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Showing papers on "Non-rapid eye movement sleep published in 2005"


Journal ArticleDOI
26 Oct 2005-Nature
TL;DR: The functions of mammalian sleep remain unclear, but theories suggest a role for non-rapid eye movement sleep in energy conservation and in nervous system recuperation.
Abstract: The functions of mammalian sleep remain unclear. Most theories suggest a role for non-rapid eye movement (NREM) sleep in energy conservation and in nervous system recuperation. Theories of REM sleep have suggested a role for this state in periodic brain activation during sleep, in localized recuperative processes and in emotional regulation. Across mammals, the amount and nature of sleep are correlated with age, body size and ecological variables, such as whether the animals live in a terrestrial or an aquatic environment, their diet and the safety of their sleeping site. Sleep may be an efficient time for the completion of a number of functions, but variations in sleep expression indicate that these functions may differ across species.

901 citations


Book ChapterDOI
01 Jan 2005
TL;DR: In this article, a nightly pattern of sleep in mature humans sleeping on a regular schedule includes several reliable characteristics: sleep begins in NREM and progresses through deeper NREM stages (stages 2, 3, and 4 using the classic definitions, or stages N2 and N3 using the updated definitions) before the first episode of REM sleep occurs approximately 80 to 100 minutes later.
Abstract: Normal human sleep comprises two states—rapid eye movement (REM) and non–REM (NREM) sleep— that alternate cyclically across a sleep episode. State characteristics are well defined: NREM sleep includes a variably synchronous cortical electroencephalogram (EEG; including sleep spindles, Kcomplexes, and slow waves) associated with low muscle tonus and minimal psychological activity; the REM sleep EEG is desynchronized, muscles are atonic, and dreaming is typical. A nightly pattern of sleep in mature humans sleeping on a regular schedule includes several reliable characteristics: Sleep begins in NREM and progresses through deeper NREM stages (stages 2, 3, and 4 using the classic definitions, or stages N2 and N3 using the updated definitions) before the first episode of REM sleep occurs approximately 80 to 100 minutes later. Thereafter, NREM sleep and REM sleep cycle with a period of approximately 90 minutes. NREM stages 3 and 4 (or stage N3) concentrate in the early NREM cycles, and REM sleep episodes lengthen across the night. Age-related changes are also predictable: Newborn humans enter REM sleep (called active sleep) before NREM (called quiet sleep) and have a shorter sleep cycle (approximately 50 minutes); coherent sleep stages emerge as the brain matures during the first year. At birth, active sleep is approximately 50% of total sleep and declines over the first 2 years to approximately 20% to 25%. NREM sleep slow waves are not present at birth but emerge in the first 2 years. Slow-wave sleep (stages 3 and 4) decreases across adolescence by 40% from preteen years and continues a slower decline into old age, particularly in men and less so in women. REM sleep as a percentage of total sleep is approximately 20% to 25% across childhood, adolescence, adulthood, and into old age except in dementia. Other factors predictably alter sleep, such as previous sleep-wake history (e.g., homeostatic load), phase of the circadian timing system, ambient temperature, drugs, and sleep disorders. A clear appreciation of the normal characteristics of sleep provides a strong background and template for understanding clinical conditions in which “normal” characteristics are altered, as well as for interpreting certain consequences of sleep disorders. In this chapter, the normal young adult sleep pattern is described as a working baseline pattern. Normative changes due to aging and other factors are described with that background in mind. Several major sleep disorders are highlighted by their differences from the normative pattern.

813 citations


Journal ArticleDOI
TL;DR: Evidence is provided that overnight verbal memory retention is highly correlated with the number of sleep spindles detected by an automatic algorithm over left frontocentral areas, and theories suggesting a link between sleep spindle activity and verbal memory consolidation are supported.

