network by changing the cytokine mix, but does not completely disrupt sleep due to the redundant nature of the cytokine network. The cytokine network operates in a paracrine/autocrine fashion and is responsive to neuronal use. Finally, cytokines elicit their somnogenic actions via endocrine and neurotransmitter systems as well as having direct effects neurons and glia. Evidence in support of these postulates is reviewed in this essay.
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Sleep apnea is a common disorder that causes your breathing to stop or get very shallow. Breathing ... an hour. The most common type is obstructive sleep apnea. It causes your airway to collapse or ...
Schreck, Kimberly A; Richdale, Amanda L
Evidence demonstrates that health professionals have limited knowledge about childhood sleep, frequently do not screen for these problems and often rely on parents to raise sleep issues at clinic visits. However, little is known about parents' sleep knowledge. The goal of this study was to assess parents' knowledge of sleep and specifically: (i) sleep aspects related to the age of children; (ii) developmentally normal sleep; and (iii) sleep problems that may lead to parents' ability to raise sleep issues at clinic visits. This study evaluated the knowledge of 170 parents of children aged 2-17 years about infant, child and adolescent sleep patterns and problems. The majority of parents could not answer correctly questions about developmental sleep patterns or sleep problems, but were more likely to answer correctly questions about normal infant sleep patterns and about sleep problems during waking hours. Parents also were more likely to answer 'don't know' to questions about: (i) older children and adolescents; (ii) sleep apnea; and (iii) dreams and nightmares. The implications of these findings for the identification, intervention and prevention of childhood sleep problems are discussed.
Roth, T; Roehrs, T; Zwyghuizen-Doorenbos, A; Stepanski, E; Wittig, R
Generally sleep is considered a time of amnesia. It is not uncommon for an individual to experience 8 h of sleep and have no memory for events during that time. Similarly, a substantial proportion of the population has no memory for dreams that occurred during the night, despite the fact that the literature on awakening during rapid eye movement (REM) sleep clearly shows that individuals normally have four to six "dream experiences" a night. Research on this issue seems to indicate that the lack of memory cannot be explained by the organisms' inability to perceive stimuli. The data indicate that although perceptual thresholds are elevated, organisms can clearly perceive stimuli, and, in fact, can discriminate between them during sleep. The amnesia also cannot be explained by a defect in long-term memory, as studies have indicated that stimuli put into the memory during wakefulness are more efficiently retrieved after a sleep period than after a comparable period of wakefulness. The most likely explanation for the amnestic property of sleep seems to be the inability of organisms to transfer information from short-term memory to long-term memory during sleep. There are several sources of evidence to support this hypothesis. First, the probability of remembering a stimulus given during wakefulness is related to the proximity of sleep onset to the stimulus. Generally, information put into the system within 5 min of sleep onset is lost from memory. Secondly, disorders of excessive daytime somnolence which cause individuals to have frequent microsleeps are often associated with complains of memory problems.(ABSTRACT TRUNCATED AT 250 WORDS)
Hilakivi, L A; Taira, T; Hilakivi, I
To examine the functional significance of early postnatal active sleep for the development of behavioural reactivity to auditory stimuli, rat pups were daily injected i.p. from the 7th to the 18th postnatal days with 5 mg kg-1 (6.6 mmol l-1) desipramine or 25 mg kg-1 (12.2 mmol l-1) zimeldine. Sleep-wake behaviour was recorded with a static-charge-sensitive bed (SCSB) method. Both desipramine and zimeldine suppressed the percentage of active sleep relative to the total recording time throughout the treatment period. In addition, these drugs increased the percentage of quiet state and waking. At the age of 38 days the zimeldine-treated rats showed more motor activity in the open field than the controls. At the age of 39 and 78 days all rat groups behaved similarly in the open field. Startle measures and motor activation, provoked by auditory stimulation, were determined by the SCSB method when the rats were 4 months of age. Auditory stimuli, consisting of a series of ten clicks, induced a greater number of startles as well as strong movement responses in the control rats than in the desipramine- or zimeldine-treated rats. The number of small movement responses did not differ between the rat groups. These findings indicate that early postnatal active sleep and the monoaminergic systems regulating it may be important for the normal development of neuronal circuitry associated with later reactivity to auditory stimuli.
Mezza, D.; Allahgholi, A.; Delfs, A.; Dinapoli, R.; Goettlicher, P.; Graafsma, H.; Greiffenberg, D.; Hirsemann, H.; Klyuev, A.; Laurus, T.; Marras, A.; Mozzanica, A.; Perova, I.; Poehlsen, J.; Schmitt, B.; Sheviakov, I.; Shi, X.; Trunk, U.; Xia, Q.; Zhang, J.; Zimmer, M.
AGIPD (adaptive gain integrating pixel detector) is a detector system developed for the European XFEL (XFEL.EU), which is currently being constructed in Hamburg, Germany. The XFEL.EU will operate with bunch trains at a repetition rate of 10 Hz. Each train consists of 2700 bunches with a temporal separation of 220 ns corresponding to a rate of 4.5 MHz. Each photon pulse has a duration of < 100 fs (rms) and contains up to 1012 photons in an energy range between 0.25 and 25 keV . In order to cope with the large dynamic range, the first stage of each bump-bonded AGIPD ASIC is a charge sensitive preamplifier with three different gain settings that are dynamically switched during the charge integration. Dynamic gain switching allows single photon resolution in the high gain stage and can cover a dynamic range of 104 × 12.4 keV photons in the low gain stage. The burst structure of the bunch trains forces to have an intermediate in-pixel storage of the signals. The full scale chip has 352 in-pixel storage cells inside the pixel area of 200 × 200 μm2. This contribution will report on the measurements done with the new calibration circuitry of the AGIPD1.1 chip (without sensor). These results will be compared with the old version of the chip (AGIPD1.0). A new calibration method (that is not AGIPD specific) will also be shown.
Schmitt, Karen; Holsboer-Trachsler, Edith; Eckert, Anne
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.
Brown, Ritchie E.; Basheer, Radhika; McKenna, James T.; Strecker, Robert E.; McCarley, Robert W.
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
Brown, Ritchie E; Basheer, Radhika; McKenna, James T; Strecker, Robert E; McCarley, Robert W
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.
Miller, Michelle A.
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
Qureshi, Irfan A; Mehler, Mark F
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.
Sorensen, Gertrud Laura; Knudsen, Stine; Jennum, Poul
Study Objectives: Narcolepsy is characterized by instability of sleep-wake, tonus, and rapid eye movement (REM) sleep regulation. It is associated with severe hypothalamic hypocretin deficiency, especially in patients with cataplexy (loss of tonus). As the hypocretin neurons coordinate and stabilize the brain's sleep-wake pattern, tonus, and REM flip-flop neuronal centers in animal models, we set out to determine whether hypocretin deficiency and/or cataplexy predicts the unstable sleep-wake and REM sleep pattern of the human phenotype. Design: We measured the frequency of transitions in patients with narcolepsy between sleep-wake states and to/from REM and NREM sleep stages. Patients were subdivided by the presence of +/- cataplexy and +/- hypocretin-1 deficiency. Setting: Sleep laboratory studies conducted from 2001-2011. Patients: In total 63 narcolepsy patients were included in the study. Cataplexy was present in 43 of 63 patients and hypocretin-1 deficiency was present in 37 of 57 patients. Measurements and Results: Hypocretin-deficient patients with narcolepsy had a significantly higher frequency of sleep-wake transitions (P = 0.014) and of transitions to/from REM sleep (P = 0.044) than patients with normal levels of hypocretin-1. Patients with cataplexy had a significantly higher frequency of sleep-wake transitions (P = 0.002) than those without cataplexy. A multivariate analysis showed that transitions to/from REM sleep were predicted mainly by hypocretin-1 deficiency (P = 0.011), whereas sleep-wake transitions were predicted mainly by cataplexy (P = 0.001). Conclusions: In human narcolepsy, hypocretin deficiency and cataplexy are both associated with signs of destabilized sleep-wake and REM sleep control, indicating that the disorder may serve as a human model for the sleep-wake and REM sleep flip-flop switches. Citation: Sorensen GL; Knudsen S; Jennum P. Sleep transitions in hypocretin-deficient narcolepsy. SLEEP 2013;36(8):1173-1177. PMID:23904677
Abrams, Robert M
Sleep deprivation occurs when inadequate sleep leads to decreased performance, inadequate alertness, and deterioration in health. It is incompletely understood why humans need sleep, although some theories include energy conservation, restoration, and information processing. Sleep deprivation has many deleterious health effects. Residency programs have enacted strict work restrictions because of medically related errors due to sleep deprivation. Because obstetrics is an unpredictable specialty with long irregular hours, enacting a hospitalist program enhances patient safety, decreases malpractice risk, and improves the physician's quality of life by allowing obstetricians to get sufficient rest.
West, John B.; Elliott, Ann R.; Prisk, G. Kim; Paiva, Manuel
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
Lin, D. Y.; Wu, J. D.; Chang, Y. J.; Wu, J. S.
Practical and cost-effective circuitry with high sensitivity has been developed to measure a small capacitance using current compensation method. The circuitry uses an electronic switch to periodically connect or separate the capacitor under test (Cx) from a reference capacitor (Cr). When Cx is connected in parallel with Cr the total capacitance becomes Cx+Cr. On the other hand, as Cx is separated from Cr, the total capacitance is only Cr. This periodic change of the capacitance generates a periodic square-wave output with an amplitude in proportion to the capacitance of Cx. A high sensitivity of ΔV /ΔC=202.2mV/pF has been achieved, making the circuitry a powerful tool in measuring small capacitances. Three applications have been performed to present its capability: (a) displacement, (b) height of liquid, and (c) angle of tilt. The experimental results demonstrate the performance of the circuitry.
Johns, M W
In recent years the effectiveness of hypnotic drugs has had to be assessed in terms of a greatly increased knowledge of the physiology and pathology of sleep. The normal pattern of sleep and wakefulness involves a cyclic alternation between three rather than two basically dissimilar states of the brain and body - alert wakefulness, rapid-eye-movement (REM) sleep and non-rapid-eye-movement (NREM) sleep. The pattern of this alternation in individual people results from the interaction of many influences - biological (including genetic, early developmental and later degenerative influences), psychological, social and environmental factors, various physical and psychiatric disorders, and most drugs which affect the central nervous system. The quality of sleep is not related in any simple or constant manner either to its duration or to the proprotions of time spent in each stage of sleep. Among the disorders of sleep, insomnia is a far more common problem of medical management than are enuresis, narcolepsy, somnambulism or nightmares. With a few exceptions, most hypnotic drugs now in widespread use cease to be effective in treating insomnia after the first few nights. However, the ineffective treatment is often continued because insomnia will be even worse during the initial period of drug withdrawal. These factors and the toxicity of hypnotic drugs when taken in overdose make the long-term treatment of insomnia more difficult than was previously supposed. Barbiturates should no longer be prescribed. Some of the non-barbiturates, such as glutethimide and methaqualone, have no advantage over the barbiturates. The benzodiazepine hypnotics, nitrazepam and flurazepam, are less toxic in overdose and are relatively effective in treating insomnia. Chloral hydrate and its derivates are useful alternative drugs for short-term use. Measures to improve sleep without drugs deserve greater emphasis than they have had in the past.
Kotter, Dale K [Shelley, ID; Spencer, David F [Idaho Falls, ID; Roybal, Lyle G [Idaho Falls, ID; Rohrbaugh, David T [Idaho Falls, ID
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.
This review examines the biological background to the development of ideas on rapid eye movement sleep (REM sleep), so-called paradoxical sleep (PS), and its relation to dreaming. Aspects of the phenomenon which are discussed include physiological changes and their anatomical location, the effects of total and selective sleep deprivation in the human and animal, and REM sleep behavior disorder, the latter with its clinical manifestations in the human. Although dreaming also occurs in other sleep phases (non-REM or NREM sleep), in the human, there is a contingent relation between REM sleep and dreaming. Thus, REM is taken as a marker for dreaming and as REM is distributed ubiquitously throughout the mammalian class, it is suggested that other mammals also dream. It is suggested that the overall function of REM sleep/dreaming is more important than the content of the individual dream; its function is to place the dreamer protagonist/observer on the topographical world. This has importance for the developing infant who needs to develop a sense of self and separateness from the world which it requires to navigate and from which it is separated for long periods in sleep. Dreaming may also serve to maintain a sense of ‘I’ness or “self” in the adult, in whom a fragility of this faculty is revealed in neurological disorders.
i.e., the mean duration of a normal normal room light (about 150 lux) upon NREM - REM sleep cycle), minimizing the awakening did not improve performance...Badia, 1988; awakenings have greater negative effects on Rosa et al., 1983; Rosa & Bonnet, 1985). A subsequent performance than REM sleep more accurate...slow Neurophysiology, 102, 125-131. wave versus REM sleep . Labuc S. (1978) A study of performance Psychophysiology, 5, 231. upon sudden awakening
Di Mauro, Federica; Lollobrigida, Valeria; Di Fraia, Marco; Savastano, Vincenzo; Loffredo, Lorenzo; Nicita, Francesco; Spalice, Alberto; Duse, Marzia
Introduction Studies on Mean Platelet Volume (MPV) in children with Sleep Disordered Breathing (SDB) report conflicting results and the hypothesis of an intermittent hypoxemia leading to a systemic inflammation is reaching consensus. Vitamin D exerts anti-inflammatory properties and its deficiency has been supposed to play a role in sleep disorders. Emerging interest is rising about Primary Snoring (PS) since it is reasonable that also undetectable alteration of hypoxia might predispose to an increased production of inflammatory mediators. In this perspective, in a group of children affected by SDB, our aim was to investigate MPV, vitamin D and C Reactive Protein (CRP) levels, which had been previously evaluated separately in different studies focused only on Obstructive Sleep Apnea Syndrome (OSAS). Materials and Methods We enrolled 137 children: 70 healthy controls (HC), 67 affected by SDB undergoing a polysomnographic evaluation, 22 with a diagnosis of PS and 45 with a diagnosis of OSAS. All patients underwent routine biochemical evaluations including blood cell counts, CRP and vitamin D. Results Children affected by SDB had a mean age of 8.49±2.19 and were prevalently males (23 females, 34%; 44 males, 66%). MPV levels were higher in OSAS and PS when compared to HC; platelet count (PLT) and CRP levels were higher while Vitamin D levels were lower in children with SDB when compared to HC. MPV levels were correlated with PLT (r = -0.54; p<0.001), vitamin D (r = -0.39; p<0.001) and CRP (r = 0.21; p<0.01). A multiple regression was run to predict MPV levels from vitamin D, CRP and PLT and these variables significantly predicted MPV (F = 17.42, p<0.0001; adjusted R2 = 0.37). Only platelet count and vitamin D added statistically significantly to the prediction (p<0.05). Conclusion The present study provides evidence of higher MPV and lower vitamin D levels in children with PS as well as in children with OSAS, and supports the underlying inflammation, hence
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Cologan, Victor; Schabus, Manvel; Ledoux, Didier; Moonen, Gustave; Maquet, Pierre; Laureys, Steven
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.
Beltrami, Flávia Gabe; Nguyen, Xuân-Lan; Pichereau, Claire; Maury, Eric; Fleury, Bernard; Fagondes, Simone
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
This report was confined to considering the effects of sleep deprivation , in man, with particular reference to studies of the resulting biochemical...have a limited value when taken separately: the biochemical and physiological changes that occur in response to sleep deprivation may depend...three separate heads: first, the biochemical changes resulting from sleep deprivation ; secondly, the physiological ones; and last, the changes in performance and behaviour. (Author)
The ON-OFF direction selective ganglion cells (DSGCs) in the mammalian retina code image motion by responding much more strongly to movement in one direction. They do so by receiving inhibitory inputs selectively from a particular sector of processes of the overlapping starburst amacrine cells, a type of retinal interneuron. The mechanisms of establishment and regulation of this selective connection are unknown. Here, we report that in the rat retina, the morphology, physiology of the ON-OFF DSGCs and the circuitry for coding motion directions develop normally with pharmacological blockade of GABAergic, cholinergic activity and/or action potentials for over two weeks from birth. With recent results demonstrating light independent formation of the retinal DS circuitry, our results strongly suggest the formation of the circuitry, i.e., the connections between the second and third order neurons in the visual system, can be genetically programmed, although emergence of direction selectivity in the visual cortex appears to require visual experience. PMID:21573161
Barton, Cynthia K.; Williams, Anthony J.
This research analyzed and proposed development of the computerized Electrical Circuitry Program (ECP). ECP is proposed to assist U.S. Army Corps of Engineers (USACE) in-house electrical engineers in performing the required analysis during facilities concept design phase. The program would include features which allow the user to design a thorough power system with minimum effort. The program would also allow the user to graphically determine outlet locations for luminaries, establish receptacle locations and types, select switch locations and types, lay out wiring diagrams for the system, and locate and describe the features of the panelboards. ECP would be equipped to perform voltage drop, short circuit, and wire length calculations to insure the system design's efficiency. Using the information entered into the program, ECP would create summary reports and panel schedules to be submitted with design documents.
Goldstein, Jill M.; Jerram, Matthew; Abbs, Brandon; Whitfield-Gabrieli, Susan; Makris, Nikos
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
Fietze, Ingo; Strauch, Jutta; Holzhausen, Martin; Glos, Martin; Theobald, Christiane; Lehnkering, Hanna; Penzel, Thomas
Ballet dancers are competitive athletes who undergo extreme physical and mental stress and work according to an irregular schedule, with long days of training, rehearsal, and performance. Their most significant potential risks entail physical injury and altered sleep. The elaborate training requirements for ballet dancers do not allow regular chronobiological patterns or a normal sleep-wake rhythm. Our aim was to investigate the sleep-wake rhythm and sleep quality during rehearsal phases prior to a ballet premiere. We used wrist actigraphy and sleep diaries for a period of 67 days before the ballet premiere performance to study 24 classical ballet dancers. We likewise applied the Epworth Sleepiness Score (ESS), Pittsburgh Sleep Quality Index (PSQI), SF-12 Quality of life Assessment, and d2 Test of Attention to assess quality of sleep, aspects of cognitive performance, and health status. We found significant reduction in sleep duration, from 418+/-43 min to 391+/-42 min, and sleep efficiency, from 81+/-4% to 79+/-5%, over the 67-day course of the rehearsal. We also found a decline in time in bed and an increase in wakefulness after sleep onset. Sleep onset latency did not change. However, the changes in sleep as documented by actigraphy were not reflected by the subjective data of the sleep diaries and sleep scores. As a result of the facts that total sleep efficiency and sleep duration values were already lower than usual for the dancers' age group at the beginning of the study and that mental acuity, concentration, and speed were likewise impaired, we observed exacerbated health deterioration in terms of sleep deprivation in ballet dancers during preparation for a premier. We conclude that individual activity-rest schedules, including daytime naps, may be helpful, especially during the stressful training and rehearsal experienced prior to ballet premieres.
Bearer, Elaine L.; Zhang, Xiaowei; Janvelyan, Davit; Boulat, Benoit; Jacobs, Russell E.
The serotonin transporter (SERT) modulates the entire serotonergic system in the brain and influences both the dopaminergic and norepinephrinergic systems. These three systems are intimately involved in normal physiological functioning of the brain and implicated in numerous pathological conditions. Here we use high-resolution magnetic resonance imaging (MRI) and spectroscopy to elucidate the effects of disruption of the serotonin transporter in an animal model system: the SERT knock-out mouse. Employing manganese-enhanced MRI, we injected Mn2+ into the prefrontal cortex and obtained 3D MR images at specific time points in cohorts of SERT and normal mice. Statistical analysis of co-registered datasets demonstrated that active circuitry originating in the prefrontal cortex in the SERT knock-out is dramatically altered, with a bias towards more posterior areas (substantia nigra, ventral tegmental area, and Raphé nuclei) directly involved in the reward circuit. Injection site and tracing were confirmed with traditional track tracers by optical microscopy. In contrast, metabolite levels were essentially normal in the SERT knock-out by in vivo magnetic resonance spectroscopy and little or no anatomical differences between SERT knock-out and normal mice were detected by MRI. These findings point to modulation of the limbic cortical-ventral striatopallidal by disruption of SERT function. Thus, molecular disruptions of SERT that produce behavioral changes also alter the functional anatomy of the reward circuitry in which all the monoamine systems are involved. PMID:19306930
Abdullah, Haslaile; Holland, Gerard; Cosic, Irena; Cvetkovic, Dean
Sleep apnoea is a sleep breathing disorder which causes changes in cardiac and neuronal activity and discontinuities in sleep pattern when observed via electrocardiogram (ECG) and electroencephalogram (EEG). This paper presents a pilot study result of assessing the correlation between EEG frequency bands and ECG Heart Rate Variability (HRV) in normal and sleep apnoea human clinical patients at different sleep stages. In sleep apnoea patients, the results have shown that EEG delta, sigma and beta bands exhibited a strong correlation with cardiac HRV parameters at different sleep stages.
In 40 aquanauts, a prolonged stay under increased pressure (11 to 46 kgs/cm2) of the oxygen-helium-nitrogen mixture did not affect the average duration of sleep. Slow-wave sleep, mostly its 3 rd and 4 th stages, and paradoxical sleep were significantly decreased whereas the light sleep/profound sleep ratio increased. The cyclic structure of sleep became altered. The longer the exposure to high pressure led to an augmentation of the slow-wave sleep and REM-phase, but the normal cycles terminating with a REM-phase could not be formed during the experiment.
Lacey, J H; Stanley, P; Hartmann, M; Koval, J; Crisp, A H
This study examined the immediate influence of intravenous amino acids and glucose on sleep as measured by all-night EEG recording. The study on 9 normal female subjects was of a latin-square design. Slow wave sleep (SWS) was increased by both solutions whilst dream sleep (REM) was decreased by amino acids and increased by glucose. Total sleep time was not affected. Subjective feelings as to restlessness, quality and depth of sleep under the impact of the various solutions were gathered. The work further elucidates the effect of nutrition on sleep and supports certain theories as to the function of the main sleep component.
Marchand, William R; Lee, James N; Suchy, Yana; Garn, Cheryl; Johnson, Susanna; Wood, Nicole; Chelune, Gordon
Normal human aging is associated with declining motor control and function. It is thought that dysfunction of the cortico-basal ganglia circuitry may contribute to age-related sensorimotor impairment, however the underlying mechanisms are poorly characterized. The aim of this study was to enhance our understanding of age-related changes in the functional architecture of these circuits. Fifty-nine subjects, consisting of a young, middle and old group, were studied using functional MRI and a motor activation paradigm. Functional connectivity analyses and examination of correlations of connectivity strength with performance on the activation task as well as neurocognitive tasks completed outside of magnet were conducted. Results indicated that increasing age is associated with changes in the functional architecture of the cortico-basal ganglia circuitry. Connectivity strength increased between subcortical nuclei and cortical motor and sensory regions but no changes were found between subcortical components of the circuitry. Further, increased connectivity was correlated with poorer performance on a neurocognitive task independently of age. This result suggests that increased connectivity reflects a decline in brain function rather than a compensatory process. These findings advance our understanding of the normal aging process. Further, the methods employed will likely be useful for future studies aimed at disambiguating age-related versus illness progression changes associated with neuropsychiatric disorders that involve the cortico-basal ganglia circuitry.
Lin, Qiong; Chauvistré, Heike; Costa, Ivan G.; Gusmao, Eduardo G.; Mitzka, Saskia; Hänzelmann, Sonja; Baying, Bianka; Klisch, Theresa; Moriggl, Richard; Hennuy, Benoit; Smeets, Hubert; Hoffmann, Kurt; Benes, Vladimir; Seré, Kristin; Zenke, Martin
Dendritic cells (DC) are professional antigen presenting cells that develop from hematopoietic stem cells through successive steps of lineage commitment and differentiation. Multipotent progenitors (MPP) are committed to DC restricted common DC progenitors (CDP), which differentiate into specific DC subsets, classical DC (cDC) and plasmacytoid DC (pDC). To determine epigenetic states and regulatory circuitries during DC differentiation, we measured consecutive changes of genome-wide gene expression, histone modification and transcription factor occupancy during the sequel MPP-CDP-cDC/pDC. Specific histone marks in CDP reveal a DC-primed epigenetic signature, which is maintained and reinforced during DC differentiation. Epigenetic marks and transcription factor PU.1 occupancy increasingly coincide upon DC differentiation. By integrating PU.1 occupancy and gene expression we devised a transcription factor regulatory circuitry for DC commitment and subset specification. The circuitry provides the transcription factor hierarchy that drives the sequel MPP-CDP-cDC/pDC, including Irf4, Irf8, Tcf4, Spib and Stat factors. The circuitry also includes feedback loops inferred for individual or multiple factors, which stabilize distinct stages of DC development and DC subsets. In summary, here we describe the basic regulatory circuitry of transcription factors that drives DC development. PMID:26476451
Barron, Carole C.; Fleming, James G.; Montague, Stephen
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.
Kavanau, J Lee
Biotelemetry has revealed daily 15-h behavioral sleep periods in a cubomedusan jellyfish, Chironex fleckeri. Its sleep is expected to be phylogenetically most primitive, since jellyfish possess only two germ layers. They belong to the phylum Cnidaria, the 'simplest' multicellular organisms with an organized nervous system. Cubomedusae have a complex visual system with 24 eyes of four different types, each type specialized for a different task. Input to these eyes during visually guided fast-swimming predation requires enormous amounts of neural processing, possibly nearly saturating the capacity of their comparatively simple nervous system. These heavy neural demands may account for the need for fifteen hours of sleep. C. fleckeri is the only animal known for which sleep may be either present or absent, dependent on lifestyle. Limited knowledge of behavior of some other cubomedusae suggests that they also possess this faculty. The finding of sleep in C. fleckeri supports current proposals of sleep's origin and basic function. Evolutionary analyses link sleep to a conflict produced by excessive processing demands on multifunctional neural circuitry for detailed focal vision by complex lensed eyes. The conflict arises between the enormous demands of complex visual analysis and needs for split-second control of actions, on the one hand, and non-urgent processing of memories of ongoing and stored events, on the other. Conflict is resolved by deferring the non-urgent processing to periods of sleep. Without sleep, selection would favor the evolution of circuitry 'dedicated' to single or but few tasks, with corresponding lesser efficiency. Had complex lensed eyes of medusae originated as a consequence of selection for increased mating success of males pursuing females, it could have occurred before the evolution of fast-swimming bilateral (three-germ-layered) prey. But if it was a consequence of selection for increased prey-hunting success, the origin of such eyes
Jehan, Shazia; Auguste, Evan; Hussain, Mahjabeen; Pandi-Perumal, Seithikurippu R.; Brzezinski, Amon; Gupta, Ravi; Attarian, Hrayr; Jean-Louis, Giradin; McFarlane, Samy I.
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
Kales, J D; Kales, A
Modern sleep research studies have provided the practicing physician with considerable new information concerning the basic psychophysiology of sleep, the effects of medical conditions on sleep and the role of maturational and emotional factors in producing certain sleep disorders. Medical and psychiatric disorders, sleep disorders and drug-induced sleep stage alterations are studied in the sleep laboratory using the same techniques developed to analyze sleep patterns in normal subjects. After initial sleep laboratory adaptation, a profile of the sleep characteristics of various clinical conditions is obtained. This profile can be compared to sleep profiles of normal subjects as well as to the effects on sleep of subsequent experimental or therapeutic procedures. Various studies have shown that coronary artery, duodenal ulcer and nocturnal headache patients experience angina, increased gastric acid secretion and migraine or cluster headaches, respectively during REM sleep. Adult nocturnal asthamtic episodes occur out of all sleep stages while attacks of dyspnea in asthmatic children occur in all stages except stage 4 sleep. Hypothyroid patients show decreases in stages 3 and 4 sleep, while in hyperthyroid patients the percentage of time spent in stages 3 and 4 sleep is markedly increased. Enuretic episodes occur predominantly in non-rapid eye movement (NREM) sleep. Sleepwalking and night terror episodes occur exclusively out of NREM sleep, particularly from stages 3 and 4 sleep. Most child somnambulists and children with night terrors "outgrow" this disorder, suggesting a delayed maturation of the central nervous system. Stimulant drugs are effective in the treatment of the sleep attacks of narcolepsy and in treating certain cases of hypersomnia, while imipramine is an effective treatment for the auxillary symptoms of narcolepsy. Psychological disturbances are frequent in adult somnambulism and night terrors as well as in hypersomnia and insomnia. Proper
Samaitienė, Rūta; Norkūnienė, Jolita; Tumienė, Birutė; Grikinienė, Jurgita
Although patients with benign childhood epilepsy with centrotemporal spikes exhibit a benign course of the disease, some of them display sleep and behavioral problems. Sixty-one patients with rolandic epilepsy, aged 6-11 years, were included in this study. The patients were divided into two subgroups according to the presence of seizures over the preceding 6 months. The control group comprised 25 patients without epilepsy and with similar characteristics in terms of age and sex. All patients underwent evaluation of sleep (Sleep Disturbance Scale for Children) and behavior (Lithuanian version of the Child Behaviour Checklist). Only patients who had had seizures over the preceding 6 months displayed significantly higher scores for sleep problems (disorders of excessive daytime sleepiness, disorders of sleep-wake transition, and scores for total sleep problems), worse sleep quality (longer sleep-onset latency), and behavioral problems (anxiety/depression, social problems, thought problems, attention problems, and aggressive behavior) than the patients of the control group. Our data add to evidence that active epilepsy has an impact on sleep and behavior. Clinically significant sleep problems were related to the higher risk of behavioral problems. Parents' ratings for existing sleep problems were sensitive to Sleep Disturbance Scale for Children scores above normal values.
Mazwi, Nicole L; Fusco, Heidi; Zafonte, Ross
Sleep disturbances affect more than half of survivors of traumatic brain injury (TBI) and have the potential to undermine rehabilitation, recovery, and outcomes. Normal sleep architecture has been well-described and the neurophysiology of sleep is becoming better understood in recent years, though this complex process continues to be dissected for better appreciation. There are numerous types of sleep disorder, most of which fall under two categories: dyssomnias and parasomnias. In more challenging scenarios patients may be plagued with more than one dyssomnia and/or parasomnia simultaneously, complicating the diagnostic and therapeutic approach. Objective and subjective methods are used to evaluate sleep disorders and help distinguish them from psychiatric and environmental contributors to poor sleep. There are several pharmacologic and nonpharmacologic treatments options for sleep disturbances after TBI, many of which have been particularly helpful in restoring adequate quantity and quality of sleep for survivors. However, to date no consensus has been established regarding how to treat this entity, and it may be that a multimodal approach is ultimately best.
Kayser, Matthew S; Biron, David
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.
Benzodiazepines; Sedatives; Hypnotics; Sleeping pills; Insomnia - medicines; Sleep disorder - medicines ... the-counter (OTC) sleeping pills contain antihistamines. These medicines are commonly used to treat allergies. While these ...
Kim, Bowon; Kocsis, Bernat; Hwang, Eunjin; Kim, Youngsoo; Strecker, Robert E.; McCarley, Robert W.; Choi, Jee Hyun
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
Hamlet, J. F. (Inventor)
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.
... normal, but the body clock loses its normal circadian cycle. People with changing work shifts and travelers who ... Abbott SM, Reid KJ, Zee PC. Circadian disorders of the sleep-wake ... Medicine . 6th ed. Philadelphia, PA: Elsevier; 2017:chap 40. ...
Singh, A; Subhashini, N; Sharma, S; Mallick, B N
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.
Westermann, Jürgen; Lange, Tanja; Textor, Johannes; Born, Jan
Sleep benefits the consolidation of psychological memory, and there are hints that sleep likewise supports immunological memory formation. Comparing psychological and immunological domains, we make the case for active system consolidation that is similarly established in both domains and partly conveyed by the same sleep-associated processes. In the psychological domain, neuronal reactivation of declarative memory during slow-wave sleep (SWS) promotes the redistribution of representations initially stored in hippocampal circuitry to extra-hippocampal circuitry for long-term storage. In the immunological domain, SWS seems to favor the redistribution of antigenic memories initially held by antigen-presenting cells, to persisting T cells serving as a long-term store. Because storage capacities are limited in both systems, system consolidation presumably reduces information by abstracting 'gist' for long-term storage.
Everson, Carol A.; Henchen, Christopher J.; Szabo, Aniko; Hogg, Neil
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
Bamne, Mikhil N.; Mansour, Hader; Monk, Timothy H.; Buysse, Daniel J.; Nimgaonkar, Vishwajit L.
Sleep and circadian rhythms are complex and inter-connected physiological processes. Relative to the remarkable progress made in identifying the genetic basis of circadian rhythms and some specific sleep disorders, efforts to identify genetic variants associated with normal variation in sleep have progressed more slowly. Two key issues concerning the design of such studies must be addressed in order to facilitate further progress. The first concerns the sleep related traits to be targeted. The second issue is the choice of the gene mapping method (linkage, candidate gene association or genome-wide association). This paper discusses these issues, reviews published studies of sleep phenotypes, and recommends cost-effective methods to advance knowledge of the genetic determinants of normal sleep patterns. PMID:20299255
Sawicka, E H; Branthwaite, M A
Eleven subjects with non-paralytic and 10 with paralytic kyphoscoliosis and nine normal control subjects were studied during sleep. The Cobb angle of those with kyphoscoliosis varied from 60 degrees to 140 degrees (median 100 degrees) and the vital capacity varied from 17% to 56% (median 28%) of the value predicted on the basis of span. Recordings made during sleep included expired carbon dioxide tension at the nose, gas flow at the mouth, arterial oxygen saturation, chest wall movement, and the electroencephalogram, electro-oculogram, and electrocardiogram. In three subjects transcutaneous carbon dioxide tension was measured simultaneously. Patients with kyphoscoliosis hypoventilated during sleep, particularly in rapid eye movement sleep, resulting in a rise in end tidal and transcutaneous carbon dioxide tension, and a reduction in oxygen saturation to a degree not observed in normal subjects. Reduced chest wall movement was the major cause of these episodes, which were more frequent and occupied a greater proportion of sleep time in those with kyphoscoliosis than in normal subjects. Serious cardiac arrhythmias were rarely associated. It is concluded that disturbances of respiration during sleep occur in patients with kyphoscoliosis and that these may be important in the pathogenesis of cardiorespiratory failure. PMID:3424256
Disrupted sleep is probably the most common complaint of parents with a new baby. Night waking increases in the second half of the first year of infant life and is more pronounced for breastfed infants. Sleep-related phenotypes of infants with Prader-Willi and Angelman syndromes suggest that imprinted genes of paternal origin promote greater wakefulness whereas imprinted genes of maternal origin favor more consolidated sleep. All these observations are consistent with a hypothesis that waking at night to suckle is an adaptation of infants to extend their mothers’ lactational amenorrhea, thus delaying the birth of a younger sib and enhancing infant survival. PMID:24610432
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.
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
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.
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
Wang, Yi-Qun; Li, Rui; Zhang, Meng-Qi; Zhang, Ze; Qu, Wei-Min; Huang, Zhi-Li
Most depressed patients suffer from sleep abnormalities, which are one of the critical symptoms of depression. They are robust risk factors for the initiation and development of depression. Studies about sleep electroencephalograms have shown characteristic changes in depression such as reductions in non-rapid eye movement sleep production, disruptions of sleep continuity and disinhibition of rapid eye movement (REM) sleep. REM sleep alterations include a decrease in REM sleep latency, an increase in REM sleep duration and REM sleep density with respect to depressive episodes. Emotional brain processing dependent on the normal sleep-wake regulation seems to be failed in depression, which also promotes the development of clinical depression. Also, REM sleep alterations have been considered as biomarkers of depression. The disturbances of norepinephrine and serotonin systems may contribute to REM sleep abnormalities in depression. Lastly, this review also discusses the effects of different antidepressants on REM sleep disturbances in depression.
Wang, Yi-Qun; Li, Rui; Zhang, Meng-Qi; Zhang, Ze; Qu, Wei-Min; Huang, Zhi-Li
Most depressed patients suffer from sleep abnormalities, which are one of the critical symptoms of depression. They are robust risk factors for the initiation and development of depression. Studies about sleep electroencephalograms have shown characteristic changes in depression such as reductions in non-rapid eye movement sleep production, disruptions of sleep continuity and disinhibition of rapid eye movement (REM) sleep. REM sleep alterations include a decrease in REM sleep latency, an increase in REM sleep duration and REM sleep density with respect to depressive episodes. Emotional brain processing dependent on the normal sleep-wake regulation seems to be failed in depression, which also promotes the development of clinical depression. Also, REM sleep alterations have been considered as biomarkers of depression. The disturbances of norepinephrine and serotonin systems may contribute to REM sleep abnormalities in depression. Lastly, this review also discusses the effects of different antidepressants on REM sleep disturbances in depression. PMID:26412074
Ramezani, Ryan J.; Stacpoole, Peter W.
