Showing papers on "Slow-wave sleep published in 2004"
TL;DR: In adults, it appeared that sleep latency, percentages of stage 1 and stage 2 significantly increased with age while percentage of REM sleep decreased, and effect sizes for the different sleep parameters were greatly modified by the quality of subject screening, diminishing or even masking age associations with differentSleep parameters.
Abstract: Objectives: The purposes of this study were to identify age-related changes in objectively recorded sleep patterns across the human life span in healthy individuals and to clarify whether sleep latency and percentages of stage 1, stage 2, and rapid eye movement (REM) sleep significantly change with age. Design: Review of literature of articles published between 1960 and 2003 in peer-reviewed journals and meta-analysis. Participants: 65 studies representing 3,577 subjects aged 5 years to 102 years. Measurement: The research reports included in this meta-analysis met the following criteria: (1) included nonclinical participants aged 5 years or older; (2) included measures of sleep characteristics by “all night” polysomnography or actigraphy on sleep latency, sleep efficiency, total sleep time, stage 1 sleep, stage 2 sleep, slow-wave sleep, REM sleep, REM latency, or minutes awake after sleep onset; (3) included numeric presentation of the data; and (4) were published between 1960 and 2003 in peer-reviewed journals. Results: In children and adolescents, total sleep time decreased with age only in studies performed on school days. Percentage of slow-wave sleep was significantly negatively correlated with age. Percentages of stage 2 and REM sleep significantly changed with age. In adults, total sleep time, sleep efficiency, percentage of slow-wave sleep, percentage of REM sleep, and REM latency all significantly decreased with age, while sleep latency, percentage of stage 1 sleep, percentage of stage 2 sleep, and wake after sleep onset significantly increased with age. However, only sleep efficiency continued to significantly decrease after 60 years of age. The magnitudes of the effect sizes noted changed depending on whether or not studied participants were screened for mental disorders, organic diseases, use of drug or alcohol, obstructive sleep apnea syndrome, or other sleep disorders. Conclusions: In adults, it appeared that sleep latency, percentages of stage 1 and stage 2 significantly increased with age while percentage of REM sleep decreased. However, effect sizes for the different sleep parameters were greatly modified by the quality of subject screening, diminishing or even masking age associations with different sleep parameters. The number of studies that examined the evolution of sleep parameters with age are scant among school-aged children, adolescents, and middle-aged adults. There are also very few studies that examined the effect of race on polysomnographic sleep parameters.
2,601 citations
TL;DR: It is shown that sleep homeostasis indeed has a local component, which can be triggered by a learning task involving specific brain regions, and that the local increase in SWA after learning correlates with improved performance of the task after sleep.
Abstract: Human sleep is a global state whose functions remain unclear. During much of sleep, cortical neurons undergo slow oscillations in membrane potential, which appear in electroencephalograms as slow wave activity (SWA) of <4 Hz1. The amount of SWA is homeostatically regulated, increasing after wakefulness and returning to baseline during sleep2. It has been suggested that SWA homeostasis may reflect synaptic changes underlying a cellular need for sleep3. If this were so, inducing local synaptic changes should induce local SWA changes, and these should benefit neural function. Here we show that sleep homeostasis indeed has a local component, which can be triggered by a learning task involving specific brain regions. Furthermore, we show that the local increase in SWA after learning correlates with improved performance of the task after sleep. Thus, sleep homeostasis can be induced on a local level and can benefit performance.
1,658 citations
TL;DR: It is shown that, in humans, hippocampal areas that are activated during route learning in a virtual town are likewise activated during subsequent slow wave sleep, and that the amount of hippocampal activity expressed during slow waveSleep positively correlates with the improvement of performance in route retrieval on the next day.
727 citations
TL;DR: Men, but not women, show evidence of poorer sleep with aging, suggesting important sex differences in sleep physiology, and sleep architecture varies with sex, age, ethnicity, and SDB.
Abstract: Background Polysomnography is used to assess sleep quality and to gauge the functional effect of sleep disorders. Few population-based data are available to estimate the variation in sleep architecture across the population and the extent to which sleep-disordered breathing (SDB), a common health condition, contributes to poor sleep independent of other factors. The objective of this study was to describe the population variability in sleep quality and to quantify the independent associations with SDB. Methods Cross-sectional analyses were performed on data from 2685 participants, aged 37 to 92 years, in a community-based multicenter cohort study. Dependent measures included the percentage time in each sleep stage, the arousal index, and sleep efficiency. Independent measures were age, sex, ethnicity, comorbidity status, and the respiratory disturbance index. Results Lighter sleep was found in men relative to women and in American Indians and blacks relative to other ethnic groups. Increasing age was associated with impaired sleep in men, with less consistent associations in women. Notably, women had, on average, 106% more slow wave sleep. Sleep-disordered breathing was associated with poorer sleep; however, these associations were generally smaller than associations with sex, ethnicity, and age. Current smokers had lighter sleep than ex-smokers or never smokers. Obesity had little effect on sleep. Conclusions Sleep architecture varies with sex, age, ethnicity, and SDB. Individual assessment of the effect of SDB on sleep quality needs to account for other host characteristics. Men, but not women, show evidence of poorer sleep with aging, suggesting important sex differences in sleep physiology.