387 citations


Journal ArticleDOI
01 Nov 2005-Sleep
TL;DR: Maturational changes of homeostatic sleep regulation are permissive of the sleep phase delay in the course of adolescence as well as aspects of sleep homeostasis.
Abstract: STUDY OBJECTIVES: To examine the effects of total sleep deprivation on adolescent sleep and the sleep electroencephalogram (EEG) and to study aspects of sleep homeostasis. DESIGN: Subjects were studied during baseline and recovery sleep after 36 hours of wakefulness. SETTING: Four-bed sleep research laboratory. PARTICIPANTS: Seven prepubertal or early pubertal children (pubertal stage Tanner 1 or 2 = Tanner 1/2; mean age 11.9 years, SD +/- 0.8, 2 boys) and 6 mature adolescents (Tanner 5; 14.2 years, +/- 1.4, 2 boys). INTERVENTIONS: Thirty-six hours of sleep deprivation. MEASUREMENTS: All-night polysomnography was performed. EEG power spectra (C3/A2) were calculated using a Fast Fourier transform routine. RESULTS: In both groups, sleep latency was shorter, sleep efficiency was higher, non-rapid eye movement (NREM) sleep stage 4 was increased, and waking after sleep onset was reduced in recovery relative to baseline sleep. Spectral power of the NREM sleep EEG was enhanced after sleep deprivation in the low-frequency range (1.6-3.6 Hz in Tanner 1/2; 0.8-6.0 Hz in Tanner 5) and reduced in the sigma range (11-15 Hz). Sleep deprivation resulted in a stronger increase of slow-wave activity (EEG power 0.6-4.6 Hz, marker for sleep homeostatic pressure) in Tanner 5 (39% above baseline) than in Tanner 1/2 adolescents (18% above baseline). Sleep homeostasis was modeled according to the two-process model of sleep regulation. The build-up of homeostatic sleep pressure during wakefulness was slower in Tanner 5 adolescents (time constant of exponential saturating function 15.4 +/- 2.5 hours) compared with Tanner 1/2 children (8.9 +/- 1.2 hours). In contrast, the decline of the homeostatic process was similar in both groups. CONCLUSION: Maturational changes of homeostatic sleep regulation are permissive of the sleep phase delay in the course of adolescence.

383 citations


Journal ArticleDOI
01 Jan 2005-Drugs
TL;DR: In general, the objectively measured sleep of depressed patients improves during 3–4 weeks of effective antidepressant treatment with most agents, as does their subjective impression of their sleep.
Abstract: Most antidepressants change sleep; in particular, they alter the physiological patterns of sleep stages recorded overnight with EEG and other physiological measures. These effects are greatest and most consistent on rapid eye movement (REM) sleep, and tend to be in the opposite direction to the sleep abnormalities found in major depression, but are usually of greater degree. Reductions in the amount of REM sleep and increases in REM sleep onset latency are seen after taking antidepressants, both in healthy volunteers and in depressed patients. Antidepressants that increase serotonin function by blocking reuptake or by inhibiting metabolism have the greatest effect on REM sleep. The decrease in amount of REM sleep appears to be greatest early in treatment, and gradually diminishes during long-term treatment, except after monoamine oxidase inhibitors when REM sleep is often absent for many months. Sleep initiation and maintenance are also affected by antidepressants, but the effects are much less consistent between drugs. Some antidepressants such as clomipramine and the selective serotonin receptor inhibitors (SSRIs), particularly fluoxetine, are sleep-disturbing early in treatment and some others such as amitriptyline and the newer serotonin 5-HT2-receptor antagonists are sleep promoting. However, these effects are fairly short-lived and there are very few significant differences between drugs after a few weeks of treatment. In general, the objectively measured sleep of depressed patients improves during 3-4 weeks of effective antidepressant treatment with most agents, as does their subjective impression of their sleep. Sleep improvement earlier in treatment may be an important clinical goal in some patients, perhaps when insomnia is particularly distressing, or to ensure compliance. In these patients, the choice of a safely used and effective antidepressant which improves sleep in short term is indicated. Patients with other sleep disorders such as restless legs syndrome and REM sleep behaviour disorder should be identified before choosing a treatment, as some antidepressants worsen these conditions. Conversely, there is evidence that some antidepressants may be useful in the treatment of sleep disorders such as night terrors.