Study Objectives: 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. Design: We examined publications 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. Measurements and Results: 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 hypercapnia that was not considered due to weakness of the intrinsic muscles of respiration. Conclusions: 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 hypercapnia. 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. Citation: Ramezani RJ
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... sleeping References Balserak BI, Lee KA. Sleep and sleep disorders associated with pregnancy. In: Kryger M, Roth T, ... Elsevier; 2017:chap 156. Ibrahim S, Foldvary-Shaefer N. Sleep disorders in pregnancy: implications, evaluation, and treatment. Neurologic Clinics . ...
... Feeding Your 1- to 2-Year-Old Obstructive Sleep Apnea KidsHealth > For Parents > Obstructive Sleep Apnea Print ... kids and teens can develop it, too. About Sleep Apnea Sleep apnea happens when a person stops ...
Sleep apnea - obstructive - adults; Apnea - obstructive sleep apnea syndrome - adults; Sleep-disordered breathing - adults; OSA - adults ... When you sleep, all of the muscles in your body become more relaxed. This includes the muscles that help keep your ...
Sleep apnea - pediatric; Apnea - pediatric sleep apnea syndrome; Sleep-disordered breathing - pediatric ... During sleep, all of the muscles in the body become more relaxed. This includes the muscles that help keep ...
... Old Feeding Your 1- to 2-Year-Old Sleeping During Pregnancy KidsHealth > For Parents > Sleeping During Pregnancy ... have trouble getting enough deep, uninterrupted sleep. Why Sleeping Can Be Difficult The first and most pressing ...
American Sleep Apnea Association Learn About the CPAP Assistance Program About ASAA News about ASAA Who we are Leadership Team Supporting the ASAA Financials Learn Healthy sleep Sleep apnea Other sleep disorders Personal stories Treat Test Yourself ...
... on. Feature: Back to School, the Healthy Way Exercise & Sleep Past Issues / Fall 2012 Table of Contents ... helps kids. Photo: iStock 6 "Bests" About Kids' Exercise At least one hour of physical activity a ...
Slopper, D. K.
Circuitry limits storage in the memory of a stored program general purpose digital computer by permitting storage or writing to certain, specified areas of memory. The limit register used in the computer is easily set under program control, and the memory block size and position is readily changed to suit each specific program.
Persson, Laura; Witt, Rochelle M; Galligan, Meghan; Greer, Paul L; Eisner, Adriana; Pazyra-Murphy, Maria F; Datta, Sandeep R; Segal, Rosalind A
The olfactory system relies on precise circuitry connecting olfactory sensory neurons (OSNs) and appropriate relay and processing neurons of the olfactory bulb (OB). In mammals, the exact correspondence between specific olfactory receptor types and individual glomeruli enables a spatially precise map of glomerular activation that corresponds to distinct odors. However, the mechanisms that govern the establishment and maintenance of the glomerular circuitry are largely unknown. Here we show that high levels of Sonic Hedgehog (Shh) signaling at multiple sites enable refinement and maintenance of olfactory glomerular circuitry. Mice expressing a mutant version of Shh (Shh(Ala/Ala)), with impaired binding to proteoglycan co-receptors, exhibit disproportionately small olfactory bulbs containing fewer glomeruli. Notably, in mutant animals the correspondence between individual glomeruli and specific olfactory receptors is lost, as olfactory sensory neurons expressing different olfactory receptors converge on the same glomeruli. These deficits arise at late stages in post-natal development and continue into adulthood, indicating impaired pruning of erroneous connections within the olfactory bulb. In addition, mature Shh(Ala/Ala) mice exhibit decreased proliferation in the subventricular zone (SVZ), with particular reduction in neurogenesis of calbindin-expressing periglomerular cells. Thus, Shh interactions with proteoglycan co-receptors function at multiple locations to regulate neurogenesis and precise olfactory connectivity, thereby promoting functional neuronal circuitry.
Persson, Laura; Witt, Rochelle M.; Galligan, Meghan; Greer, Paul L.; Eisner, Adriana; Pazyra-Murphy, Maria F.; Datta, Sandeep R.; Segal, Rosalind A.
The olfactory system relies on precise circuitry connecting olfactory sensory neurons (OSNs) and appropriate relay and processing neurons of the olfactory bulb (OB). In mammals, the exact correspondence between specific olfactory receptor types and individual glomeruli enables a spatially precise map of glomerular activation that corresponds to distinct odors. However, the mechanisms that govern the establishment and maintenance of the glomerular circuitry are largely unknown. Here we show that high levels of Sonic Hedgehog (Shh) signaling at multiple sites enable refinement and maintenance of olfactory glomerular circuitry. Mice expressing a mutant version of Shh (ShhAla/Ala), with impaired binding to proteoglycan co-receptors, exhibit disproportionately small olfactory bulbs containing fewer glomeruli. Notably, in mutant animals the correspondence between individual glomeruli and specific olfactory receptors is lost, as olfactory sensory neurons expressing different olfactory receptors converge on the same glomeruli. These deficits arise at late stages in post-natal development and continue into adulthood, indicating impaired pruning of erroneous connections within the olfactory bulb. In addition, mature ShhAla/Ala mice exhibit decreased proliferation in the subventricular zone (SVZ), with particular reduction in neurogenesis of calbindin-expressing periglomerular cells. Thus, Shh interactions with proteoglycan co-receptors function at multiple locations to regulate neurogenesis and precise olfactory connectivity, thereby promoting functional neuronal circuitry. PMID:24913191
Dichter, Gabriel S.; Richey, J. Anthony; Rittenberg, Alison M.; Sabatino, Antoinette; Bodfish, James W.
The aim of this study was to investigate reward circuitry responses in autism during reward anticipation and outcomes for monetary and social rewards. During monetary anticipation, participants with autism spectrum disorders (ASDs) showed hypoactivation in right nucleus accumbens and hyperactivation in right hippocampus, whereas during monetary…
Webb, W. B.; Agnew, H. W., Jr.
Various experimental studies on sleep are described. The following areas are discussed: (1) effect of altered day length on sleep, (2) effect of a partial loss of sleep on subsequent nocturnal sleep; (3) effect of rigid control over sleep-wake-up times; (4) sleep and wakefulness in a time-free environment; (5) distribution of spindles during a full night of sleep; and (6) effect on sleep and performance of swiftly changing shifts of work.
Dimsdale, Joel E.
Some of our best descriptions of sleep disorders come from literature. While Shakespeare is well known for his references to insomnia and sleep walking, his works also demonstrate a keen awareness of many other sleep disorders. This paper examines sleep themes in Shakespeare's play Othello. The play indicates Shakespeare's astute eye for sleep deprivation, sexual parasomnias, and effects of stress and drugs on sleep. Citation: Dimsdale JE. Sleep in Othello. J Clin Sleep Med 2009;5(3):280-281. PMID:19960651
Corallino, Salvatore; Malabarba, Maria Grazia; Zobel, Martina; Di Fiore, Pier Paolo; Scita, Giorgio
The ability of cells to alter their phenotypic and morphological characteristics, known as cellular plasticity, is critical in normal embryonic development and adult tissue repair and contributes to the pathogenesis of diseases, such as organ fibrosis and cancer. The epithelial-to-mesenchymal transition (EMT) is a type of cellular plasticity. This transition involves genetic and epigenetic changes as well as alterations in protein expression and post-translational modifications. These changes result in reduced cell-cell adhesion, enhanced cell adhesion to the extracellular matrix, and altered organization of the cytoskeleton and of cell polarity. Among these modifications, loss of cell polarity represents the nearly invariable, distinguishing feature of EMT that frequently precedes the other traits or might even occur in their absence. EMT transforms cell morphology and physiology, and hence cell identity, from one typical of cells that form a tight barrier, like epithelial and endothelial cells, to one characterized by a highly motile mesenchymal phenotype. Time-resolved proteomic and phosphoproteomic analyses of cells undergoing EMT recently identified thousands of changes in proteins involved in many cellular processes, including cell proliferation and motility, DNA repair, and - unexpectedly - membrane trafficking (1). These results have highlighted a picture of great complexity. First, the EMT transition is not an all-or-none response but rather a gradual process that develops over time. Second, EMT events are highly dynamic and frequently reversible, involving both cell-autonomous and non-autonomous mechanisms. The net results is that EMT generates populations of mixed cells, with partial or full phenotypes, possibly accounting (at least in part) for the physiological as well as pathological cellular heterogeneity of some tissues. Endocytic circuitries have emerged as complex connectivity infrastructures for numerous cellular networks required for the
Nakazawa, Y; Kotorii, M; Arikawa, K; Horikawa, S; Hasuzawa, H
In a sleep study of 14 normal healthy adults an investigation was made of sleep measurements of a baseline record for its eventual relationship to the percentage of increase of REM percentage of the 1st recovery night following partial differential REM deprivation (PDRD), as well as to personality characteristics. The percentage of change in NREM sleep of the 1st recovery night was compared with the baseline record andthen compared with corresponding values of REM sleep. The results are summarized as follows. No significant correlation exists between the percentage of increase in the REM percentage of the 1st recovery night and sleep measures of the baseline record. An investigation of the relationship between sleep measures of the baseline record and personality characteristics revealed that stage SWS(%) was significantly greater in the introvert than in the extrovert, in the neurotic than in the non-neurotic, and in the nervous than in the optimistic. Comparison of the changes in NREM and REM sleep percentages of the 1st recovery night with the baseline record was made between paired personality characteristics. A significantly high percentage of increase in REM percentage was almost always associated with a significantly high percentage of decrease in stage 2 percentage. From these results it was inferred that an increase in REM percentage occurs at the expense of stage 2 percentage.
Hamidovic, Ajna; de Wit, Harriet
Loss of sleep may impair the ability to abstain from drug use, through any of a number of mechanisms. Sleep loss may increase drug use by impairing attention and inhibitory control, increasing the value of drug rewards over other rewards, or by inducing mood states that facilitate use of a drug. In the present study, we examined whether sleep deprivation (SD) would increase smoking in cigarette smokers, and whether it would do so by impairing attention or inhibitory control. Healthy cigarette smokers (N=14) were tested in a two-session within subject study, after overnight SD or after a normal night's sleep. Subjects were tested in both conditions in randomized order, after abstaining from cigarettes for 48 hours. The procedure was designed to model the human relapse situation. On each 6-h laboratory session after sleep or no sleep, subjects completed mood and craving questionnaires, tasks measuring behavioral inhibition and attention, and a choice procedure in which they chose between money and smoking cigarettes. SD increased self-reported fatigue and decreased arousal, it increased the number of cigarettes subjects chose to smoke, impaired behavioral inhibition and attention. However, the impairments in inhibition or attention were not related to the increase in smoking. It is possible that SD increases smoking because smokers expect that it will reduce sleepiness. Thus, the findings suggest that sleep loss may increase the likelihood of smoking during abstinence not through inhibitory or attentional mechanisms but because of the potential of nicotine to reduce subjective sleepiness.
Saxvig, Ingvild W; Wilhelmsen-Langeland, Ane; Pallesen, Ståle; Vedaa, Oystein; Nordhus, Inger H; Sørensen, Eli; Bjorvatn, Bjørn
Delayed sleep phase disorder is characterized by a delay in the timing of the major sleep period relative to conventional norms. The sleep period itself has traditionally been described as normal. Nevertheless, it is possible that sleep regulatory mechanism disturbances associated with the disorder may affect sleep duration and/or architecture. Polysomnographic data that may shed light on the issue are scarce. Hence, the aim of this study was to examine polysomnographic measures of sleep in adolescents and young adults with delayed sleep phase disorder, and to compare findings to that of healthy controls. A second aim was to estimate dim light melatonin onset as a marker of circadian rhythm and to investigate the phase angle relationship (time interval) between dim light melatonin onset and the sleep period. Data from 54 adolescents and young adults were analysed, 35 diagnosed with delayed sleep phase disorder and 19 healthy controls. Results show delayed timing of sleep in participants with delayed sleep phase disorder, but once sleep was initiated no group differences in sleep parameters were observed. Dim light melatonin onset was delayed in participants with delayed sleep phase disorder, but no difference in phase angle was observed between the groups. In conclusion, both sleep and dim light melatonin onset were delayed in participants with delayed sleep phase disorder. The sleep period appeared to occur at the same circadian phase in both groups, and once sleep was initiated no differences in sleep parameters were observed.
Astronauts Kathryn D. Sullivan, left, and Sally K. Ride display a 'bag of worms.' The 'bag' is a sleep restraint and the majority of the 'worms' are springs and clips used with the sleep restraint in its normal application. Clamps, a bungee cord and velcro strips are other recognizable items in the 'bag.'
Pace-Schott, Edward F.; Germain, Anne; Milad, Mohammed R.
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
display a currently valid OMB control number. PLEASE DO NOT RETURN YOUR FORM TO THE ABOVE ADDRESS. 1. REPORT DATE (DD-MM-YYYY) 01-02-2007 2. REPORT...human therapeutic Carbamazepine is a potent sleep-deprivation agent in flies. Current data indicate that its effects are mediated through the Rdl...between flies and humans (Hendricks et al., 2000; Shaw et al., 2000), but there is little current understanding of the circuitry or channels that
Rattenborg, Niels C; Voirin, Bryson; Cruz, Sebastian M.; Tisdale, Ryan; Dell'Omo, Giacomo; Lipp, Hans-Peter; Wikelski, Martin; Vyssotski, Alexei L.
Many birds fly non-stop for days or longer, but do they sleep in flight and if so, how? It is commonly assumed that flying birds maintain environmental awareness and aerodynamic control by sleeping with only one eye closed and one cerebral hemisphere at a time. However, sleep has never been demonstrated in flying birds. Here, using electroencephalogram recordings of great frigatebirds (Fregata minor) flying over the ocean for up to 10 days, we show that they can sleep with either one hemisphere at a time or both hemispheres simultaneously. Also unexpectedly, frigatebirds sleep for only 0.69 h d−1 (7.4% of the time spent sleeping on land), indicating that ecological demands for attention usually exceed the attention afforded by sleeping unihemispherically. In addition to establishing that birds can sleep in flight, our results challenge the view that they sustain prolonged flights by obtaining normal amounts of sleep on the wing. PMID:27485308
Zhdanova, Irina V.; Tucci, Valter
Experimental data show a close relationship among melatonin, circadian rhythms, and sleep. Low-dose melatonin treatment, increasing circulating melatonin levels to those normally observed at night, promotes sleep onset and sleep maintenance without changing sleep architecture. Melatonin treatment can also advance or delay the phase of the circadian clock if administered in the evening or in the morning, respectively. If used in physiologic doses and at appropriate times, melatonin can be helpful for those suffering from insomnia or circadian rhythm disorders. This may be especially beneficial for individuals with low melatonin production, which is established by measuring individual blood or saliva melatonin levels. However, high melatonin doses (over 0.3 mg) may cause side effects and disrupt the delicate mechanism of the circadian system, dissociating mutually dependent circadian body rhythms. A misleading labeling of the hormone melatonin as a "food supplement" and lack of quality control over melatonin preparations on the market continue to be of serious concern.
Vardar, Selma Arzu; Oztürk, Levent; Kurt, Cem; Bulut, Erdogan; Sut, Necdet; Vardar, Erdal
The aim of this study was to investigate the effects of sleep deprivation induced anxiety on anaerobic performance. Thirteen volunteer male physical education students completed the Turkish version of State Anxiety Inventory and performed Wingate anaerobic test for three times: (1) following a full-night of habitual sleep (baseline measurements), (2) following 30 hours of sleep deprivation, and (3) following partial-night sleep deprivation. Baseline measurements were performed the day before total sleep deprivation. Measurements following partial sleep deprivation were made 2 weeks later than total sleep deprivation measurements. State anxiety was measured prior to each Wingate test. The mean state anxiety following total sleep deprivation was higher than the baseline measurement (44.9 ± 12.9 vs. 27.6 ± 4.2, respectively, p = 0.02) whereas anaerobic performance parameters remained unchanged. Neither anaerobic parameters nor state anxiety levels were affected by one night partial sleep deprivation. Our results suggest that 30 hours continuous wakefulness may increase anxiety level without impairing anaerobic performance, whereas one night of partial sleep deprivation was ineffective on both state anxiety and anaerobic performance. Key pointsShort time total sleep deprivation (30 hours) increases state anxiety without any competition stress.Anaerobic performance parameters such as peak power, mean power and minimum power may not show a distinctive difference from anaerobic performance in a normal sleep day despite the high anxiety level induced by short time sleep deprivation.Partial sleep deprivation does not affect anxiety level and anaerobic performance of the next day.
Anderson, Kirstie N; Bradley, Andrew J
Sleep has been described as being of the brain, by the brain, and for the brain. This fundamental neurobiological behavior is controlled by homeostatic and circadian (24-hour) processes and is vital for normal brain function. This review will outline the normal sleep–wake cycle, the changes that occur during aging, and the specific patterns of sleep disturbance that occur in association with both mental health disorders and neurodegenerative disorders. The role of primary sleep disorders such as insomnia, obstructive sleep apnea, and REM sleep behavior disorder as potential causes or risk factors for particular mental health or neurodegenerative problems will also be discussed. PMID:23761983
Aurell, J; Elmqvist, D
Sleep was studied in nine patients for two to four days after major non-cardiac surgery by continuous polygraphic recording of electroencephalogram, electrooculogram, and electromyogram. Presumed optimal conditions for sleep were provided by a concerted effort by staff to offer constant pain relief and reduce environmental disturbance to a minimum. All patients were severely deprived of sleep compared with normal. The mean cumulative sleep time (stage 1 excluded) for the first two nights, daytime sleep included, was less than two hours a night. Stages 3 and 4 and rapid eye movement sleep were severely or completely suppressed. The sustained wakefulness could be attributed to pain and environmental disturbance to only minor degree. Sleep time as estimated by nursing staff was often grossly misjudged and consistently overestimated when compared with the parallel polygraphic recording. The grossly abnormal sleep pattern observed in these patients may suggest some fundamental disarrangement of the sleep-wake regulating mechanism. PMID:3921096
To better understand the neurobiology of sleep disorders, detailed understanding of circadian and homeostatic sleep-wake regulation in healthy volunteers is mandatory. Sleep physiology and the repercussions of experimentally-induced sleep deprivation on sleep and waking electroencephalogram (EEG), vigilance and subjective state are highly variable, even in healthy individuals. Accumulating evidence suggests that many aspects of normal sleep-wake regulation are at least in part genetically controlled. Current heritability estimates of sleep phenotypes vary between approximately 20-40 % for habitual sleep duration, to over 90 % for the spectral characteristics of the EEG in nonREM sleep. The molecular mechanisms underlying the trait-like, inter-individual variation are virtually unknown, and the human genetics of normal sleep is only at the beginning of being explored. The first studies identified distinct polymorphisms in genes contributing to the endogenous circadian clock and neurochemical systems previously implicated in sleep-wake regulation, to modulate sleep architecture and sleep EEG, vulnerability to sleep loss, and subjective and objective effects of caffeine on sleep. These insights are reviewed here. They disclose molecular mechanisms contributing to normal sleep-wake regulation in humans, and have potentially important implications for the neurobiology of sleep-wake disorders and their pharmacological treatment.
Linden, Michael; Dietz, Marie; Veauthier, Christian; Fietze, Ingo
Objective To elucidate the relationship between subjective complaints and polysomnographical parameters in psychosomatic patients. Method A convenience sample of patients from a psychosomatic inpatient unit were classified according to the Pittsburgh Sleep Quality Index (PSQI) as very poor sleepers (PSQI >10, n=80) and good sleepers (PSQI <6, n=19). They then underwent a polysomnography and in the morning rated their previous night’s sleep using a published protocol (Deutschen Gesellschaft für Schlafforschung und Schlafmedizin morning protocol [MP]). Results In the polysomnography, significant differences were found between very poor and good sleepers according to the PSQI with respect to sleep efficiency and time awake after sleep onset. When comparing objective PSG and subjective MP, the polysomnographical sleep onset latency was significantly positively correlated with the corresponding parameters of the MP: the subjective sleep onset latency in minutes and the subjective evaluation of sleep onset latency (very short, short, normal, long, very long) were positively correlated with the sleep latency measured by polysomnography. The polysomnographical time awake after sleep onset (in minutes) was positively correlated with the subjective time awake after sleep onset (in minutes), evaluation of time awake after sleep onset (seldom, normal often), and subjective restfulness. The polysomnographical total sleep time (TST) was positively correlated with the subjective TST. Conversely, the polysomnographical TST was negatively correlated with the evaluation of TST (high polysomnographical TST was correlated with the subjective evaluation of having slept short or normal and vice versa). The polysomnographical sleep efficiency was positively correlated with subjective feeling of current well-being in the morning and subjective TST and negatively with subjective restfulness, subjective sleep onset latency, subjective evaluation of sleep onset latency, and evaluation of
... COMMISSION Certain Semiconductor Chips with DRAM Circuitry, and Modules and Products Containing Same Receipt... Commission has received a complaint entitled In Re Certain Semiconductor Chips with DRAM Circuitry, and... importation of certain semiconductor chips with dram circuitry, and modules and products containing same....
Eiber, R; Friedman, S
Anorectics and bulimics often complain sleep onset insomnia and disrupted sleep. During awakenings bulimics can have binges. Conversely, eating disorders can be a clinical expression of a concomitantly occurring sleep disorder. Two clinical entities have been recently described: the Night Eating Syndrome (NES) and the Sleep Related Eating Disorders. The main goal of this literature review was to better characterize the relationships between eating disorders and sleep disturbances. No specific EEG sleep pattern emerges in anorectic and bulimic patients. However, all studies include several methodological limitations: a few number of patients, heterogeneous patient groups, various diagnostic criteria. The results of studies evaluating the impact of depression on sleep EEG in eating disorder patients are also subject to controversy. The only study examining the relationship between sleep EEG and morphological alterations in anorectics and normal weight bulimics shows that patients with enlarged cerebrospinal fluid spaces spent more time in slow wave sleep and that the duration of rapid eye movement (REM) sleep was reduced. The ventricular brain ratio was negatively correlated with REM sleep. The Night Eating Syndrome consists in insomnia, binge eating and morning anorexia. Other criteria are proposed to characterize the NES: more than 50% of the daily energy intake is consumed after the last evening meal, awakenings at least once a night, repetition of the provisional criteria for more than 3 months, subjects do not meet criteria for bulimia nervosa or binge eating disorder. Patients have no amnesia nor alteration of alertness, and no other sleep disorder. There is no modification of sleep EEG except sleep maintenance. The prevalence of the NES is 1.5% in the general population. Some neuroendocrine disturbances have been found in the NES. The delimitation with eating disorders is not yet clearly established. If it shares the compulsive features with eating disorders
Owens, Judith A; Weiss, Miriam R
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.
Tellez, Luis A.; Han, Wenfei; Zhang, Xiaobing; Ferreira, Tatiana L.; Perez, Isaac O.; Shammah-Lagnado, Sara J.; van den Pol, Anthony N.; de Araujo, Ivan E.
Sugar exerts its potent reinforcing effects via both gustatory and post-ingestive pathways. It is however unknown if sweetness and nutritional signals engage segregated brain networks to motivate ingestion. We show in mice that separate basal ganglia circuitries mediate the hedonic and nutritional actions of sugar. We found that, during sugar intake, suppressing hedonic value inhibited dopamine release in ventral but not dorsal striatum, whereas suppressing nutritional value inhibited dopamine release in dorsal but not ventral striatum. Consistently, cell-specific ablation of dopamine-excitable cells in dorsal, but not ventral, striatum inhibited sugar’s ability to drive the ingestion of unpalatable solutions. Conversely, optogenetic stimulation of dopamine-excitable cells in dorsal, but not ventral, striatum substituted for sugar in its ability to drive the ingestion of unpalatable solutions. Our data demonstrate that sugar recruits a distributed dopamine-excitable striatal circuitry that acts to prioritize energy seeking over taste quality. PMID:26807950
Tellez, Luis A; Han, Wenfei; Zhang, Xiaobing; Ferreira, Tatiana L; Perez, Isaac O; Shammah-Lagnado, Sara J; van den Pol, Anthony N; de Araujo, Ivan E
Sugar exerts its potent reinforcing effects via both gustatory and post-ingestive pathways. It is, however, unknown whether sweetness and nutritional signals engage segregated brain networks to motivate ingestion. We found in mice that separate basal ganglia circuitries mediated the hedonic and nutritional actions of sugar. During sugar intake, suppressing hedonic value inhibited dopamine release in ventral, but not dorsal, striatum, whereas suppressing nutritional value inhibited dopamine release in dorsal, but not ventral, striatum. Consistently, cell-specific ablation of dopamine-excitable cells in dorsal, but not ventral, striatum inhibited sugar's ability to drive the ingestion of unpalatable solutions. Conversely, optogenetic stimulation of dopamine-excitable cells in dorsal, but not ventral, striatum substituted for sugar in its ability to drive the ingestion of unpalatable solutions. Our data indicate that sugar recruits a distributed dopamine-excitable striatal circuitry that acts to prioritize energy-seeking over taste quality.
Dichter, Gabriel S; Richey, J Anthony; Rittenberg, Alison M; Sabatino, Antoinette; Bodfish, James W
The aim of this study was to investigate reward circuitry responses in autism during reward anticipation and outcomes for monetary and social rewards. During monetary anticipation, participants with autism spectrum disorders (ASDs) showed hypoactivation in right nucleus accumbens and hyperactivation in right hippocampus, whereas during monetary outcomes, participants with ASDs showed hyperactivation in left midfrontal and anterior cingulate gyrus. Groups did not differ in nucleus accumbens responses to faces. The ASD group demonstrated hyperactivation in bilateral amygdala during face anticipation that predicted social symptom severity and in bilateral insular cortex during face outcomes. These results add to the growing body of evidence that autism is characterized by altered functioning of reward circuitry. Additionally, atypical amygdala activation during the processing of social rewards may contribute to the development or expression of autistic features.
Yang, Hui-Di; Wang, Qian; Wang, Zuoxin; Wang, De-Hua
Mongolian gerbils (Meriones unguiculatus) display food hoarding and thus provide an opportunity to study the neuromechanisms underlying this behavior. In the present study, male gerbils exhibited a bimodal expression of food hoarding behavior-some displayed high levels of food hoarding whereas others virtually lacked this behavior under normal laboratory conditions with free access to food. Food hoarding was found to be associated with an increase in neuronal activation, indicated by Fos immunoreactive (ir) staining, in several brain areas including the nucleus accumbens, ventral tegmental area (VTA), and lateral hypothalamus. Food hoarding was also associated with increases in the number of cells labeled for tyrosine hydroxylase (TH-ir), the rate limiting enzyme for dopamine conversion, and the number of cells co-labeled for TH-ir/Fos-ir in the VTA, suggesting that dopamine in the brain reward circuitry may be involved in food hoarding. Further, we found that 22 h of food deprivation induced food hoarding in some, but not all, males that naturally did not display food hoarding. In these males, however, food hoarding did not increase TH-ir or TH-ir/Fos-ir expression in the VTA. Together, these data indicate that male Mongolian gerbils display diverse phenotypes of food hoarding behavior and that dopamine in the brain reward circuitry may be involved in the control of naturally occurring, but not food deprivation-induced, food hoarding.
Nestler, Eric J.
Increasing evidence supports an important role for the brain’s reward circuitry in controlling mood under normal conditions and contributing importantly to the pathophysiology and symptomatology of a range of mood disorders, such as depression. Here we focus on the nucleus accumbens (NAc), a critical component of the brain’s reward circuitry, in depression and other stress-related disorders. The prominence of anhedonia, reduced motivation, and decreased energy level in most individuals with depression supports the involvement of the NAc in these conditions. We concentrate on several transcription factors (CREB, ΔFosB, SRF, NFκB, and β-catenin), which are altered in the NAc in rodent depression models—and in some cases in the NAc of depressed humans, and which produce robust depression- or antidepressant-like effects when manipulated in the NAc in animal models. These studies of the NAc have established novel approaches toward modeling key symptoms of depression in animals and could enable the development of antidepressant medications with fundamentally new mechanisms of action. PMID:26472529
Bassett, Sarah M.; Lupis, Sarah B.; Gianferante, Danielle; Rohleder, Nicolas; Wolf, Jutta M.
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
Pizza, Fabio; Ferri, Raffaele; Poli, Francesca; Vandi, Stefano; Cosentino, Filomena I I; Plazzi, Giuseppe
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.
Rolls, Asya; Colas, Damien; Adamantidis, Antoine; Carter, Matt; Lanre-Amos, Tope; Heller, H Craig; de Lecea, Luis
Memory consolidation has been proposed as a function of sleep. However, sleep is a complex phenomenon characterized by several features including duration, intensity, and continuity. Sleep continuity is disrupted in different neurological and psychiatric conditions, many of which are accompanied by memory deficits. This finding has raised the question of whether the continuity of sleep is important for memory consolidation. However, current techniques used in sleep research cannot manipulate a single sleep feature while maintaining the others constant. Here, we introduce the use of optogenetics to investigate the role of sleep continuity in memory consolidation. We optogenetically targeted hypocretin/orexin neurons, which play a key role in arousal processes. We used optogenetics to activate these neurons at different intervals in behaving mice and were able to fragment sleep without affecting its overall amount or intensity. Fragmenting sleep after the learning phase of the novel object recognition (NOR) task significantly decreased the performance of mice on the subsequent day, but memory was unaffected if the average duration of sleep episodes was maintained at 62-73% of normal. These findings demonstrate the use of optogenetic activation of arousal-related nuclei as a way to systematically manipulate a specific feature of sleep. We conclude that regardless of the total amount of sleep or sleep intensity, a minimal unit of uninterrupted sleep is crucial for memory consolidation.
Radomski, M W; Buguet, A; Doua, F; Bogui, P; Tapie, P
Human African trypanosomiasis (sleeping sickness) is a unique disease model of disrupted circadian rhythms in the sleep-wake cycle and cortisol and prolactin secretion. This study examined the temporal relationship between growth hormone (GH) secretion and the sleep-wake cycle in 8 infected African patients and 6 healthy indigenous African subjects. Twenty-four-hour sleep patterns were recorded by polysomnography and hourly blood samples analyzed for plasma GH. No relationships between the mean normalized plasma GH levels (Z scores) and the sleep stages (wakefulness, sleep stages 1 and 2 ('light' sleep), slow-wave sleep (stages 3 and 4, SWS), and rapid eye movement (REM) sleep) were found in the patients or healthy subjects. However, when the time of sampling of the plasma GH concentrations was lagged by 16 min with respect to the occurrence of the various sleep stages, significant correlations were found between plasma GH concentrations and SWS in both healthy subjects and patients. Thus, the association between SWS and GH secretion persisted even in the presence of disrupted circadian rhythms, further supporting the concept that sleep and the stimulation of GH secretion are outputs of a common mechanism.
Frank, Marcos G
The visual cortex has provided key insights into how experience shapes cortical circuitry. Scientists have identified how different manipulations of visual experience trigger distinct forms of plasticity as well as many of the underlying cellular and molecular mechanisms. Intriguingly, experience is not the only factor driving plasticity in the visual system. Sleep is also required for the full expression of plasticity in the developing visual cortex. In this review, I discuss what we have learned about the role of sleep in visual cortical plasticity and what it tells us about sleep function.
Carskadon, Mary A.
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
Pigarev, Ivan N; Pigareva, Marina L
Inability to solve complex problems or errors in decision making is often attributed to poor brain processing, and raises the issue of brain augmentation. Investigation of neuronal activity in the cerebral cortex in the sleep-wake cycle offers insights into the mechanisms underlying the reduction in mental abilities for complex problem solving. Some cortical areas may transit into a sleep state while an organism is still awake. Such local sleep would reduce behavioral ability in the tasks for which the sleeping areas are crucial. The studies of this phenomenon have indicated that local sleep develops in high order cortical areas. This is why complex problem solving is mostly affected by local sleep, and prevention of local sleep might be a potential way of augmentation of brain function. For this approach to brain augmentation not to entail negative consequences for the organism, it is necessary to understand the functional role of sleep. Our studies have given an unexpected answer to this question. It was shown that cortical areas that process signals from extero- and proprioreceptors during wakefulness, switch to the processing of interoceptive information during sleep. It became clear that during sleep all "computational power" of the brain is directed to the restoration of the vital functions of internal organs. These results explain the logic behind the initiation of total and local sleep. Indeed, a mismatch between the current parameters of any visceral system and the genetically determined normal range would provide the feeling of tiredness, or sleep pressure. If an environmental situation allows falling asleep, the organism would transit to a normal total sleep in all cortical areas. However, if it is impossible to go to sleep immediately, partial sleep may develop in some cortical areas in the still behaviorally awake organism. This local sleep may reduce both the "intellectual power" and the restorative function of sleep for visceral organs.
Pigarev, Ivan N.; Pigareva, Marina L.
Inability to solve complex problems or errors in decision making is often attributed to poor brain processing, and raises the issue of brain augmentation. Investigation of neuronal activity in the cerebral cortex in the sleep-wake cycle offers insights into the mechanisms underlying the reduction in mental abilities for complex problem solving. Some cortical areas may transit into a sleep state while an organism is still awake. Such local sleep would reduce behavioral ability in the tasks for which the sleeping areas are crucial. The studies of this phenomenon have indicated that local sleep develops in high order cortical areas. This is why complex problem solving is mostly affected by local sleep, and prevention of local sleep might be a potential way of augmentation of brain function. For this approach to brain augmentation not to entail negative consequences for the organism, it is necessary to understand the functional role of sleep. Our studies have given an unexpected answer to this question. It was shown that cortical areas that process signals from extero- and proprioreceptors during wakefulness, switch to the processing of interoceptive information during sleep. It became clear that during sleep all “computational power” of the brain is directed to the restoration of the vital functions of internal organs. These results explain the logic behind the initiation of total and local sleep. Indeed, a mismatch between the current parameters of any visceral system and the genetically determined normal range would provide the feeling of tiredness, or sleep pressure. If an environmental situation allows falling asleep, the organism would transit to a normal total sleep in all cortical areas. However, if it is impossible to go to sleep immediately, partial sleep may develop in some cortical areas in the still behaviorally awake organism. This local sleep may reduce both the “intellectual power” and the restorative function of sleep for visceral organs. PMID
... of other risk factors linked to a higher risk of heart disease. The conditions that make up metabolic syndrome include high blood pressure, abnormal cholesterol, high blood sugar and an increased waist circumference. Complications with medications and surgery. Obstructive sleep apnea ...
This article describes the two-process model of sleep regulation. The 24-hour sleep-wake cycle is regulated by a homeostatic process and an endogenous, 2 oscillators, circadian process, under the influence of external synchronisers. These two processes are partially independent but influence each other, as shown in the two-sleep-process auto-regulation model. A reciprocal inhibition model of two interconnected neuronal groups, "SP on" and "SP off", explains the regular recurrence of paradoxical sleep. Sleep studies have primarily depended on observation of the subject and have determined the optimal conditions for sleep (position, external conditions, sleep duration and need) and have studied the consequences of sleep deprivation or modifications of sleep schedules. Then, electrophysiological recordings permitted the classification of sleep stages according to the observed EEG patterns. The course of a night's sleep is reported on a "hypnogram". The adult subject falls asleep in non-REM sleep (N1), then sleep deepens progressively to stages N2 and N3 with the appearance of spindles and slow waves (N2). Slow waves become more numerous in stage N3. Every 90minutes REM sleep recurs, with muscle atonia and rapid eye movements. These adult sleep patterns develop progressively during the 2 first years of life as total sleep duration decreases, with the reduction of diurnal sleep and of REM sleep. Around 2 to 4 months, spindles and K complexes appear on the EEG, with the differentiation of light and deep sleep with, however, a predominance of slow wave sleep.