608 citations
TL;DR: Effects of tDCS involve enhanced generation of slow oscillatory EEG activity considered to facilitate processes of neuronal plasticity, which may facilitate sleep-dependent consolidation of declarative memories.
Abstract: In humans, weak transcranial direct current stimulation (tDCS) modulates excitability in the motor, visual, and prefrontal cortex. Periods rich in slow-wave sleep (SWS) not only facilitate the consolidation of declarative memories, but in humans, SWS is also accompanied by a pronounced endogenous transcortical DC potential shift of negative polarity over frontocortical areas. To experimentally induce widespread extracellular negative DC potentials, we applied anodal tDCS (0.26 mA) [correction] repeatedly (over 30 min) bilaterally at frontocortical electrode sites during a retention period rich in SWS. Retention of declarative memories (word pairs) and also nondeclarative memories (mirror tracing skills) learned previously was tested after this period and compared with retention performance after placebo stimulation as well as after retention intervals of wakefulness. Compared with placebo stimulation, anodal tDCS during SWS-rich sleep distinctly increased the retention of word pairs (p < 0.005). When applied during the wake retention interval, tDCS did not affect declarative memory. Procedural memory was also not affected by tDCS. Mood was improved both after tDCS during sleep and during wake intervals. tDCS increased sleep depth toward the end of the stimulation period, whereas the average power in the faster frequency bands (,alpha, and beta) was reduced. Acutely, anodal tDCS increased slow oscillatory activity <3 Hz. We conclude that effects of tDCS involve enhanced generation of slow oscillatory EEG activity considered to facilitate processes of neuronal plasticity. Shifts in extracellular ionic concentration in frontocortical tissue (expressed as negative DC potentials during SWS) may facilitate sleep-dependent consolidation of declarative memories.
528 citations
TL;DR: There is increasing evidence that sleep deprivation has detrimental effects on the immune response, indicating that sleep should be considered a vital part of the immune system and that there is a reciprocal relationship between sleep and immunity.
Abstract: It is a common belief that we are more susceptible to infections when deprived of sleep. Consistent with this, there is increasing evidence that sleep deprivation has detrimental effects on the immune response, indicating that sleep should be considered a vital part of the immune system and that there is a reciprocal relationship between sleep and immunity. This relationship is important because, over recent decades, there has been a documented decrease in the mean duration and quality of sleep in the population. The concept that lack of sleep might be compromising immunity in the population has far-reaching public-health implications for both individuals and society.
481 citations
TL;DR: Understanding the role of arousals and CAP and the relationship between physiologic and pathologic MA can shed light on the adaptive properties of the sleeping brain and provide insight into the pathomechanisms of sleep disturbances.
Abstract: The role of arousals in sleep is gaining interest among both basic researchers and clinicians. In the last 20 years increasing evidence shows that arousals are deeply involved in the pathophysiology of sleep disorders. The nature of arousals in sleep is still a matter of debate. According to the conceptual framework of the American Sleep Disorders Association criteria, arousals are a marker of sleep disruption representing a detrimental and harmful feature for sleep. In contrast, our view indicates arousals as elements weaved into the texture of sleep taking part in the regulation of the sleep process. In addition, the concept of micro-arousal (MA) has been extended, incorporating, besides the classical low-voltage fast-rhythm electroencephalographic (EEG) arousals, high-amplitude EEG bursts, be they like delta-like or K-complexes, which reflects a special kind of arousal process, mobilizing parallely antiarousal swings. In physiologic conditions, the slow and fast MA are not randomly scattered but appear structurally distributed within sleep representing state-specific arousal responses. MA preceded by slow waves occurs more frequently across the descending part of sleep cycles and in the first cycles, while the traditional fast type of arousals across the ascending slope of cycles prevails during the last third of sleep. The uniform arousal characteristics of these two types of MAs is supported by the finding that different MAs are associated with an increasing magnitude of vegetative activation ranging hierarchically from the weaker slow EEG types (coupled with mild autonomic activation) to the stronger rapid EEG types (coupled with a vigorous autonomic activation). Finally, it has been ascertained that MA are not isolated events but are basically endowed with a periodic nature expressed in non-rapid eye movement (NREM) sleep by the cyclic alternating pattern (CAP). Understanding the role of arousals and CAP and the relationship between physiologic and pathologic MA can shed light on the adaptive properties of the sleeping brain and provide insight into the pathomechanisms of sleep disturbances. Functional significance of arousal in sleep, and particularly in NREM sleep, is to ensure the reversibility of sleep, without which it would be identical to coma. Arousals may connect the sleeper with the surrounding world maintaining the selection of relevant incoming information and adapting the organism to the dangers and demands of the outer world. In this dynamic perspective, ongoing phasic events carry on the one hand arousal influences and on the other elements of information processing. The other function of arousals is tailoring the more or less stereotyped endogenously determined sleep process driven by chemical influences according to internal and external demands. In this perspective, arousals shape the individual course of night sleep as a variation of the sleep program.