329 citations


Journal ArticleDOI
TL;DR: The results suggest that playing an exciting computer game affects sleep latency and REM sleep but that a bright display does not affect sleep variables.
Abstract: Epidemiological studies have shown that playing a computer game at night delays bedtime and shortens sleeping hours, but the effects on sleep architecture and quality have remained unclear. In the present study, the effects of playing a computer game and using a bright display on nocturnal sleep were examined in a laboratory. Seven male adults (24.7+/-5.6 years old) played exciting computer games with a bright display (game-BD) and a dark display (game-DD) and performed simple tasks with low mental load as a control condition in front of a BD (control-BD) and DD (control-DD) between 23:00 and 1:45 hours in randomized order and then went to bed at 2:00 hours and slept until 8:00 hours. Rectal temperature, electroencephalogram (EEG), heart rate and subjective sleepiness were recorded before sleep and a polysomnogram was recorded during sleep. Heart rate was significantly higher after playing games than after the control conditions, and it was also significantly higher after using the BD than after using the DD. Subjective sleepiness and relative theta power of EEG were significantly lower after playing games than after the control conditions. Sleep latency was significantly longer after playing games than after the control conditions. REM sleep was significantly shorter after the playing games than after the control conditions. No significant effects of either computer games or BD were found on slow-wave sleep. These results suggest that playing an exciting computer game affects sleep latency and REM sleep but that a bright display does not affect sleep variables.

304 citations


Journal ArticleDOI
TL;DR: Functional magnetic resonance imaging data is presented demonstrating a change in the representation of a motor memory after a night of sleep, which holds important implications for acquiring real-life skills and in clinical rehabilitation following brain trauma, such as stroke.

296 citations


Journal ArticleDOI
TL;DR: Sleep restriction practiced on a chronic basis induces cumulative performance deficits of the same order of magnitude as observed during total sleep deprivation, and there are also considerable individual differences in the degree of vulnerability to performance impairment from sleep loss.

276 citations


Journal ArticleDOI
TL;DR: The development and optimization of an automatic classification system that is based on one central EEG channel, two EOG channels and one chin EMG channel and proved the high reliability and validity of the Somnolyzer 24 × 7 and demonstrated its applicability in clinical routine and sleep studies.
Abstract: To date, the only standard for the classification of sleep-EEG recordings that has found worldwide acceptance are the rules published in 1968 by Rechtschaffen and Kales. Even though several attempts have been made to automate the classification process, so far no method has been published that has proven its validity in a study including a sufficiently large number of controls and patients of all adult age ranges. The present paper describes the development and optimization of an automatic classification system that is based on one central EEG channel, two EOG channels and one chin EMG channel. It adheres to the decision rules for visual scoring as closely as possible and includes a structured quality control procedure by a human expert. The final system (Somnolyzer 24 x 7) consists of a raw data quality check, a feature extraction algorithm (density and intensity of sleep/wake-related patterns such as sleep spindles, delta waves, SEMs and REMs), a feature matrix plausibility check, a classifier designed as an expert system, a rule-based smoothing procedure for the start and the end of stages REM, and finally a statistical comparison to age- and sex-matched normal healthy controls (Siesta Spot Report). The expert system considers different prior probabilities of stage changes depending on the preceding sleep stage, the occurrence of a movement arousal and the position of the epoch within the NREM/REM sleep cycles. Moreover, results obtained with and without using the chin EMG signal are combined. The Siesta polysomnographic database (590 recordings in both normal healthy subjects aged 20-95 years and patients suffering from organic or nonorganic sleep disorders) was split into two halves, which were randomly assigned to a training and a validation set, respectively. The final validation revealed an overall epoch-by-epoch agreement of 80% (Cohen's kappa: 0.72) between the Somnolyzer 24 x 7 and the human expert scoring, as compared with an inter-rater reliability of 77% (Cohen's kappa: 0.68) between two human experts scoring the same dataset. Two Somnolyzer 24 x 7 analyses (including a structured quality control by two human experts) revealed an inter-rater reliability close to 1 (Cohen's kappa: 0.991), which confirmed that the variability induced by the quality control procedure, whereby approximately 1% of the epochs (in 9.5% of the recordings) are changed, can definitely be neglected. Thus, the validation study proved the high reliability and validity of the Somnolyzer 24 x 7 and demonstrated its applicability in clinical routine and sleep studies.

275 citations


Journal ArticleDOI
26 Oct 2005-Nature
TL;DR: Contrary to common assumptions, wakefulness, rapid eye movement (REM) and non-REM sleep are not mutually exclusive states, and this striking realization explains a fascinating range of clinical phenomena.
Abstract: Problems with sleep are one of the commonest reasons for seeking medical attention. Knowledge gained from basic research into sleep in animals has led to marked advances in the understanding of human sleep, with important diagnostic and therapeutic implications. At the same time, research guided by human sleep disorders is leading to important basic sleep concepts. For example, sleep may not be a global, but rather a local, brain phenomenon. Furthermore, contrary to common assumptions, wakefulness, rapid eye movement (REM) and non-REM sleep are not mutually exclusive states. This striking realization explains a fascinating range of clinical phenomena.

