Showing papers on "Non-rapid eye movement 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: The evidence supportive of P2 being the result of independent processes is described and several features, such as its persistence from wakefulness into sleep, the general consensus that unlike most other EEG phenomena it increases with age, and the fact that it can be generated using respiratory stimuli are highlighted.
727 citations
TL;DR: Subjectively disturbed sleep in patients with insomnia is associated with greater brain metabolism, and daytime fatigue may reflect decreased activity in the prefrontal cortex resulting from inefficient sleep.
Abstract: OBJECTIVE: The authors investigated the neurobiological basis of poor sleep and daytime fatigue in insomnia. METHOD: [18F]Fluorodeoxyglucose positron emission tomography was used to assess regional cerebral glucose metabolism of seven patients with insomnia and 20 healthy subjects. RESULTS: Compared with healthy subjects, patients with insomnia showed greater global cerebral glucose metabolism during sleep and while awake, a smaller decline in relative metabolism from waking to sleep states in wake-promoting regions, and reduced relative metabolism in the prefrontal cortex while awake. CONCLUSIONS: Subjectively disturbed sleep in patients with insomnia is associated with greater brain metabolism. The inability to fall asleep may be related to a failure of arousal mechanisms to decline in activity from waking to sleep states. Further, daytime fatigue may reflect decreased activity in the prefrontal cortex resulting from inefficient sleep.
635 citations
TL;DR: Results indicate that increased sleep stage 2 spindle activity is related to an increase in recall performance and, thus, may reflect memory consolidation in stage 2 sleep.
Abstract: Study Objectives: Functional significance of stage 2 sleep spindle activity for declarative memory consolidation. Design: Randomized, within-subject, multicenter. Setting: Weekly sleep laboratory visits, actigraphy, and sleep diary (4 weeks). Participants: Twenty-four healthy subjects (12 men) aged between 20 and 30 years. Interventions: Declarative memory task or nonlearning control task before sleep. Measurement and Results: This study measured spindle activity during stage 2 sleep following a (declarative) word-pair association task as compared to a control task. Participants performed a cued recall in the evening after learning (160 word pairs) as well as in the subsequent morning after 8 hours of undisturbed sleep with full polysomnography. Overnight change in the number of recalled words, but not absolute memory performance, correlated significantly with increased spindle activity during the experimental night (r 24 =.63, P <.01). Time spent in each sleep stage could not account for this relationship. Conclusion: A growing body of evidence supports the active role of sleep for information reprocessing. Whereas past research focused mainly on the distinct rapid eye movement and slow-wave sleep, these results indicate that increased sleep stage 2 spindle activity is related to an increase in recall performance and, thus, may reflect memory consolidation.
532 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: Results show a behavioral dissociation, based upon an individual's awareness for having learned a sequence of finger movements, which is sleep dependent for explicit skills but time dependent for implicit skills.
429 citations
TL;DR: It is demonstrated that the fragmented wakefulness of orexin deficiency is not a consequence of abnormal sleep homeostasis, poor circadian control, or defective fundamental arousal systems, and may be best described as behavioral state instability, with apparently low thresholds to transition between states.
Abstract: Narcolepsy is caused by a lack of orexin (hypocretin), but the physiologic process that underlies the sleepiness of narcolepsy is unknown. Using orexin knock-out (KO) mice as a model of narcolepsy, we critically tested the three leading hypotheses: poor circadian control of sleep and wakefulness, inadequate activation of arousal regions, or abnormal sleep homeostasis. Compared with wild-type (WT) littermates, orexin KO mice had essentially normal amounts of sleep and wake, but wake and non-rapid eye movement (NREM) bouts were very brief, with many more transitions between all behavioral states. In constant darkness, orexin KO mice had normal amplitude and timing of sleep-wake rhythms, providing no evidence for disordered circadian control. When placed in a new, clean cage, both groups of mice remained awake for approximately 45 min, demonstrating that, even in the absence of orexin, fundamental arousal regions can be engaged to produce sustained wakefulness. After depriving mice of sleep for 2-8 hr, orexin KO mice recovered their NREM and rapid eye movement sleep deficits at comparable rates and to the same extent as WT mice, with similar increases in EEG delta power, suggesting that their homeostatic control of sleep is normal. These experiments demonstrate that the fragmented wakefulness of orexin deficiency is not a consequence of abnormal sleep homeostasis, poor circadian control, or defective fundamental arousal systems. Instead, the fragmented behavior of orexin KO mice may be best described as behavioral state instability, with apparently low thresholds to transition between states.