481 citations
TL;DR: In this article, the modified multiple platform (MMP) technique was used for sleep deprivation in social stable groups of rats and showed significant reduction in paradoxical sleep (PS) and slow wave sleep (SWS).
334 citations
TL;DR: Critically ill patients exhibit more frequent arousals and awakenings than is normal, and decreases in rapid eye movement and slow wave sleep, and measures to improve the quantity and quality of sleep in critically ill patients include careful attention to mode of mechanical ventilation, decreasing noise, and sedative agents (although the latter are double-edged swords).
Abstract: Abnormalities of sleep are extremely common in critically ill patients, but the mechanisms are poorly understood. About half of total sleep time occurs during the daytime, and circadian rhythm is markedly diminished or lost. Judgments based on inspection consistently overestimate sleep time and do not detect sleep disruption. Accordingly, reliable polygraphic recordings are needed to measure sleep quantity and quality in critically ill patients. Critically ill patients exhibit more frequent arousals and awakenings than is normal, and decreases in rapid eye movement and slow wave sleep. The degree of sleep fragmentation is at least equivalent to that seen in patients with obstructive sleep apnea. About 20% of arousals and awakenings are related to noise, 10% are related to patient care activities, and the cause for the remainder is not known; severity of underlying disease is likely an important factor. Mechanical ventilation can cause sleep disruption, but the precise mechanism has not been defined. Sleep disruption can induce sympathetic activation and elevation of blood pressure, which may contribute to patient morbidity. In healthy subjects, sleep deprivation can decrease immune function and promote negative nitrogen balance. Measures to improve the quantity and quality of sleep in critically ill patients include careful attention to mode of mechanical ventilation, decreasing noise, and sedative agents (although the latter are double-edged swords).
318 citations
01 Jan 2004
TL;DR: Findings indicate that the MMP technique is effective in inducing PS deprivation (PSD), however, the fact that slow wave sleep (SWS) is also affected may have implications for conclusions on paradoxical sleep function based upon paradoxicalSleep deprivation.
Abstract: Vigilance status was continually monitored in socially stable groups of rats exposed to the modified multiple platform (MMP) technique for sleep deprivation. For comparison, sleep parameters were also monitored in socially isolated rats deprived of sleep by the single platform (SP) method. In all cases, sleep was continuously recorded during baseline, during 96 h of sleep deprivation and during 4 days of recovery. Both multiple- and single-platform techniques completely abolished paradoxical sleep (PS) during the deprivation period, but also resulted in significant decreases in slow wave sleep (SWS) (31% and 37%, respectively). Unexpectedly, animals on large platforms, which are normally intended as controls, also showed significant reductions in PS and SWS, and these effects were more pronounced in rats deprived in groups than in animals deprived in isolation. Another control preparation, rats placed on wire-mesh grids in the deprivation tank, also showed PS reduction (39%) but no loss of SWS during the 4 test days. Paradoxical sleep rebound was observed in the first 24 h in all groups, except for grid controls. Overall, no significant differences were found between single- and multiple-platform procedures during the 4 days of deprivation. However, sleep rebound was more pronounced in MMP-deprived rats than in SP-deprived rats. Sleep loss in both control groups may reflect residual effect of stress that remain in the platform technique. These findings indicate that the MMP technique is effective in inducing PS deprivation (PSD). However, the fact that SWS is also affected may have implications for conclusions on paradoxical sleep function based upon paradoxical sleep deprivation. D 2004 Elsevier B.V. All rights reserved. Theme: Neural basis of behavior Topic: Biological rhythms and sleep
283 citations
TL;DR: The predominance of FRs within the epileptogenic zone not only during NREM sleep, but also during epileptiform‐suppressing desynchronized episodes of waking and REM sleep supports the view that FRs are the product of pathological neuronal hypersynchronization associated with seizure‐generating areas.