264 citations


Journal ArticleDOI
TL;DR: This review provides brief tutorials on the elements of the innate immune system that detect infection, how sleep is characterized in the laboratory, issues regarding the interpretation of sleep effects on immune function, the interaction of sleep with circadian rhythms and stress, and some of the microbial products, cytokines, and neuropeptides associated with sleep regulation.
Abstract: Sleep is a fundamental physiologic process with unknown functions. It is divided into 2 distinct states: non-rapid-eye-movement sleep and rapid-eye-movement sleep. After acute infection with nonneurotropic agents, there are stereotypic changes in non-rapid-eye-movement sleep, particularly increased time spent in slow-wave sleep, and often a reduction of time spent in rapid-eye-movement sleep. It is now recognized that both infection-associated sleep and spontaneous sleep are regulated, in part, by immune mediators called cytokines. This review provides brief tutorials on the elements of the innate immune system that detect infection, how sleep is characterized in the laboratory, issues regarding the interpretation of sleep effects on immune function, the interaction of sleep with circadian rhythms and stress, and some of the microbial products, cytokines, and neuropeptides associated with sleep regulation. We also summarize our current understanding of the role of sleep in host defense and asthma exacerbation.

Journal ArticleDOI
TL;DR: This model provides an explanation for why the acquisition of various types of skills and priming effects, subserved by different brain structures but all designated by the generic term of implicit or non‐declarative memory, may not benefit from the same sleep stages.
Abstract: Sleep function remains elusive despite our rapidly increasing comprehension of the processes generating and maintaining the different sleep stages. Several lines of evidence support the hypothesis that sleep is involved in the off-line reprocessing of recently-acquired memories. In this review, we summarize the main results obtained in the field of sleep and memory consolidation in both animals and humans, and try to connect sleep stages with the different memory systems. To this end, we have collated data obtained using several methodological approaches, including electrophysiological recordings of neuronal ensembles, post-training modifications of sleep architecture, sleep deprivation and functional neuroimaging studies. Broadly speaking, all the various studies emphasize the fact that the four long-term memory systems (procedural memory, perceptual representation system, semantic and episodic memory, according to Tulving's SPI model; Tulving, 1995) benefit either from non-rapid eye movement (NREM) (not just SWS) or rapid eye movement (REM) sleep, or from both sleep stages. Tulving's classification of memory systems appears more pertinent than the declarative/non-declarative dichotomy when it comes to understanding the role of sleep in memory. Indeed, this model allows us to resolve several contradictions, notably the fact that episodic and semantic memory (the two memory systems encompassed in declarative memory) appear to rely on different sleep stages. Likewise, this model provides an explanation for why the acquisition of various types of skills (perceptual-motor, sensory-perceptual and cognitive skills) and priming effects, subserved by different brain structures but all designated by the generic term of implicit or non-declarative memory, may not benefit from the same sleep stages.

Journal ArticleDOI
TL;DR: Evidence is presented which points to a significant role for unstable, central respiratory motor output as a significant contributor to upper airway narrowing and obstruction during sleep.
Abstract: This brief review addresses the characteristics, lability and the mechanisms underlying the hypocapnic-induced apnoeic threshold which is unmasked during NREM sleep. The role of carotid chemoreceptors as fast, sensitive detectors of dynamic changes in CO2 is emphasized and placed in historical context of the long-held debate over central vs. peripheral contributions to CO2 sensing and to apnoea. Finally, evidence is presented which points to a significant role for unstable, central respiratory motor output as a significant contributor to upper airway narrowing and obstruction during sleep.

Journal ArticleDOI
TL;DR: It is shown that, like a "fingerprint", a particular topographic distribution of the electroencephalogram (EEG) power along the antero-posterior cortical axis distinguishes each individual during non-REM sleep, and this individual EEG-trait is substantially invariant across six consecutive nights characterized by large experimentally induced changes of sleep architecture.