Harrison, Yvonne; Espelid, Erik
It has been argued that one night of sleep loss in young healthy adults produces changes similar to that associated with normal, healthy ageing--in particular, that young sleep-deprived adults perform similarly to 60-year-old sleep-satiated adults on some tasks of frontal lobe function. This proposition was examined using a protocol viewed by many to be a direct probe of nonvolitional attention mechanisms associated with frontal lobe function. A negative priming (NP) procedure was used to compare performance between non-sleep-deprived (NSD) and sleep-deprived (SD, 34 hr) young, healthy adults. This protocol allowed for exploration of two theories of the NP effect based on inhibitory or memorial processes. Under conditions believed to facilitate inhibitory processes a normal NP effect was found for NSD(16 ms) and SD (9 ms) participants. Under conditions believed to rely on memorial processes there was no NP effect following SD, compared with a normal NP effect for NSD participants (11 ms). Distractor interference was also greater following SD. These findings do not suggest a similar pattern of change following sleep loss in healthy young adults to that of normal, healthy, non-sleep-deprived aged groups.
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.
Mullington, Janet M.; Haack, Monika; Toth, Maria; Serrador, Jorge; Meier-Ewert, Hans
That insufficient sleep is associated with poor attention and performance deficits is becoming widely recognized. Fewer people are aware that chronic sleep complaints in epidemiological studies have also been associated with an increase in overall mortality and morbidity. This article summarizes findings of known effects of insufficient sleep on cardiovascular risk factors including blood pressure, glucose metabolism, hormonal regulation and inflammation with particular emphasis on experimental sleep loss, using models of total and partial sleep deprivation, in healthy individuals who normally sleep in the range of 7-8 hours and have no sleep disorders. These studies show that insufficient sleep alters established cardiovascular risk factors in a direction that is known to increase the risk of cardiac morbidity. PMID:19110131
A growing body of research has identified significant sleep problems in children with autism. Disturbed sleep-wake patterns and abnormal hormone profiles in children with autism suggest an underlying impairment of the circadian timing system. Reviewing normal and dysfunctional relationships between sleep and circadian rhythms will enable comparisons to sleep problems in children with autism, prompt a reexamination of existing literature and offer suggestions for future inquiry. In addition, sleep and circadian rhythms continue to change over the course of development even in typical, healthy humans. Therefore, exploring the dynamic relationship between circadian rhythms and sleep throughout development provides valuable insight into those sleep problems associated with autism. Ultimately, a better understanding of sleep and circadian rhythms in children with autism may help guide appropriate treatment strategies and minimize the negative impact of these disturbances on both the children and their families.
Reilly, Thomas; Edwards, Ben
Sleep-waking cycles are fundamental in human circadian rhythms and their disruption can have consequences for behaviour and performance. Such disturbances occur due to domestic or occupational schedules that do not permit normal sleep quotas, rapid travel across multiple meridians and extreme athletic and recreational endeavours where sleep is restricted or totally deprived. There are methodological issues in quantifying the physiological and performance consequences of alterations in the sleep-wake cycle if the effects on circadian rhythms are to be separated from the fatigue process. Individual requirements for sleep show large variations but chronic reduction in sleep can lead to immuno-suppression. There are still unanswered questions about the sleep needs of athletes, the role of 'power naps' and the potential for exercise in improving the quality of sleep.
Roehrs, Timothy; Roth, Thomas
Disturbed sleep is a key complaint of people experiencing acute and chronic pain. These two vital functions, sleep and pain, interact in complex ways that ultimately impact the biological and behavioral capacity of the individual. Polysomnographic studies of patients experiencing acute pain during postoperative recovery show shortened and fragmented sleep with reduced amounts of slow wave and rapid eye movement (REM) sleep, and the recovery is accompanied by normalization of sleep. Objective assessments of sleep in patients with various chronic pain conditions have been less definitive with some studies showing fragmented and shortened sleep and others showing normal sleep. Although daytime fatigue is a frequent complaint associated with complaints of pain-related disturbed sleep, objective assessments of daytime sleepiness reveal minimally elevated levels of sleepiness and emphasize the importance of distinguishing sleepiness and fatigue. The pain-sleep nexus has been modeled in healthy pain-free subjects and the studies have demonstrated the bidirectionality of the sleep-pain relation. Given this bidirectionality, treatment must focus on alleviation of both the pain and sleep disturbance. Few of the treatment studies have done such, and as a result no clear consensus on treatment approaches, much less on differential etiology-based treatment strategies, has emerged.
Bassett, Sarah M; Lupis, Sarah B; Gianferante, Danielle; Rohleder, Nicolas; Wolf, Jutta M
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.
During a sleep study the sleep cycles and stages of sleep are monitored. Electrodes are placed to monitor continuous recordings of brain waves, electrical activity of muscles, eye movement, respiratory ...
Sleep paralysis - isolated; Parasomnia - isolated sleep paralysis ... Episodes of isolated sleep paralysis last from a few seconds to 1 or 2 minutes. During these episodes the person is unable to move or ...
... begins with a sleep stage called non-rapid eye movement (NREM) sleep. During this stage, your brain waves, ... your brain activity picks up again, and rapid eye movement (REM) sleep begins. Most dreaming occurs during REM ...
... Old Feeding Your 1- to 2-Year-Old Sleep and Your Preschooler KidsHealth > For Parents > Sleep and ... child chattering away, playing through the entire naptime. Sleeping Problems Preschoolers may have nightmares or night terrors , ...
Carskadon, Mary A.
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
Carskadon, Mary A.
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
Lucke-Wold, Brandon P.; Smith, Kelly E.; Nguyen, Linda; Turner, Ryan C.; Logsdon, Aric F.; Jackson, Garrett J.; Huber, Jason D.; Rosen, Charles L.; Miller, Diane B.
Sleep disruption, which includes a loss of sleep as well as poor quality fragmented sleep, frequently follows traumatic brain injury (TBI) impacting a large number of patients each year in the United States. Fragmented and/or disrupted sleep can worsen neuropsychiatric, behavioral, and physical symptoms of TBI. Additionally, sleep disruption impairs recovery and can lead to cognitive decline. The most common sleep disruption following TBI is insomnia, which is difficulty staying asleep. The consequences of disrupted sleep following injury range from deranged metabolomics and blood brain barrier compromise to altered neuroplasticity and degeneration. There are several theories for why sleep is necessary (e.g., glymphatic clearance and metabolic regulation) and these may help explain how sleep disruption contributes to degeneration within the brain. Experimental data indicate disrupted sleep allows hyperphosphorylated tau and amyloid β plaques to accumulate. As sleep disruption may act as a cellular stressor, target areas warranting further scientific investigation include the increase in endoplasmic reticulum and oxidative stress following acute periods of sleep deprivation. Potential treatment options for restoring the normal sleep cycle include melatonin derivatives and cognitive behavioral therapy. PMID:25956251
Lucke-Wold, Brandon P; Smith, Kelly E; Nguyen, Linda; Turner, Ryan C; Logsdon, Aric F; Jackson, Garrett J; Huber, Jason D; Rosen, Charles L; Miller, Diane B
Sleep disruption, which includes a loss of sleep as well as poor quality fragmented sleep, frequently follows traumatic brain injury (TBI) impacting a large number of patients each year in the United States. Fragmented and/or disrupted sleep can worsen neuropsychiatric, behavioral, and physical symptoms of TBI. Additionally, sleep disruption impairs recovery and can lead to cognitive decline. The most common sleep disruption following TBI is insomnia, which is difficulty staying asleep. The consequences of disrupted sleep following injury range from deranged metabolomics and blood brain barrier compromise to altered neuroplasticity and degeneration. There are several theories for why sleep is necessary (e.g., glymphatic clearance and metabolic regulation) and these may help explain how sleep disruption contributes to degeneration within the brain. Experimental data indicate disrupted sleep allows hyperphosphorylated tau and amyloid β plaques to accumulate. As sleep disruption may act as a cellular stressor, target areas warranting further scientific investigation include the increase in endoplasmic reticulum and oxidative stress following acute periods of sleep deprivation. Potential treatment options for restoring the normal sleep cycle include melatonin derivatives and cognitive behavioral therapy.
Kohls, Gregor; Yerys, Benjamin; Schultz, Robert T.
RRBIs, like insistence on sameness, compulsions and rituals, to become such a force so as to impact the growth trajectory of an evolutionarily ancient brain structure like the caudate nucleus? This question ties in with a long-standing debate among clinicians and scientists concerning the potential functions that the myriad of RRBIs might serve in individuals with ASD. While several plausible ideas have been advanced7, convincing support for any specific one is lacking. One hypothesis that is gaining increased research attention, however, involves the effects of alterations of the balance between social and nonsocial motivation in reward circuitry on RRBIs8. This model suggests that ASD is in part a disorder of “behavioral dependency” to RRBIs because of the rewarding effects they induce1. Indeed, insistence on sameness and preoccupying restricted interests are reported to be quite pleasurable by affected individuals1. The dorsal striatum with caudate nucleus, in particular, is believed to mediate reward value for purposeful actions5. Functional imaging studies show that the brain's reward circuitry in ASD, particularly striatum and ventral prefrontal cortices, selectively over-reacts to objects that may comprise an intense special interest, whereas it under-reacts to more typical desires such as social reward and money6. This may indicate that the brain in ASD cares less for conventional rewards. It is not yet known if an initial lack of social reward motivation opens the door for enhanced rewarding effects of certain circumscribed objects, topics, and routines, or whether the reverse is true – that the dominating reward effects of nonsocial objects, topic and routines diminishes the reward value of social engagement. The rewarding effects of RRBIs are thought to be fueled by the preference of those with ASD for predictability in their environment, where they can exercise more control; social encounters are in many ways the antithesis of this, as these are often
Ardito Marretta, R M; Barbaraci, G
This study, through a typical aerospace systems architecture, suggests an engineering design of a human cancer cell circuitry in which a digital optimal control matrix is assigned to repair the DNA damage level and/or to trigger its apoptosis. Here, the conceived machinery is proposed taking into account the state of the art in cancer investigation. However, it could be further generalized. The most recent studies on cancer pathologies give a predominant role to the oncosuppressor protein p53 and its antagonist, the oncogene Mdm2. Experimental and theoretical approaches are in agreement in deducing a "digital" response of the p53 when genomic integrity is damaged. Once DNA damage is present, the mutual influence of p53 and its antagonist, the Mdm2 oncogene, is closed in a feedback loop. In this work, starting from these current results, a novel molecular mechanism is proposed, based on a digital optimal control law, whereby p53 and Mdm2 proteins activities can be represented by appropriate circuitry and governed by the optimal control law of digital systems. This procedure obtains a real-time sequence evaluation of protein oscillations and an unexpected and relevant acceleration in the DNA repairing when suitable digital control matrix is implemented. Those effects suggest interesting perspectives for future scientific investigations. First of all, the proposed digital circuitry, receiving the p53 signal from a damaged cell, is able to repair the current level of genomic alteration. Moreover, the cell fate is newly conceived and bound by the modified pulsing mechanism of p53.
Sundelin, Tina; Lekander, Mats; Kecklund, Göran; Van Someren, Eus J. W.; Olsson, Andreas; Axelsson, John
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
Narcolepsy is a disabling neurologic condition affecting 1 in 2000 individuals, characterized by sleepiness, cataplexy, and transitions from wakefulness into rapid-eye-movement sleep. Current treatments include amphetamine-like stimulants and antidepressants. Human narcolepsy is HLA-associated, multigenic, and environmentally influenced. Positional cloning was used to isolate narcolepsy genes in canine families with autosomal recessive narcolepsy transmission. Three mutations in the G-protein-coupled hypocretin (orexin) receptor-2 (Hcrtr-2) gene were identified. In humans, most cases of narcolepsy are not linked to hypocretin (Hcrt) ligand or receptor mutations but are associated with undetectable cerebrospinal fluid Hcrt-1 levels. A single Hcrt gene/narcolepsy mutation was identified in narcoleptic patients. Hcrt-1 is wake-promoting in vivo, and studies in sporadic human narcolepsy indicate a loss of brain Hcrt-1 and Hcrt-2 and a disappearance of Hcrt-1-containing cells in the hypothalamus. Narcolepsy with cataplexy may therefore be due to Hcrt deficiency. The HLA association in humans suggests possible autoimmune activity against hypothalamic Hcrt-containing cells. Hypocretins may also have roles in regulating normal sleep, appetite, neuroendocrine function and energy metabolism, uniquely positioning them as a link between multiple important behaviors. Abnormal Hcrt transmission is also found in neurologic disorders featuring excessive daytime sleepiness and/or hypothalamic abnormalities. Pharmacologic manipulations of Hcrts may have multiple therapeutic applications.
To advance our understanding of how the brain makes food decisions, it is essential to combine knowledge from two fields that have not yet been well integrated: the neuro-computational basis of decision-making and the homeostatic regulators of feeding. This Review integrates these two literatures from a neuro-computational perspective, with an emphasis in describing the variables computed by different neural systems and how they affect dietary choice. We highlight what is unique about feeding decisions, the mechanisms through which metabolic and endocrine factors affect the decision-making circuitry, why making healthy food choices is difficult for many people, and key processes at work in the obesity epidemic.
This paper starts by overviewing results dealing with the approximation capabilities of neural networks, as well as bounds on the size of threshold gate circuits. Based on a constructive solution for Kolmogorov`s superpositions the authors show that implementing Boolean functions can be done using neurons having an identity transfer function. Because in this case the size of the network is minimized, it follows that size-optimal solutions for implementing Boolean functions can be obtained using analog circuitry. Conclusions and several comments on the required precision are ending the paper.
Exposure to cocaine, and likely other drugs of abuse, generates α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor-silent glutamatergic synapses in the nucleus accumbens. These immature synaptic contacts evolve after drug withdrawal to redefine the neurocircuital properties. These results raise at least three critical questions: (1) what are the molecular and cellular mechanisms that mediate drug-induced generation of silent synapses; (2) how are neurocircuits remodeled upon generation and evolution of drug-generated silent synapses; and (3) what behavioral consequences are produced by silent synapse-based circuitry remodeling? This short review analyzes related experimental results, and extends them to some speculations. PMID:26721952
Wilmott, C. M.
The Fibonacci sequence is a famously well-known integer sequence from the thirteenth century which has transcended its original motivation. It possesses many interested and varied applications within architecture, engineering and science. Less well known is the Narayana sequence which itself has interesting and wide-ranging Fibonacci-type connections. In this paper, we shall recall Narayana's original motivation that gives rise to the sequence bearing his name. We also provide an interesting application of this sequence to the construction to quantum gate circuitry used in quantum computation.
Arrigoni, Elda; Chen, Michael C; Fuller, Patrick M
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.
Holst, Sebastian C; Valomon, Amandine; Landolt, Hans-Peter
Research spanning (genetically engineered) animal models, healthy volunteers, and sleep-disordered patients has identified the neurotransmitters and neuromodulators dopamine, serotonin, norepinephrine, histamine, hypocretin, melatonin, glutamate, acetylcholine, γ-amino-butyric acid, and adenosine as important players in the regulation and maintenance of sleep-wake-dependent changes in neuronal activity and the sleep-wake continuum. Dysregulation of these neurochemical systems leads to sleep-wake disorders. Most currently available pharmacological treatments are symptomatic rather than causal, and their beneficial and adverse effects are often variable and in part genetically determined. To evaluate opportunities for evidence-based personalized medicine with present and future sleep-wake therapeutics, we review here the impact of known genetic variants affecting exposure of and sensitivity to drugs targeting the neurochemistry of sleep-wake regulation and the pathophysiology of sleep-wake disturbances. Many functional polymorphisms modify drug response phenotypes relevant for sleep. To corroborate the importance of these and newly identified variants for personalized sleep-wake therapy, human sleep pharmacogenetics should be complemented with pharmacogenomic investigations, research about sleep-wake-dependent pharmacological actions, and studies in mice lacking specific genes. These strategies, together with future knowledge about epigenetic mechanisms affecting sleep-wake physiology and treatment outcomes, may lead to potent and safe novel therapies for the increasing number of sleep-disordered patients (e.g., in aged populations).
Thakurela, Sudhir; Tiwari, Neha; Schick, Sandra; Garding, Angela; Ivanek, Robert; Berninger, Benedikt; Tiwari, Vijay K
Pax6 is a highly conserved transcription factor among vertebrates and is important in various aspects of the central nervous system development. However, the gene regulatory circuitry of Pax6 underlying these functions remains elusive. We find that Pax6 targets a large number of promoters in neural progenitors cells. Intriguingly, many of these sites are also bound by another progenitor factor, Sox2, which cooperates with Pax6 in gene regulation. A combinatorial analysis of Pax6-binding data set with transcriptome changes in Pax6-deficient neural progenitors reveals a dual role for Pax6, in which it activates the neuronal (ectodermal) genes while concurrently represses the mesodermal and endodermal genes, thereby ensuring the unidirectionality of lineage commitment towards neuronal differentiation. Furthermore, Pax6 is critical for inducing activity of transcription factors that elicit neurogenesis and repress others that promote non-neuronal lineages. In addition to many established downstream effectors, Pax6 directly binds and activates a number of genes that are specifically expressed in neural progenitors but have not been previously implicated in neurogenesis. The in utero knockdown of one such gene, Ift74, during brain development impairs polarity and migration of newborn neurons. These findings demonstrate new aspects of the gene regulatory circuitry of Pax6, revealing how it functions to control neuronal development at multiple levels to ensure unidirectionality and proper execution of the neurogenic program. PMID:27462442
Lee, Michelle; Manders, Toby R.; Eberle, Sarah E.; Su, Chen; D'amour, James; Yang, Runtao; Lin, Hau Yueh; Deisseroth, Karl; Froemke, Robert C.
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
Napadow, Vitaly; Li, Ang; Loggia, Marco L; Kim, Jieun; Schalock, Peter C; Lerner, Ethan; Tran, Thanh-Nga; Ring, Johannes; Rosen, Bruce R; Kaptchuk, Ted J; Pfab, Florian
Itch is an aversive sensory experience and while systemic therapies, such as acupuncture, have shown promise in alleviating itch in patients suffering from chronic itch, their antipruritic mechanisms are unknown. As several lines of evidence implicate brain-focused mechanisms, we applied functional magnetic resonance imaging and our validated temperature-modulation itch model to evaluate the underlying brain circuitry supporting allergen-induced itch reduction in atopic dermatitis patients by acupuncture, antihistamine, and respective placebo treatments. Brain response to allergen itch demonstrated phase dependency. During an increasing itch phase, activation was localized in anterior insula and striatum, regions associated with salience/interoception and motivation processing. Once itch reached peak plateau, robust activation was noted in prefrontal cognitive and premotor areas. Acupuncture reduced itch and itch-evoked activation in the insula, putamen, and premotor and prefrontal cortical areas. Neither itch sensation nor itch-evoked brain response was altered following antihistamine or placebo acupuncture. Greater itch reduction following acupuncture was associated with greater reduction in putamen response, a region implicated in motivation and habitual behavior underlying the urge to scratch, specifically implicating this region in acupuncture's antipruritic effects. Understanding brain circuitry underlying itch reduction following acupuncture and related neuromodulatory therapies will significantly impact the development and applicability of novel therapies to reduce an itch.
Gearheart, Christy M; Arazi, Benjamin; Rouchka, Eric C
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.
Peppler, Kylie; Glosson, Diane
Central to our understanding of learning is the relationship between various tools and technologies and the structuring of disciplinary subject matter. One of the staples of early science education curriculum is the use of electrical circuit toolkits to engage students in broader discussions of energy. Traditionally, these concepts are introduced to youth using battery packs, insulated wire and light bulbs. However, there are affordances and limitations in the way this toolset highlights certain conceptual aspects while obscuring others, which we argue leads to common misconceptions about electrical circuitry. By contrast, we offer an alternative approach utilizing an e-textiles toolkit for developing understanding of electrical circuitry, testing the efficacy of this approach for learning in elective settings to pave the way for later classroom adoption. This study found that youth who engaged in e-textile design demonstrated significant gains in their ability to diagram a working circuit, as well as significant gains in their understanding of current flow, polarity and connections. The implications for rethinking our current toolkits for teaching conceptual understanding in science are discussed.
Luyster, Faith S.; Strollo, Patrick J.; Zee, Phyllis C.; Walsh, James K.
Chronic sleep deficiency, defined as a state of inadequate or mistimed sleep, is a growing and underappreciated determinant of health status. Sleep deprivation contributes to a number of molecular, immune, and neural changes that play a role in disease development, independent of primary sleep disorders. These changes in biological processes in response to chronic sleep deficiency may serve as etiological factors for the development and exacerbation of cardiovascular and metabolic diseases and, ultimately, a shortened lifespan. Sleep deprivation also results in significant impairments in cognitive and motor performance which increase the risk of motor vehicle crashes and work-related injuries and fatal accidents. The American Academy of Sleep Medicine and the Sleep Research Society have developed this statement to communicate to national health stakeholders the current knowledge which ties sufficient sleep and circadian alignment in adults to health. Citation: Luyster FS; Strollo PJ; Zee PC; Walsh JK. Sleep: a health imperative. SLEEP 2012;35(6):727-734. PMID:22654183
Sexton-Radek, Kathy; Hartley, Andrew
College students regularly report increased sleep disturbances as well as concomitant reductions in performance (e.g., academic grades) upon entering college. Sleep hygiene refers to healthy sleep practices that are commonly used as first interventions in sleep disturbances. One widely used practice of this sort involves arranging the sleep environment to minimize disturbances from excessive noise and light at bedtime. Communal sleep situations such as those in college residence halls do not easily support this intervention. Following several focus groups, a questionnaire was designed to gather self-reported information on sleep disturbances in a college population. The present study used The Young Adult Sleep Environment Inventory (YASEI) and sleep logs to investigate the sleep environment of college students living in residential halls. A summary of responses indicated that noise and light are significant sleep disturbances in these environments. Recommendations are presented related to these findings.
Baweja, R; Calhoun, S; Baweja, R; Singareddy, R
Sleep complaints and sleep disorders are common during childhood and adolescence. The impact of not getting enough sleep may affect children's' physical health as well emotional, cognitive and social development. Insomnia, sleep-disordered breathing, parasomnias and sleep disturbances associated with medical and psychiatric disorders are some of the commonly encountered sleep disorders in this age group. Changes in sleep architecture and the amount of sleep requirement associated with each stage of development should be considered during an evaluation of sleep disorders in children. Behavioral treatments should be used initially wherever possible especially considering that most pharmacologic agents used to treat pediatric sleep disorders are off-label. In this review we address the most common sleep problems in children/adolescents as they relate to prevalence, presentation and symptoms, evaluation and management.
Sehgal, Amita; Mignot, Emmanuel
Sleep remains one of the least understood phenomena in biology – even its role in synaptic plasticity remains debatable. Since sleep was recognized to be regulated genetically, intense research has launched on two fronts: the development of model organisms for deciphering the molecular mechanisms of sleep and attempts to identify genetic underpinnings of human sleep disorders. In this Review, we describe how unbiased, high-throughput screens in model organisms are uncovering sleep regulatory mechanisms and how pathways, such as the circadian clock network and specific neurotransmitter signals, have conserved effects on sleep from Drosophila to humans. At the same time, genome-wide association (GWA) studies have uncovered ~14 loci increasing susceptibility to sleep disorders, such as narcolepsy and restless leg syndrome. To conclude, we discuss how these different strategies will be critical to unambiguously defining the function of sleep. PMID:21784243
Zarcone, V.; De La Pena, A.; Dement, W. C.
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.
Mattis, Joanna; Sehgal, Amita
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. Mechanisms underlying the connection between circadian/sleep dysregulation and neurodegeneration remain unclear, but several recent studies provide interesting possibilities. While mechanistic analysis is underway, it is worth considering treatment of circadian/sleep disruption as a means to alleviate symptoms of neurodegenerative disorders. PMID:26947521
Mattis, Joanna; Sehgal, Amita
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.
Goudard, Anaïs; Lalande, Laure; Bertin, Camille; Sautereau, Marie; Le Borgne, Marc; Cabelguenne, Delphine
In a French prison, most inmates reported not being satisfied with their sleep. Life habits between good and bad sleepers were not significantly different except for television and smoking. The most frequently reported symptom of insomnia was several awakenings at night, and the most frequently cited etiologies were rumination of thoughts and noise. Most patients reported that their sleeping problems began or worsened after incarceration. A quarter of the inmates were following a hypnotic treatment, and most of these treatments began in prison. Only 42% of patients were satisfied with its effectiveness. These observations enabled us to make recommendations for healthy sleep patterns such as respecting normal night-and-day cycles, encouraging to stop smoking, and promoting appropriate use of hypnotic treatments.
Urry, Emily; Landolt, Hans-Peter
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.
Thakkar, Mahesh M; Sharma, Rishi; Sahota, Pradeep
Alcohol is a potent somnogen and one of the most commonly used "over the counter" sleep aids. In healthy non-alcoholics, acute alcohol decreases sleep latency, consolidates and increases the quality (delta power) and quantity of NREM sleep during the first half of the night. However, sleep is disrupted during the second half. Alcoholics, both during drinking periods and during abstinences, suffer from a multitude of sleep disruptions manifested by profound insomnia, excessive daytime sleepiness, and altered sleep architecture. Furthermore, subjective and objective indicators of sleep disturbances are predictors of relapse. Finally, within the USA, it is estimated that societal costs of alcohol-related sleep disorders exceeds $18 billion. Thus, although alcohol-associated sleep problems have significant economic and clinical consequences, very little is known about how and where alcohol acts to affect sleep. In this review, we have described our attempts to unravel the mechanism of alcohol-induced sleep disruptions. We have conducted a series of experiments using two different species, rats and mice, as animal models. We performed microdialysis, immunohistochemical, pharmacological, sleep deprivation and lesion studies which suggest that the sleep-promoting effects of alcohol may be mediated via alcohol's action on the mediators of sleep homeostasis: adenosine (AD) and the wake-promoting cholinergic neurons of the basal forebrain (BF). Alcohol, via its action on AD uptake, increases extracellular AD resulting in the inhibition of BF wake-promoting neurons. Since binge alcohol consumption is a highly prevalent pattern of alcohol consumption and disrupts sleep, we examined the effects of binge drinking on sleep-wakefulness. Our results suggest that disrupted sleep homeostasis may be the primary cause of sleep disruption observed following binge drinking. Finally, we have also shown that sleep disruptions observed during acute withdrawal, are caused due to impaired
Davidson, J R; Moldofsky, H; Lue, F A
The study investigated secretory patterns of growth hormone (GH) and cortisol in relation to sleep and wakefulness. Plasma hormone levels were monitored in 10 young men during baseline waking and sleeping, during 40 hours of wakefulness, and during sleep following deprivation. The normal nocturnal GH surge disappeared with sleep deprivation, and was intensified following sleep deprivation. Mean GH levels were higher during slow wave sleep (SWS) compared with other sleep stages. During sleep after deprivation, GH secretion was prolonged, and second GH peaks occurred in three subjects which were not associated with SWS. Average 24-hour cortisol levels were not altered by sleep deprivation or sleep following deprivation, but the nocturnal cortisol rise occurred approximately one hour earlier with sleep deprivation and one hour later with resumed sleep, compared to baseline. This effect on the timing of the rise is consistent with an initial inhibitory influence of sleep on cortisol secretion. The results demonstrate that: the nocturnal growth hormone surge is largely sleep-dependent; temporal associations between GH and SWS are not reliable after sleep deprivation; although the cortisol rhythm is not sleep-dependent, the timing of the cortisol rise may be influenced by sudden changes in the sleep-wake schedule. PMID:1911740
Noland, Heather; Price, James H.; Dake, Joseph; Telljohann, Susan K.
Background: Sleep duration affects the health of children and adolescents. Shorter sleep durations have been associated with poorer academic performance, unintentional injuries, and obesity in adolescents. This study extends our understanding of how adolescents perceive and deal with their sleep issues. Methods: General education classes were…
Vail III, William Banning
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.
Kyung Lee, Elliott; Douglass, Alan B
Although the precise function of sleep is unknown, decades of research strongly implicate that sleep has a vital role in central nervous system (CNS) restoration, memory consolidation, and affect regulation. Slow-wave sleep (SWS) and rapid eye movement (REM) sleep have been of significant interest to psychiatrists; SWS because of its putative role in CNS energy recuperation and cognitive function, and REM sleep because of its suggested involvement in memory, mood regulation, and possible emotional adaptation. With the advent of the polysomnogram, researchers are now beginning to understand some of the consequences of disrupted sleep and sleep deprivation in psychiatric disorders. The same neurochemistry that controls the sleep-wake cycle has also been implicated in the pathophysiology of numerous psychiatric disorders. Thus it is no surprise that several psychiatric disorders have prominent sleep symptoms. This review will summarize normal sleep architecture, and then examine sleep abnormalities and comorbid sleep disorders seen in schizophrenia, as well as anxiety, cognitive, and substance abuse disorders.
Tarullo, Amanda R.; Balsam, Peter D.; Fifer, William P.
Human neonates spend the majority of their time sleeping. Despite the limited waking hours available for environmental exploration, the first few months of life are a time of rapid learning about the environment. The organization of neonate sleep differs qualitatively from adult sleep, and the unique characteristics of neonatal sleep may promote…
Sleep quality and duration are strong indicators of an individual’s health and quality of lifebut they are difficult to track in everyday life. Mobile apps such as Sleep as Android leverage smartphone sensors to track sleep patterns and make recommendations to improve sleeping habits. PMID:28293622
Edalat-Nejad, M.; Haqhverdi, F.; Hossein-Tabar, T.; Ahmadian, M.
Disturbed sleep is common in end-stage renal disease (ESRD). Exogenous melatonin has somniferous properties in normal subjects and can improve sleep quality (SQ) in several clinical conditions. Recent studies have shown that melatonin may play a role in improving sleep in patients undergoing dialysis. The goal of the present study was to assess the effect of exogenous melatonin administration on SQ improvement in daytime hemodialysis patients. Lipid profile and the required dose of erythropoietin (EPO) are also reported as secondary outcomes. In a 6-week randomized, double-blind cross-over clinical trial, 3 mg melatonin or placebo was administered to 68 patients at bedtime. A 72-h washout preceded the switch from melatonin to placebo, or vice versa. SQ was assessed by the Pittsburgh sleep quality index (PSQI). Sixty-eight patients completed the study protocol and were included in the final analysis. Melatonin treatment significantly improved the global PSQI scores (P < 0.001), particularly subjective SQ (P < 0.001), sleep efficiency (P = 0.005) and sleep duration (P < 0.001). No differences in sleep latency and daytime sleepiness were observed. Melatonin also increased the high-density lipoprotein (HDL) cholesterol (P = 0.003). The need for EPO prescription decreased after melatonin treatment (P < 0.001). We conclude that melatonin can improve sleep in ESRD. The modest increase in HDL cholesterol and decrease in the EPO requirement are other benefits associated with this treatment PMID:23960341
Girard, Todd A; Cheyne, J Allan
The objective of this prospective naturalistic field study was to determine the distribution of naturally occurring sleep-paralysis (SP) episodes over the course of nocturnal sleep and their relation to bedtimes. Regular SP experiencers (N = 348) who had previously filled out a screening assessment for SP as well as a general sleep survey were recruited. Participants reported, online over the World Wide Web, using a standard reporting form, bedtimes and subsequent latencies of spontaneous episodes of SP occurring in their homes shortly after their occurrence. The distribution of SP episodes over nights was skewed to the first 2 h following bedtime. Just over one quarter of SP episodes occurred within 1 h of bedtime, although episodes were reported throughout the night with a minor mode around the time of normal waking. SP latencies following bedtimes were moderately consistent across episodes and independent of bedtimes. Additionally, profiles of SP latencies validated self-reported hypnagogic, hypnomesic, and hypnopompic SP categories, as occurring near the beginning, middle, and end of the night/sleep period respectively. Results are consistent with the hypothesis that SP timing is controlled by mechanisms initiated at or following sleep onset. These results also suggest that SP, rather than uniquely reflecting anomalous sleep-onset rapid eye movement (REM) periods, may result from failure to maintain sleep during REM periods at any point during the sleep period. On this view, SP may sometimes reflect the maintenance of REM consciousness when waking and SP hallucinations the continuation of dream experiences into waking life.
DeFelipe, J.; Arellano, J. I.; Merchan-Perez, A.; Gonzalez-Albo, M. C.; Walton, K.; Llinas, R.
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.
Averette, Anna F.; Lee, Soo Chan; Kim, Taeyup; Bahn, Yong-Sun; Robbins, Nicole; Heitman, Joseph; Cowen, Leah E.
Fungal pathogens have evolved diverse strategies to sense host-relevant cues and coordinate cellular responses, which enable virulence and drug resistance. Defining circuitry controlling these traits opens new opportunities for chemical diversity in therapeutics, as the cognate inhibitors are rarely explored by conventional screening approaches. This has great potential to address the pressing need for new therapeutic strategies for invasive fungal infections, which have a staggering impact on human health. To explore this approach, we focused on a leading human fungal pathogen, Candida albicans, and screened 1,280 pharmacologically active compounds to identify those that potentiate the activity of echinocandins, which are front-line therapeutics that target fungal cell wall synthesis. We identified 19 compounds that enhance activity of the echinocandin caspofungin against an echinocandin-resistant clinical isolate, with the broad-spectrum chelator DTPA demonstrating the greatest synergistic activity. We found that DTPA increases susceptibility to echinocandins via chelation of magnesium. Whole genome sequencing of mutants resistant to the combination of DTPA and caspofungin identified mutations in the histidine kinase gene NIK1 that confer resistance to the combination. Functional analyses demonstrated that DTPA activates the mitogen-activated protein kinase Hog1, and that NIK1 mutations block Hog1 activation in response to both caspofungin and DTPA. The combination has therapeutic relevance as DTPA enhanced the efficacy of caspofungin in a mouse model of echinocandin-resistant candidiasis. We found that DTPA not only reduces drug resistance but also modulates morphogenesis, a key virulence trait that is normally regulated by environmental cues. DTPA induced filamentation via depletion of zinc, in a manner that is contingent upon Ras1-PKA signaling, as well as the transcription factors Brg1 and Rob1. Thus, we establish a new mechanism by which metal chelation
Kishi, Akifumi; Struzik, Zbigniew R.; Natelson, Benjamin H.; Togo, Fumiharu; Yamamoto, Yoshiharu
Sleep dynamics emerges from complex interactions between neuronal populations in many brain regions. Annotated sleep stages from electroencephalography (EEG) recordings could potentially provide a non-invasive way to obtain valuable insights into the mechanisms of these interactions, and ultimately into the very nature of sleep regulation. However, to date, sleep stage analysis has been restricted, only very recently expanding the scope of the traditional descriptive statistics to more dynamical concepts of the duration of and transitions between vigilance states and temporal evaluation of transition probabilities among different stages. Physiological and/or pathological implications of the dynamics of sleep stage transitions have, to date, not been investigated. Here, we study detailed duration and transition statistics among sleep stages in healthy humans and patients with chronic fatigue syndrome, known to be associated with disturbed sleep. We find that the durations of waking and non-REM sleep, in particular deep sleep (Stages III and IV), during the nighttime, follow a power-law probability distribution function, while REM sleep durations follow an exponential function, suggestive of complex underlying mechanisms governing the onset of light sleep. We also find a substantial number of REM to non-REM transitions in humans, while this transition is reported to be virtually non-existent in rats. Interestingly, the probability of this REM to non-REM transition is significantly lower in the patients than in controls, resulting in a significantly greater REM to awake, together with Stage I to awake, transition probability. This might potentially account for the reported poor sleep quality in the patients because the normal continuation of sleep after either the lightest or REM sleep is disrupted. We conclude that the dynamical transition analysis of sleep stages is useful for elucidating yet-to-be-determined human sleep regulation mechanisms with a
Gross, Brooks A.; Vanderheyden, William M.; Urpa, Lea M.; Davis, Devon E.; Fitzpatrick, Christopher J.; Prabhu, Kaustubh; Poe, Gina R.