Abstract: The presence of fast ripple oscillations (FRs, 200-500 Hz) has been confirmed in rodent epilepsy models but has not been observed in nonepileptic rodents, suggesting that FRs are associated with epileptogenesis. Although studies in human epileptic patients have reported that both FRs and ripples (80-200 Hz) chiefly occur during non-rapid eye movement sleep (NREM), and that ripple oscillations in human hippocampus resemble those found in nonprimate slow wave sleep, quantitative studies of these oscillations previously have not been conducted during polysomnographically defined sleep and waking states. Spontaneous FRs and ripples were detected using automated computer techniques in patients with medial temporal lobe epilepsy during sleep and waking, and results showed that the incidence of ripples, which are thought to represent normal activity in animal and human hippocampus, was similar between epileptogenic and nonepileptogenic temporal lobe, whereas rates of FR occurrence were significantly associated with epileptogenic areas. The generation of both FRs and ripples showed the highest rates of occurrence during NREM sleep. During REM sleep, ripple rates were lowest, whereas FR rates remained elevated and were equivalent to rates observed during waking. The predominance of FRs within the epileptogenic zone not only during NREM sleep, but also during epileptiform-suppressing desynchronized episodes of waking and REM sleep supports the view that FRs are the product of pathological neuronal hypersynchronization associated with seizure-generating areas.
TL;DR: The results indicate that persistent experience-dependent neuronal reverberation is a general property of multiple forebrain structures, and does not consist of an exact replay of previous activity, but instead it defines a mild and consistent bias towards salient neural ensemble firing patterns.
Abstract: The discovery of experience-dependent brain reactivation during both slow-wave (SW) and rapid eye-movement (REM) sleep led to the notion that the consolidation of recently acquired memory traces requires neural replay during sleep. To date, however, several observations continue to undermine this hypothesis. To address some of these objections, we investigated the effects of a transient novel experience on the long-term evolution of ongoing neuronal activity in the rat forebrain. We observed that spatiotemporal patterns of neuronal ensemble activity originally produced by the tactile exploration of novel objects recurred for up to 48 h in the cerebral cortex, hippocampus, putamen, and thalamus. This novelty-induced recurrence was characterized by low but significant correlations values. Nearly identical results were found for neuronal activity sampled when animals were moving between objects without touching them. In contrast, negligible recurrence was observed for neuronal patterns obtained when animals explored a familiar environment. While the reverberation of past patterns of neuronal activity was strongest during SW sleep, waking was correlated with a decrease of neuronal reverberation. REM sleep showed more variable results across animals. In contrast with data from hippocampal place cells, we found no evidence of time compression or expansion of neuronal reverberation in any of the sampled forebrain areas. Our results indicate that persistent experience-dependent neuronal reverberation is a general property of multiple forebrain structures. It does not consist of an exact replay of previous activity, but instead it defines a mild and consistent bias towards salient neural ensemble firing patterns. These results are compatible with a slow and progressive process of memory consolidation, reflecting novelty-related neuronal ensemble relationships that seem to be context- rather than stimulus-specific. Based on our current and previous results, we propose that the two major phases of sleep play distinct and complementary roles in memory consolidation: pretranscriptional recall during SW sleep and transcriptional storage during REM sleep.
TL;DR: Subjects taking serotonergic antidepressants had more EMG activity in the submental lead during REM sleep than did controls, and this correlated with measures of REM suppression and age.
Abstract: STUDY OBJECTIVES Rapid eye movement (REM) sleep behavior disorder (RBD) is generally observed in older men and in individuals with specific neurologic diseases. There are case reports of RBD in individuals taking serotonergic antidepressants. Our objective was to assess electromyogram (EMG) activity during REM sleep in individuals taking serotonergic antidepressants and in a matched control group not on such medication. DESIGN Chart review of clinical and polysomnographic data. SETTING Sleep laboratory affiliated with a general hospital. PARTICIPANTS 15 subjects taking a serotonergic antidepressant and 15 age-matched individuals not on such medication. MEASUREMENTS Submental and anterior tibialis tonic and phasic EMG activity during REM sleep, REM latency, time in REM, apnea-hypopnea index, periodic leg movements of sleep index, and sleep-architecture measures. RESULTS Tonic, but not phasic, submental EMG activity during REM sleep was significantly more common in the antidepressant-treated group than in the control group (P < .02). Tonic REM submental EMG activity correlated with REM latency (r = .42, P = .02) and inversely with REM time (r = -.36, P = .05). Subject age correlated with tonic REM submental EMG activity (r = .58, P = .02) in the antidepressant group There were also trends for more phasic activity in the anterior tibialis (P = .09) and submental (P = .07) EMG in REM sleep in the antidepressant group than in the control group. CONCLUSIONS Subjects taking serotonergic antidepressants had more EMG activity in the submental lead during REM sleep than did controls. This correlated with measures of REM suppression and age. Individuals taking such medications may be at increased risk of developing REM sleep behavior disorder, particularly with increasing age.