Journal ArticleDOI
TL;DR: Results from the sleep laboratory do not seem to support the subjective complaints of poor sleep in patients with obsessive-compulsive disorder (OCD) and post-traumatic stress disorder (PTSD), and no significant differences were found in all sleep parameters between social phobia patients and controls.
Abstract: Many patients suffering from the majority of anxiety disorders complain about their sleep by reporting difficulties in initiating and maintaining it. Polysomnographic studies have shown that, in comparison to normal subjects, the sleep of patients with panic disorder is characterized by longer sleep latency, increased time awake and reduced sleep efficiency. Sleep architecture is normal and there are no significant changes in REM sleep measures. Nocturnal panic attacks are non-REM-related events and occur without an obvious trigger in 18-45% of panic disorder patients. Regarding generalized anxiety disorder, the patients complain of 'trouble sleeping' in 60-70%, while polysomnography has shown increased sleep latency and decreased sleep continuity measures. The findings in REM sleep and sleep architecture generally do not show any aberration to exist. In patients with obsessive-compulsive disorder (OCD) and post-traumatic stress disorder (PTSD), results from the sleep laboratory do not seem to support the subjective complaints of poor sleep. The early reports of shortened REM latency in OCD could not be replicated by recent studies. A dysregulation of the REM sleep control system has been reported for patients with PTSD. Finally, no significant differences were found in all sleep parameters between social phobia patients and controls.

Journal ArticleDOI
TL;DR: There are remarkable racial differences in reported napping and nighttime sleep patterns beginning as early as age 3 and extending to at least 8 years of age, independent of commonly investigated demographic factors.
Abstract: The first few years of life are associated with dramatic changes in sleep amount and distribution. The 15 to 17 hours of daily sleep of neonates drops to ~14 hours by the age of 1 year and then declines more gradually to ~10 hours by the age of 8 years.1–3 The polyphasic sleep/wake pattern present at birth quickly shifts to one characterized by a primary nocturnal sleep period and 2 daytime naps, 1 in the morning (which disappears at ~2 years) and 1 in the afternoon.4,5 Between the ages of 2 and 5 years, the frequency of afternoon naps declines, and the biphasic sleep/wake pattern gives way to a consolidated pattern of sleep occurring only at night.6 Changes in sleep structure also occur during this period, with an adult-like sleep architecture emerging by approximately the age of 5 years.1,3 These pronounced changes in sleep likely reflect maturation of chronobiological and homeostatic mechanisms well known to regulate sleep/wake cycling and sleep structure in adults.6,7 The actions of these mechanisms are modulated by environmental, biomedical, psychosocial, and cultural/familial factors in a way that permits sleep needs to be met and/or alertness to be maintained in widely varying circumstances. Among children, as among adults, inadequate or poor-quality sleep is closely linked to disturbances of behavior and mood.8–10 Moreover, good sleep may be important for normal cognitive and emotional development.11 This study is an investigation of the early childhood transition from a biphasic to a consolidated, or monophasic, sleep/wake pattern. Most studies have found that the proportion of children napping regularly drops gradually from close to 100% at the age of 2 years to <10% at the age of 6 years.4,5,12,13 The age-related decrease in napping is closely linked to the aforementioned reduction in total daily sleep duration. Cultural preferences may play an important role in regulation of napping behavior.6,14 For example, most Icelandic children stop napping by their fourth birthday,13 whereas the majority of American children typically stop napping between ages 4 and 5 years.4 Currently, little is known about napping beyond the descriptive level. The age at which napping is no longer obligatory has not been established, and the factors influencing when children stop (or continue) napping (eg, school schedules, home routines, regulatory systems) have not been investigated systematically. Furthermore, little is known about the benefits and consequences of biphasic versus monophasic wake/sleep patterns during childhood. The major objective of this study was to examine racial differences in caretaker-reported napping and nighttime sleep. In a recent study of 2- to 5-year-old children sampled from pediatric patient streams in a major midwestern-US population center, Lavigne et al8 found that minority (black, Hispanic, and “other”) children were reported to take substantially more and longer daytime naps and to sleep less at night than were non-Hispanic white children. It is important to determine if this finding is generalizable to minorities living in other geographic areas of the United States. The data now available to guide research and clinical practice related to children’s sleep/wake patterns have come from studies of mostly non-Hispanic white children.4,5,13,15,16 Given the increasingly complex racial makeup of the United States, normative data on children’s sleep may need to be organized by racial group. Additionally, finding an explanation for racial differences would increase our understanding of factors that regulate sleep and wakefulness in children. Racial variability in napping may be due to a number of factors including (1) differences in awareness of afternoon sleep tendency by children and/or their caretakers, (2) cultural or family-related differences in attitudes about the acceptability of a regular afternoon nap, and (3) genetic differences either in sleep need or in the functioning of the chronobiological and/or homeostatic mechanisms regulating sleep. In this study, we compared the caretaker-reported napping and nighttime sleep of non-Hispanic white and black children in a community sample of 2- to 8-year-olds. Based on findings by Lavigne et al,8 it was anticipated that black children would be reported to nap more and spend less time in bed at night than would white children of the same age. One of the specific questions posed was whether the stronger nap tendency of black children reflected greater sleep need as opposed to a difference in the way in which sleep was distributed. A second question concerned whether racial differences in sleep could be accounted for by demographic differences. A final question concerned whether variability in napping behavior in preschool children was importantly related to measures of daytime behavioral and emotional functioning.