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
Yoncheva, Yuliya N.; Castellanos, F. Xavier; Pizinger, Theresa; Kovtun, Kyle; St-Onge, Marie-Pierre
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, inpatient crossover study experimentally manipulates sleep and meal times while preserving sleep duration (7.05±0.44h for 5 nights). Resting-state functional MRI scans (2×5-minute runs) were obtained for 4 participants (3 males; 25.3±4.6 y), each completing all study phases (normal sleep/normal meal; late sleep/normal meal; normal sleep/late meal; late sleep/late meal). Normal mealtimes were 1, 5, 11, and 12.5h after awakening; late mealtimes were 4.5, 8.5, 14.5 and 16h 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 mealtime 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. PMID:27478925
Grandner, Michael A; Jackson, Nicholas; Gerstner, Jason R; Knutson, Kristen L
Short sleep duration is associated with weight gain and obesity, diabetes, cardiovascular disease, psychiatric illness, and performance deficits. Likewise, long sleep duration is also associated with poor physical and mental health. The role of a healthy diet in habitual sleep duration represents a largely unexplored pathway linking sleep and health. This study evaluated associations between habitual sleep parameters and dietary/nutritional variables obtained via the National Health and Nutrition Examination Survey (NHANES), 2007-2008. We hypothesized that habitual very short (<5h) short (5-6h) and long (9+h) sleep durations are associated with intake of a number of dietary nutrient variables. Overall, energy intake varied across very short (2036kcal), short (2201kcal), and long (1926kcal) sleep duration, relative to normal (2151kcal) sleep duration (p=0.001). Normal sleep duration was associated with the greatest food variety (17.8), compared to very short (14.0), short (16.5) and long (16.3) sleep duration (p<0.001). Associations between sleep duration were found across nutrient categories, with significant associations between habitual sleep duration and proteins, carbohydrates, vitamins and minerals. In stepwise analyses, significant contributors of unique variance included theobromine (long sleep RR=0.910, p<0.05), vitamin C (short sleep RR=0.890, p<0.05), tap water (short sleep RR=0.952, p<0.001; very short (<5h) sleep RR=0.941, p<0.05), lutein+zeaxanthin (short sleep RR=1.123, p<0.05), dodecanoic acid (long sleep RR=0.812, p<0.05), choline (long sleep RR=0.450, p=0.001), lycopene (very short (<5h) sleep RR=0.950, p<0.05), total carbohydrate (very short (<5h) sleep RR=0.494, p<0.05; long sleep RR=0.509, p<0.05), selenium (short sleep RR=0.670, p<0.01) and alcohol (long sleep RR=1.172, p<0.01). Overall, many nutrient variables were associated with short and/or long sleep duration, which may be explained by differences in food variety. Future studies should
Mims, Kimberly Nicole; Kirsch, Douglas
Evidence increasingly suggests sleep disorders are associated with higher risk of cardiovascular events, including stroke. Strong data correlate untreated sleep apnea with poorer stroke outcomes and more recent evidence implicates sleep disruption as a possible etiology for increased cerebrovascular events. Also, sleep duration may affect incidence of cardiovascular events. In addition, sleep-disordered breathing, insomnia, restless legs syndrome, and parasomnias can occur as a result of cerebrovascular events. Treatment of sleep disorders improve sleep-related symptoms and may also improve stroke recovery and risk of future events.
Driver-Dunckley, Erika D; Adler, Charles H
This article summarizes what is currently known about sleep disturbances in several movement disorders including Parkinson disease, essential tremor, parkinsonism, dystonia, Huntington disease, myoclonus, and ataxias. There is an association between movement disorders and sleep. In some cases the prevalence of sleep disorders is much higher in patients with movement disorder, such as rapid eye movement sleep behavior disorder in Parkinson disease. In other cases, sleep difficulties worsen the involuntary movements. In many cases the medications used to treat patients with movement disorder disturb sleep or cause daytime sleepiness. The importance of discussing sleep issues in patients with movement disorders cannot be underestimated.
Oyiengo, Dennis; Louis, Mariam; Hott, Beth; Bourjeily, Ghada
Sleep disturbances are common in pregnancy and may be influenced by a multitude of factors. Pregnancy physiology may predispose to sleep disruption but may also result in worsening of some underlying sleep disorders, and the de novo development of others. Apart from sleep disordered breathing, the impact of sleep disorders on pregnancy, fetal, and neonatal outcomes is poorly understood. In this article, we review the literature and discuss available data pertaining to the most common sleep disorders in perinatal women. These include restless legs syndrome, insomnia, circadian pattern disturbances, narcolepsy, and sleep-disordered breathing.
Jurkowski, Marek K; Bobek-Billewicz, Barbara
Sleep is a universal phenomenon of human and animal lives, although the importance of sleep for homeo-stasis is still unknown. Sleep disturbances influence many behavioral and physiologic processes, leading to health complications including death. On the other hand, sleep improvement can beneficially influence the course of healing of many disorders and can be a prognostic of health recovery. The factors influencing sleep have different biological and chemical origins. They are classical hormones, hypothalamic releasing and inhibitory hormones, neuropeptides, peptides and others as cytokines, prostaglandins, oleamid, adenosine, nitric oxide. These factors regulate most physiologic processes and are likely elements integrating sleep with physiology and physiology with sleep in health and disorders.
Cheng, Philip; Drake, Christopher
Sleep and circadian rhythms significantly impact almost all aspects of human behavior and are therefore relevant to occupational sleep medicine, which is focused predominantly around workplace productivity, safety, and health. In this article, 5 main factors that influence occupational functioning are reviewed: (1) sleep deprivation, (2) disordered sleep, (3) circadian rhythms, (4) common medical illnesses that affect sleep and sleepiness, and (5) medications that affect sleep and sleepiness. Consequences of disturbed sleep and sleepiness are also reviewed, including cognitive, emotional, and psychomotor functioning and drowsy driving.
Pien, Grace W; Schwab, Richard J
This paper reviews the topic of sleep disorders in pregnant women. We describe changes in sleep architecture and sleep pattern during pregnancy, discuss the impact of the physical and biochemical changes of pregnancy on sleep in pregnant women and examine whether maternal-fetal outcomes may be adversely affected in women with disordered sleep. The literature on common sleep disorders affecting pregnant women, including insomnia, sleep-disordered breathing and restless legs syndrome, is reviewed and recommendations are made for the management of these disorders during pregnancy.
and altered vigilance, and atropinic effects; (9) Case-control studies showed a statistical link between benzodiazepine use in early pregnancy and birth defects such as cleft lip. In contrast, data on the use of doxylamine during pregnancy are reassuring; (10) Other sedative psychotropics have not been adequately tested in this setting or have been shown to have a negative risk-benefit balance; (11) In practice, patients who complain of poor-quality sleep should be given appropriate information on the mechanisms of normal sleep and related misconceptions, on the best methods for getting to sleep, and on the dangers of sedative psychotropics (dependence, withdrawal syndrome). When prescribing or dispensing a benzodiazepine to a woman of child-bearing age, the risk of birth defects, although not clearly demonstrated, must be mentioned.
Villa, Chiara; Ferini-Strambi, Luigi; Combi, Romina
Sleep disorders are frequently reported in Alzheimer's disease (AD), with a significant impact on patients and caregivers and a major risk factor for early institutionalization. Although changes in sleep organization are a hallmark of the normal aging processes, sleep macro- and micro-architectural alterations are more evident in patients affected by AD. Degeneration of neural pathways regulating sleep-wake patterns and sleep architecture may contribute to sleep alterations. In return, several recent studies suggested that common sleep disorders may precede clinical symptoms of dementia and represent risk factors for cognitive decline, through impairment of sleep-dependent memory consolidation processes. Thus, a close relationship between sleep disorders and AD has been largely hypothesized. Here, sleep alterations in AD and its pre-dementia stage, mild cognitive impairment, and their complex interactions are reviewed.
Takeuchi, T; Miyasita, A; Inugami, M; Yamamoto, Y
The hypothesis that there is a strict relationship between dreams and a specific rapid eye movement (REM) sleep mechanism is controversial. Many researchers have recently denied this relationship, yet none of their studies have simultaneously controlled both sleep length and depth prior to non-REM (NREM) and REM sleep awakenings, due to the natural rigid order of the NREM--REM sleep cycle. The failure to control sleep length and depth prior to arousal has confounded interpretations of the REM-dreams relationship. We have hypothesised that different physiological mechanisms underlie dreaming during REM and NREM sleep, based on recent findings concerning the specificity of REM sleep for cognitive function. Using the Sleep Interruption Technique, we elicited sleep onset REM periods (SOREMP) from 13 normal subjects to collect SOREMP and sleep onset NREM (NREMP) dreams without the confounds described above. Regression analyses showed that SOREMP dream occurrences were significantly related to the amount of REM sleep, while NREMP dream occurrences were related to arousals from NREM sleep. Dream properties evaluated using the Dream Property Scale showed qualitative differences between SOREMP and NREMP dream reports. These results support our hypothesis and we have concluded that although 'dreaming' may occur during both REM and NREM periods as previous researchers have suggested, the dreams obtained from these distinct periods differ significantly in their quantitative and qualitative aspects and are likely to be produced by different mechanisms.
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.
MacLean, Joanna E; Fitzgerald, Dominic A; Waters, Karen A
Sleep and breathing are physiological processes that begin in utero and undergo progressive change. While the major period of change for both sleep and breathing occurs during the months after birth, considered a period of vulnerability, more subtle changes continue to occur throughout childhood. The systems that control sleep and breathing develop separately, but sleep represents an activity state during which breathing and breathing control is significantly altered. Infants and young children may spend up to 12 hours a day sleeping; therefore, the effects of sleep on breathing are fundamental to understanding both processes in childhood. This review summarizes the current literature relevant to understanding the normal development of sleep and breathing across infancy and childhood.
Imeri, Luca; Opp, Mark R.
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
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
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
Malvy, D; Chappuis, F
Human African trypanosomiasis (HAT), or sleeping sickness, is a vector-borne disease that flourishes in impoverished, rural parts of sub-Saharan Africa. It is caused by infection with the protozoan parasite Trypanosoma brucei and is transmitted by tsetse flies of the genus Glossina. The majority of cases are caused by T. b. gambiense, which gives rise to the chronic, anthroponotic endemic disease in Western and Central Africa. Infection with T. b. rhodesiense leads to the acute, zoonotic form of Eastern and Southern Africa. The parasites live and multiply extracellularly in the blood and tissue fluids of their human host. They have elaborated a variety of strategies for invading hosts, to escape the immune system and to take advantage of host growth factors. HAT is a challenging and deadly disease owing to its complex epidemiology and clinical presentation and, if left untreated, can result in high death rates. As one of the most neglected tropical diseases, HAT is characterized by the limited availability of safe and cost-effective control tools. No vaccine against HAT is available, and the toxicity of existing old and cumbersome drugs precludes the adoption of control strategies based on preventive chemotherapy. As a result, the keystones of interventions against sleeping sickness are active and passive case-finding for early detection of cases followed by treatment, vector control and animal reservoir management. New methods to diagnose and treat patients and to control transmission by the tsetse fly are needed to achieve the goal of global elimination of the disease.
Heshmati, Mitra; Russo, Scott J.
Anhedonia, or the loss of pleasure in previously rewarding stimuli, is a core symptom of major depressive disorder that may reflect an underlying dysregulation in reward processing. The mesolimbic dopamine circuit, also known as the brain’s reward circuit, is integral to processing the rewarding salience of stimuli to guide actions. Manifestation of anhedonia and associated depression symptoms like feelings of sadness, changes in appetite, and psychomotor effects, may reflect changes in the brain reward circuitry as a common underlying disease process. This review will synthesize the recent literature from human and rodent studies providing a circuit-level framework for understanding anhedonia in depression, with emphasis on the nucleus accumbens. PMID:26525751
Garverick, Steven L. (Inventor); Yu, Xinyu (Inventor)
An amplifier system can include an input amplifier configured to receive an analog input signal and provide an amplified signal corresponding to the analog input signal. A tracking loop is configured to employ delta modulation for tracking the amplified signal, the tracking loop providing a corresponding output signal. A biasing circuit is configured to adjust a bias current to maintain stable transconductance over temperature variations, the biasing circuit providing at least one bias signal for biasing at least one of the input amplifier and the tracking loop, whereby the circuitry receiving the at least one bias signal exhibits stable performance over the temperature variations. In another embodiment the biasing circuit can be utilized in other applications.
Franks, Kevin M; Russo, Marco J; Sosulski, Dara L; Mulligan, Abigail A; Siegelbaum, Steven A; Axel, Richard
In the piriform cortex, individual odorants activate a unique ensemble of neurons that are distributed without discernable spatial order. Piriform neurons receive convergent excitatory inputs from random collections of olfactory bulb glomeruli. Pyramidal cells also make extensive recurrent connections with other excitatory and inhibitory neurons. We introduced channelrhodopsin into the piriform cortex to characterize these intrinsic circuits and to examine their contribution to activity driven by afferent bulbar inputs. We demonstrated that individual pyramidal cells are sparsely interconnected by thousands of excitatory synaptic connections that extend, largely undiminished, across the piriform cortex, forming a large excitatory network that can dominate the bulbar input. Pyramidal cells also activate inhibitory interneurons that mediate strong, local feedback inhibition that scales with excitation. This recurrent network can enhance or suppress bulbar input, depending on whether the input arrives before or after the cortex is activated. This circuitry may shape the ensembles of piriform cells that encode odorant identity.
Kalivas, Benjamin C; Kalivas, Peter W
Intrusive thinking triggers clinical symptoms in many neuropsychiatric disorders. Using drug addiction as an exemplar disorder sustained in part by intrusive thinking, we explore studies demonstrating that impairments in corticostriatal circuitry strongly contribute to intrusive thinking. Neuroimaging studies have long implicated this projection in cue-induced craving to use drugs, and preclinical models show that marked changes are produced at corticostriatal synapses in the nucleus accumbens during a relapse episode. We delineate an accumbens microcircuit that mediates cue-induced drug seeking becoming an intrusive event. This microcircuit harbors many potential therapeutic targets. We focus on preclinical and clinical studies, showing that administering N-acetylcysteine restores uptake of synaptic glutamate by astroglial glutamate transporters and thereby inhibits intrusive thinking. We posit that because intrusive thinking is a shared endophenotype in many disorders, N-acetylcysteine has positive effects in clinical trials for a variety of neuropsychiatric disorders, including drug addiction, gambling, trichotillomania, and depression.
Daubert, Elizabeth A.; Condron, Barry G.
Serotonin is an important neuromodulator associated with a wide range of physiological effects in the central nervous system. The exact mechanisms for how serotonin influences brain development are not well understood, although studies in invertebrate and vertebrate model organisms are beginning to unravel a regulatory role for serotonin in neuronal morphology and circuit formation. Recent data suggests a developmental window during which altered serotonin levels permanently impact circuitry, however, the temporal constraints and molecular mechanisms responsible are still under investigation. Growing evidence suggests that alterations in early serotonin signaling contribute to a number of neurodevelopmental and neuropsychiatric disorders. Thus, understanding how altered serotonin signaling affects neuronal morphology and plasticity, and ultimately animal physiology and pathophysiology, will be of great significance. PMID:20561690
Eshel, Neir; Bukwich, Michael; Rao, Vinod; Hemmelder, Vivian; Tian, Ju; Uchida, Naoshige
Dopamine neurons are thought to facilitate learning by comparing actual and expected reward1,2. Despite two decades of investigation, little is known about how this comparison is made. To determine how dopamine neurons calculate prediction error, we combined optogenetic manipulations with extracellular recordings in the ventral tegmental area (VTA) while mice engaged in classical conditioning. By manipulating the temporal expectation of reward, we demonstrate that dopamine neurons perform subtraction, a computation that is ideal for reinforcement learning but rarely observed in the brain. Furthermore, selectively exciting and inhibiting neighbouring GABA neurons in the VTA reveals that these neurons are a source of subtraction: they inhibit dopamine neurons when reward is expected, causally contributing to prediction error calculations. Finally, bilaterally stimulating VTA GABA neurons dramatically reduces anticipatory licking to conditioned odours, consistent with an important role for these neurons in reinforcement learning. Together, our results uncover the arithmetic and local circuitry underlying dopamine prediction errors. PMID:26322583
Kalivas, Benjamin C.; Kalivas, Peter W.
Intrusive thinking triggers clinical symptoms in many neuropsychiatric disorders. Using drug addiction as an exemplar disorder sustained in part by intrusive thinking, we explore studies demonstrating that impairments in corticostriatal circuitry strongly contribute to intrusive thinking. Neuroimaging studies have long implicated this projection in cue-induced craving to use drugs, and preclinical models show that marked changes are produced at corticostriatal synapses in the nucleus accumbens during a relapse episode. We delineate an accumbens microcircuit that mediates cue-induced drug seeking becoming an intrusive event. This microcircuit harbors many potential therapeutic targets. We focus on preclinical and clinical studies, showing that administering N-acetylcysteine restores uptake of synaptic glutamate by astroglial glutamate transporters and thereby inhibits intrusive thinking. We posit that because intrusive thinking is a shared endophenotype in many disorders, N-acetylcysteine has positive effects in clinical trials for a variety of neuropsychiatric disorders, including drug addiction, gambling, trichotillomania, and depression. PMID:27069381
de Groat, W. C.; Wickens, C.
The functions of the lower urinary tract to store and periodically eliminate urine are regulated by a complex neural control system in the brain and spinal cord that coordinates the activity of the bladder and urethral outlet. Experimental studies in animals indicate that urine storage is modulated by reflex mechanisms in the spinal cord, whereas voiding is mediated by a spinobulbospinal pathway passing through a coordination centre in the rostral brain stem. Many of the neural circuits controlling micturition exhibit switch-like patterns of activity that turn on and off in an all-or-none manner. This study summarizes the anatomy and physiology of the spinal and supraspinal micturition switching circuitry and describes a computer model of these circuits that mimics the switching functions of the bladder and urethra at the onset of micturition. PMID:23033877
Sadovnikov, A. V.; Grishin, S. V. Romanenko, D. V.; Sharaevskii, Yu. P.; Davies, C. S.; Kruglyak, V. V.; Nikitov, S. A.
We demonstrate a magnonic beam splitter that works by inter-converting magnetostatic surface and backward-volume spin waves propagating in orthogonal sections of a T-shaped yttrium iron garnet structure. The inter-conversion is enabled by the overlap of the surface and volume spin wave bands. This overlap results from the demagnetising field induced along the transversely magnetised section(-s) of the structure and the quantization of the transverse wave number of the propagating spin waves (which are therefore better described as waveguide modes). In agreement with numerical micromagnetic simulations, our Brillouin light scattering imaging experiments reveal that, depending on the frequency, the incident fundamental waveguide magnonic modes may also be converted into higher order waveguide modes. The magnonic beam splitter demonstrated here is an important step towards the development of parallel logic circuitry of magnonics.
To advance our understanding of how the brain makes food decisions, it is essential to combine knowledge from two fields that have not yet been well integrated: the neuro-computational basis of decision-making and the homeostatic regulators of feeding. This Review integrates these two literatures from a neuro-computational perspective, with an emphasis in describing the variables computed by different neural systems and how they affect dietary choice. We highlight what is unique about feeding decisions, the mechanisms through which metabolic and endocrine factors affect the decision-making circuitry, why making healthy food choices is difficult for many people, and key processes at work in the obesity epidemic. PMID:24270272
Jahanshahi, Amir; Salvo, Pietro; Vanfleteren, Jan
Stretchable and curvilinear electronics has been used recently for the fabrication of micro systems interacting with the human body. The applications range from different kinds of implantable sensors inside the body to conformable electrodes and artificial skins. One of the key parameters in biocompatible stretchable electronics is the fabrication of reliable electrical interconnects. Although very recent literature has reported on the reliability of stretchable interconnects by cyclic loading, work still needs to be done on the integration of electrical circuitry composed of rigid components and stretchable interconnects in a biological environment. In this work, the feasibility of a developed technology to fabricate simple electrical circuits with meander shaped stretchable interconnects is presented. Stretchable interconnects are 200 nm thin Au layer supported with polyimide (PI). A stretchable array of light emitting diodes (LEDs) is embedded in biocompatible elastomer using this technology platform and it features a 50% total elongation.
Morairty, Stephen R; Dittrich, Lars; Pasumarthi, Ravi K; Valladao, Daniel; Heiss, Jaime E; Gerashchenko, Dmitry; Kilduff, Thomas S
Although the neural circuitry underlying homeostatic sleep regulation is little understood, cortical neurons immunoreactive for neuronal nitric oxide synthase (nNOS) and the neurokinin-1 receptor (NK1) have been proposed to be involved in this physiological process. By systematically manipulating the durations of sleep deprivation and subsequent recovery sleep, we show that activation of cortical nNOS/NK1 neurons is directly related to non-rapid eye movement (NREM) sleep time, NREM bout duration, and EEG δ power during NREM sleep, an index of preexisting homeostatic sleep drive. Conversely, nNOS knockout mice show reduced NREM sleep time, shorter NREM bouts, and decreased power in the low δ range during NREM sleep, despite constitutively elevated sleep drive. Cortical NK1 neurons are still activated in response to sleep deprivation in these mice but, in the absence of nNOS, they are unable to up-regulate NREM δ power appropriately. These findings support the hypothesis that cortical nNOS/NK1 neurons translate homeostatic sleep drive into up-regulation of NREM δ power through an NO-dependent mechanism.
Across species, the performance of vocal signals can be modulated by the social environment. Zebra finches, for example, adjust their song performance when singing to females (‘female-directed’ or FD song) compared to when singing in isolation (‘undirected’ or UD song). These changes are salient, as females prefer the FD song over the UD song. Despite the importance of these performance changes, the neural mechanisms underlying this social modulation remain poorly understood. Previous work in finches has established that expression of the immediate early gene EGR1 is increased during singing and modulated by social context within the vocal control circuitry. Here, we examined whether particular neural subpopulations within those vocal control regions exhibit similar modulations of EGR1 expression. We compared EGR1 expression in neurons expressing parvalbumin (PV), a calcium buffer that modulates network plasticity and homeostasis, among males that performed FD song, males that produced UD song, or males that did not sing. We found that, overall, singing but not social context significantly affected EGR1 expression in PV neurons throughout the vocal control nuclei. We observed differences in EGR1 expression between two classes of PV interneurons in the basal ganglia nucleus Area X. Additionally, we found that singing altered the amount of PV expression in neurons in HVC and Area X and that distinct PV interneuron types in Area X exhibited different patterns of modulation by singing. These data indicate that throughout the vocal control circuitry the singing-related regulation of EGR1 expression in PV neurons may be less influenced by social context than in other neuron types and raise the possibility of cell-type specific differences in plasticity and calcium buffering. PMID:28235074
In the awake brain, information about the external world reaches the hippocampus via the entorhinal cortex, whereas during sleep the direction of information flow is reversed: population bursts initiated in the hippocampus invade the neocortex. We suggest that neocortico-hippocampal transfer of information and the modification process in neocortical circuitries by the hippocampal output take place in a temporally discontinuous manner associated with theta/gamma oscillations. On the other hand, transfer of the stored representations to neocortical areas is carried by discrete quanta of cooperative neuronal bursts (called sharp wave bursts) initiated in the hippocampus during slow wave sleep. The spatio-temporal participation of principal cells in sharp waves is determined by experience-induced changes in the CA3 recurrent collateral matrix. The co-operative, converging pre-synaptic activity can induce localized fast spikes and associated calcium influx in the apical dendrites of CA1 pyramidal cells, a necessary condition for the induction of synaptic plasticity. In addition, the subcortical effects of hippocampal sharp wave bursts may be critical in the release of various hormones which, in turn, may affect synaptic plasticity. These observations suggest that sleep patterns in the limbic system are essential for the preservation of experience-induced synaptic modifications.
Vetrugno, Roberto; Montagna, Pasquale
Sleep is a coordinated process involving more or less simultaneous changes in sensory, motor, autonomic, hormonal, and cerebral processes. On the other hand, none of the changes occurring with sleep are invariably coupled to sleep. EEG synchrony, heat loss, sleep-related hormone secretion, and even REM-related motoneuron paralysis may occur independent of the parent state. In REM sleep behaviour disorder (RBD) the muscle tone of wakefulness intrudes into REM sleep, allowing the release of dream-enacting behaviours. Status dissociatus (SD) is a condition in which brain and mind are in disarray along the boundaries of sleep and wakefulness. The existence of such dissociated behaviours shows that they have separate neuronal control systems and indicates that the whole organization of sleep is an emergent property of the collective neuronal systems to synchronize. Insults to the brain can drastically alter the circuitries responsible for maintaining the integrity of wakefulness, NREM sleep, and REM sleep. As a consequence, the basic states of existence can become admixed and interchanged with striking disturbances of consciousness, brain electrophysiology, and the behavioural and polygraphic expression of sleep and wakefulness. The evolution of RBD into SD may result from a disarray of (brainstem) structures that orchestrate the whole brain wake-sleep conditions, but with preserved discrete systems and dissociable strategies to still place navigation in wake and sleep. Advances in the fields of genetics, neuroimaging, and behavioural neurology will expand the understanding of the mechanisms underlying the organization of the states of being along with their somatic/behavioural manifestations.
Pace-Schott, Edward F; Germain, Anne; Milad, Mohammed R
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
Bracha, H Stefan; Ralston, Tyler C; Williams, Andrew E; Yamashita, Jennifer M; Bracha, Adam S
This review discusses the clenching-grinding spectrum from the neuropsychiatric/neuroevolutionary perspective. In neuropsychiatry, signs of jaw clenching may be a useful objective marker for detecting or substantiating a self-report of current subjective emotional distress. Similarly, accelerated tooth wear may be an objective clinical sign for detecting, or substantiating, long-lasting anxiety. Clenching-grinding behaviors affect at least 8 percent of the population. We argue that during the early paleolithic environment of evolutionary adaptedness, jaw clenching was an adaptive trait because it rapidly strengthened the masseter and temporalis muscles, enabling a stronger, deeper and therefore more lethal bite in expectation of conflict (warfare) with conspecifics. Similarly, sharper incisors produced by teeth grinding may have served as weaponry during early human combat. We posit that alleles predisposing to fear-induced clenching-grinding were evolutionarily conserved in the human clade (lineage) since they remained adaptive for anatomically and mitochondrially modern humans (Homo sapiens) well into the mid-paleolithic. Clenching-grinding, sleep bruxism, myofacial pain, craniomaxillofacial musculoskeletal pain, temporomandibular disorders, oro-facial pain, and the fibromyalgia/chronic fatigue spectrum disorders are linked. A 2003 Cochrane meta-analysis concluded that dental procedures for the above spectrum disorders are not evidence based. There is a need for early detection of clenching-grinding in anxiety disorder clinics and for research into science-based interventions. Finally, research needs to examine the possible utility of incorporating physical signs into Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition posttraumatic stress disorder diagnostic criteria. One of the diagnostic criterion that may need to undergo a revision in Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition is Criterion D (persistent fear-circuitry
Kenngott, Max; McKay, Cavendish
We examine the dynamics of the two process model of human sleep regulation. In this model, sleep propensity is governed by the interaction between a periodic threshold (process C) and a saturating growth/decay (process S). We find that the parameter space of this model admits sleep cycles with a wide variety of characteristics, many of which are not observed in normal human sleepers. We also examine the effects of phase dependent feedback on this model.
Gee, Dylan G.
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…
Van Cauter, Eve; Spiegel, Karine; Tasali, Esra; Leproult, Rachel
Reduced sleep duration and quality appear to be endemic in modern society. Curtailment of the bedtime period to minimum tolerability is thought to be efficient and harmless by many. It has been known for several decades that sleep is a major modulator of hormonal release, glucose regulation and cardiovascular function. In particular, slow wave sleep (SWS), thought to be the most restorative sleep stage, is associated with decreased heart rate, blood pressure, sympathetic nervous activity and cerebral glucose utilization, compared with wakefulness. During SWS, the anabolic growth hormone is released while the stress hormone cortisol is inhibited. In recent years, laboratory and epidemiologic evidence have converged to indicate that sleep loss may be a novel risk factor for obesity and type 2 diabetes. The increased risk of obesity is possibly linked to the effect of sleep loss on hormones that play a major role in the central control of appetite and energy expenditure, such as leptin and ghrelin. Reduced leptin and increased ghrelin levels correlate with increases in subjective hunger when individuals are sleep restricted rather than well rested. Given the evidence, sleep curtailment appears to be an important, yet modifiable, risk factor for the metabolic syndrome, diabetes and obesity. The marked decrease in average sleep duration in the last 50 years coinciding with the increased prevalence of obesity, together with the observed adverse effects of recurrent partial sleep deprivation on metabolism and hormonal processes, may have important implications for public health. PMID:18929315
Van Cauter, Eve; Spiegel, Karine; Tasali, Esra; Leproult, Rachel
Reduced sleep duration and quality appear to be endemic in modern society. Curtailment of the bedtime period to minimum tolerability is thought to be efficient and harmless by many. It has been known for several decades that sleep is a major modulator of hormonal release, glucose regulation and cardiovascular function. In particular, slow wave sleep (SWS), thought to be the most restorative sleep stage, is associated with decreased heart rate, blood pressure, sympathetic nervous activity and cerebral glucose utilization, compared with wakefulness. During SWS, the anabolic growth hormone is released while the stress hormone cortisol is inhibited. In recent years, laboratory and epidemiologic evidence have converged to indicate that sleep loss may be a novel risk factor for obesity and type 2 diabetes. The increased risk of obesity is possibly linked to the effect of sleep loss on hormones that play a major role in the central control of appetite and energy expenditure, such as leptin and ghrelin. Reduced leptin and increased ghrelin levels correlate with increases in subjective hunger when individuals are sleep restricted rather than well rested. Given the evidence, sleep curtailment appears to be an important, yet modifiable, risk factor for the metabolic syndrome, diabetes and obesity. The marked decrease in average sleep duration in the last 50 years coinciding with the increased prevalence of obesity, together with the observed adverse effects of recurrent partial sleep deprivation on metabolism and hormonal processes, may have important implications for public health.
Will, Bruno; Kelche, Christian; Cassel, Jean-Christophe
Intracerebral grafting techniques of fetal neural cells have been used essentially with two main types of lesion paradigms, namely damage to long projection systems, in which the source and the target are clearly separate, and damage to neurons that are involved in local circuits within a small (sub)region of the brain. With the’first lesion paradigm, grafts placed homotopically (in the source) are not appropriate because their fibers grow poorly through the host parenchyma and fail to reach their normal target. To be successful, the grafts must be placed ectopically in the target region of the damaged projection systems, where generally they work as level-setting systems. Conversely, with the second paradigm, the grafts are supposed to compensate for a local loss of neurons and must be placed homotopically to induce functional effects that are based on the reconstruction of a point-to-point circuitry. By inserting a biological or artificial bridging-substrate between the source and the target of long projection systems, it might be possible to combine the positive effects of both homotopic and ectopic grafting by achieving both target reinnervation and normal control of the grafted neurons within the source area. These issues are illustrated and discussed in this review. PMID:10709217
McGuire, Sarah M.
One of the primary impacts of aircraft noise on a community is its disruption of sleep. Aircraft noise increases the time to fall asleep, the number of awakenings, and decreases the amount of rapid eye movement and slow wave sleep. Understanding these changes in sleep may be important as they could increase the risk for developing next-day effects such as sleepiness and reduced performance and long-term health effects such as cardiovascular disease. There are models that have been developed to predict the effect of aircraft noise on sleep. However, most of these models only predict the percentage of the population that is awakened. Markov and nonlinear dynamic models have been developed to predict an individual's sleep structure during the night. However, both of these models have limitations. The Markov model only accounts for whether an aircraft event occurred not the noise level or other sound characteristics of the event that may affect the degree of disturbance. The nonlinear dynamic models were developed to describe normal sleep regulation and do not have a noise effects component. In addition, the nonlinear dynamic models have slow dynamics which make it difficult to predict short duration awakenings which occur both spontaneously and as a result of nighttime noise exposure. The purpose of this research was to examine these sleep structure models to determine how they could be altered to predict the effect of aircraft noise on sleep. Different approaches for adding a noise level dependence to the Markov Model was explored and the modified model was validated by comparing predictions to behavioral awakening data. In order to determine how to add faster dynamics to the nonlinear dynamic sleep models it was necessary to have a more detailed sleep stage classification than was available from visual scoring of sleep data. An automatic sleep stage classification algorithm was developed which extracts different features of polysomnography data including the
... Topics CPAP High Blood Pressure Overweight and Obesity Sleep Deprivation and Deficiency Sleep Studies Send a link to ... For more information, go to the Health Topics Sleep Deprivation and Deficiency article.) If treatment and enough sleep ...
Morgan, Dionne; Tsai, Sheila C
In this article, the effect of sleep and sleep disorders on endocrine function and the influence of endocrine abnormalities on sleep are discussed. Sleep disruption and its associated endocrine consequences in the critically ill patient are also reviewed.
Morgan, Dionne; Tsai, Sheila C
In this article, the effect of sleep and sleep disorders on endocrine function and the influence of endocrine abnormalities on sleep are discussed. Sleep disruption and its associated endocrine consequences in the critically ill patient are also reviewed.
Volk, Carina; Huber, Reto
Sleep is undisputable an essential part of our life, if we do not sleep enough we feel the consequences the next day. The importance of sleep for healthy brain functioning has been well studied in adults, but less is known for the role of sleep in the paediatric age. Childhood and adolescence is a critical phase for brain development. The increased need for sleep during this developmental phase fosters the growing recognition for a central role of sleep during development. In this review we summarize the findings that demonstrate a close relationship between sleep and brain maturation, discuss the consequences of insufficient sleep during childhood and adolescence and outline initial attempts that have been made in order to improve sleep in this age range.
Webb, W. B.
Discussion of the electroencephalogram as the critical measurement procedure for sleep research, and survey of major findings that have emerged in the last decade on the presence of sleep within the twenty-four-hour cycle. Specifically, intrasleep processes, frequency of stage changes, sequence of stage events, sleep stage amounts, temporal patterns of sleep, and stability of intrasleep pattern in both man and lower animals are reviewed, along with some circadian aspects of sleep, temporal factors, and number of sleep episodes. It is felt that it is particularly critical to take the presence of sleep into account whenever performance is considered. When it is recognized that responsive performance is extremely limited during sleep, it is easy to visualize the extent to which performance is controlled by sleep itself.
Luyster, Faith S; Strollo, Patrick J; Zee, Phyllis C; Walsh, James K
Chronic sleep deficiency, defined as a state of inadequate or mistimed sleep, is a growing and underappreciated determinant of health status. Sleep deprivation contributes to a number of molecular, immune, and neural changes that play a role in disease development, independent of primary sleep disorders. These changes in biological processes in response to chronic sleep deficiency may serve as etiological factors for the development and exacerbation of cardiovascular and metabolic diseases and, ultimately, a shortened lifespan. Sleep deprivation also results in significant impairments in cognitive and motor performance which increase the risk of motor vehicle crashes and work-related injuries and fatal accidents. The American Academy of Sleep Medicine and the Sleep Research Society have developed this statement to communicate to national health stakeholders the current knowledge which ties sufficient sleep and circadian alignment in adults to health.
Sadeh, Avi; Tikotzky, Liat; Scher, Anat
Infant sleep undergoes dramatic evolution during the first year of life. This process is driven by underlying biological forces but is highly dependent on environmental cues including parental influences. In this review the links between infant sleep and parental behaviors, cognitions, emotions and relationships as well as psychopathology are examined within the context of a transactional model. Parental behaviors, particularly those related to bedtime interactions and soothing routines, are closely related to infant sleep. Increased parental involvement is associated with more fragmented sleep. Intervention based on modifying parental behaviors and cognitions have direct effect on infant sleep. It appears that parental personality, psychopathology and related cognitions and emotions contribute to parental sleep-related behaviors and ultimately influence infant sleep. However, the links are bidirectional and dynamic so that poor infant sleep may influence parental behaviors and poor infant sleep appears to be a family stressor and a risk factor for maternal depression.
Beattie, Louise; Walsh, Darragh; McLaren, Jessica; Biello, Stephany M.
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
VanHelder, T; Radomski, M W
Sleep deprivation or partial sleep loss are common in work conditions as rotating shifts and prolonged work hours, in sustained military operations and in athletes competing in events after crossing several time zones or engaged in ultramarathon or triathlon events. Although it is well established that sleep loss has negative effects on mental performance, its effects on physical performance are equivocal. This review examines the latter question in light of recent studies published on this problem. Sleep deprivation of 30 to 72 hours does not affect cardiovascular and respiratory responses to exercise of varying intensity, or the aerobic and anaerobic performance capability of individuals. Muscle strength and electromechanical responses are also not affected. Time to exhaustion, however, is decreased by sleep deprivation. Although ratings of perceived exertion always increased during exercise in sleep-deprived (30 to 60 hours) subjects compared with normal sleep, this is not a reliable assessment of a subject's ability to perform physical work as the ratings of perceived exertion are dissociated from any cardiovascular changes in sleep deprivation. Examination of the various hormonal and metabolic parameters which have been measured in the studies reviewed reveals that the major metabolic perturbations accompanying sleep deprivation in humans are an increase in insulin resistance and a decrease in glucose tolerance. This may explain the reduction in observed time to exhaustion in sleep-deprived subjects. The role of growth hormone in mediating altered carbohydrate metabolism may be of particular relevance as to how sleep deprivation alters the supply of energy substrate to the muscle.