TL;DR: The sleep disturbances of either never-medicated or previously treated schizophrenia patients are characterized by a sleep-onset and maintenance insomnia, and the atypical antipsychotics olanzapine, risperidone, and clozapine significantly increase total sleep time and stage 2 sleep.
TL;DR: In this paper, the authors hypothesize that the activity of histamine cells is linked to the maintenance of waking, in contrast to activity in noradrenergic and serotonergic neurons, which is more tightly coupled to maintenance of muscle tone in waking and its loss in REM sleep and cataplexy.
TL;DR: The decline of slow-wave sleep during adolescence may reflect developmental changes of the brain rather than changes of sleep regulatory processes.
Abstract: OBJECTIVES
To describe developmental changes of the human sleep electroencephalogram (EEG) during adolescence using EEG spectral analysis and specifically to compare the nocturnal dynamics of slow-wave activity (EEG spectral power 06-46 Hz, a marker for sleep homeostatic pressure) in prepubertal and mature adolescents
DESIGN After 10 nights on a fixed 10-hour sleep schedule without daytime naps, participants were studied during a 10-hour baseline night
SETTING Data were collected in a 4-bed sleep research laboratory
PARTICIPANTS
Eight prepubertal children (pubertal stage Tanner 1; mean age 113 years, SD +/- 12, 4 boys) and 8 mature adolescents (Tanner 5; mean age 141 years, +/- 13, 3 boys)
INTERVENTIONS Not applicable
MEASUREMENTS
All-night polysomnography was performed Sleep stages were scored according to conventional criteria EEG power spectra (of derivation C3/A2) were calculated using a fast Fourier transform routine
RESULTS
A reduction of non-rapid eye movement (NREM) sleep stage 4 (by 401%) and greater amounts of stage 2 sleep (197%) were found in mature compared to prepubertal adolescents NREM sleep EEG power was lower in the frequency ranges < 7 Hz, 118 to 126 Hz, and 162 to 168 Hz in mature adolescents A reduction of rapid eye movement sleep spectral power was present in the frequency ranges < 86 Hz and 96 to 15 Hz for mature compared to prepubertal adolescents Slow-wave activity showed identical dynamics within individual NREM sleep episodes and across the night in both developmental groups
CONCLUSIONS
The homeostatic recuperative drive during sleep remains unchanged across puberty The decline of slow-wave sleep during adolescence may reflect developmental changes of the brain rather than changes of sleep regulatory processes
TL;DR: It is suggested that caffeine attenuated the build-up of sleep propensity associated with wakefulness, and support an important role of adenosine and adenosines receptors in the homeostatic regulation of sleep.
TL;DR: The results suggest that 1) EEG markers of sleep homeostasis appear in the first postnatal months, and 2) sleepHomeostasis goes through a period of maturation.
Abstract: The development of nocturnal sleep and the sleep electroencephalogram (EEG) was investigated in a longitudinal study during infancy. All-night polysomnographic recordings were obtained at home at 2 wk and at 2, 4, 6, and 9 mo after birth (analysis of 7 infants). Total sleep time and the percentage of quiet sleep or non-rapid eye movement sleep (QS/NREMS) increased with age, whereas the percentage of active sleep or rapid eye movement sleep (AS/REMS) decreased. Spectral power of the sleep EEG was higher in QS/NREMS than in AS/REMS over a large part of the 0.75- to 25-Hz frequency range. In both QS/NREMS and AS/REMS, EEG power increased with age in the frequency range 17 Hz. The largest rise occurred between 2 and 6 mo. A salient feature of the QS/NREMS spectrum was the emergence of a peak in the sigma band (12-14 Hz) at 2 mo that corresponded to the appearance of sleep spindles. Between 2 and 9 mo, low-frequency delta activity (0.75-1.75 Hz) showed an alternating pattern with a high level occurring in every other QS/NREMS episode. At 6 mo, sigma activity showed a similar pattern. In contrast, theta activity (6.5-9 Hz) exhibited a monotonic decline over consecutive QS/NREMS episodes, a trend that at 9 mo could be closely approximated by an exponential function. The results suggest that 1) EEG markers of sleep homeostasis appear in the first postnatal months, and 2) sleep homeostasis goes through a period of maturation. Theta activity and not delta activity seems to reflect the dissipation of sleep propensity during infancy.