Journal ArticleDOI
TL;DR: Although daytime fatigue is a frequent complaint associated with complaints of pain-related disturbed sleep, objective assessments of daytime sleepiness reveal minimally elevated levels ofSleepiness and emphasize the importance of distinguishing sleepiness and fatigue.
Abstract: 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.

Journal ArticleDOI
TL;DR: In this article, a rat EEG was recorded during 6 hours of sleep deprivation in the first half of the light period (SDL, n = 7) and the EEG showed an increase in the delta (1.5-4 Hz) and low theta (5-6.5 Hz) bands.

Journal ArticleDOI
TL;DR: A strong association was observed between rCBF in the ventromedial prefrontal regions and delta power, in agreement with electrophysiological studies, supporting the notion that delta activity is a valuable prominent feature of NREM sleep.

Journal ArticleDOI
TL;DR: Evidence is shown that mobile phone exposure prior to sleep may promote rapid eye movement sleep and modify the sleep electroencephalogram in the first non-rapid eye movementSleep period.
Abstract: Previous research has suggested that exposure to radiofrequency electromagnetic fields increases electroencephalogram spectral power in non-rapid eye movement sleep. Other sleep parameters have also been affected following exposure. We examined whether aspects of sleep architecture show sensitivity to electromagnetic fields emitted by digital mobile phone handsets. Fifty participants were exposed to electromagnetic fields for 30 min prior to sleep. Results showed a decrease in rapid eye movement sleep latency and increased electroencephalogram spectral power in the 11.5-12.25 Hz frequency range during the initial part of sleep following exposure. These results are evidence that mobile phone exposure prior to sleep may promote rapid eye movement sleep and modify the sleep electroencephalogram in the first non-rapid eye movement sleep period.

Journal ArticleDOI
TL;DR: The majority of studies indicate that stage 4 sleep and rapid eye movement (REM) latency are reduced in schizophrenia, whereas REM sleep duration tends to remain unchanged, and the characterization of the neurotransmitter systems involved remains a challenging dilemma.
Abstract: Insomnia is a common symptom in schizophrenia, although it is seldom the predominant complaint Sleep-onset and maintenance insomnia is a characteristic feature of schizophrenic patients regardless of either their medication status (drug-naive or previously treated) or the phase of the clinical course (acute or chronic) Regarding sleep architecture, the majority of studies indicate that stage 4 sleep and rapid eye movement (REM) latency are reduced in schizophrenia, whereas REM sleep duration tends to remain unchanged Insomnia in schizophrenic patients could be partly related to the presumed over-activity of the dopaminergic system However, there is a possibility that the GABAergic system is also involved in sleep disturbance in schizophrenia Since many signal transmission systems within the CNS can be implicated in the reduction of REM latency in schizophrenia, the characterization of the neurotransmitter systems involved remains a challenging dilemma