Greenhill, L; Puig-Antich, J; Goetz, R; Hanlon, C; Davies, M
A 2-night polysomnographic study of 9 rigorously assessed prepubertal children who fit Diagnostic Statistical Manual-III criteria for attention deficit disorder with hyperactivity (ADDH) and a contrast group of 11 control children is reported. Despite the fact that 57% of the ADDH group were reported to experience restless sleep on structured parental rating forms, they did not show any sleep architecture abnormalities on polysomnographic recordings when compared with the normals at baseline other than decreased rapid eye movement (REM) activity. Seven of the ADDH boys were restudied after 6 months of continuous methylphenidate therapy (mean daily dose of 34.4 +/- 14.0 mg or 1.4 +/- 0.7 mg/kg). Across and within (pre-post) group comparisons showed that methylphenidate therapy was associated with delayed sleep onset, lengthened sleep, and changes in certain REM sleep variables.
Conte, F.; Carobbi, G.; Errico, B. M.; Ficca, G.
Several studies have consistently shown that pre-sleep learning is associated to changes of sleep structure. Whereas previous research has mainly focused on sleep states, namely REM and NREM amount, very little attention has been paid to the hypothesis that pre-sleep learning might improve sleep continuity, stability, and cyclic organization, which are often impaired in aging. Thus, aim of this research was to assess, in a sample of 18 healthy elderly subjects, whether a memory task administered at bedtime would determine changes in any sleep parameter, with special regard to sleep continuity, stability, and organization. To this purpose, a baseline sleep (BL), i.e., a normal sleep with 9-h time in bed (TIB), was compared to a post-training sleep (TR), with the same TIB but preceded by an intensive training session. For the latter, a verbal declarative task was used, consisting in learning paired-word lists, rehearsed, and recalled for three times in a row. To control for individual learning abilities, subjects were administered several sets of lists with increasing difficulty, until they reached an error rate ≥20% at third recall. Relative to BL, TR shows a significant reduction in the frequency of brief awakenings, arousals, state transitions, “functional uncertainty” (FU) periods, and in the percentage of time in FU over total sleep time (TST). A significant increase in the number of complete cycles, total cycle time (TCT), and TCT/TST proportion was also found. All these changes are evenly distributed over the sleep episode. No sleep stage measure display significant changes, apart from a slight reduction in the percentage of Stage 1. Scores at retest are negatively correlated with both the frequency of arousals and of state transitions. Our data suggest that pre-sleep learning can yield a beneficial re-organizing effect on elderlies’ sleep quality. The inverse correlation between recall scores and the measures of sleep continuity and stability provides
Conte, F; Carobbi, G; Errico, B M; Ficca, G
Several studies have consistently shown that pre-sleep learning is associated to changes of sleep structure. Whereas previous research has mainly focused on sleep states, namely REM and NREM amount, very little attention has been paid to the hypothesis that pre-sleep learning might improve sleep continuity, stability, and cyclic organization, which are often impaired in aging. Thus, aim of this research was to assess, in a sample of 18 healthy elderly subjects, whether a memory task administered at bedtime would determine changes in any sleep parameter, with special regard to sleep continuity, stability, and organization. To this purpose, a baseline sleep (BL), i.e., a normal sleep with 9-h time in bed (TIB), was compared to a post-training sleep (TR), with the same TIB but preceded by an intensive training session. For the latter, a verbal declarative task was used, consisting in learning paired-word lists, rehearsed, and recalled for three times in a row. To control for individual learning abilities, subjects were administered several sets of lists with increasing difficulty, until they reached an error rate ≥20% at third recall. Relative to BL, TR shows a significant reduction in the frequency of brief awakenings, arousals, state transitions, "functional uncertainty" (FU) periods, and in the percentage of time in FU over total sleep time (TST). A significant increase in the number of complete cycles, total cycle time (TCT), and TCT/TST proportion was also found. All these changes are evenly distributed over the sleep episode. No sleep stage measure display significant changes, apart from a slight reduction in the percentage of Stage 1. Scores at retest are negatively correlated with both the frequency of arousals and of state transitions. Our data suggest that pre-sleep learning can yield a beneficial re-organizing effect on elderlies' sleep quality. The inverse correlation between recall scores and the measures of sleep continuity and stability provides
Killick, Roo; Hoyos, Camilla M.; Melehan, Kerri; Dungan, George C.; Poh, Jonathon; Liu, Peter Y.
Summary Objective Acutely restricting sleep worsens insulin sensitivity in healthy individuals whose usual sleep is normal in duration and pattern. The effect of recovery or weekend ‘catch-up’ sleep on insulin sensitivity and metabolically active hormones in individuals with chronic sleep restriction who regularly ‘catch-up’ on sleep at weekends is as yet unstudied. Design 19 men (mean ± SEM age 28.6±2.0years, BMI 26.0±0.8kg/m2) with at least 6 months’ history (5.1±0.9years) of lifestyle driven, restricted sleep during the working week (373±6.6 min/night) with regular weekend ‘catch up’ sleep (weekend sleep extension 37.4±2.3%) completed an in-laboratory, randomised, cross-over study comprising 2 of 3 conditions, stratified by age. Conditions were 3 weekend nights of 10 hours, 6 hours or 10 hours time-in-bed with slow wave sleep suppression using targeted acoustic stimuli. Measurements Insulin sensitivity was measured in the morning following the 3rd intervention night by minimal modelling of 19 samples collected during a 2 hour oral glucose tolerance test. Glucose, insulin, c-peptide, leptin, peptide YY, ghrelin, cortisol, testosterone and luteinising hormone (LH) were measured from daily fasting blood samples; HOMA-IR, HOMA-β and QUICKI were calculated. Results Insulin sensitivity was higher following 3 nights of sleep extension compared to sustained sleep restriction. Fasting insulin, c-peptide, HOMA-IR, HOMA-β, leptin and PYY decreased with ‘catch-up’ sleep, QUICKI and testosterone increased, while morning cortisol and LH did not change. Targeted acoustic stimuli reduced SWS by 23%, but did not alter insulin sensitivity. Conclusions Three nights of ‘catch-up’ sleep improved insulin sensitivity in men with chronic, repetitive sleep restriction. Methods to improve metabolic health by optimising sleep are plausible. PMID:25683266
Ferreira, Teresa; Prabhakar, Sudesh; Kharbanda, Parampreet S.
Context: Parkinson's disease (PD) is associated with sleep disturbances, attributed to the neurodegenerative process and therapeutic drugs. Studies have found levodopa to increase wakefulness in some patients while increasing sleepiness in others. Aims: To confirm sleep disturbances in drug naïve PD patients and understand the impact of levodopa on their sleep. Materials and Methods: Twenty-three drug naïve PD patients and 31 age-gender matched controls were compared using the Parkinson's Disease Sleep Scale (PDSS) and Epworth Sleepiness Scale (ESS). A polysomnogram objectively compared sleep quality. Of the 23 patients, the 12 initiated on levodopa were reassessed subjectively and through polysomnography after 2 months of therapy. Statistical Analysis: Data was expressed as mean ± standard deviation, median, and range. Continuous variables were analyzed by Student's T test for normally distributed data and Mann–Whitney U test for skewed data. Discrete variables were compared by Chi Square tests (Pearson Chi square Test or Fisher's Exact Test). Wilcoxon signed ranks test was applied in the analysis of paired data pre- and post-levodopa. A P value < 0.05 was considered as statistically significant. Statistical analysis of the data was done using the Statistical Package for the Social Sciences (SPSS) version 12. Results: Drug naïve PD patients had lower PDSS scores than controls. The sleep architecture changes observed on polysomnogram were reduced NREM Stage III and REM sleep and increased sleep latency and wake after sleep onset time. Following levodopa, improved sleep efficiency with reduced sleep latency and wake after sleep onset time was noted, coupled with improved PDSS scores. However, NREM Stage III and REM sleep duration did not increase. Discussion: PD patients take longer to fall asleep and have difficulty in sleep maintenance. Sleep maintenance is affected by nocturia, REM behavioral disorder, nocturnal cramps, akinesia, and tremors, as observed in
Bayon, V; Léger, D
The presence of insomnia in patients with sleep apnea seems paradoxical as excessive sleepiness is one of the major symptoms of sleep apnea. However, recent research has shown that about half of patients with sleep disorder breathing experience insomnia. Moreover, patients complaining of insomnia or non-restorative sleep may also present with moderate to severe sleep apnea syndromes. Thus, in recent years, clinicians have become more aware of the possible association between insomnia and sleep apnea. This article reviews data published on different aspects of this co-occurrence.
Rains, Jeanetta C; Poceta, J Steven
Irrespective of diagnosis, chronic daily, morning, or "awakening" headache patterns are soft signs of a sleep disorder. Sleep apnea headache may emerge de novo or may present as an exacerbation of cluster, migraine, tension-type, or other headache. Insomnia is the most prevalent sleep disorder in chronic migraine and tension-type headache, and increases risk for depression and anxiety. Sleep disturbance (e.g., sleep loss, oversleeping, schedule shift) is an acute headache trigger for migraine and tension-type headache. Snoring and sleep disturbance are independent risk factors for progression from episodic to chronic headache.
Al-Biltagi, Mohammed A
Sleep and epilepsy are two well recognized conditions that interact with each other in a complex bi-directional way. Some types of epilepsies have increased activity during sleep disturbing it; while sleep deprivation aggravates epilepsy due to decreased seizure threshold. Epilepsy can deteriorate the sleep-related disorders and at the same time; the parasomnias can worsen the epilepsy. The secretion of sleep-related hormones can also be affected by the occurrence of seizures and supplementation of epileptic patients with some of these sleep-related hormones may have a beneficial role in controlling epilepsy. PMID:25254184
El Shakankiry, Hanan M
Sleep has long been considered as a passive phenomenon, but it is now clear that it is a period of intense brain activity involving higher cortical functions. Overall, sleep affects every aspect of a child’s development, particularly higher cognitive functions. Sleep concerns are ranked as the fifth leading concern of parents. Close to one third of all children suffer from sleep disorders, the prevalence of which is increased in certain pediatric populations, such as children with special needs, children with psychiatric or medical diagnoses and children with autism or pervasive developmental disorders. The paper reviews sleep physiology and the impact, classification, and management of sleep disorders in the pediatric age group. PMID:23616721
Iranzo, Alex; Santamaria, Joan; de Riquer, Martín
In Don Quijote de la Mancha, Miguel de Cervantes presents Don Quixote as an amazing character of the 17th century who suffers from delusions and illusions, believing himself to be a medieval knight errant. Besides this neuropsychiatric condition, Cervantes included masterful descriptions of several sleep disorders such as insomnia, sleep deprivation, disruptive loud snoring and rapid eye movement sleep behaviour disorder. In addition, he described the occurrence of physiological, vivid dreams and habitual, post-prandial sleepiness--the siesta. Cervantes' concept of sleep as a passive state where all cerebral activities are almost absent is in conflict with his description of abnormal behaviours during sleep and vivid, fantastic dreams. His concept of sleep was shared by his contemporary, Shakespeare, and could have been influenced by the reading of the classical Spanish book of psychiatry Examen de Ingenios (1575).
Tamura, Yoshiyuki; Matsuda, Mika; Chiba, Shigeru
Actigraphy is a method that utilizes a miniaturized computerized wristwatch-like device to monitor and collect data generated by body movements over extended periods of time. It allows estimation of sleep and wakefulness based on motor activity. It provides a noninvasive, objective, and longitudinal method for the diagnostic and post-treatment evaluation of patients with sleep disorders in the ambulatory setting. It has been used for researchers to study sleep disturbances in a variety of populations, most frequently for the evaluation of insomnia, paradoxical insomnia, and circadian rhythm sleep disorders. In addition, it is particularly useful in populations where polysomnography would be difficult to record, such as in patients with dementia and delirium. Actigraphy should be extensively carried out in sleep medicine as well as sleep research.
Anderson, James R; Jones, Bryan W; Yang, Jia-Hui; Shaw, Marguerite V; Watt, Carl B; Koshevoy, Pavel; Spaltenstein, Joel; Jurrus, Elizabeth; UV, Kannan; Whitaker, Ross T; Mastronarde, David; Tasdizen, Tolga; Marc, Robert E
Circuitry mapping of metazoan neural systems is difficult because canonical neural regions (regions containing one or more copies of all components) are large, regional borders are uncertain, neuronal diversity is high, and potential network topologies so numerous that only anatomical ground truth can resolve them. Complete mapping of a specific network requires synaptic resolution, canonical region coverage, and robust neuronal classification. Though transmission electron microscopy (TEM) remains the optimal tool for network mapping, the process of building large serial section TEM (ssTEM) image volumes is rendered difficult by the need to precisely mosaic distorted image tiles and register distorted mosaics. Moreover, most molecular neuronal class markers are poorly compatible with optimal TEM imaging. Our objective was to build a complete framework for ultrastructural circuitry mapping. This framework combines strong TEM-compliant small molecule profiling with automated image tile mosaicking, automated slice-to-slice image registration, and gigabyte-scale image browsing for volume annotation. Specifically we show how ultrathin molecular profiling datasets and their resultant classification maps can be embedded into ssTEM datasets and how scripted acquisition tools (SerialEM), mosaicking and registration (ir-tools), and large slice viewers (MosaicBuilder, Viking) can be used to manage terabyte-scale volumes. These methods enable large-scale connectivity analyses of new and legacy data. In well-posed tasks (e.g., complete network mapping in retina), terabyte-scale image volumes that previously would require decades of assembly can now be completed in months. Perhaps more importantly, the fusion of molecular profiling, image acquisition by SerialEM, ir-tools volume assembly, and data viewers/annotators also allow ssTEM to be used as a prospective tool for discovery in nonneural systems and a practical screening methodology for neurogenetics. Finally, this framework
Beyaert, Lisa; Greggers, Uwe; Menzel, Randolf
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.
Carter, Matthew E; Brill, Julia; Bonnavion, Patricia; Huguenard, John R; Huerta, Ramon; de Lecea, Luis
Current models of sleep/wake regulation posit that Hypocretin (Hcrt)-expressing neurons in the lateral hypothalamus promote and stabilize wakefulness by projecting to subcortical arousal centers. However, the critical downstream effectors of Hcrt neurons are unknown. Here we use optogenetic, pharmacological, and computational tools to investigate the functional connectivity between Hcrt neurons and downstream noradrenergic neurons in the locus coeruleus (LC) during nonrapid eye movement (NREM) sleep. We found that photoinhibiting LC neurons during Hcrt stimulation blocked Hcrt-mediated sleep-to-wake transitions. In contrast, when LC neurons were optically stimulated to increase membrane excitability, concomitant photostimulation of Hcrt neurons significantly increased the probability of sleep-to-wake transitions compared with Hcrt stimulation alone. We also built a conductance-based computational model of Hcrt-LC circuitry that recapitulates our behavioral results using LC neurons as the main effectors of Hcrt signaling. These results establish the Hcrt-LC connection as a critical integrator-effector circuit that regulates NREM sleep/wake behavior during the inactive period. This coupling of distinct neuronal systems can be generalized to other hypothalamic integrator nuclei with downstream effector/output populations in the brain.
Amici, R; Bastianini, S; Berteotti, C; Cerri, M; Del Vecchio, F; Lo Martire, V; Luppi, M; Perez, E; Silvani, A; Zamboni, G; Zoccoli, G
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.
Martinez, Jacqueline; Cowings, Patricia S.; Toscano, William B.
In space, astronauts may experience effects of cumulative sleep loss due to demanding work schedules that can result in cognitive performance impairments, mood state deteriorations, and sleep-wake cycle disruption. Individuals who experience sleep deprivation of six hours beyond normal sleep times experience detrimental changes in their mood and performance states. Hence, the potential for life threatening errors increases exponentially with sleep deprivation. We explored the effects of 36-hours of sleep deprivation on cognitive performance, mood states, and physiological responses to identify which metrics may best predict fatigue induced performance decrements of individuals.
Diambra, L.; Malta, C. P.; Capurro, A.
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.
Schwartz, Michael D; Nguyen, Alexander T; Warrier, Deepti R; Palmerston, Jeremiah B; Thomas, Alexia M; Morairty, Stephen R; Neylan, Thomas C; Kilduff, Thomas S
Hypocretin 1 and 2 (Hcrts; also known as orexin A and B), excitatory neuropeptides synthesized in cells located in the tuberal hypothalamus, play a central role in the control of arousal. Hcrt inputs to the locus coeruleus norepinephrine (LC NE) system and the posterior hypothalamic histaminergic tuberomammillary nuclei (TMN HA) are important efferent pathways for Hcrt-induced wakefulness. The LC expresses Hcrt receptor 1 (HcrtR1), whereas HcrtR2 is found in the TMN. Although the dual Hcrt/orexin receptor antagonist almorexant (ALM) decreases wakefulness and increases NREM and REM sleep time, the neural circuitry that mediates these effects is currently unknown. To test the hypothesis that ALM induces sleep by selectively disfacilitating subcortical wake-promoting populations, we ablated LC NE neurons (LCx) or TMN HA neurons (TMNx) in rats using cell-type-specific saporin conjugates and evaluated sleep/wake following treatment with ALM and the GABAA receptor modulator zolpidem (ZOL). Both LCx and TMNx attenuated the promotion of REM sleep by ALM without affecting ALM-mediated increases in NREM sleep. Thus, eliminating either HcrtR1 signaling in the LC or HcrtR2 signaling in the TMN yields similar effects on ALM-induced REM sleep without affecting NREM sleep time. In contrast, neither lesion altered ZOL efficacy on any measure of sleep-wake regulation. These results contrast with those of a previous study in which ablation of basal forebrain cholinergic neurons attenuated ALM-induced increases in NREM sleep time without affecting REM sleep, indicating that Hcrt neurotransmission influences distinct aspects of NREM and REM sleep at different locations in the sleep-wake regulatory network.
Phillips, A. J. K.; Robinson, P. A.
A physiologically based model of the mechanisms that control the human sleep-wake cycle is formulated in terms of an equivalent nonconservative mechanical potential. The potential is analytically simplified and reduced to a quartic two-well potential, matching the bifurcation structure of the original model. This yields a dynamics-based model that is analytically simpler and has fewer parameters than the original model, allowing easier fitting to experimental data. This model is first demonstrated to semiquantitatively match the dynamics of the physiologically based model from which it is derived, and is then fitted directly to a set of experimentally derived criteria. These criteria place rigorous constraints on the parameter values, and within these constraints the model is shown to reproduce normal sleep-wake dynamics and recovery from sleep deprivation. Furthermore, this approach enables insights into the dynamics by direct analogies to phenomena in well studied mechanical systems. These include the relation between friction in the mechanical system and the timecourse of neurotransmitter action, and the possible relation between stochastic resonance and napping behavior. The model derived here also serves as a platform for future investigations of sleep-wake phenomena from a dynamical perspective.
Morris, Christopher J.; Aeschbach, Daniel; Scheer, Frank A.J.L.
Levels of numerous hormones vary across the day and night. Such fluctuations are not only attributable to changes in sleep/wakefulness and other behaviors but also to a biological timing system governed by the suprachiasmatic nucleus of the hypothalamus. Sleep has a strong effect on levels of some hormones such as growth hormone but little effect on others which are more strongly regulated by the biological timing system (e.g., melatonin). Whereas the exact mechanisms through which sleep affects circulating hormonal levels are poorly understood, more is known about how the biological timing system influences the secretion of hormones. The suprachiasmatic nucleus exerts its influence on hormones via neuronal and humoral signals but it is also now apparent that peripheral cells can rhythmically secrete hormones independent of signals from the suprachiasmatic nucleus. Under normal circumstances, behaviors and the biological timing system are synchronized and consequently hormonal systems are exquisitely regulated. However, many individuals (e.g., shift-workers) frequently undergo circadian misalignment by desynchronizing their sleep/wake cycle from the biological timing system. Recent experiments indicate that circadian misalignment has an adverse effect on metabolic and hormonal factors such as glucose and insulin. Further research is needed to determine the underlying mechanisms that cause the negative effects induced by circadian misalignment. Such research could aid the development of countermeasures for circadian misalignment. PMID:21939733
Forlano, Paul M.; Kim, Spencer D.; Krzyminska, Zuzanna M.; Sisneros, Joseph A.
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
Vandrey, Ryan; Smith, Michael T.; McCann, Una D.; Budney, Alan J.; Curran, Erin M.
Background Sleep difficulty is a common symptom of cannabis withdrawal, but little research has objectively measured sleep or explored the effects of hypnotic medication on sleep during cannabis withdrawal. Methods Twenty daily cannabis users completed a within-subject crossover study. Participants alternated between periods of ad-libitum cannabis use and short-term cannabis abstinence (3 days). Placebo was administered at bedtime during one abstinence period (withdrawal test) and extended-release zolpidem, a non-benzodiazepine GABAA receptor agonist, was administered during the other. Polysomnographic (PSG) sleep architecture measures, subjective ratings, and cognitive performance effects were assessed each day. Results During the placebo-abstinence period, participants had decreased sleep efficiency, total sleep time, percent time spent in Stage 1 and Stage 2 sleep, REM latency and subjective sleep quality, as well as increased sleep latency and time spent in REM sleep compared with when they were using cannabis. Zolpidem attenuated the effects of abstinence on sleep architecture and normalized sleep efficiency scores, but had no effect on sleep latency. Zolpidem was not associated with any significant side effects or next-day cognitive performance impairments. Conclusions These data extend prior research that indicates abrupt abstinence from cannabis can lead to clinically significant sleep disruption in daily users. The findings also indicate that sleep disruption associated with cannabis withdrawal can be attenuated by zolpidem, suggesting that hypnotic medications might be useful adjunct pharmacotherapies in the treatment of cannabis use disorders. PMID:21296508
Sturm, Anna; Czisch, Michael; Spoormaker, Victor I
Impaired fear extinction and disturbed sleep coincide in post-traumatic stress disorder (PTSD), but the nature of this relationship is unclear. Rapid eye movement (REM) sleep deprivation impairs fear extinction recall in rodents and young healthy subjects, and animal models have demonstrated both disrupted sleep after fear conditioning and normalized sleep after extinction learning. As a correlation between unconditioned stimulus (US) responding and subsequent sleep architecture has been observed in healthy subjects, the goal of this study was to test whether US intensity would causally affect subsequent sleep. Twenty-four young healthy subjects underwent a fear conditioning session with skin conductance response measurements before an afternoon session of polysomnographically recorded sleep (up to 120 min) in the sleep laboratory. Two factors were manipulated experimentally in a 2 × 2 design: US (electrical shock) was set at high or low intensity, and subjects did or did not receive an extinction session after fear conditioning. We observed that neither factor affected REM sleep amount, that high US intensity nominally increased sleep fragmentation (more Stage 1 sleep, stage shifts and wake after sleep onset), and that extinction increased Stage 4 amount. Moreover, reduced Stage 1 and increased Stage 4 and REM sleep were associated with subjective sleep quality of the afternoon nap. These results provide evidence for the notion that US intensity and extinction affect subsequent sleep architecture in young healthy subjects, which may provide a translational bridge from findings in animal studies to correlations observed in PTSD patients.
Verhaert, Vincent; Haex, Bart; De Wilde, Tom; Berckmans, Daniel; Verbraecken, Johan; de Valck, Elke; Vander Sloten, Jos
This study combines concepts of bed design and sleep registrations to investigate how quality of spine support affects the manifestation of sleep in healthy subjects. Altogether, 17 normal sleepers (nine males, eight females; age 24.3±7.1 years) participated in an anthropometric screening, prior to the actual sleep experiments, during which personalised sleep system settings were determined according to individual body measures. Sleep systems (i.e. mattress and supporting structure) with an adjustable stiffness distribution were used. Subjects spent three nights of 8 h in bed in the sleep laboratory in a counterbalanced order (adaptation, personalised support and sagging support). During these nights, polysomnography was performed. Subjective sleep data were gathered by means of questionnaires. Results show that individual posture preferences are a determinant factor in the extent that subjects experience a negative effect while sleeping on a sagging sleep system. STATEMENT OF RELEVANCE: This study investigated how spine support affects sleep in healthy subjects, finding that the relationship between bedding and sleep quality is affected by individual anthropometry and sleep posture. In particular, results indicate that a sagging sleep system negatively affects sleep quality for people sleeping in a prone or lateral posture.
Sassin, J. F.; Weitzman, E. D.; Kapen, S.; Frantz, A. G.
Human prolactin was measured in plasma by radioimmunoassay at 20-minute intervals for a 24-hour period in each of six normal adults, whose sleep-wake cycles were monitored polygraphically. A marked diurnal variation in plasma concentrations was demonstrated, with highest values during sleep. Periods of episodic release occurred throughout the 24 hours.
Astronauts Kathryn D. Sullivan, left, and Sally K. Ride display a 'bag of worms'. The 'bag' is a sleep restraint and the majority of the 'worms' are springs and clips used with the sleep restraint in its normal application. Clamps, a bungee cord and velcro strips are other recognizable items in the 'bag'.
Buxton, Orfeu M.; Cain, Sean W.; O’Connor, Shawn P.; Porter, James H.; Duffy, Jeanne F.; Wang, Wei; Czeisler, Charles A.; Shea, Steven A.
Epidemiological studies link short sleep and circadian disruption with risk of metabolic syndrome and diabetes. We tested the hypotheses that prolonged sleep restriction with concurrent circadian disruption, as can occur with shift work, impairs glucose regulation and metabolism. Healthy adults spent >5 weeks in controlled laboratory conditions including: sleep extension (baseline), 3-week sleep restriction (5.6 h sleep/24 h) combined with circadian disruption (recurring 28-h ‘days’), and 9-day recovery sleep with circadian re-entrainment. Prolonged sleep restriction with concurrent circadian disruption significantly decreased resting metabolic rate, and increased postprandial plasma via inadequate pancreatic beta cell responsivity; these normalized with 9 days of recovery sleep and stable circadian reentrainment. Thus, in humans, prolonged sleep restriction with concurrent circadian disruption alters metabolism and could increase risk of obesity and diabetes. PMID:22496545
Swanson, Larry W.
The basic plan of nervous system organization has been investigated since classical antiquity. The first model centered on pneumas pumped from sensory nerves through the ventricular system and out motor nerves to muscles. It was popular well into the seventeenth century and diverted attention from the organization of brain parenchyma itself. Willis focused on gray matter production and white matter conduction of pneumas in 1664, and by the late nineteenth century a clear cellular model of nervous system organization based on sensory, motor, and association neuron classes transmitting nerve impulses was elaborated by Cajal and his contemporaries. Today, revolutionary advances in experimental pathway tracing methods, molecular genetics, and computer science inspire systems neuroscience. Seven minimal requirements are outlined for knowledge management systems capable of describing, analyzing, and modeling the basic plan of nervous system circuitry in general, and the plan evolved for vertebrates, for mammals, and ultimately for humans in particular. The goal remains a relatively simple, easy to understand model analogous to the one Harvey elaborated in 1628 for circulation in the cardiovascular system. As Cajal wrote in 1909, “To extend our understanding of neural function to the most complex human physiological and psychological activities, it is essential that we first generate a clear and accurate view of the structure of the relevant centers, and of the human brain itself, so that the basic plan—the overview—can be grasped in the blink of an eye.” PMID:17267046
Li, Yue; Liberal, Iñigo; Della Giovampaola, Cristian; Engheta, Nader
Engineering optical nanocircuits by exploiting modularization concepts and methods inherited from electronics may lead to multiple innovations in optical information processing at the nanoscale. We introduce the concept of “waveguide metatronics,” an advanced form of optical metatronics that uses structural dispersion in waveguides to obtain the materials and structures required to construct this class of circuitry. Using numerical simulations, we demonstrate that the design of a metatronic circuit can be carried out by using a waveguide filled with materials with positive permittivity. This includes the implementation of all “lumped” circuit elements and their assembly in a single circuit board. In doing so, we extend the concepts of optical metatronics to frequency ranges where there are no natural plasmonic materials available. The proposed methodology could be exploited as a platform to experimentally validate optical metatronic circuits in other frequency regimes, such as microwave frequency setups, and/or to provide a new route to design optical nanocircuitry. PMID:27386566
Petrovich, Gorica D.
Appetite and eating are not only controlled by energy needs, but also by extrinsic factors that are not directly related to energy balance. Environmental signals that acquire motivational properties through associative learning—learned cues—can override homeostatic signals and stimulate eating in sated states, or inhibit eating in states of hunger. Such influences are important, as environmental factors are believed to contribute to the increased susceptibility to overeating and the rise in obesity in the developed world. Similarly, environmental and social factors contribute to the onset and maintenance of anorexia nervosa and other eating disorders through interactions with the individual genetic background. Nevertheless, how learning enables environmental signals to control feeding, and the underlying brain mechanisms are poorly understood. We developed two rodent models to study how learned cues are integrated with homeostatic signals within functional forebrain networks, and how these networks are modulated by experience. In one model, a cue previously paired with food when an animal was hungry induces eating in sated rats. In the other model, food-deprived rats inhibit feeding when presented with a cue that signals danger, a tone previously paired with footshocks. Here evidence will be reviewed that the forebrain network formed by the amygdala, lateral hypothalamus and medial prefrontal cortex mediates cue-driven feeding, while a parallel amygdalar circuitry mediates suppression of eating by the fear cue. Findings from the animal models may be relevant for understanding aspects of human appetite and eating, and maladaptive mechanisms that could lead to overeating and anorexia. PMID:21549730
Swanson, Larry W
The basic plan of nervous system organization has been investigated since classical antiquity. The first model centered on pneumas pumped from sensory nerves through the ventricular system and out motor nerves to muscles. It was popular well into the 17th century and diverted attention from the organization of brain parenchyma itself. Willis focused on gray matter production and white matter conduction of pneumas in 1664, and by the late 19th century a clear cellular model of nervous system organization based on sensory, motor, and association neuron classes transmitting nerve impulses was elaborated by Cajal and his contemporaries. Today, revolutionary advances in experimental pathway tracing methods, molecular genetics, and computer science inspire systems neuroscience. Seven minimal requirements are outlined for knowledge management systems capable of describing, analyzing, and modeling the basic plan of nervous system circuitry in general, and the plan evolved for vertebrates, for mammals, and ultimately for humans in particular. The goal remains a relatively simple, easy to understand model analogous to the one Harvey elaborated in 1628 for blood circulation in the cardiovascular system. As Cajal wrote in 1909, "To extend our understanding of neural function to the most complex human physiological and psychological activities, it is essential that we first generate a clear and accurate view of the structure of the relevant centers, and of the human brain itself, so that the basic plan--the overview--can be grasped in the blink of an eye."
Russell, Ronan; Ilg, Marcus; Lin, Qiong; Wu, Guangming; Lechel, André; Bergmann, Wendy; Eiseler, Tim; Linta, Leonhard; Kumar P., Pavan; Klingenstein, Moritz; Adachi, Kenjiro; Hohwieler, Meike; Sakk, Olena; Raab, Stefanie; Moon, Anne; Zenke, Martin; Seufferlein, Thomas; Schöler, Hans R.; Illing, Anett; Liebau, Stefan; Kleger, Alexander
Summary Pluripotency represents a cell state comprising a fine-tuned pattern of transcription factor activity required for embryonic stem cell (ESC) self-renewal. TBX3 is the earliest expressed member of the T-box transcription factor family and is involved in maintenance and induction of pluripotency. Hence, TBX3 is believed to be a key member of the pluripotency circuitry, with loss of TBX3 coinciding with loss of pluripotency. We report a dynamic expression of TBX3 in vitro and in vivo using genetic reporter tools tracking TBX3 expression in mouse ESCs (mESCs). Low TBX3 levels are associated with reduced pluripotency, resembling the more mature epiblast. Notably, TBX3-low cells maintain the intrinsic capability to switch to a TBX3-high state and vice versa. Additionally, we show TBX3 to be dispensable for induction and maintenance of naive pluripotency as well as for germ cell development. These data highlight novel facets of TBX3 action in mESCs. PMID:26651606
Petrovich, Gorica D
Appetite and eating are not only controlled by energy needs, but also by extrinsic factors that are not directly related to energy balance. Environmental signals that acquire motivational properties through associative learning-learned cues-can override homeostatic signals and stimulate eating in sated states, or inhibit eating in states of hunger. Such influences are important, as environmental factors are believed to contribute to the increased susceptibility to overeating and the rise in obesity in the developed world. Similarly, environmental and social factors contribute to the onset and maintenance of anorexia nervosa and other eating disorders through interactions with the individual genetic background. Nevertheless, how learning enables environmental signals to control feeding, and the underlying brain mechanisms are poorly understood. We developed two rodent models to study how learned cues are integrated with homeostatic signals within functional forebrain networks, and how these networks are modulated by experience. In one model, a cue previously paired with food when an animal was hungry induces eating in sated rats. In the other model, food-deprived rats inhibit feeding when presented with a cue that signals danger, a tone previously paired with footshocks. Here evidence will be reviewed that the forebrain network formed by the amygdala, lateral hypothalamus and medial prefrontal cortex mediates cue-driven feeding, while a parallel amygdalar circuitry mediates suppression of eating by the fear cue. Findings from the animal models may be relevant for understanding aspects of human appetite and eating, and maladaptive mechanisms that could lead to overeating and anorexia.
De Dreu, Carsten K W; Baas, Matthijs; Roskes, Marieke; Sligte, Daniel J; Ebstein, Richard P; Chew, Soo Hong; Tong, Terry; Jiang, Yushi; Mayseless, Naama; Shamay-Tsoory, Simone G
Creativity enables humans to adapt flexibly to changing circumstances, to manage complex social relations and to survive and prosper through social, technological and medical innovations. In humans, chronic, trait-based as well as temporary, state-based approach orientation has been linked to increased capacity for divergent rather than convergent thinking, to more global and holistic processing styles and to more original ideation and creative problem solving. Here, we link creative cognition to oxytocin, a hypothalamic neuropeptide known to up-regulate approach orientation in both animals and humans. Study 1 (N = 492) showed that plasma oxytocin predicts novelty-seeking temperament. Study 2 (N = 110) revealed that genotype differences in a polymorphism in the oxytocin receptor gene rs1042778 predicted creative ideation, with GG/GT-carriers being more original than TT-carriers. Using double-blind placebo-controlled between-subjects designs, Studies 3-6 (N = 191) finally showed that intranasal oxytocin (vs matching placebo) reduced analytical reasoning, and increased holistic processing, divergent thinking and creative performance. We conclude that the oxytonergic circuitry sustains and enables the day-to-day creativity humans need for survival and prosperity and discuss implications.
Bryant, Richard A; Das, Pritha
Little is understood about neural networks associated with conversion disorders. This case study reports the first investigation of the neural circuitry associated with the recovery of chronic conversion disorder. A patient with a four year history of hysterical mutism was assessed with functional MRI (fMRI) during a vocalization task, and then provided psychotherapy that attempted to reduce motivational factors that maintained mutism. The patient resumed full speech, and was readministered the fMRI vocalization task. Vocalization during mutism and following recovery of speech resulted in increases in speech-related networks, including the inferior frontal gyrus (IFG), middle frontal, and supplementary motor area of the frontal cortex, temporal and parietal cortices, and also in the primary and sensory motor regions. Following speech recovery but not during mutism, the IFG was correlated positively with the anterior cingulate cortex and negatively with the amygdala. This pattern suggests that during the conversion disorder there was impaired connectivity between speech networks and networks that regulate anxiety.
Katz, Paul S.; Calin-Jageman, Robert; Dhawan, Akshaye; Frederick, Chad; Guo, Shuman; Dissanayaka, Rasanjalee; Hiremath, Naveen; Ma, Wenjun; Shen, Xiuyn; Wang, Hsui C.; Yang, Hong; Prasad, Sushil; Sunderraman, Rajshekhar; Zhu, Ying
The basic unit of any nervous system is the neuron. Therefore, understanding the operation of nervous systems ultimately requires an inventory of their constituent neurons and synaptic connectivity, which form neural circuits. The presence of uniquely identifiable neurons or classes of neurons in many invertebrates has facilitated the construction of cellular-level connectivity diagrams that can be generalized across individuals within a species. Homologous neurons can also be recognized across species. Here we describe NeuronBank.org, a web-based tool that we are developing for cataloging, searching, and analyzing neuronal circuitry within and across species. Information from a single species is represented in an individual branch of NeuronBank. Users can search within a branch or perform queries across branches to look for similarities in neuronal circuits across species. The branches allow for an extensible ontology so that additional characteristics can be added as knowledge grows. Each entry in NeuronBank generates a unique accession ID, allowing it to be easily cited. There is also an automatic link to a Wiki page allowing an encyclopedic explanation of the entry. All of the 44 previously published neurons plus one previously unpublished neuron from the mollusc, Tritonia diomedea, have been entered into a branch of NeuronBank as have 4 previously published neurons from the mollusc, Melibe leonina. The ability to organize information about neuronal circuits will make this information more accessible, ultimately aiding research on these important models. PMID:20428500
... about getting enough sleep. You learn to change negative thoughts and beliefs about sleep into positive thoughts ... problems, such as anxiety or depression . Loss of social support . Alcohol use (drinking). Side effects of medicines. Conditions ...