TL;DR: The nocturnal increase in ghrelin levels is more likely to be caused by sleep-associated processes than by circadian influences, and secretion during the first hours of sleep correlated positively with peak hGH concentrations.
Abstract: Ghrelin, an endogenous ligand of the growth hormone secretagogue receptor, has been shown to promote slow-wave sleep (SWS, non-REM sleep stages 3 and 4). Plasma levels of ghrelin are dependent on food intake and increase in sleeping subjects during the early part of the night. It is unknown whether sleep itself affects ghrelin levels or whether circadian networks are involved. Therefore, we studied the effect of sleep deprivation on nocturnal ghrelin secretion. In healthy male volunteers, plasma levels of ghrelin, cortisol, and human growth hormone (hGH) were measured during two experimental sessions of 24 h each: once when the subjects were allowed to sleep between 2300 and 0700 and once when they were kept awake throughout the night. During sleep, ghrelin levels increased during the early part of the night and decreased in the morning. This nocturnal increase was blunted during sleep deprivation, and ghrelin levels increased only slightly until the early morning. Ghrelin secretion during the first hours of sleep correlated positively with peak hGH concentrations. We conclude that the nocturnal increase in ghrelin levels is more likely to be caused by sleep-associated processes than by circadian influences. During the first hours of sleep, ghrelin might promote sleep-associated hGH secretion and contribute to the promotion of SWS.
TL;DR: These observations provide first evidence that ‘negative’ BOLD signal changes during human sleep are associated with electrophysiological indicators of altered neuronal activity, and suggest true cortical deactivation upon stimulus presentation.
Abstract: Prominent local decreases in blood oxygenation level (BOLD) can be observed by functional magnetic resonance imaging (fMRI) upon acoustic stimulation during sleep. The goal of this study was to further characterize this BOLD signal decrease with respect to corresponding neurophysiological phenomena using a simultaneous electroencephalography (EEG)/fMRI approach in sleeping human subjects. Healthy volunteers were subjected to acoustic stimulation during non-rapid eye movement (NREM) sleep. On the basis of statistical parametric maps, the correlations between the fMRI response (both amplitude and extent of the BOLD response) and the concomittant changes in the EEG (delta power and K-complexes) were calculated. Amplitude and extent of the stimulus-induced negative BOLD effect correlated positively with measures of EEG synchronization, namely an increase in the number of K-complexes and EEG delta power. Stimulus-induced BOLD decreases were most prominent during light (stage 2) NREM sleep and disappeared during slow wave sleep, indicating an influence of the baseline degree of hyperpolarization. Our observations provide first evidence that 'negative' BOLD signal changes during human sleep are associated with electrophysiological indicators of altered neuronal activity. Increased number of K-complexes and delta power reflecting hyperpolarization suggests true cortical deactivation upon stimulus presentation. This sleep stage-dependent deactivation might serve to protect the brain from arousing stimuli, particularly during the light phases of sleep shortly after sleep onset.
TL;DR: Robust, direct sleep‐facilitating and circadian effects of melatonin are demonstrated without concomitant changes in sleep duration, and support the use ofmelatonin in the treatment of sleep disorders in which the circadian melatonin rhythm is delayed relative to desired sleep time.
Abstract: The rhythm of plasma melatonin originating from the pineal gland and driven by the circadian pacemaker located in the suprachiasmatic nucleus is closely associated with the circadian (approximately 24 h) variation in sleep propensity and sleep spindle activity in humans. We investigated the contribution of melatonin to variation in sleep propensity, structure, duration and EEG activity in a protocol in which sleep was scheduled to begin during the biological day, i.e. when endogenous melatonin concentrations are low. The two 14 day trials were conducted in an environmental scheduling facility. Each trial included two circadian phase assessments, baseline sleep and nine 16 h sleep opportunities (16.00–08.00 h) in near darkness. Eight healthy male volunteers (24.4 ± 4.4 years) without sleep complaints were recruited, and melatonin (1.5 mg) or placebo was administered at the start of the first eight 16 h sleep opportunities. During melatonin treatment, sleep in the first 8 h of the 16 h sleep opportunities was increased by 2 h. Sleep per 16 h was not significantly different and approached asymptotic values of 8.7 h in both conditions. The percentage of rapid eye movement (REM) sleep was not affected by melatonin, but the percentage of stage 2 sleep and sleep spindle activity increased, and the percentage of stage 3 sleep decreased. During the washout night, the melatonin-induced advance in sleep timing persisted, but was smaller than on the preceding treatment night and was consistent with the advance in the endogenous melatonin rhythm. These data demonstrate robust, direct sleep-facilitating and circadian effects of melatonin without concomitant changes in sleep duration, and support the use of melatonin in the treatment of sleep disorders in which the circadian melatonin rhythm is delayed relative to desired sleep time.