Journal ArticleDOI
TL;DR: If many factors, including pain, disease process per se, as well as medication, could disturb sleep, sleep disturbances may also adversely affect the natural course of the painful disease.
Abstract: Objective Clinical experiences as well as specific investigations show that pain and sleep disturbances are closely correlated. The aims of this review are first to describe sleep disturbances related to painful medical diseases and analgesics and secondly to propose management possibilities for these sleep disturbances. Method The viewpoints presented were based mainly on objective rest activity and sleep studies using actigraphy and polysomnography. Results Polysomnographic and actigraphic studies have described significant sleep disturbances in patients suffering from different pain disorders. These disturbances are: reduced sleep efficiency and altered sleep architecture characterized by increased wakefulness and stage 1 non-rapid eye movement sleep, associated with diminished slow wave sleep and rapid eye movement sleep. Sleep disturbances may be related to pain and to the analgesic or sedative medications administered. Conclusion If many factors, including pain, disease process per se, as well as medication, could disturb sleep, sleep disturbances may also adversely affect the natural course of the painful disease. Improving sleep quantity and quality in patients with painful disorders may break this vicious circle and as consequence enhance the patients' overall health and quality of life.

Journal ArticleDOI
TL;DR: The data indicate that age-related changes in sleep propensity are clearly related to a reduced circadian signal opposing the homeostatic drive for sleep.

Journal ArticleDOI
TL;DR: The role of KC providing gating functions in idiopathic generalized epilepsies and other, different, sleep disorders are characterised and the relationship of KC with synchronisation-type and desynchronisation- type micro-arousals, and the 'cyclic alternating pattern', will be discussed.

Journal ArticleDOI
TL;DR: The recognition of RBD has shed additional scientific light on the "bumps in the night"; expanded knowledge of states of being and state dissociation; opened up new areas of research on brain and mind dysfunction during sleep; and reaffirmed the vital link between basic research and clinical medicine.

Journal ArticleDOI
TL;DR: In this paper, the subjective estimates of sleep in depressed patients are discussed, and the differential effects of various classes of antidepressants on subjective sleep parameters, as well as on sleep onset latency, continuity of sleep, sleep efficiency and rapid eye movement (REM) sleep verified with sleep recordings.
Abstract: Depressed patients often report sleep problems, which usually include difficulties with initiation and maintenance of sleep, as well as poor subjective quality of sleep. Such reports are confirmed by objective analysis of depressed patients’ sleep through polysomnography, although there is no exact correspondence between subjective and objective measurements. In the present paper, we discuss some methodological problems related to the subjective estimates of sleep. Further, we review the differential effects of the various classes of antidepressants on subjective sleep parameters, as well as on sleep onset latency, continuity of sleep, sleep efficiency and rapid eye movement (REM) sleep verified with sleep recordings. Finally, we discuss the attempts to use these and other indices, such as delta sleep ratio (DSR), as signposts of the course of the illness, and predictors of response to treatment.

Journal ArticleDOI
TL;DR: The homeostatic response of the lower-range SWA was markedly and specifically reduced after NA depletion, suggesting that the wake-dependent accumulation of sleep need is causally related to cellular changes dependent on NA release, such as the induction of LTP-related genes, and support the hypothesis that sleep SWA homeostasis may be related to synaptic potentiation during wakefulness.
Abstract: Sleep intensity is regulated by the duration of previous wakefulness, suggesting that waking results in the progressive accumulation of sleep need (Borbely and Achermann, 2000). In mammals, sleep intensity is reflected by slow-wave activity (SWA) in the nonrapid eye movement (NREM) sleep electroencephalogram, which increases in proportion to the time spent awake. However, the mechanisms responsible for the increase of NREM SWA after wakefulness remain unclear. According to a recent hypothesis (Tononi and Cirelli, 2003), the increase in SWA occurs because during wakefulness, many cortical circuits undergo synaptic potentiation, as evidenced by the widespread induction of long-term potentiation (LTP)-related genes in the brain of awake animals. A direct prediction of this hypothesis is that manipulations interfering with the induction of LTP-related genes should result in a blunted SWA response. Here, we examined SWA response in rats in which cortical norepinephrine (NA) was depleted, a manipulation that greatly reduces the induction of LTP-related genes during wakefulness (Cirelli and Tononi, 2004). We found that the homeostatic response of the lower-range SWA was markedly and specifically reduced after NA depletion. These data suggest that the wake-dependent accumulation of sleep need is causally related to cellular changes dependent on NA release, such as the induction of LTP-related genes, and support the hypothesis that sleep SWA homeostasis may be related to synaptic potentiation during wakefulness.