Vigeta, Sônia Maria Garcia; Hachul, Helena; Tufik, Sergio; de Oliveira, Eleonora Menicucci
The aim of this study was to identify factors that most influence the perception of sleep quality in postmenopausal women. We used the methodological strategy of the Collective Subject Discourse (CSD), which is based on a theoretical framework of social representations theory. We obtained the data by interviewing 22 postmenopausal Brazilian women who were experiencing insomnia. The women gave accounts of their difficulties with sleep; a variety of dimensions were identified within the data. The onset of sleep disorders might have occurred during childhood or in situations considered to be stressful, and were not necessarily associated with menopause. We found that hormonal alterations occurring during menopause, psychosocial factors, and sleep-breathing disorders triggered occasional sleep disturbances during this time of life. Participants were aware of the consequences of sleep deprivation. In addition, inadequate sleep hygiene habits figured prominently as determinants in the persistence of sleep disturbances.
... to locate sleep centers in your area. Search radius (in miles): 10 25 50 Share: Essentials in ... to locate sleep centers in your area. Search radius: Treatment & Therapy CPAP Titration Study This type of ...
... this page: //medlineplus.gov/ency/article/004018.htm Aging changes in sleep To use the sharing features ... cycle is repeated several times during the night. AGING CHANGES With aging, sleep patterns tend to change. ...
... medlineplus.gov/ency/patientinstructions/000872.htm Teenagers and sleep To use the sharing features on this page, ... need. What Makes it Hard for Teens to Sleep? Several factors make it hard for teens to ...
... the sleep-wake process and our circadian biologic clock -- regulate our sleep. They program our bodies to ... on the time spent awake. Our circadian biologic clock is a 24-hour body rhythm affected by ...
... 12-Month-Old Bed-Sharing All About Sleep Sleep and Your 1- to 2-Year-Old Communication and Your Newborn Medical Care and Your Newborn Your Newborn's Growth Choosing Safe Baby Products: Cribs Flat Head Syndrome ( ...
Allison, Kelly C; Spaeth, Andrea; Hopkins, Christina M
Insomnia is related to an increased risk of eating disorders, while eating disorders are related to more disrupted sleep. Insomnia is also linked to poorer treatment outcomes for eating disorders. However, over the last decade, studies examining sleep and eating disorders have relied on surveys, with no objective measures of sleep for anorexia nervosa or bulimia nervosa, and only actigraphy data for binge eating disorder. Sleep disturbance is better defined for night eating syndrome, where sleep efficiency is reduced and melatonin release is delayed. Studies that include objectively measured sleep and metabolic parameters combined with psychiatric comorbidity data would help identify under what circumstances eating disorders and sleep disturbance produce an additive effect for symptom severity and for whom poor sleep would increase risk for an eating disorder. Cognitive behavior therapy for insomnia may be a helpful addition to treatment of those with both eating disorder and insomnia.
Sleep and Health (0:36) Dr. Orfeu Buxton describes how animal and human studies suggest that adequate sleep is crucial for a long and healthy life. choose settings to watch video: Windows Media Player - high | low ...
Tarullo, Amanda R; Balsam, Peter D; Fifer, William P
Human neonates spend the majority of their time sleeping. Despite the limited waking hours available for environmental exploration, the first few months of life are a time of rapid learning about the environment. The organization of neonate sleep differs qualitatively from adult sleep, and the unique characteristics of neonatal sleep may promote learning. Sleep contributes to infant learning in multiple ways. First, sleep facilitates neural maturation, thereby preparing infants to process and explore the environment in increasingly sophisticated ways. Second, sleep plays a role in memory consolidation of material presented while the infant was awake. Finally, emerging evidence indicates that infants process sensory stimuli and learn about contingencies in their environment even while asleep. As infants make the transition from reflexive to cortically mediated control, learned responses to physiological challenges during sleep may be critical adaptations to promote infant survival.
Nedelcovych, Michael T; Gould, Robert W; Zhan, Xiaoyan; Bubser, Michael; Gong, Xuewen; Grannan, Michael; Thompson, Analisa T; Ivarsson, Magnus; Lindsley, Craig W; Conn, P Jeffrey; Jones, Carrie K
Hyperarousal and sleep disturbances are common, debilitating symptoms of post-traumatic stress disorder (PTSD). PTSD patients also exhibit abnormalities in quantitative electroencephalography (qEEG) power spectra during wake as well as rapid eye movement (REM) and non-REM (NREM) sleep. Selective serotonin reuptake inhibitors (SSRIs), the first-line pharmacological treatment for PTSD, provide modest remediation of the hyperarousal symptoms in PTSD patients, but have little to no effect on the sleep-wake architecture deficits. Development of novel therapeutics for these sleep-wake architecture deficits is limited by a lack of relevant animal models. Thus, the present study investigated whether single prolonged stress (SPS), a rodent model of traumatic stress, induces PTSD-like sleep-wake and qEEG spectral power abnormalities that correlate with changes in central serotonin (5-HT) and neuropeptide Y (NPY) signaling in rats. Rats were implanted with telemetric recording devices to continuously measure EEG before and after SPS treatment. A second cohort of rats was used to measure SPS-induced changes in plasma corticosterone, 5-HT utilization, and NPY expression in brain regions that comprise the neural fear circuitry. SPS caused sustained dysregulation of NREM and REM sleep, accompanied by state-dependent alterations in qEEG power spectra indicative of cortical hyperarousal. These changes corresponded with acute induction of the corticosterone receptor co-chaperone FK506-binding protein 51 and delayed reductions in 5-HT utilization and NPY expression in the amygdala. SPS represents a preclinical model of PTSD-related sleep-wake and qEEG disturbances with underlying alterations in neurotransmitter systems known to modulate both sleep-wake architecture and the neural fear circuitry.
Wilhelm, Ines; Metzkow-Meszaros, Maila; Knapp, Susanne; Born, Jan
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…
Berryman, Matthew J.; Coussens, Scott W.; Pamula, Yvonne; Kennedy, Declan; Lushington, Kurt; Shalizi, Cosma; Allison, Andrew; Martin, A. James; Saint, David; Abbott, Derek
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.
Sulman, Cecille G.
Adenotonsillectomy is the most common surgery performed for sleep disordered breathing with good outcomes. Children with obesity, craniofacial disorders, and neurologic impairment are at risk for persistent sleep apnea after adenotonsillectomy. Techniques exist to address obstructive lesions of the palate, tongue base, or craniofacial skeleton in children with persistent sleep apnea. Children with obstructive sleep apnea have a higher rate of peri-operative complications. PMID:24926473
Adey, W. R.
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.
112. 17 D. C. Kay, R. B. Eisenstein and D. R. Jasinski, Morphine effects on human REM state, waking state, and NREM sleep . Psychopharmacologia, 14...recording days. The EEG state data showed an increase in waking and decrease in both slow wave and REM sleep during acute heroin withdrawal. Total sleep ...was maximally suppressed on withdrawal days 2 and 3 and was still below normal control values on with- drawal days 5 - 7. REM sleep was more
Pelayo, Rafael; Yuen, Kin
This article reviews common sleep disorders in children and pharmacologic options for them. Discussions of pediatric sleep pharmacology typically focus on treatment of insomnia. Although insomnia is a major concern in this population, other conditions of concern in children are presented, such as narcolepsy, parasomnias, restless legs syndrome, and sleep apnea.
... use the bed only for sleep Discourage watching television during periods of wakefulness Medications for sleep changes In some cases, non-drug approaches fail to work or the sleep changes are accompanied by disruptive nighttime behaviors. For those individuals who do require medication, experts ...
Carley, David W; Farabi, Sarah S
IN BRIEF Far from a simple absence of wakefulness, sleep is an active, regulated, and metabolically distinct state, essential for health and well-being. In this article, the authors review the fundamental anatomy and physiology of sleep and its regulation, with an eye toward interactions between sleep and metabolism.
Giganti, F; Zilli, I; Aboudan, S; Salzarulo, P
This chapter will discuss the relationship between yawning, sleep onset, awakening and sleepiness. Models concerning wake-sleep regulation will be discussed in relation to yawning. Yawning close to sleep, before and after, will be examined in several conditions and populations. Also, the time course of yawning and sleepiness assessed by subjective estimates will be described.
... Old Feeding Your 1- to 2-Year-Old Sleep and Your Preschooler KidsHealth > For Parents > Sleep and Your Preschooler A A A What's in ... Preschoolers need about 11 to 12 hours of sleep each day, which can include a nap. There's ...
... Get Enough Sleep There are many reasons why sleep is in such short supply. Busy schedules. Evening activities, whether it is ... inflammation, two things that can damage your heart. Obesity . When you do not get enough rest from sleep, you are more prone to overeat. It is ...
... eye movement) sleep. These stages progress in a cycle from stage 1 to REM sleep, then the cycle starts over again with stage 1 ( see figure ... minutes after we fall asleep. A complete sleep cycle takes 90 to 110 minutes on average. The ...
Segal, J.D.; Kenney, C.J.; Parker, S.I.; Aw, C.H.; Snoeys, W.J.; Wooley, B.; Plummer, J.D.; /Stanford U., Elect. Eng. Dept.
A second-generation monolithic silicon radiation sensor has been built and characterized. This pixel detector has CMOS circuitry fabricated directly in the high-resistivity floatzone substrate. The bulk is fully depleted from bias applied to the backside diode. Within the array, PMOS pixel circuitry forms the first stage amplifiers. Full CMOS circuitry implementing further amplification as well as column and row logic is located in the periphery of the pixel array. This allows a sparse-field readout scheme where only pixels with signals above a certain threshold are readout. We describe the fabrication process, circuit design, system performance, and results of gamma-ray radiation tests.
Ross, R J; Ball, W A; Dinges, D F; Kribbs, N B; Morrison, A R; Silver, S M; Mulvaney, F D
A subjective disturbance of sleep, including the occurrence of repetitive, stereotypical anxiety dreams, is characteristic of posttraumatic stress disorder (PTSD). The phenomenology of the PTSD anxiety dream has seemed most consistent with an underlying rapid eye movement (REM) sleep dysfunction. However, motor behavior reportedly can accompany PTSD dreams, and normal REM sleep typically involves a nearly total paralysis of the body musculature. As a means of understanding this discrepancy, anterior tibialis muscle activity during sleep was studied in a group of Vietnam combat veterans with current PTSD and in an age-matched normal control group. The PTSD subjects had a higher percentage of REM sleep epochs with at least one prolonged twitch burst; they also were more likely to have periodic limb movements in sleep, during nonrapid eye movement sleep. Both these forms of muscle activation also have been observed in REM behavior disorder (RBD), a parasomnia characterized by the actual enactment of dream sequences during REM sleep. The identification of RBD-like signs in PTSD adds to the evidence for a fundamental disturbance of REM sleep phasic mechanisms in PTSD.
Deschenes, Cynthia L.; McCurry, Susan M.
Sleep disturbances are widespread among older adults. Degenerative neurologic disorders that cause dementia, such as Alzheimer's disease and Parkinson's disease, exacerbate age-related changes in sleep, as do many common comorbid medical and psychiatric conditions. Medications used to treat chronic illness and insomnia have many side effects that can further disrupt sleep and place patients at risk for injury. This article reviews the neurophysiology of sleep in normal aging and sleep changes associated with common dementia subtypes and comorbid conditions. Current pharmacologic and nonpharmacologic evidence-based treatment options are discussed, including the use of light therapy, increased physical and social activity, and multicomponent cognitive-behavioral interventions for improving sleep in institutionalized and community-dwelling adults with dementia. PMID:19187704
Nicholson, Anthony N.; Pascoe, Peta A.; Spencer, Michael B.; Stone, Barbara M.; Green, Roger L.
The nocturnal sleep and daytime alertness of aircrew were studied by electroencephalography and the multiple sleep latency test. After a transmeridian flight from London To San Francisco, sleep onset was faster and, although there was increased wakefulness during the second half of the night, sleep duration and efficiency over the whole night were not changed. The progressive decrease in sleep latencies observed normally in the multiple sleep latency test during the morning continued throughout the day after arrival. Of the 13 subjects, 12 took a nap of around 1-h duration in the afternoon preceding the return flight. These naps would have been encouraged by the drowsiness at this time and facilitated by the departure of the aircraft being scheduled during the early evening. An early evening departure had the further advantage that the circadian increase in vigilance expected during the early part of the day would occur during the latter part of the return flight.
Colrain, Ian M; Baker, Fiona C
Adolescence is marked by dramatic changes in sleep. Older adolescents go to bed later, have an increased preference for evening activities, and sleep less than younger adolescents. This behavior change is driven by external factors, notably increased pressures from academic, social, and extracurricular activities and by biological circadian factors. There are also substantial changes in sleep architecture across adolescence, with dramatic declines in slow wave sleep, and slow wave activity (delta, ~ 0.5-4.5 Hz). These changes are associated with underlying changes in brain structure and organization, with a decrease in synaptic density likely underlying the reduction in high amplitude slow waveforms. While changes in sleep across adolescence are a normal part of development, many adolescents are getting insufficient sleep and are consequently, less likely to perform well at school, more likely to develop mood-related disturbances, be obese, and are at greater risk for traffic accidents, alcohol and drug abuse.
Díaz-Muñoz, M; Hernández-Muñoz, R; Suárez, J; Vidrio, S; Yááñez, L; Aguilar-Roblero, R; Rosenthal, L; Villalobos, L; Fernández-Cancino, F; Drucker-Colín, R; Chagoya De Sanchez, V
Blood adenosine metabolism, including metabolites and metabolizing enzymes, was studied during the sleep period in human volunteers. Searching for significant correlations among biochemical parameters found: adenosine with state 1 of slow-wave sleep (SWS); activity of 5'-nucleotidase with state 2 of SWS; inosine and AMP with state 3-4 of SWS; and activity of 5'-nucleotidase and lactate with REM sleep. The correlations were detected in all of the subjects that presented normal hypnograms, but not in those who had fragmented sleep the night of the experiment. The data demonstrate that it is possible to obtain information of complex brain operations such as sleep by measuring biochemical parameters in blood. The results strengthen the notion of a role played by adenosine, its metabolites and metabolizing enzymes, during each of the stages that constitute the sleep process in humans.
Li, Junxin; Gooneratne, Nalaka
Insomnia and other sleep complaints are highly prevalent in community-dwelling older adults yet often go under detected. Age-related physiological changes may affect sleep, but sleep disturbances and complaints should not be considered normal in this population. Various physiological, psychological, and social consequences have been associated with insomnia and sleep complaints. Treatment options are available so it is imperative to diagnose and treat these individuals to promote healthy aging. Exercise is known to have a wide variety of health benefits, but unfortunately most older adults engage in less exercise with advancing age. This paper describes age-related changes in sleep, clinical correlates of insomnia, consequences of untreated insomnia, and nonpharmacological treatments for insomnia in older adults, with a focus on the relationship between exercise and sleep in community-dwelling older adults with insomnia or sleep complaints. Possible mechanisms explaining the relationship between exercise and sleep are discussed. While the research to date shows promising evidence for exercise as a safe and effective treatment for insomnia and sleep complaints in community-dwelling older adults, future research is needed before exercise can be a first-line treatment for insomnia and sleep complaints in this population. PMID:27088071
Martin, B J
Acute loss of sleep produces few apparent physiological effects at rest. Nevertheless, many anecdotes suggest that adequate sleep is essential for optimum endurance athletic performance. To investigate this question, heavy exercise performance after 36 h without sleep was compared with that after normal sleep in eight subjects. During prolonged treadmill walking at about 80% of the VO2 max, sleep loss reduced work time to exhaustion by an average of 11% (p = 0.05). This decrease occurred despite doubling monetary incentives for subjects during work after sleeplessness. Subjects appeared to fall into "resistant" and "susceptible" categories: four showed less than a 5% change in performance after sleep loss, while four others showed decrements in exercise tolerance ranging from 15 to 40%. During the walk, sleep loss resulted in significantly greater perceived exertion (p less than 0.05), even though exercise heart rate and metabolic rate (VO2 and VCO2) were unchanged. Minute ventilation was significantly elevated during exercise after sleep loss ( p less than 0.05). Sleep loss failed to alter the continuous slow rises in VE and heart rate that occurred as work was prolonged. These findings suggest that the psychological effects of acute sleep loss may contribute to decreased tolerance of prolonged heavy exercise.
Sanchez-Ortiz, Efrain; Yui, Daishi; Song, Dongli; Li, Yun; Rubenstein, John L.; Reichardt, Louis F.; Parada, Luis F.
Dysfunction of basal forebrain cholinergic neurons (BFCNs) is an early pathological hallmark of Alzheimer's disease (AD). Numerous studies have indicated that nerve growth factor (NGF) supports survival and phenotypic differentiation of BFCNs. Consistent with a potential link to AD pathogenesis, TrkA, a NGF receptor, is expressed in cholinergic forebrain neuronal populations including those in basal forebrain (BF) and striatum, and is markedly reduced in individuals with mild cognitive impairment (MCI) without dementia and early-stage AD. To investigate the role of TrkA in the development, connectivity, and function of the BF cholinergic system and its contribution to AD pathology, we have generated a forebrain-specific conditional TrkA knockout mouse line. Our findings show a key role for TrkA signaling in establishing the BF cholinergic circuitry through the ERK pathway, and demonstrate that the normal developmental increase of choline acetyltransferase (ChAT) expression becomes critically dependent on TrkA signaling before neuronal connections are established. Moreover, the anatomical and physiological deficits caused by lack of TrkA signaling in BFCNs have selective impact on cognitive activity. These data demonstrate that TrkA loss results in cholinergic BF dysfunction and cognitive decline that is reminiscent of MCI and early AD. PMID:22442072
Stopper, Colin M.; Floresco, Stan B.
Abnormal reinforcement learning and representations of reward value are present in schizophrenia, and these impairments can manifest as deficits in risk/reward decision making. These abnormalities may be due in part to dopaminergic dysfunction within cortico-limbic-striatal circuitry. Evidence from studies with laboratory animal have revealed that normal DA activity within different nodes of these circuits is critical for mediating dissociable processes that can refine decision biases. Moreover, both phasic and tonic dopamine transmission appear to play separate yet complementary roles in these processes. Tonic dopamine release within the prefrontal cortex and nucleus accumbens, serves as a “running rate-meter” of reward and reflects contextual information such as reward uncertainty and overt choice behavior. On the other hand, manipulations of outcome-related phasic dopamine bursts and dips suggest these signals provide rapid feedback to allow for quick adjustments in choice as reward contingencies change. The lateral habenula is a key input to the DA system that phasic signals is necessary for expressing subjective decision biases; as suppression of activity within this nucleus leads to catastrophic impairments in decision making and random patterns of choice behavior. As schizophrenia is characterized by impairments in using positive and negative feedback to appropriately guide decision making, these findings suggest that these deficits in these processes may be mediated, at least in part, by abnormalities in both tonic and phasic dopamine transmission. PMID:25406370
Dubowy, Christine; Moravcevic, Katarina; Yue, Zhifeng; Wan, Joy Y.; Van Dongen, Hans P.A.; Sehgal, Amita
Study Objectives: Sleep rebound—the increase in sleep that follows sleep deprivation—is a hallmark of homeostatic sleep regulation that is conserved across the animal kingdom. However, both the mechanisms that underlie sleep rebound and its relationship to habitual daily sleep remain unclear. To address this, we developed an efficient thermogenetic method of inducing sleep deprivation in Drosophila that produces a substantial rebound, and applied the newly developed method to assess sleep rebound in a screen of 1,741 mutated lines. We used data generated by this screen to identify lines with reduced sleep rebound following thermogenetic sleep deprivation, and to probe the relationship between habitual sleep amount and sleep following thermogenetic sleep deprivation in Drosophila. Methods: To develop a thermogenetic method of sleep deprivation suitable for screening, we thermogenetically stimulated different populations of wake-promoting neurons labeled by Gal4 drivers. Sleep rebound following thermogenetically-induced wakefulness varies across the different sets of wake-promoting neurons that were stimulated, from very little to quite substantial. Thermogenetic activation of neurons marked by the c584-Gal4 driver produces both strong sleep loss and a substantial rebound that is more consistent within genotypes than rebound following mechanical or caffeine-induced sleep deprivation. We therefore used this driver to induce sleep deprivation in a screen of 1,741 mutagenized lines generated by the Drosophila Gene Disruption Project. Flies were subjected to 9 h of sleep deprivation during the dark period and released from sleep deprivation 3 h before lights-on. Recovery was measured over the 15 h following sleep deprivation. Following identification of lines with reduced sleep rebound, we characterized baseline sleep and sleep depth before and after sleep deprivation for these hits. Results: We identified two lines that consistently exhibit a blunted increase in the
Fournier, Michèle; Bourriquen, Gaëlle; Lamaze, Fabien C.; Côté, Maxime C.; Fournier, Éric; Joly-Beauparlant, Charles; Caron, Vicky; Gobeil, Stéphane; Droit, Arnaud; Bilodeau, Steve
Controlling the transcriptional program is essential to maintain the identity and the biological functions of a cell. The Mediator and Cohesin complexes have been established as central cofactors controlling the transcriptional program in normal cells. However, the distribution, recruitment and importance of these complexes in cancer cells have not been fully investigated. Here we show that FOXA and master transcription factors are part of the core transcriptional regulatory circuitry of cancer cells and are essential to recruit M ediator and Cohesin. Indeed, Mediator and Cohesin occupied the enhancer and promoter regions of actively transcribed genes and maintained the proliferation and colony forming potential. Through integration of publically available ChIP-Seq datasets, we predicted the core transcriptional regulatory circuitry of each cancer cell. Unexpectedly, for all cells investigated, the pioneer transcription factors FOXA1 and/or FOXA2 were identified in addition to cell-specific master transcription factors. Loss of both types of transcription factors phenocopied the loss of Mediator and Cohesin. Lastly, the master and pioneer transcription factors were essential to recruit Mediator and Cohesin to regulatory regions of actively transcribed genes. Our study proposes that maintenance of the cancer cell state is dependent on recruitment of Mediator and Cohesin through FOXA and master transcription factors.
Fournier, Michèle; Bourriquen, Gaëlle; Lamaze, Fabien C; Côté, Maxime C; Fournier, Éric; Joly-Beauparlant, Charles; Caron, Vicky; Gobeil, Stéphane; Droit, Arnaud; Bilodeau, Steve
Controlling the transcriptional program is essential to maintain the identity and the biological functions of a cell. The Mediator and Cohesin complexes have been established as central cofactors controlling the transcriptional program in normal cells. However, the distribution, recruitment and importance of these complexes in cancer cells have not been fully investigated. Here we show that FOXA and master transcription factors are part of the core transcriptional regulatory circuitry of cancer cells and are essential to recruit M ediator and Cohesin. Indeed, Mediator and Cohesin occupied the enhancer and promoter regions of actively transcribed genes and maintained the proliferation and colony forming potential. Through integration of publically available ChIP-Seq datasets, we predicted the core transcriptional regulatory circuitry of each cancer cell. Unexpectedly, for all cells investigated, the pioneer transcription factors FOXA1 and/or FOXA2 were identified in addition to cell-specific master transcription factors. Loss of both types of transcription factors phenocopied the loss of Mediator and Cohesin. Lastly, the master and pioneer transcription factors were essential to recruit Mediator and Cohesin to regulatory regions of actively transcribed genes. Our study proposes that maintenance of the cancer cell state is dependent on recruitment of Mediator and Cohesin through FOXA and master transcription factors.
Fournier, Michèle; Bourriquen, Gaëlle; Lamaze, Fabien C.; Côté, Maxime C.; Fournier, Éric; Joly-Beauparlant, Charles; Caron, Vicky; Gobeil, Stéphane; Droit, Arnaud; Bilodeau, Steve
Controlling the transcriptional program is essential to maintain the identity and the biological functions of a cell. The Mediator and Cohesin complexes have been established as central cofactors controlling the transcriptional program in normal cells. However, the distribution, recruitment and importance of these complexes in cancer cells have not been fully investigated. Here we show that FOXA and master transcription factors are part of the core transcriptional regulatory circuitry of cancer cells and are essential to recruit M ediator and Cohesin. Indeed, Mediator and Cohesin occupied the enhancer and promoter regions of actively transcribed genes and maintained the proliferation and colony forming potential. Through integration of publically available ChIP-Seq datasets, we predicted the core transcriptional regulatory circuitry of each cancer cell. Unexpectedly, for all cells investigated, the pioneer transcription factors FOXA1 and/or FOXA2 were identified in addition to cell-specific master transcription factors. Loss of both types of transcription factors phenocopied the loss of Mediator and Cohesin. Lastly, the master and pioneer transcription factors were essential to recruit Mediator and Cohesin to regulatory regions of actively transcribed genes. Our study proposes that maintenance of the cancer cell state is dependent on recruitment of Mediator and Cohesin through FOXA and master transcription factors. PMID:27739523
Smeyatsky, N; Baldwin, D; Botros, W; Gura, R; Kurian, T; Lambert, M T; Patel, A G; Steinert, J; Priest, R G
Narcolepsy is clinically associated with cataplexy, sleep paralysis and hypnagogic hallucinations. It is treated by reassurance (that there is no physical disease) and by stimulants such as ephedrine and amphetamine on an intermittent basis. The special tricyclic antidepressant clomipramine is also used, and mono-amine oxidase inhibitors (MAOIs) are useful in theory. Obstructive sleep apnoea is an important and often unrecognised cause of daytime somnolence. It is treated by weight reduction (pickwickian syndrome), hormones, or recently, with continuous positive pressure apparatus. Night terrors (pavor nocturnus) and sleepwalking typically occur during deep sleep (stage 3 and 4 throughout the episode) in children. In a night terror the child sits up with a scream, with eyes open, but inaccessible. He eventually falls asleep calmly. Sleepwalking, too, shows the features of inaccessibility and subsequent amnesia for the episode. Both conditions are normally treated with reassurance (to the parents) but may occasionally warrant benzodiazepines. Enuresis usually occurs in non-rapid eye movement (NREM) sleep, especially stages 3 and 4. The reason for the efficacy of tricyclic antidepressants is not precisely known. Delirium tremens (DT) is treated as a rebound excess of REM sleep, with benzodiazepines and other drugs. It is the withdrawal syndrome (with or without major seizures) to the barbiturate-alcohol group of drugs, which includes alcohol, chloral, paraldehyde, glutethimide, methylprylone, ethchlorvynol, meprobamate and meprobamate-diphenhydramine. Insomnia may be treated by the above drugs, by analgesics, antidepressants, major tranquillisers (neuroleptics) and miscellaneous other compounds. For the majority of patients, however, the most suitable group seems to be the benzodiazepines. The benzodiazepines are much safer than their predecessors, in both acute and chronic usage.(ABSTRACT TRUNCATED AT 250 WORDS)
Opp, Mark R
Personal experience indicates we sleep differently when sick. Data reviewed demonstrate the extent to which sleep is altered during the course of infection of host organisms by several classes of pathogens. One important unanswered question is whether or not the alterations in sleep during infection are of functional relevance. That is, does the way we sleep when sick facilitate or impede recovery? One retrospective, preclinical study suggests that sleep changes during infection are of functional relevance. Toth and colleagues  analyzed sleep responses of rabbits to three different microbial infections. Those rabbits that exhibited robust increases in NREM sleep were more likely to survive than those that exhibited long periods of NREM sleep suppression. These tantalizing data suggest that the precise alterations in sleep through the course of infection are important determinants of morbidity and mortality. Data from healthy subjects demonstrate a role for at least two cytokines in the regulation of spontaneous, physiologic NREM sleep. A second critical yet unanswered question is whether or not cytokines mediate infection-induced alterations in sleep. The hypothesis that cytokines mediate infection-induced alterations in sleep is logical based on observations of the impact of infection on levels of cytokines in the peripheral immune system and in the brain. No attempts have been made to intervene with cytokine systems in brain during the course of infection to determine if there is an impact on infection-induced alterations in sleep. Although substantial progress has been made in elucidating the myriad mechanisms by which cytokines regulate and modulate sleep, much remains to be determined with respect to mechanistic and functional aspects of infection-induced alterations in sleep.
Hall, F. Scott; Uhl, George R.; Bearer, Elaine L.; Jacobs, Russell E.
Synaptic levels of the monoamine neurotransmitters dopamine, serotonin, and norepinephrine are modulated by their respective plasma membrane transporters, albeit with a few exceptions. Monoamine transporters remove monoamines from the synaptic cleft and thus influence the degree and duration of signaling. Abnormal concentrations of these neuronal transmitters are implicated in a number of neurological and psychiatric disorders, including addiction, depression, and attention deficit/hyperactivity disorder. This work concentrates on the norepinephrine transporter (NET), using a battery of in vivo magnetic resonance imaging techniques and histological correlates to probe the effects of genetic deletion of the norepinephrine transporter on brain metabolism, anatomy and functional connectivity. MRS recorded in the striatum of NET knockout mice indicated a lower concentration of NAA that correlates with histological observations of subtle dysmorphisms in the striatum and internal capsule. As with DAT and SERT knockout mice, we detected minimal structural alterations in NET knockout mice by tensor-based morphometric analysis. In contrast, longitudinal imaging after stereotaxic prefrontal cortical injection of manganese, an established neuronal circuitry tracer, revealed that the reward circuit in the NET knockout mouse is biased toward anterior portions of the brain. This is similar to previous results observed for the dopamine transporter (DAT) knockout mouse, but dissimilar from work with serotonin transporter (SERT) knockout mice where Mn2+ tracings extended to more posterior structures than in wildtype animals. These observations correlate with behavioral studies indicating that SERT knockout mice display anxiety-like phenotypes, while NET knockouts and to a lesser extent DAT knockout mice display antidepressant-like phenotypic features. Thus, the mainly anterior activity detected with manganese-enhanced MRI in the DAT and NET knockout mice is likely indicative of
Hubscher, C H; Gupta, D S; Brink, T S
Despite common comorbidity of sexual and urinary dysfunctions, the interrelationships between the neural control of these functions are poorly understood. The medullary reticular formation (MRF) contributes to both mating/arousal functions and micturition, making it a good site to test circuitry interactions. Urethane-anesthetized adult Wistar rats were used to examine the impact of electrically stimulating different nerve targets [dorsal nerve of the penis (DNP) or clitoris (DNC); L6/S1 trunk] on responses of individual extracellularly recorded MRF neurons. The effect of bladder filling on MRF neurons was also examined, as was stimulation of DNP on bladder reflexes via cystometry. In total, 236 MRF neurons responded to neurostimulation: 102 to DNP stimulation (12 males), 64 to DNC stimulation (12 females), and 70 to L6/S1 trunk stimulation (12 males). Amplitude thresholds were significantly different at DNP (15.0 ± 0.6 μA), DNC (10.5 ± 0.7 μA), and L6/S1 trunk (54.2 ± 4.6 μA), whereas similar frequency responses were found (max responses near 30-40 Hz). In five males, filling/voiding cycles were lengthened with DNP stimulation (11.0 ± 0.9 μA), with a maximal effective frequency plateau beginning at 30 Hz. Bladder effects lasted ≈ 2 min after DNP stimulus offset. Many MRF neurons receiving DNP/DNC input responded to bladder filling (35.0% and 68.3%, respectively), either just before (43%) or simultaneously with (57%) the voiding reflex. Taken together, MRF-evoked responses with neurostimulation of multiple nerve targets along with different responses to bladder infusion have implications for the role of MRF in multiple aspects of urogenital functions.
Amongst the most significant questions we are confronted with today include the integration of the brain's micro-circuitry, our ability to build the complex social networks that underpin society and how our society impacts on our ecological environment. In trying to unravel these issues one place to begin is at the level of the individual: to consider how we accumulate information about our environment, how this information leads to decisions and how our individual decisions in turn create our social environment. While this is an enormous task, we may already have at hand many of the tools we need. This article is intended to review some of the recent results in neuro-cognitive research and show how they can be extended to two very specific and interrelated types of expertise: perceptual expertise and social cognition. These two cognitive skills span a vast range of our genetic heritage. Perceptual expertise developed very early in our evolutionary history and is a highly developed part of all mammals' cognitive ability. On the other hand social cognition is most highly developed in humans in that we are able to maintain larger and more stable long term social connections with more behaviorally diverse individuals than any other species. To illustrate these ideas I will discuss board games as a toy model of social interactions as they include many of the relevant concepts: perceptual learning, decision-making, long term planning and understanding the mental states of other people. Using techniques that have been developed in mathematical psychology, I show that we can represent some of the key features of expertise using stochastic differential equations (SDEs). Such models demonstrate how an expert's long exposure to a particular context influences the information they accumulate in order to make a decision.These processes are not confined to board games, we are all experts in our daily lives through long exposure to the many regularities of daily tasks and social
Shapiro, Rebecca S.; Robbins, Nicole; Cowen, Leah E.
Summary: Pathogenic fungi have become a leading cause of human mortality due to the increasing frequency of fungal infections in immunocompromised populations and the limited armamentarium of clinically useful antifungal drugs. Candida albicans, Cryptococcus neoformans, and Aspergillus fumigatus are the leading causes of opportunistic fungal infections. In these diverse pathogenic fungi, complex signal transduction cascades are critical for sensing environmental changes and mediating appropriate cellular responses. For C. albicans, several environmental cues regulate a morphogenetic switch from yeast to filamentous growth, a reversible transition important for virulence. Many of the signaling cascades regulating morphogenesis are also required for cells to adapt and survive the cellular stresses imposed by antifungal drugs. Many of these signaling networks are conserved in C. neoformans and A. fumigatus, which undergo distinct morphogenetic programs during specific phases of their life cycles. Furthermore, the key mechanisms of fungal drug resistance, including alterations of the drug target, overexpression of drug efflux transporters, and alteration of cellular stress responses, are conserved between these species. This review focuses on the circuitry regulating fungal morphogenesis and drug resistance and the impact of these pathways on virulence. Although the three human-pathogenic fungi highlighted in this review are those most frequently encountered in the clinic, they represent a minute fraction of fungal diversity. Exploration of the conservation and divergence of core signal transduction pathways across C. albicans, C. neoformans, and A. fumigatus provides a foundation for the study of a broader diversity of pathogenic fungi and a platform for the development of new therapeutic strategies for fungal disease. PMID:21646428
Edwards, Adrianne N; Patterson-Fortin, Laura M; Vakulskas, Christopher A; Mercante, Jeffrey W; Potrykus, Katarzyna; Vinella, Daniel; Camacho, Martha I; Fields, Joshua A; Thompson, Stuart A; Georgellis, Dimitris; Cashel, Michael; Babitzke, Paul; Romeo, Tony
CsrA protein regulates important cellular processes by binding to target mRNAs and altering their translation and/or stability. In Escherichia coli, CsrA binds to sRNAs, CsrB and CsrC, which sequester CsrA and antagonize its activity. Here, mRNAs for relA, spoT and dksA of the stringent response system were found among 721 different transcripts that copurified with CsrA. Many of the transcripts that copurified with CsrA were previously determined to respond to ppGpp and/or DksA. We examined multiple regulatory interactions between the Csr and stringent response systems. Most importantly, DksA and ppGpp robustly activated csrB/C transcription (10-fold), while they modestly activated csrA expression. We propose that CsrA-mediated regulation is relieved during the stringent response. Gel shift assays confirmed high affinity binding of CsrA to relA mRNA leader and weaker interactions with dksA and spoT. Reporter fusions, qRT-PCR and immunoblotting showed that CsrA repressed relA expression, and (p)ppGpp accumulation during stringent response was enhanced in a csrA mutant. CsrA had modest to negligible effects on dksA and spoT expression. Transcription of dksA was negatively autoregulated via a feedback loop that tended to mask CsrA effects. We propose that the Csr system fine-tunes the stringent response and discuss biological implications of the composite circuitry.