TL;DR: Although mPer1 and mPer2 represent key elements of the molecular clock in the SCN, they are not required for homeostatic regulation of the daily amounts of waking, slow-wave sleep (SWS), or REM sleep.
Abstract: In mammals, sleep is regulated by circadian and homeostatic mechanisms. The circadian component, residing in the suprachiasmatic nucleus (SCN), regulates the timing of sleep, whereas homeostatic fa...
TL;DR: Results suggest that consolidation of truly episodic memories mainly involves REM sleep, and the effects of sleep deprivation during the first or second half of the night on episodic memory consolidation is examined.
Abstract: STUDY OBJECTIVES: The aim of this study is to examine the effects of sleep deprivation during the first or second half of the night on episodic memory consolidation. Episodic memory is defined as memory for events located in time and space. It is also characterized by autonoetic consciousness, which gives a subject the conscious sensation of traveling back in time to relive the original event and forward into the future. DESIGN: Consolidation of episodic information was tested after 4-hour retention intervals, which followed learning and occurred during either the early or late half night, respectively dominated by slow wave sleep (SWS) or rapid eye movement (REM) sleep, or corresponding periods of wakefulness. SETTING: Data collection occurred in the sleep laboratory. PARTICIPANTS: Forty-three young healthy subjects: 9 men and 34 women, age ranging from 18 to 26 years (mean 20.18 +/- 1.94 years) were included in this study. INTERVENTIONS: Waking after a 4-hour retention interval filled with early or late sleep, or 4-hour sleep deprivation, during early or late period of night. MEASUREMENTS AND RESULTS: The cognitive task, named the What-Where-When test, was specially designed to assess factual, spatial, and temporal components of episodic memory. This task was associated with the Remember/Know paradigm to assess autonoetic consciousness. We measured performance on immediate free recall, delayed free recall (after a 4-hour interval of wakefulness or sleep), and delayed recognition. We also calculated a forgetting rate for each feature (factual, spatial, and temporal) and, for the recognition task, scores of autonoetic consciousness (R responses). REM-sleep deprivation was associated with significantly lower recall of spatial information compared to SWS deprivation (P < .01) or late sleep (P < .05) conditions. REM-sleep deprivation was also associated with a higher forgetting rate of temporal information as compared to the early sleep condition (P< .01). Finally, REM-sleep deprivation led subjects to give significantly fewer R responses, indicative of true memories, as compared to SWS deprivation (P < .05). CONCLUSIONS: These results suggest that consolidation of truly episodic memories mainly involves REM sleep. Language: en
TL;DR: All patients receiving efavirenz had longer sleep latencies and shorter duration of deep sleep, although poor sleepers also showed reduced sleep efficiency and shorterduration of rapid eye movement sleep.
Abstract: Ambulatory electroencephalogram monitoring was performed for 18 HIV-infected subjects treated with efavirenz with and without insomnia and for 13 healthy control subjects. All patients receiving efavirenz had longer sleep latencies and shorter duration of deep sleep, although poor sleepers also showed reduced sleep efficiency and shorter duration of rapid eye movement sleep. Efavirenz plasma levels were higher in patients with insomnia and/or reduced sleep efficiency.
TL;DR: The complex effects of dopamine (DA) on normal and pathological waking–sleeping are summarized and a diencephalospinal DA system may have an additional important role in mediating state-specific sensorimotor activity that is relevant to periodic limb movements and restless legs syndrome.
Abstract: In Parkinson's disease (PD), waking is frequently punctuated by sleep episodes, including rapid eye movement (REM) (i.e., dream) sleep, and sleep is interrupted by motor activities such as periodic limb movements and REM sleep behavior disorder. Because these pathologic behaviors are unaccounted for by contemporary models, this review summarizes the complex effects of dopamine (DA) on normal and pathological waking-sleeping. Maintenance of wakefulness is probably promoted by mesocorticolimbic DA circuits, and suppression of nocturnal movement appears to be influenced by indirect pathways linking midbrain DA neurons with pre-motor structures in the mesopontine tegmentum and ventromedial medulla. A diencephalospinal DA system may have an additional important role in mediating state-specific sensorimotor activity that is relevant to periodic limb movements and restless legs syndrome.
TL;DR: Preliminary data from a sleep study of adults with GH deficiency using wrist actigraphy for 6 nights at home and polysomnography in the laboratory indeed show decreased total sleep time and increased sleep fragmentation in GH-deficient patients as compared with normal controls.