Journal ArticleDOI
TL;DR: Findings confirm the presence of extensive variability in the sleep of chronic insomniacs and that poor sleep may be predictable for some of them and that sleep patterns could be classified in three clusters.
Abstract: SUMMARY Sleep of chronic insomniacs is often characterized by extensive night-to-nightvariability. To date, no study has examined this variability with long series of dailysleep data. The present study examined night-to-night variability with a sample of 106participants meeting DSM-IV diagnostic criteria for persistent primary insomnia.Participants completed daily sleep diaries for an average of 31 days (range: 18–56).Sleep efficiency, sleep onset latency and wake after sleep onset were derived from thismeasure. Despite evidence of extensive night variability, results showed that sleeppatterns could be classified in three clusters. The first one was characterized by a highprobability of having poor sleep, the second one by a low and decreasing probability,and the third one by a constant median probability of having a poor sleep, which is anunpredictable sleep pattern. In the first cluster, poor sleep was expected each night forpatients with a predominance mixed insomnia including the three insomnia subtypes. Inthe second cluster, patients presented moderate insomnia, sleep-onset latency below thethreshold level and a predominance of sleep-maintenance insomnia. In the thirdpattern, poor nights seemed unpredictable for patients with moderate to severeinsomnia associated with the lowest proportion of sleep-maintenance insomnia.Overall, sleep was predictable for about two-thirds of individuals, whereas it wasunpredictable for about one-third. These findings confirm the presence of extensivevariability in the sleep of chronic insomniacs and that poor sleep may be predictable forsome of them. Additional research is needed to characterize those sleep patterns interms of clinical features and temporal course.keywords insomnia, night-to-night variability, predictability, sleep, sleep pattern

Journal ArticleDOI
TL;DR: Sleep paralysis accompanied by hypnopompic (‘upon awakening’) hallucinations is an often-frightening manifestation of discordance between the cognitive/perceptual and motor aspects of rapid eye movement (REM) sleep.
Abstract: Sleep paralysis accompanied by hypnopompic ('upon awakening') hallucinations is an often-frightening manifestation of discordance between the cognitive/perceptual and motor aspects of rapid eye movement (REM) sleep. Awakening sleepers become aware of an inability to move, and sometimes experience intrusion of dream mentation into waking consciousness (e.g. seeing intruders in the bedroom). In this article, we summarize two studies. In the first study, we assessed 10 individuals who reported abduction by space aliens and whose claims were linked to apparent episodes of sleep paralysis during which hypnopompic hallucinations were interpreted as alien beings. In the second study, adults reporting repressed, recovered, or continuous memories of childhood sexual abuse more often reported sleep paralysis than did a control group. Among the 31 reporting sleep paralysis, only one person linked it to abuse memories. This person was among the six recovered memory participants who reported sleep paralysis (i.e. 17% rate of interpreting it as abuse-related). People rely on personally plausible cultural narratives to interpret these otherwise baffling sleep paralysis episodes.

Journal ArticleDOI
01 Jul 2005-Sleep
TL;DR: A daytime short nap containing 3 minutes of stage 2 sleep has recuperative effects, whereas these effects are limited following only stage 1 sleep.
Abstract: Study objectives The recuperative effect of a nap of less than 30 minutes has been confirmed. Such naps consist mainly of stages 1 and 2 sleep. The present study examined whether sleep stage 1 or 2 contributed to the recuperative effect of a short nap. Design Repeated-measurement within-subject design. After sleep was restricted to 1.5 hours less than their usual nocturnal sleep, participants took a rest (No-nap condition) or a nap at 2:00 PM. In the nap condition, they were awakened after 5 minutes of stage 1 sleep (S1-nap condition) or 3 minutes after stage 2 sleep appeared (S2-nap condition). Setting University sleep laboratory. Participants Ten healthy university students (aged 19 to 24 years). Measurements Subjective mood, performance on visual detection and symbol-digit substitution tasks, and the number of slow eye movements during a performance task were measured before and after the nap or rest. Results In the No-nap condition, subjective mood and performance deteriorated, and Slow eye movements increased during mid-afternoon, suggesting that the post-lunch dip occurred. In contrast, subjective alertness and performance improved and slow eye movements rarely occurred in the S2-nap condition. Although subjective sleepiness and fatigue improved, performance deteriorated and slow eye movements increased in the S1-nap condition. Conclusion A daytime short nap containing 3 minutes of stage 2 sleep has recuperative effects, whereas these effects are limited following only stage 1 sleep.