Edwards, Adrianne N.; Patterson-Fortin, Laura M.; Vakulskas, Christopher A.; Mercante, Jeffrey W.; Potrykus, Katarzyna; Vinella, Daniel; Camacho, Martha I.; Fields, Joshua A.; Thompson, Stuart A.; Georgellis, Dimitris; Cashel, Michael; Babitzke, Paul; Romeo, Tony
Summary CsrA protein regulates important cellular processes by binding to target mRNAs and altering their translation and/or stability. In Escherichia coli, CsrA binds to sRNAs, CsrB and CsrC, which sequester CsrA and antagonize its activity. Here, mRNAs for relA, spoT and dksA of the stringent response system were found among 721 different transcripts that copurified with CsrA. Many of the transcripts that copurified with CsrA were previously determined to respond to ppGpp and/or DksA. We examined multiple regulatory interactions between the Csr and stringent response systems. Most importantly, DksA and ppGpp robustly activated csrB/C transcription (10-fold), while they modestly activated csrA expression. We propose that CsrA-mediated regulation is relieved during the stringent response. Gel shift assays confirmed high affinity binding of CsrA to relA mRNA leader and weaker interactions with dksA and spoT. Reporter fusions, qRT-PCR, and immunoblotting showed that CsrA repressed relA expression, and (p)ppGpp accumulation during stringent response was enhanced in a csrA mutant. CsrA had modest to negligible effects on dksA and spoT expression. Transcription of dksA was negatively autoregulated via a feedback loop that tended to mask CsrA effects. We propose that the Csr system fine-tunes the stringent response and discuss biological implications of the composite circuitry. PMID:21488981
Grandner, Michael A
Biological needs for sleep are met by engaging in behaviors that are largely influenced by the environment, social norms and demands, and societal influences and pressures. Insufficient sleep duration and sleep disorders such as insomnia and sleep apnea are highly prevalent in the US population. This article outlines some of these downstream factors, including cardiovascular and metabolic disease risk, neurocognitive dysfunction, and mortality, as well as societal factors such as age, sex, race/ethnicity, and socioeconomics. This review also discusses societal factors related to sleep, such as globalization, health disparities, public policy, public safety, and changing patterns of use of technology.
Pace-Schott, Edward F.; Milad, Mohammed R.; Orr, Scott P.; Rauch, Scott L.; Stickgold, Robert; Pitman, Roger K.
Study Objective: To examine the effects of sleep on fear conditioning, extinction, extinction recall, and generalization of extinction recall in healthy humans. Design: During the Conditioning phase, a mild, 0.5-sec shock followed conditioned stimuli (CS+s), which consisted of 2 differently colored lamps. A third lamp color was interspersed but never reinforced (CS-). Immediately after Conditioning, one CS+ was extinguished (CS+E) by presentation without shocks (Extinction phase). The other CS+ went unextinguished (CS+U). Twelve hours later, following continuous normal daytime waking (Wake group, N = 27) or an equal interval containing a normal night's sleep (Sleep group, N = 26), conditioned responses (CRs) to all CSs were measured (Extinction Recall phase). It was hypothesized that the Sleep versus Wake group would show greater extinction recall and/or generalization of extinction recall from the CS+E to the CS+U. Setting: Academic medical center. Subjects: Paid normal volunteers. Measurements and Results: Square-root transformed skin conductance response (SCR) measured conditioned responding. During Extinction Recall, the Group (Wake or Sleep) × CS+ Type (CS+E or CS+U) interaction was significant (P = 0.04). SCRs to the CS+E did not differ between groups, whereas SCRs to the CS+U were significantly smaller in the Sleep group. Additionally, SCRs were significantly larger to the CS+U than CS+E in the Wake but not the Sleep group. Conclusions: After sleep, extinction memory generalized from an extinguished conditioned stimulus to a similarly conditioned but unextinguished stimulus. Clinically, adequate sleep may promote generalization of extinction memory from specific stimuli treated during exposure therapy to similar stimuli later encountered in vivo. Citation: Pace-Schott EF; Milad MR; Orr SP; Rauch SL; Stickgold R; Pitman RK. Sleep promotes generalization of extinction of conditioned fear. SLEEP 2009;32(1):19-26. PMID:19189775
Fernandes, Carina; Rocha, Nuno Barbosa F.; Rocha, Susana; Herrera-Solís, Andrea; Salas-Pacheco, José; García-García, Fabio; Murillo-Rodríguez, Eric; Yuan, Ti-Fei; Machado, Sergio; Arias-Carrión, Oscar
Adult mammalian brains continuously generate new neurons, a phenomenon called adult neurogenesis. Both environmental stimuli and endogenous factors are important regulators of adult neurogenesis. Sleep has an important role in normal brain physiology and its disturbance causes very stressful conditions, which disrupt normal brain physiology. Recently, an influence of sleep in adult neurogenesis has been established, mainly based on sleep deprivation studies. This review provides an overview on how rhythms and sleep cycles regulate hippocampal and subventricular zone neurogenesis, discussing some potential underlying mechanisms. In addition, our review highlights some interacting points between sleep and adult neurogenesis in brain function, such as learning, memory, and mood states, and provides some insights on the effects of antidepressants and hypnotic drugs on adult neurogenesis. PMID:25926773
Hackius, Marc; Werth, Esther; Sürücü, Oguzkan; Baumann, Christian R; Imbach, Lukas L
Patients with Parkinson's disease (PD) and REM sleep behavior disorder (RBD) show mostly unimpaired motor behavior during REM sleep, which contrasts strongly to coexistent nocturnal bradykinesia. The reason for this sudden amelioration of motor control in REM sleep is unknown, however. We set out to determine whether movements during REM sleep are processed by different motor networks than movements in the waking state. We recorded local field potentials in the subthalamic nucleus (STN) and scalp EEG (modified 10/20 montage) during sleep in humans with PD and RBD. Time-locked event-related β band oscillations were calculated during movements in REM sleep compared with movements in the waking state and during NREM sleep. Spectral analysis of STN local field potentials revealed elevated β power during REM sleep compared with NREM sleep and β power in REM sleep reached levels similar as in the waking state. Event-related analysis showed time-locked β desynchronization during WAKE movements. In contrast, we found significantly elevated β activity before and during movements in REM sleep and NREM sleep. Corticosubthalamic coherence was reduced during REM and NREM movements. We conclude that sleep-related movements are not processed by the same corticobasal ganglia network as movements in the waking state. Therefore, the well-known seemingly normal motor performance during RBD in PD patients might be generated by activating alternative motor networks for movement initiation. These findings support the hypothesis that pathological movement-inhibiting basal ganglia networks in PD patients are bypassed during sleep.
This study investigated the effects of inhalation aromatherapy on sleep disturbance in elderly individuals with dementia. In 19 subjects, normal sleep was observed for a 20-day control period, inhalation aromatherapy was then applied for a 20-day intervention period, and the control and intervention periods were compared. During the intervention period, essential oils were placed nightly on towels around the subjects' pillows. The measured sleep conditions were sleep latency, total sleep time, sleep efficacy, duration of the longest sustained sleep period, wake time after sleep onset, early morning awakening, total daytime sleep, and the Neuropsychiatric Inventory. Total sleep time was significantly longer in the intervention period than in the control period (p < 0.05). The duration of the longest sustained sleep period was significantly longer in the intervention period than in the control period (p < 0.05). Early morning awakening in the intervention period was significantly less compared to that in the control period (p < 0.05). Total daytime sleep could not be adequately measured and was omitted from the analysis. No significant differences in other sleep conditions were observed. These results indicated positive effects of inhalation aromatherapy on symptoms of sleep disturbance in elderly individuals with dementia.
Yaugher, Ashley C.; Alexander, Gerianne M.
Research on psychopathology and experimental studies of sleep restriction support a relationship between sleep disruption and both internalizing and externalizing disorders. The objective of the current study was to extend this research by examining sleep, impulsivity, antisocial personality traits, and internalizing traits in a university sample. Three hundred and eighty six individuals (161 males) between the ages of 18 and 27 years (M = 18.59, SD = 0.98) wore actigraphs for 7 days and completed established measures of disorder-linked personality traits and sleep quality (i.e., Personality Assessment Inventory (PAI), Triarchic Psychopathy Measure, Barratt Impulsiveness Scale-11, and the Pittsburgh Sleep Quality Index). As expected, sleep measures and questionnaire scores fell within the normal range of values and sex differences in sleep and personality were consistent with previous research results. Similar to findings in predominantly male forensic psychiatric settings, higher levels of impulsivity predicted poorer subjective sleep quality in both women and men. Consistent with well-established associations between depression and sleep, higher levels of depression in both sexes predicted poorer subjective sleep quality. Bidirectional analyses showed that better sleep efficiency decreases depression. Finally, moderation analyses showed that gender does have a primary role in sleep efficiency and marginal effects were found. The observed relations between sleep and personality traits in a typical university sample add to converging evidence of the relationship between sleep and psychopathology and may inform our understanding of the development of psychopathology in young adulthood. PMID:26500575
Troxel, Wendy M.; Shih, Regina A.; Pedersen, Eric R.; Geyer, Lily; Fisher, Michael P.; Griffin, Beth Ann; Haas, Ann C.; Kurz, Jeremy; Steinberg, Paul S.
Abstract Sleep disturbances are a common reaction to stress and are linked to a host of physical and mental health problems. Given the unprecedented demands placed on U.S. military forces since 2001, there has been growing concern about the prevalence and consequences of sleep problems for servicemembers. Sleep problems often follow a chronic course, persisting long after servicemembers return home from combat deployments, with consequences for their reintegration and the readiness and resiliency of the force. Therefore, it is critical to understand the role of sleep problems in servicemembers’ health and functioning and the policies and programs available to promote healthy sleep. This study provides the first comprehensive review of sleep-related policies and programs across the U.S. Department of Defense (DoD), along with a set of actionable recommendations for DoD, commanders, researchers, and medical professionals who treat U.S. servicemembers. The two-year multimethod study also examined the rates and correlates of sleep problems among post-deployed servicemembers, finding negative effects on mental health, daytime impairment, and perceived operational readiness. The research reviewed evidence-based interventions to treat sleep disturbances among servicemembers and veterans and exposed several individual- and system-level barriers to achieving healthy sleep. Implementing evidence-based treatments is just one step toward improving sleep across the force; as the research recommendations highlight, it is equally important that policies and programs also focus on preventing sleep problems and their consequences. PMID:28083395
Sleep duration has gradually diminished during the last decade while obesity and type 2 diabetes have become epidemics. Experimental sleep curtailment leads to increased appetite, hormonal disturbances and, especially, insulin resistance. Numerous epidemiological studies have therefore examined whether habitual short sleep is associated with obesity and type 2 diabetes. A large majority of cross-sectional studies have confirmed an association between short, and also long sleep duration and obesity in adults more than in the elderly. Short sleep is strongly associated to obesity in children and adolescents. Prospective studies, including studies in children, are not conclusive with regard to the effect of short sleep on the incidence of obesity. Both short and long sleep durations are associated with diabetes, but only short sleep duration seems predictive of future diabetes. Insomnia seems to be a strong contributor to short sleep duration but the association of insomnia with obesity is not clear. Insomnia is associated with type 2 diabetes and also predictive of a higher incidence. Other studies have shown that short sleep duration and insomnia are associated with, and sometime predictive of, other components of the metabolic syndrome, especially hypertension and the risk of coronary disease. The treatment of short sleep duration and insomnia with regard to their effects on the metabolic syndrome merits further study.
Du Mond, Courtney; Mindell, Jodi A.
Sleep is an important aspect of a child's early development and is essential to family well-being. During their first 3 years, infants and toddlers spend more than 50% of their lives sleeping. However, concerns about sleep and sleep problems are among the most common issues brought to the attention of pediatricians. Although sleep is one of the…
Krystal, Andrew D.
SYNOPSIS Psychiatric disorders and sleep are related in important ways. In contrast to the longstanding view of this relationship which viewed sleep problems as symptoms of psychiatric disorders, there is growing experimental evidence that the relationship between psychiatric disorders and sleep is complex and includes bi-directional causation. In this article we provide the evidence that supports this point of view, reviewing the data on the sleep disturbances seen in patients with psychiatric disorders but also reviewing the data on the impact of sleep disturbances on psychiatric conditions. Although much has been learned about the psychiatric disorders-sleep relationship, additional research is needed to better understand these relationships. This work promises to improve our ability to understand both of these phenomena and to allow us to better treat the many patients with sleep disorders and with psychiatric disorders. PMID:23099143
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.
... From the Federal Register Online via the Government Publishing Office ] INTERNATIONAL TRADE COMMISSION Certain Semiconductor Chips With Dram Circuitry, and Modules and Products Containing Same: Notice of Commission Determination To Terminate the Investigation Based on Settlement AGENCY:...
Heffner, Kathi L.; France, Christopher R.; Trost, Zina; Mei Ng, H.; Pigeon, Wilfred R.
Objectives Sleep disturbance is a common co-morbidity of chronic pain. Inflammatory processes are dysregulated in sleep disturbance and also contribute to pain sensitivity. Thus, inflammation may play an important role in bi-directional associations between pain and sleep. Little is known about concurrent relationships among chronic pain, sleep, and inflammation. The aim of our study was to examine associations among sleep disturbance and circulating levels of the inflammatory cytokine, interleukin-6 (IL-6), in individuals with and without chronic low back pain. Methods Gender and age-matched adults with chronic low back pain (CLBP; n = 25) or without chronic pain (controls; n = 25) completed measures of sleep quality in the past month and depressive symptoms in the past week, and provided a blood draw for IL-6. The next morning, participants reported their sleep quality the previous night and their current experience of morning pain. Results Individuals with CLBP had more sleep disturbance than controls. Circulating IL-6 levels were similar for the two groups; however, in adults with CLBP, poorer sleep quality was associated with higher IL-6 levels, and both sleep and IL-6 related to pain reports. Unlike CLBP participants, controls showed normal, age-related increases in IL-6 levels, whereas sleep quality was unrelated to IL-6 levels. Depressive symptoms could not fully explain the observed associations. Discussion Inflammatory processes may play a significant role in cycles of pain and sleep disturbance. Clinical interventions that improve sleep and reduce concomitant inflammatory dysregulation hold promise for chronic pain management. PMID:21188850
Solomonova, Elizaveta; Stenstrom, Philippe; Schon, Emilie; Duquette, Alexandra; Dubé, Simon; O'Reilly, Christian; Nielsen, Tore
Face recognition is a highly specialized capability that has implicit and explicit memory components. Studies show that learning tasks with facial components are dependent on rapid eye movement and non-rapid eye movement sleep features, including rapid eye movement sleep density and fast sleep spindles. This study aimed to investigate the relationship between sleep-dependent consolidation of memory for faces and partial rapid eye movement sleep deprivation, rapid eye movement density, and fast and slow non-rapid eye movement sleep spindles. Fourteen healthy participants spent 1 night each in the laboratory. Prior to bed they completed a virtual reality task in which they interacted with computer-generated characters. Half of the participants (REMD group) underwent a partial rapid eye movement sleep deprivation protocol and half (CTL group) had a normal amount of rapid eye movement sleep. Upon awakening, they completed a face recognition task that contained a mixture of previously encountered faces from the task and new faces. Rapid eye movement density and fast and slow sleep spindles were detected using in-house software. The REMD group performed worse than the CTL group on the face recognition task; however, rapid eye movement duration and rapid eye movement density were not related to task performance. Fast and slow sleep spindles showed differential relationships to task performance, with fast spindles being positively and slow spindles negatively correlated with face recognition. The results support the notion that rapid eye movement and non-rapid eye movement sleep characteristics play complementary roles in face memory consolidation. This study also raises the possibility that fast and slow spindles contribute in opposite ways to sleep-dependent memory consolidation.
Varga, Andrew W; Kishi, Akifumi; Mantua, Janna; Lim, Jason; Koushyk, Viachaslau; Leibert, David P; Osorio, Ricardo S; Rapoport, David M; Ayappa, Indu
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.
... A-STEP equips students with the knowledge and skills they need to excel in the profession of sleep technology. Sleep Education SleepEducation.org provides patients and the general public with comprehensive, accurate information about healthy sleep and sleep disorders, along with ...
BaHammam, Ahmed S.
Sleep medicine is a relatively new scientific specialty. Sleep is an important topic in Islamic literature, and the Quran and Hadith discuss types of sleep, the importance of sleep, and good sleep practices. Islam considers sleep as one of the signs of the greatness of Allνh (God) and encourages followers to explore this important sign. The Quran describes different types of sleep, and these correspond with sleep stages identified by modern science. The Quran discusses the beneficial effects of sleep and emphasizes the importance of maintaining a pattern of light and darkness. A mid-day nap is an important practice for Muslims, and the Prophet Muhammad peace be upon him (pbuh) promoted naps as beneficial. In accordance with the practice and instructions of Muhammad (pbuh), Muslims have certain sleep habits and these sleep habits correspond to some of the sleep hygiene rules identified by modern science. Details during sleep include sleep position, like encouraging sleep on the right side and discouraging sleep in the prone position. Dream interpretation is an established science in the Islamic literature and Islamic scholars have made significant contributions to theories of dream interpretation. We suggest that sleep scientists examine religious literature in general and Islamic literature in particular, to understand the views, behaviors, and practices of ancient people about the sleep and sleep disorders. Such studies may help to answer some unresolved questions in sleep science or lead to new areas of inquiry. PMID:21977062
Bahammam, Ahmed S
Sleep medicine is a relatively new scientific specialty. Sleep is an important topic in Islamic literature, and the Quran and Hadith discuss types of sleep, the importance of sleep, and good sleep practices. Islam considers sleep as one of the signs of the greatness of Allνh (God) and encourages followers to explore this important sign. The Quran describes different types of sleep, and these correspond with sleep stages identified by modern science. The Quran discusses the beneficial effects of sleep and emphasizes the importance of maintaining a pattern of light and darkness. A mid-day nap is an important practice for Muslims, and the Prophet Muhammad peace be upon him (pbuh) promoted naps as beneficial. In accordance with the practice and instructions of Muhammad (pbuh), Muslims have certain sleep habits and these sleep habits correspond to some of the sleep hygiene rules identified by modern science. Details during sleep include sleep position, like encouraging sleep on the right side and discouraging sleep in the prone position. Dream interpretation is an established science in the Islamic literature and Islamic scholars have made significant contributions to theories of dream interpretation. We suggest that sleep scientists examine religious literature in general and Islamic literature in particular, to understand the views, behaviors, and practices of ancient people about the sleep and sleep disorders. Such studies may help to answer some unresolved questions in sleep science or lead to new areas of inquiry.
Ha, Young-Geun; Everaerts, Ken; Hersam, Mark C; Marks, Tobin J
Recent advances in semiconductor performance made possible by organic π-electron molecules, carbon-based nanomaterials, and metal oxides have been a central scientific and technological research focus over the past decade in the quest for flexible and transparent electronic products. However, advances in semiconductor materials require corresponding advances in compatible gate dielectric materials, which must exhibit excellent electrical properties such as large capacitance, high breakdown strength, low leakage current density, and mechanical flexibility on arbitrary substrates. Historically, conventional silicon dioxide (SiO2) has dominated electronics as the preferred gate dielectric material in complementary metal oxide semiconductor (CMOS) integrated transistor circuitry. However, it does not satisfy many of the performance requirements for the aforementioned semiconductors due to its relatively low dielectric constant and intransigent processability. High-k inorganics such as hafnium dioxide (HfO2) or zirconium dioxide (ZrO2) offer some increases in performance, but scientists have great difficulty depositing these materials as smooth films at temperatures compatible with flexible plastic substrates. While various organic polymers are accessible via chemical synthesis and readily form films from solution, they typically exhibit low capacitances, and the corresponding transistors operate at unacceptably high voltages. More recently, researchers have combined the favorable properties of high-k metal oxides and π-electron organics to form processable, structurally well-defined, and robust self-assembled multilayer nanodielectrics, which enable high-performance transistors with a wide variety of unconventional semiconductors. In this Account, we review recent advances in organic-inorganic hybrid gate dielectrics, fabricated by multilayer self-assembly, and their remarkable synergy with unconventional semiconductors. We first discuss the principals and functional
Park, Silvia J.H.; Borghuis, Bart G.; Rahmani, Pouyan; Zeng, Qiang
Visual processing in the retina depends on coordinated signaling by interneurons. Photoreceptor signals are relayed to ∼20 ganglion cell types through a dozen excitatory bipolar interneurons, each responsive to light increments (ON) or decrements (OFF). ON and OFF bipolar cell pathways become tuned through specific connections with inhibitory interneurons: horizontal and amacrine cells. A major obstacle for understanding retinal circuitry is the unknown function of most of the ∼30–40 amacrine cell types, each of which synapses onto a subset of bipolar cell terminals, ganglion cell dendrites, and other amacrine cells. Here, we used a transgenic mouse line in which vasoactive intestinal polypeptide-expressing (VIP+) GABAergic interneurons express Cre recombinase. Targeted whole-cell recordings of fluorescently labeled VIP+ cells revealed three predominant types: wide-field bistratified and narrow-field monostratified cells with somas in the inner nuclear layer (INL) and medium-field monostratified cells with somas in the ganglion cell layer (GCL). Bistratified INL cells integrated excitation and inhibition driven by both ON and OFF pathways with little spatial tuning. Narrow-field INL cells integrated excitation driven by the ON pathway and inhibition driven by both pathways, with pronounced hyperpolarizations at light offset. Monostratified GCL cells integrated excitation and inhibition driven by the ON pathway and showed center-surround spatial tuning. Optogenetic experiments showed that, collectively, VIP+ cells made strong connections with OFF δ, ON-OFF direction-selective, and W3 ganglion cells but weak, inconsistent connections with ON and OFF α cells. Revealing VIP+ cell morphologies, receptive fields and synaptic connections advances our understanding of their role in visual processing. SIGNIFICANCE STATEMENT The retina is a model system for understanding nervous system function. At the first stage, rod and cone photoreceptors encode light and
Respiratory function undergoes sleep-associated changes which in normal subjects leave it unaffected. However in some cases they may be more marked than usual or may be superimposed on a pre-existing disease, thus giving rise to sleep-related ventilation disorders. These include obstructive sleep apnea syndrome (OSAS), nocturnal desaturation events of chronic obstructive pulmonary disease (COPD) and restrictive syndromes, as well as nocturnal asthmatic attacks. OSAS is a condition characterized by the frequent recurrence of interruptions of oronasal flow (greater than 10 s.) due to upper airway occlusion induced by a reduction in pharyngeal muscle tone. This phenomenon, particularly prominent in REM sleep, results in oxyhemoglobin desaturation and marked cardiovascular consequences (arrhythmias, increases in pulmonary and systemic arterial pressure), as well as symptoms (loud intermittent snoring, daytime sleepiness, intellectual deterioration etc.). Obesity is often associated with OSAS or may lead to a sleep-related hypoventilation syndrome. Treatment is based on weight loss, surgery of upper airway abnormalities, if present, and on splinting of the upper airway by the application of nasal continuous positive airway pressure. In COPD and restrictive disorders, nocturnal hypoxemia is mainly due to REM-associated loss of respiratory muscle tone, as well as in the sleep-related exaggeration of functional defects due to COPD (low chemoreceptor sensitivity, high closing volume etc.). Treatment is based on oxygen administration, provided that possible side-effects are carefully monitored. Nocturnal asthma is due to circadian changes in hormonal secretion (catecholamines, cortisol), as well as supine posture, reduced muco-ciliary clearance, gastro-esophageal reflux etc. Sleep itself plays some role through a depressed arousal reaction in slow wave sleep, resulting in more marked and prolonged attacks in this stage. Slow-release theophylline or beta-mimetic medications
Wilhelm, I; Prehn-Kristensen, A; Born, J
Extensive research has been accumulated demonstrating that sleep is essential for processes of memory consolidation in adults. In children and infants, a great capacity to learn and to memorize coincides with longer and more intense sleep. Here, we review the available data on the influence of sleep on memory consolidation in healthy children and infants, as well as in children with attention-deficit/hyperactivity disorder (ADHD) as a model of prefrontal impairment, and consider possible mechanisms underlying age-dependent differences. Findings indicate a major role of slow wave sleep (SWS) for processes of memory consolidation during early development. Importantly, longer and deeper SWS during childhood appears to produce a distinctly superior strengthening of hippocampus-dependent declarative memories, but concurrently prevents an immediate benefit from sleep for procedural memories, as typically observed in adults. Studies of ADHD children point toward an essential contribution of prefrontal cortex to the preferential consolidation of declarative memory during SWS. Developmental studies of sleep represent a particularly promising approach for characterizing the supra-ordinate control of memory consolidation during sleep by prefrontal-hippocampal circuitry underlying the encoding of declarative memory.
Molfese, Victoria J; Rudasill, Kathleen M; Prokasky, Amanda; Champagne, Carly; Holmes, Molly; Molfese, Dennis L; Bates, John E
Two sources of information (parent-reported sleep diaries and actigraph records) were used to investigate how toddler sleep characteristics (bed time/sleep onset, wake time/sleep offset, total nighttime sleep, and total sleep time) are related to sleep problems and temperament. There were 64 toddler participants in the study. Consistent with studies of older children, parent reports differed from actigraph-based records. The findings that parent-reported and actigraph-recorded sleep characteristics varied as a function of parent report of toddler sleep problems and temperament add needed information on toddler sleep. Such information may contribute to improving parents' awareness of their child's sleep characteristics and correlates of problem sleep.
Kloss, Jacqueline D; Nash, Christina O; Walsh, Colleen M; Culnan, Elizabeth; Horsey, Sarah; Sexton-Radek, Kathy
Sensitizing young adults about sleep hygiene knowledge and helpful sleep attitudes may have the potential to instill long-lasting healthy sleep practices. Towards these ends, evaluation of psychoeducational program "Sleep 101" tailored to college students was undertaken. Following two weeks of sleep-log recordings, participants were randomly assigned to a Sleep 101 (experimental) condition or a sleep monitoring (control) condition. The Sleep 101 condition was comprised of two 90-minute workshops aimed to educate students about healthy sleep practices, helpful thoughts about sleep, and ways to improve sleep. The sleep monitoring group received a sleep hygiene handout and completed sleep logs for the study duration. Sleep 101 participants endorsed fewer maladaptive beliefs and attitudes about sleep, increased sleep hygiene knowledge, and reduced sleep onset latency compared to the sleep monitoring participants. Brief psychoeducational courses may be a cost-effective way to alleviate current, and/or prevent future, sleep problems in young adults.
Porter, Verna R; Buxton, William G; Avidan, Alon Y
The older patient population is growing rapidly around the world and in the USA. Almost half of seniors over age 65 who live at home are dissatisfied with their sleep, and nearly two-thirds of those residing in nursing home facilities suffer from sleep disorders. Chronic and pervasive sleep complaints and disturbances are frequently associated with excessive daytime sleepiness and may result in impaired cognition, diminished intellect, poor memory, confusion, and psychomotor retardation all of which may be misinterpreted as dementia. The key sleep disorders impacting patients with dementia include insomnia, hypersomnolence, circadian rhythm misalignment, sleep disordered breathing, motor disturbances of sleep such as periodic leg movement disorder of sleep and restless leg syndrome, and parasomnias, mostly in the form of rapid eye movement (REM) sleep behavior disorder (RBD). RBD is a pre-clinical marker for a class of neurodegenerative diseases, the "synucleinopathies", and requires formal polysomnographic evaluation. Untreated sleep disorders may exacerbate cognitive and behavioral symptoms in patients with dementia and are a source of considerable stress for bed partners and family members. When left untreated, sleep disturbances may also increase the risk of injury at night, compromise health-related quality of life, and precipitate and accelerate social and economic burdens for caregivers.
Chouchou, F; Lavigne, G-J
The placebo response is a psychobiological phenomenon for clinical benefits following the administration of an inert substance whatever its form. This phenomenon can be attributed to a wide range of neurobiological processes, such as expectations of relief, the Pavlovian conditioning and learning, emotional regulation, and reward mechanisms, which are themselves under the influence of processes that take place during sleep. The study of placebo analgesia in healthy from a placebo conditioning associated with analgesic suggestions has highlighted a relationship between sleep, expectations of relief and placebo analgesia: when the induction is persuasive before sleep, expectations of relief modulate placebo response the next morning and paradoxical sleep correlates negatively with both expectations and the placebo response. When the analgesic experience before sleep is less persuasive, expectations of relief are still present but no longer interact with placebo analgesia while paradoxical sleep no longer correlates with the analgesic placebo response. Sleep-processes especially during paradoxical sleep seem to influence the relationship between expectations of relief and placebo analgesia. In this review, we describe the relationship between sleep and placebo analgesia, the mechanisms involved in the placebo response (e.g., conditioning, learning, memory, reward) and their potential link with sleep that could make it a special time for the building placebo response.
Markov, Dimitri; Doghramji, Karl
Sleep disorders are becoming more prevalent. There is an overlap of symptoms related to obstructive sleep apnea syndrome (OSAS) and many psychiatric conditions. Complaints of excessive sleepiness, insomnia, cognitive dysfunction, and depressive symptoms can be related to both disease states. Obstructive sleep apnea syndrome is characterized by repetitive disruption of sleep by cessation of breathing and was first described in the 19th century by bedside observation during sleep. Physicians observed this cessation of breathing while the patient slept and postulated that these episodes were responsible for subsequent complaints of sleepiness. OSAS can coexist with major depressive disorder, exacerbate depressive symptoms, or be responsible for a large part of the symptom complex of depression. Additionally, in schizophrenia, sleep apnea may develop as a result of chronic neuroleptic treatment and its effect on gains in body weight, a major risk factor for the development of OSAS. It is important to recognize the signs and symptoms of sleep apnea, namely excessive daytime sleepiness, snoring, and witnessed apneas. Recognition of the existence of sleep apnea, prompt referral to a sleep specialist, and ultimately treatment of an underlying sleep disorder, such as OSAS, can ameliorate symptoms of psychiatric disease. PMID:20975818
Moldofsky, H; Gilbert, R; Lue, F A; MacLean, A W
We hypothesized that sleep-related violent behavior associated with parasomnias occurs as the result of a diathesis and is precipitated by stressors and mediated by disturbed nonrapid eye movement (NREM) sleep physiology. Sixty-four consecutive adult patients (mean age 30 years) who were investigated for sleepwalking or sleep terrors were categorized according to clinical history into three groups: serious violence during sleep to other people or to property or self (n = 26); harmful, but not destructive behavior (n = 12); and nonviolent behavior (n = 26). Log linear analysis showed that a diathesis (childhood parasomnia and/or family history of parasomnia) and a stressor (psychologic distress, substance abuse and sleep schedule disorder) predicted the presence of sleepwalking or night terror. Serious violent acts were more likely to occur with males (p < 0.004) who showed sleep schedule disorder (p < 0.03). Both harmful and serious violent sleep behavior occurred with drug abuse (p < 0.009). In comparison to all other groups, those who were violent to other people were males who experienced more stressors (p < 0.02), drank excessive caffeinated beverages, abused drugs (p < 0.03) and showed less stage 4 sleep (p < 0.02) and less alpha (7.5-11 Hz) electroencephalogram NREM sleep (p < 0.02) on polysomnography. Being male and having < 2% stage 4 sleep provided 89% sensitivity, 80% specificity and 81% diagnostic accuracy for individuals who were violent to others. The forensic implications of these findings are discussed.
Kim, Min Ju; Lee, Jung Hie; Duffy, Jeanne F.
Objective To review circadian rhythm sleep disorders, including underlying causes, diagnostic considerations, and typical treatments. Methods Literature review and discussion of specific cases. Results Survey studies 1,2 suggest that up to 3% of the adult population suffers from a circadian rhythm sleep disorder (CRSD). However, these sleep disorders are often confused with insomnia, and an estimated 10% of adult and 16% of adolescent sleep disorders patients may have a CRSD 3-6. While some CRSD (such as jet lag) can be self-limiting, others when untreated can lead to adverse medical, psychological, and social consequences. The International Classification of Sleep Disorders classifies CRSD as dyssomnias, with six subtypes: Advanced Sleep Phase Type, Delayed Sleep Phase Type, Irregular Sleep Wake Type, Free Running Type, Jet Lag Type, and Shift Work Type. The primary clinical characteristic of all CRSD is an inability to fall asleep and wake at the desired time. It is believed that CRSD arise from a problem with the internal biological clock (circadian timing system) and/or misalignment between the circadian timing system and the external 24-hour environment. This misalignment can be the result of biological and/or behavioral factors. CRSD can be confused with other sleep or medical disorders. Conclusions Circadian rhythm sleep disorders are a distinct class of sleep disorders characterized by a mismatch between the desired timing of sleep and the ability to fall asleep and remain asleep. If untreated, CRSD can lead to insomnia and excessive daytime sleepiness, with negative medical, psychological, and social consequences. It is important for physicians to recognize potential circadian rhythm sleep disorders so that appropriate diagnosis, treatment, and referral can be made. PMID:25368503
Oishi, Yo; Takata, Yohko; Taguchi, Yujiro; Kohtoh, Sayaka; Urade, Yoshihiro; Lazarus, Michael
Recording of the epidural electroencephalogram (EEG) and electromyogram (EMG) in small animals, like mice and rats, has been pivotal to study the homeodynamics and circuitry of sleep-wake regulation. In many laboratories, a cable-based sleep recording system is used to monitor the EEG and EMG in freely behaving mice in combination with computer software for automatic scoring of the vigilance states on the basis of power spectrum analysis of EEG data. A description of this system is detailed herein. Steel screws are implanted over the frontal cortical area and the parietal area of 1 hemisphere for monitoring EEG signals. In addition, EMG activity is monitored by the bilateral placement of wires in both neck muscles. Non-rapid eye movement (Non-REM; NREM) sleep is characterized by large, slow brain waves with delta activity below 4 Hz in the EEG, whereas a shift from low-frequency delta activity to a rapid low-voltage EEG in the theta range between 6 and 10 Hz can be observed at the transition from NREM to REM sleep. By contrast, wakefulness is identified by low- to moderate-voltage brain waves in the EEG trace and significant EMG activity.
Sleep is necessary for normal psychological functioning, and psychological function in turn affects sleep integrity. Recent investigations delineate the relation of sleep to a broad array of processes ranging from learning and memory to emotional reactivity and mood, and use a variety of methodological approaches (imaging, electrophysiological, behavioral) to reveal the complex relations between sleep and the functioning of the awake brain. The articles in this issue advance our fundamental knowledge of the relation of sleep to psychological function. In addition, several of the articles discuss how sleep is affected by or affects human clinical conditions, including insomnia, epilepsy, mild cognitive impairment, bipolar disorder, and cancer. Together, the articles of this special issue highlight recent progress in understanding the behavioral neuroscience of sleep and identify promising areas for future research, including the possibility of sleep-based interventions to improve psychological health. (PsycINFO Database Record
Pace-Schott, E F; Kaji, J; Stickgold, R; Hobson, J A
The Nightcap is a home-based sleep monitoring device that reliably differentiates rapid eye movement sleep, nonrapid eye movement sleep and wake states using eyelid and body movement measurements. This study documents its capacity to measure differences in sleep latency and sleep efficiency between self-described good and poor sleepers drawn from a normal population. Ten self-described "good" sleepers and 11 self-described "poor" sleepers were selected from a pool of college students. These groups differed significantly on selection parameters and on subjective estimates of sleep quality obtained each morning during the study. Each subject wore the Nightcap at home for 12-17 nights. Statistically significant differences in Nightcap-measured sleep latency and sleep efficiency were obtained between groups using individual subject means. In individual subjects, Nightcap measurements of sleep latency were correlated with subjective estimates of sleep latency. Poor sleepers were less accurate in estimating their sleep onset latency than were good sleepers. The demonstrated sensitivity of the Nightcap to good and poor sleep in these normal subjects augurs well for its application in a clinical setting.
Nakatani, Masahiro; Okada, Shima; Shimizu, Sachiko; Mohri, Ikuko; Ohno, Yuko; Taniike, Masako; Makikawa, Masaaki
In recent years, the amount of children with sleep disorders that cause arousal during sleep or light sleep is increasing. Attention-deficit hyperactivity disorder (ADHD) is a cause of this sleep disorder; children with ADHD have frequent body movement during sleep. Therefore, we investigated the body movement during sleep of children with and without ADHD using video imaging. We analysed large gross body movements (GM) that occur and obtained the GM rate and the rest duration. There were differences between the body movements of children with ADHD and normally developed children. The children with ADHD moved frequently, so their rest duration was shorter than that of the normally developed children. Additionally, the rate of gross body movement indicated a significant difference in REM sleep (p < 0.05). In the future, we will develop a new device that can easily diagnose children with ADHD, using video image processing.