Abstract: For more than 30 years, growth hormone (GH) has been observed to be preferentially secreted during deep, slow-wave sleep (SWS). However, the mechanisms that underlie this robust relationship that links anabolic processes in the body with behavioral rest and decreased cerebral metabolism remain to be elucidated. Current evidence indicates that GH secretion during the beginning of sleep appears to be primarily regulated by GH-releasing hormone (GHRH) stimulation occurring during a period of relative somatostatin withdrawal, which also is associated with elevated levels of circulating ghrelin. Apparently, two populations of GHRH neurons need to be simultaneously active to stimulate, in a coordinated fashion, SWS and pituitary GH release. Pharmacological interventions that are capable of increasing the duration and/or the intensity of SWS such as oral administration of gamma-hydroxybutyrate (GHB), also increase the rate of GH release. Because the normal negative feedback exerted by GH on central GHRH is inoperative in patients with GH deficiency, it is possible that the decreased energy levels and fatigue often reported by GH-deficient adults partly reflect an alteration in sleep-wake regulation. Preliminary data from a sleep study of adults with GH deficiency using wrist actigraphy for 6 nights at home and polysomnography in the laboratory indeed show decreased total sleep time and increased sleep fragmentation in GH-deficient patients as compared with normal controls.
TL;DR: In this paper, age-related changes of the EEG response to sleep deprivation along the antero-posterior axis (Fz, Cz, Pz, Oz) under constant routine conditions were investigated.
Abstract: Sleep loss has marked and selective effects on brain wave activity during subsequent recovery sleep. The electroencephalogram (EEG) responds to sleep deprivation with a relative increase in power density in the delta and theta range during non-rapid eye movement sleep. We investigated age-related changes of the EEG response to sleep deprivation along the antero-posterior axis (Fz, Cz, Pz, Oz) under constant routine conditions. Both healthy young (20-31 years) and older (57-74 years) participants manifested a significant relative increase in EEG power density in the delta and theta range after 40 h of sleep deprivation, indicating a sustained capacity of the sleep homeostat to respond to sleep loss in ageing. However, the increase in relative EEG delta activity (1.25-3.75 Hz) following sleep deprivation was significantly more pronounced in frontal than parietal brain regions in the young, whereas such a frontal predominance was diminished in the older volunteers. This age-related decrease of frontal delta predominance was most distinct at the beginning of the recovery sleep episode. Furthermore, the dissipation of homeostatic sleep pressure during the recovery night, as indexed by EEG delta activity, exhibited a significantly shallower decline in the older group. Activation of sleep regulatory processes in frontal brain areas by an extension of wakefulness from 16 to 40 h appears to be age-dependent. These findings provide quantitative evidence for the hypothesis that frontal brain regions are particularly vulnerable to the effects of elevated sleep pressure ('prefrontal tiredness') and ageing ('frontal ageing').
TL;DR: STN DBS seems to be an effective therapeutic option for the treatment of advanced Parkinson's disease because it improves the cardinal symptoms and also seems to improve sleep architecture.
TL;DR: These findings support the hypothesis that the SCN consolidate the sleep-wake cycle by generating a signal of arousal during the subjective night (ie. the active period), thereby having the capacity to alter baseline sleep amount.
Abstract: Context: Sleep is regulated by circadian and homeostatic processes. The circadian pacemaker, located in the suprachiasmatic nuclei (SCN), regulates the timing and consolidation of the sleep-wake cycle, while a homeostatic mechanism governs the accumulation of sleep debt and sleep, recovery. Recent studies using. mice with deletions or mutations of circadian genes show that components of the circadian pacemaker can influence the total amount of baseline sleep and recovery from sleep deprivation, indicating a broader role for the SCN in sleep regulation. Objective: To further investigate the role of the circadian pacemaker in sleep regulation in mice, we recorded sleep in sham and SCN-lesioned mice under baseline conditions and following sleep deprivation. Results: Compared to sham controls, SCN-lesioned mice exhibited a decrease in sleep consolidation and a decrease in wakefulness during the dark phase. Following sleep deprivation, SCN-lesioned mice exhibited an attenuated increase in non-rapid eye movement sleep time but an increase in non-rapid eye movement sleep electroencephalographic delta power that was similar to that of the sham controls. Conclusions: These findings support the hypothesis that the SCN consolidate the sleep-wake cycle by generating a signal of arousal during the subjective night (ie. the active period), thereby having the capacity to alter baseline sleep amount. Although the SCN are not involved in sleep homeotasis as defined by the increase in. electroencephalographic delta power after sleep deprivation, the SCN does play a central role in the regulation of sleep and wakefulness beyond just the timing of vigilance states.
TL;DR: The results confirm previous findings that apprehension of a difficult next day is associated with decreased amount of slow wave sleep, increased percentage of stage 2 sleep, bedtime state anxiety and subjectively poor sleep.