Alzoubi, Karem H; Khabour, Omar F; Albawaana, Amal S; Alhashimi, Farah H; Athamneh, Rabaa Y
Sleep deprivation is associated with oxidative stress that causes learning and memory impairment. Tempol is a nitroxide compound that promotes the metabolism of many reactive oxygen species (ROS) and has antioxidant and neuroprotective effect. The current study investigated whether chronic administration of tempol can overcome oxidative stress and prevent learning and memory impairment induced by sleep deprivation. Sleep deprivation was induced in rats using multiple platform model. Tempol was administered to rats via oral gavages. Behavioral studies were conducted to test the spatial learning and memory using radial arm water maze. The hippocampus was dissected; antioxidant biomarkers (GSH, GSSG, GSH/GSSG ratio, GPx, SOD, and catalase) were assessed. The result of this project revealed that chronic sleep deprivation impaired both short and long term memory (P<0.05), while tempol treatment prevented such effect. Furthermore, tempol normalized chronic sleep deprivation induced reduction in the hippocampus activity of catalase, GPx, and SOD (P<0.05). Tempol also enhanced the ratio of GSH/GSSG in chronically sleep deprived rats treated with tempol as compared with only sleep deprived rats (P<0.05). In conclusion chronic sleep deprivation induced memory impairment, and treatment with tempol prevented this impairment probably through normalizing antioxidant mechanisms in the hippocampus.
Kong, Danyang; Soon, Chun Siong; Chee, Michael W L
Multiple experiments have found sleep deprivation to lower task-related parietal and extrastriate visual activation, suggesting a reduction of visual processing capacity in this state. The perceptual load theory of attention (Lavie, 1995) predicts that our capacity to process unattended distractors will be reduced by increasing perceptual difficulty of task-relevant stimuli. Here, we evaluated the effects of sleep deprivation and perceptual load on visual processing capacity by measuring neural repetition-suppression to unattended scenes while healthy volunteers attended to faces embedded in face-scene pictures. Perceptual load did not affect repetition suppression after a normal night of sleep. Sleep deprivation reduced repetition suppression in the parahippocampal place area (PPA) in the high but not low perceptual load condition. Additionally, the extent to which task-related fusiform face area (FFA) activation was reduced after sleep deprivation correlated with behavioral performance and lowered repetition suppression in the PPA. The findings concerning correct responses indicate that a portion of stimulus related activation following a normal night of sleep contributes to potentially useful visual processing capacity that is attenuated following sleep deprivation. Finally, when unattended stimuli are not highly intrusive, sleep deprivation does not appear to increase distractibility.
Dijk, Derk-Jan; Lockley, Steven W.
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.
... page: //medlineplus.gov/ency/patientinstructions/000029.htm Dementia - behavior and sleep problems To use the sharing features on this ... get to sleep and stay asleep Tips for Behavior and Sleep Problems Having a daily routine may help. Calmly ...
This chapter reviews studies relating biological and mental activity during sleep and discusses how sleep affects waking behavior. The research shows that sleep and waking behaviors—-both physiological and cognitive--are more directly related than previously imagined....
... essential aspect of chronic disease prevention and health promotion. How much sleep is enough? Sleep needs vary ... National Center for Chronic Disease Prevention and Health Promotion. *Data from the National Institutes of Health Sleep ...
... of the chemicals and hormones that help us sleep well (growth hormone and melatonin).Some lifestyle habits (such as smoking and drinking alcohol or caffeinated drinks) can cause sleep problems.Sleep problems may be caused by illness, ...
Johnson, Dayna A.; Lisabeth, Lynda; Hickson, DeMarc; Johnson-Lawrence, Vicki; Samdarshi, Tandaw; Taylor, Herman; Diez Roux, Ana V.
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
Gardner, Benjamin; Strus, Ewa; Meng, Qing Cheng; Coradetti, Thomas; Naidoo, Nirinjini N.; Kelz, Max B.; Williams, Julie A.
Background Shared neurophysiologic features between sleep and anesthetic-induced hypnosis indicate a potential overlap in neuronal circuitry underlying both states. Previous studies in rodents indicate that pre-existing sleep debt discharges under propofol anesthesia. We explored the hypothesis that propofol anesthesia also dispels sleep pressure in the fruit fly. To our knowledge, this constitutes the first time propofol has been tested in the genetically tractable model, Drosophila melanogaster. Methods Daily sleep was measured in Drosophila using a standard locomotor activity assay. Propofol was administered by transferring flies onto food containing various doses of propofol or equivalent concentrations of vehicle. High-Performance Liquid Chromatography (HPLC) was used to measure tissue concentrations of ingested propofol. To determine if propofol anesthesia substitutes for natural sleep, we subjected flies to 10 hours (h) sleep deprivation (SD), followed by 6h propofol exposure, and monitored subsequent sleep. Results Oral propofol treatment causes anesthesia in flies as indicated by a dose-dependent reduction in locomotor activity (n=11–41 flies from each group) and increased arousal threshold (n=79–137). Recovery sleep in flies fed propofol after SD was delayed until after flies had emerged from anesthesia (n=30–48). SD was also associated with a significant increase in mortality in propofol-fed flies (n=44–46). Conclusions Together, these data indicate that fruit flies are effectively anesthetized by ingestion of propofol, and suggest that homologous molecular and neuronal targets of propofol are conserved in Drosophila. However, behavioral measurements indicate that propofol anesthesia does not satisfy the homeostatic need for sleep, and may compromise the restorative properties of sleep. PMID:26556728
Kharakoz, D P
Temperature as a regulator of sleep is considered. Phenomenological data are presented indicating that there is a causal (not just a correlative) relationship between the changes in brain temperature and sleep phases in the wake-sleep cycle. An earlier suggested phase-transitional concept of the recovery function of sleep was shown to be the theoretical background for this relationship. According to the concept, sleep is an evolutionary developed mechanism of purification of the molecular composition of membranes in fast synapses, whose exocytosis depends on fluid-to-solid phase transition in the membrane. The concept suggests the answer to the question of why the recovery function is incompatible with the wake state and it states that the temperature changes (its decrease during the slow-wave sleep) is a necessary condition of the recovery process. Finally, some practically valuable issues from the concept are considered, including those that at first glance may seem paradoxical.
Siclari, Francesca; Khatami, Ramin; Urbaniok, Frank; Nobili, Lino; Mahowald, Mark W; Schenck, Carlos H; Cramer Bornemann, Michel A; Bassetti, Claudio L
Although generally considered as mutually exclusive, violence and sleep can coexist. Violence related to the sleep period is probably more frequent than generally assumed and can be observed in various conditions including parasomnias (such as arousal disorders and rapid eye movement sleep behaviour disorder), epilepsy (in particular nocturnal frontal lobe epilepsy) and psychiatric diseases (including delirium and dissociative states). Important advances in the fields of genetics, neuroimaging and behavioural neurology have expanded the understanding of the mechanisms underlying violence and its particular relation to sleep. The present review outlines the different sleep disorders associated with violence and aims at providing information on diagnosis, therapy and forensic issues. It also discusses current pathophysiological models, establishing a link between sleep-related violence and violence observed in other settings.
Kelly, Michael L; Peters, Richard A; Tisdale, Ryan K; Lesku, John A
Reduced vigilance is the conspicuous cost of sleep in most animals. To mitigate against this cost, some birds and aquatic mammals have evolved the ability to sleep with one-half of their brain at a time, a phenomenon known as unihemispheric sleep. During unihemispheric sleep the eye neurologically connected to the 'awake' hemisphere remains open while the other eye is closed. Such unilateral eye closure (UEC) has been observed across avian and non-avian reptiles, but has received little attention in the latter. Here, we explored the use of UEC in juvenile saltwater crocodiles (1) under baseline conditions, and in the presence of (2) other young crocodiles and (3) a human. Crocodiles increased the amount of UEC in response to the human, and preferentially oriented their open eye towards both stimuli. These results are consistent with observations on unihemispherically sleeping cetaceans and birds, and could have implications for our understanding of the evolution of unihemispheric sleep.
Kalmbach, David A; Pillai, Vivek; Roth, Thomas; Drake, Christopher L
Little attention has been paid to the relation between daily affect and sleep, as most prior studies have focused instead on the role of pathological mood in the context of sleep disturbance. However, understanding the transaction between normal variations in emotional experiences and sleep can shed light on the premorbid vulnerabilities that trigger the evolution of affect and sleep into more problematic states. The present study used a 2-week daily sampling approach to examine the impact of day-to-day variations in positive and negative affect on nightly self-reported sleep-onset latency, sleep duration and sleep quality in a sample of young women. Hierarchical linear modelling revealed temporal relations between positive and negative affect states and sleep parameters. Specifically, different aspects of both positive and negative affect were uniquely predictive of sleep indices, with sadness and serenity acting as the most consistent predictors. Additionally, better sleep quality was predictive of greater happiness the following day. These results highlight the importance of how our daily emotional experiences influence our nightly sleep and, in turn, how our sleep has an impact on our daily affect. Moreover, our findings may offer insight into the progression of normative levels of affect and sleep as they develop into comorbid depression, anxiety and insomnia.
Alberca-Reina, Esther; Cantero, Jose L; Atienza, Mercedes
Encoding and memory consolidation are influenced by factors such as sleep and congruency of newly learned information with prior knowledge (i.e., schema). However, only a few studies have examined the contribution of sleep to enhancement of schema-dependent memory. Based on previous studies showing that total sleep deprivation specifically impairs hippocampal encoding, and that coherent schemas reduce the hippocampal consolidation period after learning, we predict that sleep loss in the pre-training night will mainly affect schema-unrelated information whereas sleep restriction in the post-training night will have similar effects on schema-related and unrelated information. Here, we tested this hypothesis by presenting participants with face-face associations that could be semantically related or unrelated under different sleep conditions: normal sleep before and after training, and acute sleep restriction either before or after training. Memory was tested one day after training, just after introducing an interference task, and two days later, without any interference. Significant results were evident on the second retesting session. In particular, sleep restriction before training enhanced memory for semantically congruent events in detriment of memory for unrelated events, supporting the specific role of sleep in hippocampal memory encoding. Unexpectedly, sleep restriction after training enhanced memory for both related and unrelated events. Although this finding may suggest a poorer encoding during the interference task, this hypothesis should be specifically tested in future experiments. All together, the present results support a framework in which encoding processes seem to be more vulnerable to sleep loss than consolidation processes.
Sawant, Neena S; Parkar, Shubhangi R; Tambe, Ravindra
Sleep paralysis (SP) is a cardinal symptom of narcolepsy. However, little is available in the literature about isolated sleep paralysis. This report discusses the case of a patient with isolated sleep paralysis who progressed from mild to severe SP over 8 years. He also restarted drinking alcohol to be able to fall asleep and allay his anxiety symptoms. The patient was taught relaxation techniques and he showed complete remission of the symptoms of SP on follow up after 8 months.
Poryazova, R; Bassetti, C L
The three different states of being (wakefulness, NREM and REM sleep) are associated with profound neurophysiological and neurochemical changes in the brain. These changes explain the existence of movement disorders appearing only or preferentially during sleep, and the effects of sleep on movement disorders. Sleep-related movement disorders are of clinical relevance for multiple reasons: 1) high frequency (e.g. restless legs syndrome (RLS)); 2) diagnostic relevance (e.g. REM sleep behavior disorder (RBD) as first manifestation of Parkinson disorder); 3) diagnostic uncertainty (e.g. parasomnias vs nocturnal epilepsy); 4) association with injuries (e.g. RBD, sleepwalking), sleep disruption/daytime sleepiness (e.g. RLS), and psycho-social burden (e.g. enuresis); 5) requirement of specific treatments (e.g. nocturnal epilepsy, stridor, RBD). This article gives an overview on clinical manifestations, pathophysiology, work-up and treatment of sleep-related movement disorders (e.g. RLS, bruxism), parasomnias (e.g. sleepwalking, RBD), sleep-related epilepsies, and on sleep-associated manifestations of movement disorders (e.g. Parkinson disease, multiple system atrophy).
Headaches and sleep disorders are associated in a complex manner. Both the disorders are common in the general population, but the relationship between the two is more than coincidental. Sleep disorders can exacerbate headache sand the converse is also true. Treatment of sleep disorders can have a positive impact on the treatment of headaches. Screening for sleep disorders should be considered in all patients with headaches. This can be accomplished with brief screening tools. Those who screen positively can be further evaluated or referred to asleep specialist.
Frenette, Eric; Guilleminault, Christian
Events occurring during nighttime sleep in children can be easily mislabeled, as witnesses are usually not immediately available. Even when observers are present, description of the events can be sketchy, as these individuals are frequently aroused from their own sleep. Errors of perception are thus common and can lead to diagnosis of epilepsy where other sleep-related conditions are present, sometimes initiating unnecessary therapeutic interventions, especially with antiepileptic drugs. Often not acknowledged, paroxysmal nonepileptic behavioral and motor episodes in sleep are encountered much more frequently than their epileptic counterpart. The International Classification of Sleep Disorders (ICSD) 2nd edition displays an extensive list of such conditions that can be readily mistaken for epilepsy. The most prevalent ones are reviewed, such as nonrapid eye movement (NREM) sleep parasomnias, comprised of sleepwalking, confusional arousals and sleep terrors, periodic leg movements of sleep, repetitive movement disorders, benign neonatal myoclonus, and sleep starts. Apnea of prematurity is also briefly reviewed. Specific issues regarding management of these selected disorders, both for diagnostic consideration and for therapeutic intervention, are addressed.
Monk, T. H.; Reynolds CF, 3. d.; Kupfer, D. J.; Buysse, D. J.; Coble, P. A.; Hayes, A. J.; Machen, M. A.; Petrie, S. R.; Ritenour, A. M.
Increasingly, there is a need in both research and clinical practice to document and quantify sleep and waking behaviors in a comprehensive manner. The Pittsburgh Sleep Diary (PghSD) is an instrument with separate components to be completed at bedtime and waketime. Bedtime components relate to the events of the day preceding the sleep, waketime components to the sleep period just completed. Two-week PghSD data is presented from 234 different subjects, comprising 96 healthy young middle-aged controls, 37 older men, 44 older women, 29 young adult controls and 28 sleep disorders patients in order to demonstrate the usefulness, validity and reliability of various measures from the instrument. Comparisons are made with polysomnographic and actigraphic sleep measures, as well as personality and circadian type questionnaires. The instrument was shown to have sensitivity in detecting differences due to weekends, age, gender, personality and circadian type, and validity in agreeing with actigraphic estimates of sleep timing and quality. Over a 12-31 month delay, PghSD measures of both sleep timing and sleep quality showed correlations between 0.56 and 0.81 (n = 39, P < 0.001).
How, C H; Hsu, P P; Tan, K L
Most people spend a third of their lives sleeping, and thus, sleep has a major impact on all of us. As sleep is a function and not a structure, it is challenging to treat and prevent its complications. Sleep apnoea is one such complication, with serious and potentially life-threatening consequences. Local studies estimate that about 15% of Singapore's population is afflicted with sleep apnoea. The resulting sleep fragmentation may result in poor quality of sleep, leading to daytime sleepiness. Sleep apnoea may also be the underlying cause of high blood pressure, memory loss, poor concentration and work performance, motor vehicle accidents, and marital problems. Evaluation involves a sleep study, followed by patient education, and an individualised step-wise management approach should be explored. Many patients will require follow-up for a long period of time, as management options may not offer a permanent cure; other contributory causes may arise at different phases of their lives, compounded by genetic and hormonal issues, ethnicity and the modern hazards of a fast-paced society.
Brick, Cameron A; Seely, Darbi L; Palermo, Tonya M
The aim of this study was to determine whether subjective sleep quality was reduced in medical students, and whether demographics and sleep hygiene behaviors were associated with sleep quality. A Web-based survey was completed by 314 medical students, containing questions about demographics, sleep habits, exercise habits, caffeine, tobacco and alcohol use, and subjective sleep quality (using the Pittsburgh Sleep Quality Index). Correlation and regression analyses tested for associations among demographics, sleep hygiene behaviors, and sleep quality. As hypothesized, medical students' sleep quality was significantly worse than a healthy adult normative sample (t = 5.13, p < .001). Poor sleep quality in medical students was predicted by several demographic and sleep hygiene variables, and future research directions are proposed.
Anderson, Kirstie N; Smith, Ian E; Shneerson, John M
Sleep-related rhythmic movements (head banging or body rocking) are extremely common in normal infants and young children, but less than 5% of children over the age of 5 years old exhibit these stereotyped motor behaviors. They characteristically occur during drowsiness or sleep onset rather than in deep sleep or rapid eye movement (REM) sleep. We present a 27-year-old man with typical rhythmic movement disorder that had persisted into adult life and was restricted to REM sleep. This man is the oldest subject with this presentation reported to date and highlights the importance of recognizing this nocturnal movement disorder when it does occur in adults.
Sasazawa, Y.; Kawada, T.; Kiryu, Y.
This study was designed to assess the effects of daytime physical exercise on the quality of objective and subjective sleep by examining all-night sleep EEGs. The subjects were five male students, aged 19 to 20 years, who were in the habit of performing regular daytime exercise. The sleep polygraphic parameters in this study were sleep stage time as a percentage of total sleep time (%S1, %S2, %S(3+4), %SREM, %MT), time in bed (TIB), sleep time (ST), total sleep time (TST), sleep onset latency (SOL), waking from sleep, sleep efficiency, number of awakenings, number of stage shifts, number of spindles, and percentages of α and δ waves, all of which were determined by an automatic computer analysis system. The OSA questionnaire was used to investigate subjective sleep. The five scales of the OSA used were sleepiness, sleep maintenance, worry, integrated sleep feeling, and sleep initiation. Each sleep parameter was compared in the exercise and the non-exercise groups. Two-way analysis of variance was applied using subject factor and exercise factor. The main effect of the subject was significant in all parameters and the main effect of exercise in %S(3+4), SOL and sleep efficiency, among the objective sleep parameters. The main effects of the subject, except sleepiness, were significant, as was the main effect of exercise on sleep initiation, among the subjective sleep parameters. These findings suggest that daytime exercise shortened sleep latency and prolonged slow-wave sleep, and that the subjects fell asleep more easily on exercise days. There were also significant individual differences in both the objective and subjective sleep parameters.
Song, Seungmoon; Geyer, Hartmut
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
Poe, Gina R.; Walsh, Christine M.; Bjorness, Theresa E.
Mechanism is at the heart of understanding, and this chapter addresses underlying brain mechanisms and pathways of cognition and the impact of sleep on these processes, especially those serving learning and memory. This chapter reviews the current understanding of the relationship between sleep/waking states and cognition from the perspective afforded by basic neurophysiological investigations. The extensive overlap between sleep mechanisms and the neurophysiology of learning and memory processes provide a foundation for theories of a functional link between the sleep and learning systems. Each of the sleep states, with its attendant alterations in neurophysiology, is associated with facilitation of important functional learning and memory processes. For rapid eye movement (REM) sleep, salient features such as PGO waves, theta synchrony, increased acetylcholine, reduced levels of monoamines and, within the neuron, increased transcription of plasticity-related genes, cumulatively allow for freely occurring bidirectional plasticity (long-term potentiation (LTP) and its reversal, depotentiation). Thus, REM sleep provides a novel neural environment in which the synaptic remodeling essential to learning and cognition can occur, at least within the hippocampal complex. During nonREM sleep Stage 2 spindles, the cessation and subsequent strong bursting of noradrenergic cells and coincident reactivation of hippocampal and cortical targets would also increase synaptic plasticity, allowing targeted bidirectional plasticity in the neocortex as well. In delta nonREM sleep, orderly neuronal reactivation events in phase with slow wave delta activity, together with high protein synthesis levels, would facilitate the events that convert early LTP to long lasting LTP. Conversely, delta sleep does not activate immediate early genes associated with de novo LTP. This nonREM sleep-unique genetic environment combined with low acetylcholine levels may serve to reduce the strength of
Poe, Gina R; Walsh, Christine M; Bjorness, Theresa E
Mechanism is at the heart of understanding, and this chapter addresses underlying brain mechanisms and pathways of cognition and the impact of sleep on these processes, especially those serving learning and memory. This chapter reviews the current understanding of the relationship between sleep/waking states and cognition from the perspective afforded by basic neurophysiological investigations. The extensive overlap between sleep mechanisms and the neurophysiology of learning and memory processes provide a foundation for theories of a functional link between the sleep and learning systems. Each of the sleep states, with its attendant alterations in neurophysiology, is associated with facilitation of important functional learning and memory processes. For rapid eye movement (REM) sleep, salient features such as PGO waves, theta synchrony, increased acetylcholine, reduced levels of monoamines and, within the neuron, increased transcription of plasticity-related genes, cumulatively allow for freely occurring bidirectional plasticity, long-term potentiation (LTP) and its reversal, depotentiation. Thus, REM sleep provides a novel neural environment in which the synaptic remodelling essential to learning and cognition can occur, at least within the hippocampal complex. During non-REM sleep Stage 2 spindles, the cessation and subsequent strong bursting of noradrenergic cells and coincident reactivation of hippocampal and cortical targets would also increase synaptic plasticity, allowing targeted bidirectional plasticity in the neocortex as well. In delta non-REM sleep, orderly neuronal reactivation events in phase with slow wave delta activity, together with high protein synthesis levels, would facilitate the events that convert early LTP to long-lasting LTP. Conversely, delta sleep does not activate immediate early genes associated with de novo LTP. This non-REM sleep-unique genetic environment combined with low acetylcholine levels may serve to reduce the strength of
Worthman, Carol M.; Brown, Ryan A.
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
Lauer, Christoph J; Krieg, Jürgen-Christian
Sleep research on eating disorders has addressed two major questions: (1) the effects of chronic starvation in anorexia nervosa and of rapidly fluctuating eating patterns in bulimia nervosa on the sleep regulating processes and (2) the search for a significant neurobiological relationship between eating disorders and major depression. At present, the latter question appears to be resolved, since most of the available evidences clearly underline the notion that eating disorders (such as anorexia and bulimia nervosa) and affective disorders are two distinct entities. Regarding the effects of starvation on sleep regulation, recent research in healthy humans and in animals demonstrates that such a condition results in a fragmentation of sleep and a reduction of slow wave sleep. Although several peptides are supposed to be involved in these regulatory processes (i.e. CCK, orexin, leptin), their mode of action is still poorly understood. In opposite to these experimentally induced sleep disturbances are the findings that the sleep patterns in eating disorder patients per se do not markedly differ from those in healthy subjects. However, when focusing on the so-called restricting anorexics, who maintain their chronic underweight by strictly dieting, the expected effects of malnutrition on sleep can be ascertained. Furthermore, at least partial weight restoration results in a 'deepening' of nocturnal sleep in the anorexic patients. However, our knowledge about the neurobiological systems (as well as their circadian pattern of activity) that transmit the effects of starvation and of weight restoration on sleep is still limited and should be extended to metabolic signals mediating sleep.
Alkadhi, Karim; Zagaar, Munder; Alhaider, Ibrahim; Salim, Samina; Aleisa, Abdulaziz
Although the physiological function of sleep is not completely understood, it is well documented that it contributes significantly to the process of learning and memory. Ample evidence suggests that adequate sleep is essential for fostering connections among neuronal networks for memory consolidation in the hippocampus. Sleep deprivation studies are extremely valuable in understanding why we sleep and what are the consequences of sleep loss. Experimental sleep deprivation in animals allows us to gain insight into the mechanism of sleep at levels not possible to study in human subjects. Many useful approaches have been utilized to evaluate the effect of sleep loss on cognitive function, each with relative advantages and disadvantages. In this review we discuss sleep and the detrimental effects of sleep deprivation mostly in experimental animals. The negative effects of sleep deprivation on various aspects of brain function including learning and memory, synaptic plasticity and the state of cognition-related signaling molecules are discussed. PMID:24179461
Chen, Zhe; Wimmer, Ralf D; Wilson, Matthew A; Halassa, Michael M
The correlation between sleep integrity and attentional performance is normally interpreted as poor sleep causing impaired attention. Here, we provide an alternative explanation for this correlation: common thalamic circuits regulate sensory processing across sleep and attention, and their disruption may lead to correlated dysfunction. Using multi-electrode recordings in mice, we find that rate and rhythmicity of thalamic reticular nucleus (TRN) neurons are predictive of their functional organization in sleep and suggestive of their participation in sensory processing across states. Surprisingly, TRN neurons associated with spindles in sleep are also associated with alpha oscillations during attention. As such, we propose that common thalamic circuit principles regulate sensory processing in a state-invariant manner and that in certain disorders, targeting these circuits may be a more viable therapeutic strategy than considering individual states in isolation.
Yoncheva, Y N; Castellanos, F X; Pizinger, T; Kovtun, K; St-Onge, M-P
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.
Mascetti, Gian Gastone
Sleep is a behavior characterized by a typical body posture, both eyes’ closure, raised sensory threshold, distinctive electrographic signs, and a marked decrease of motor activity. In addition, sleep is a periodically necessary behavior and therefore, in the majority of animals, it involves the whole brain and body. However, certain marine mammals and species of birds show a different sleep behavior, in which one cerebral hemisphere sleeps while the other is awake. In dolphins, eared seals, and manatees, unihemispheric sleep allows them to have the benefits of sleep, breathing, thermoregulation, and vigilance. In birds, antipredation vigilance is the main function of unihemispheric sleep, but in domestic chicks, it is also associated with brain lateralization or dominance in the control of behavior. Compared to bihemispheric sleep, unihemispheric sleep would mean a reduction of the time spent sleeping and of the associated recovery processes. However, the behavior and health of aquatic mammals and birds does not seem at all impaired by the reduction of sleep. The neural mechanisms of unihemispheric sleep are unknown, but assuming that the neural structures involved in sleep in cetaceans, seals, and birds are similar to those of terrestrial mammals, it is suggested that they involve the interaction of structures of the hypothalamus, basal forebrain, and brain stem. The neural mechanisms promoting wakefulness dominate one side of the brain, while those promoting sleep predominates the other side. For cetaceans, unihemispheric sleep is the only way to sleep, while in seals and birds, unihemispheric sleep events are intermingled with bihemispheric and rapid eye movement sleep events. Electroencephalogram hemispheric asymmetries are also reported during bihemispheric sleep, at awakening, and at sleep onset, as well as being associated with a use-dependent process (local sleep). PMID:27471418
Fernandez-Mendoza, Julio; Calhoun, Susan; Bixler, Edward O.; Pejovic, Slobodanka; Karataraki, Maria; Liao, Duanping; Vela-Bueno, Antonio; Ramos-Platon, Maria J.; Sauder, Katherine A.; Vgontzas, Alexandros N.
Study Objectives: To examine the joint effect of insomnia and objective short sleep duration on neuropsychological performance. Design: Representative cross-sectional study. Setting: Sleep laboratory. Participants: 1,741 men and women randomly selected from central Pennsylvania. Interventions: None. Measurements: Insomnia (n = 116) was defined by a complaint of insomnia with a duration ≥ 1 year and the absence of sleep disordered breathing (SDB), while normal sleep (n = 562) was defined as the absence of insomnia, excessive daytime sleepiness, and SDB. Both groups were split according to polysomnographic sleep duration into 2 categories: ≥ 6 h of sleep (“normal sleep duration”) and < 6 h of sleep (“short sleep duration”). We compared the groups' performance on a comprehensive neuropsychological battery that measured processing speed, attention, visual memory, and verbal fluency, while controlling for age, race, gender, education, body mass index, and physical and mental health. Results: No significant differences were detected between insomniacs and controls. However, the insomnia with short sleep duration group compared to the control with normal or short sleep duration groups showed poorer neuropsychological performance in variables such as processing speed, set-switching attention, and number of visual memory errors and omissions. In contrast, the insomnia with normal sleep duration group showed no significant deficits. Conclusions: Insomnia with objective short sleep duration is associated with deficits in set-switching attentional abilities, a key component of the “executive control of attention.” These findings suggest that objective sleep duration may predict the severity of chronic insomnia, including its effect on neurocognitive function. Citation: Fernandez-Mendoza J; Calhoun S; Bixler EO; Pejovic S; Karataraki M; Liao D; Vela-Bueno A; Ramos-Platon MJ; Sauder KA; Vgontzas AN. Insomnia with objective short sleep duration is associated with
Caldwell, J L; Caldwell, J A
Twelve subjects were studied to determine the after-effects of using three 10-mg doses of dextroamphetamine to sustain alertness during sleep deprivation. Sleep architecture during recovery sleep was evaluated by comparing post-deprivation sleep after placebo. Performance and mood recovery were assessed by comparing volunteers who received dextroamphetamine first (during sleep deprivation) to those who received placebo first. Stages 1 and 2 sleep, movement time, REM latency, and sleep latency increased on the night after sleep deprivation with dextroamphetamine vs. placebo. Stage 4 was unaffected. Comparisons to baseline revealed more stage 1 during baseline than during either post-deprivation sleep period and more stage 2 during baseline than during sleep following placebo. Stage 4 sleep was lower during baseline and after dextroamphetamine than after placebo. Sleep onset was slowest on the baseline night. Next-day performance and mood were not different as a function of whether subjects received dextroamphetamine or placebo during deprivation. These data suggest dextroamphetamine alters post-deprivation sleep architecture when used to sustain alertness during acute sleep loss, but next-day performance and subjective mood ratings are not substantially affected. A recovery sleep period of only 8 h appears to be adequate to regain baseline performance levels after short-term sleep deprivation.
... Because OSA makes it hard to get a good night's sleep, kids might have a hard time waking in the morning, be tired throughout the day, and have attention or other behavior problems. As a result, sleep apnea can hurt school performance. Teachers and others may think a child has attention ...
Yanik, G.M. Jr.
Behavioral and biochemical approaches have been used to determine the relative contribution of endogenous adenosine and adenosine receptors to the sleep-wake cycle in the rat. Adenosine concentrations in specific areas of the rat brain were not affected by 24 hours of total sleep deprivation, or by 24 or 48 hours of REM sleep deprivation. In order to assess the effect of REM sleep deprivation on adenosine A/sub 1/ receptors, /sup 3/H-L-PIA binding was measured. The Bmax values for /sup 3/H-L-PIA binding to membrane preparations of the cortices and corpus striata from 48 hour REM sleep-deprived animals were increased 14.8% and 23%, respectively. These increases were not maintained following the cessation of sleep deprivation and recovered within 2 hours. The results of a 96 hour REM deprivation experiment were similar to those of the 48 hour REM sleep deprivation experiment. However, these increases were not evident in similar structures taken from stress control animals, and conclusively demonstrated that the changes in /sup 3/H-L-PIA binding resulted from REM sleep deprivation and not from stress.
Harrelson, Orvis A.; And Others
The first part of this booklet concerns why sleep and exercise are necessary. It includes a discussion of what occurs during sleep and what dreams are. It also deals with the benefits of exercise, fatigue, posture, and the correlation between exercise and personality. The second part concerns nutrition and the importance of food. This part covers…
... as while talking on the phone or driving. Risk factors for sleep apnea include being overweight and having a large neck. Losing even 10 percent of body weight can help reduce the ... be at increased risk for sleep apnea. Smoking and alcohol use increase ...
Fisher, H. T.
Schematic outlines are presented with various design requirements for the accommodation of the spacecrew of Space Stations. The primary concern is for sleeping accommodations. Some other general requirements given are for a rest place, entertainment, dressing area, personal item stowage, body restraint, total privacy, external viewing, and grooming provisions. Several plans are given for sleep quarters concepts.
... During the study, medical staff will watch your child sleep. Several sensors will be attached to your child ... your family. Last Updated 11/21/2015 Source Sleep Apnea and Your Child (Copyright © 2003 American Academy of Pediatrics) Updated 10/ ...
Morselli, Lisa L.; Guyon, Aurore; Spiegel, Karine
Evidence for the role of sleep on metabolic and endocrine function has been reported more than four decades ago. In the past 30 years, the prevalence of obesity and diabetes has greatly increased in industrialized countries, and self-imposed sleep curtailment, now very common, is starting to be recognized as a contributing factor, alongside with increased caloric intake and decreased physical activity. Furthermore, obstructive sleep apnea, a chronic condition characterized by recurrent upper airway obstruction leading to intermittent hypoxemia and sleep fragmentation, has also become highly prevalent as a consequence of the epidemic of obesity and has been shown to contribute, in a vicious circle, to the metabolic disturbances observed in obese patients. In this article, we summarize the current data supporting the role of sleep in the regulation of glucose homeostasis and the hormones involved in the regulation of appetite. We also review the results of the epidemiologic and laboratory studies that investigated the impact of sleep duration and quality on the risk of developing diabetes and obesity, as well as the mechanisms underlying this increased risk. Finally, we discuss how obstructive sleep apnea affects glucose metabolism and the beneficial impact of its treatment, the continuous positive airway pressure. In conclusion, the data available in the literature highlight the importance of getting enough good sleep for metabolic health. PMID:22101912
... is linked to an increased risk for the development of Type 2 diabetes. Specifically, sleep duration and quality have emerged as predictors of levels of Hemoglobin A1c , an important marker of blood sugar control. Recent research suggests that optimizing sleep ...
Han, Kuem Sun; Kim, Lin
The purpose of this study was to review potential, physiological, hormonal and neuronal mechanisms that may mediate the sleep changes. This paper investigates the literatures regarding the activity of the hypothalamic-pituitary-adrenal (HPA) axis, one of the main neuroendocrine stress systems during sleep in order to identify relations between stress and sleep disorder and the treatment of stress-induced insomnia. Sleep and wakefulness are regulated by the aminergic, cholinergic brainstem and hypothalamic systems. Activation of the HPA and/or the sympathetic nervous systems results in wakefulness and these hormones including corticotropin-releasing hormone (CRH), adrenocorticotropic hormone (ACTH), cortisol or corticosterone, noradrenaline, and adrenaline, are associated with attention and arousal. Stress-related insomnia leads to a vicious circle by activating the HPA system. An awareness of the close interaction between sleep and stress systems is emerging and the hypothalamus is now recognized as a key center for sleep regulation, with hypothalamic neurontransmitter systems providing the framework for therapeutic advances. An updated understanding of these systems may allow researchers to elucidate neural mechanisms of sleep disorder and to develop effective intervention for sleep disorder. PMID:23319874
Wu, Meng-Ni; Lai, Chiou-Lian; Liu, Ching-Kuan; Yen, Chen-Wen; Liou, Li-Min; Hsieh, Cheng-Fang; Tsai, Ming-Ju; Chen, Sharon C-J; Hsu, Chung-Yao
Because the impact of periodic limb movements in sleep (PLMS) is controversial, no consensus has been reached on the therapeutic strategy for PLMS in obstructive sleep apnea (OSA). To verify the hypothesis that PLMS is related to a negative impact on the cardiovascular system in OSA patients, this study investigated the basal autonomic regulation by heart rate variability (HRV) analysis. Sixty patients with mild-to-moderate OSA who underwent polysomnography (PSG) and completed sleep questionnaires were analysed retrospectively and divided into the PLMS group (n = 30) and the non-PLMS group (n = 30). Epochs without any sleep events or continuous effects were evaluated using HRV analysis. No significant difference was observed in the demographic data, PSG parameters or sleep questionnaires between the PLMS and non-PLMS groups, except for age. Patients in the PLMS group had significantly lower normalized high frequency (n-HF), high frequency (HF), square root of the mean of the sum of the squares of difference between adjacent NN intervals (RMSSD) and standard deviation of all normal to normal intervals index (SDNN-I), but had a higher normalized low frequency (n-LF) and LF/HF ratio. There was no significant difference in the Epworth Sleepiness Scale, the Pittsburgh Sleep Quality Index, the Short-Form 36 and the Hospital Anxiety and Depression Scale between the two groups. After adjustment for confounding variables, PLMS remained an independent predictor of n-LF (β = 0.0901, P = 0.0081), LF/HF ratio (β = 0.5351, P = 0.0361), RMSSD (β = -20.1620, P = 0.0455) and n-HF (β = -0.0886, P = 0.0134). In conclusion, PLMS is related independently to basal sympathetic predominance and has a potentially negative impact on the cardiovascular system of OSA patients.
de Andrés, Isabel; Garzón, Miguel; Reinoso-Suárez, Fernando
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.
de Andrés, Isabel; Garzón, Miguel; Reinoso-Suárez, Fernando
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 b