370 citations
TL;DR: Autoregressive spectral analysis of the electrocardiogram (EKG) interbeat interval sequence was used to characterize stress-related changes in heart rate variability during sleep in 59 healthy men and women to represent one pathway to disturbed sleep.
Abstract: OBJECTIVE Although stress can elicit profound and lasting effects on sleep, the pathways whereby stress affects sleep are not well understood. In this study, we used autoregressive spectral analysis of the electrocardiogram (EKG) interbeat interval sequence to characterize stress-related changes in heart rate variability during sleep in 59 healthy men and women. METHODS Participants (N = 59) were randomly assigned to a control or stress condition, in which a standard speech task paradigm was used to elicit acute stress in the immediate presleep period. EKG was collected throughout the night. The high frequency component (0.15-0.4 Hz Eq) was used to index parasympathetic modulation, and the ratio of low to high frequency power (0.04-0.15 Hz Eq/0.15-0.4 Hz Eq) of heart rate variability was used to index sympathovagal balance. RESULTS Acute psychophysiological stress was associated with decreased levels of parasympathetic modulation during nonrapid eye movement (NREM) and rapid eye movement sleep and increased levels of sympathovagal balance during NREM sleep. Parasympathetic modulation increased across successive NREM cycles in the control group; these increases were blunted in the stress group and remained essentially unchanged across successive NREM periods. Higher levels of sympathovagal balance during NREM sleep were associated with poorer sleep maintenance and lower delta activity. CONCLUSIONS Changes in heart rate variability associated with acute stress may represent one pathway to disturbed sleep. Stress-related changes in heart rate variability during sleep may also be important in association with chronic stressors, which are associated with significant morbidity and increased risk for mortality.
351 citations
TL;DR: The results showing a relationship between FIRST scores and nocturnal polysomnography and Multiple Sleep Latency Test scores suggest individuals with high FIRST scores may be predisposed to developing chronic primary insomnia and the vulnerability identified may underlie vulnerability to transient sleep disturbance associated with other sleep-disruptive factors.
Abstract: Study objectives To determine the presence of a hypothesized trait vulnerability to sleep disturbance and hyperarousal. Design Polysomnographic assessment of sleep in response to stress during a first night in the laboratory and subsequent physiologic arousal. Participants One hundred and four individuals (46% men, mean age 40.4 +/- 12.9 years) drawn from a population-based sample. Interventions Individuals were exposed to a first night in the laboratory. Measurements and results Participants completed a Likert-scale questionnaire, consisting of 27 items, that assesses sleep disturbance in response to commonly experienced stressful situations. Factor analytic techniques identified a single 9-item factor that was representative of the construct of "stress-related" vulnerability to sleep disturbance. Reliability of the resulting 9-item scale was high (Cronbach's alpha = .83). Individuals with higher scores on this scale, the Ford Insomnia Response to Stress Test (FIRST; median split), had a lower sleep efficiency (P = .001), as well as an increased latency to stage 1 sleep (P = .001) and persistent sleep (P = .002) on the first night of nocturnal polysomnography. Moreover, these high-scoring individuals showed increased arousal as evidenced by an elevated sleep latency on the Multiple Sleep Latency Test compared to individuals with low FIRST scores. Importantly, after controlling for current and past insomnia, the differences between individuals scoring high and low on the FIRST in terms of nocturnal sleep and daytime arousal remained significant. Other stages of sleep (stage 2, slow-wave, and rapid eye movement sleep) were not different between the groups. Conclusions These results showing a relationship between FIRST scores and nocturnal polysomnography and Multiple Sleep Latency Test scores have 3 potential implications: (1) the data demonstrate a characteristic that relates to vulnerability to stress-related sleep disturbance as manifested by a first night in the laboratory; (2) the elevated latencies on the Multiple Sleep Latency Test in these individuals, despite significantly disturbed sleep, support the notion of physiologic hyperarousal in these individuals and suggests they may be predisposed to developing chronic primary insomnia; and (3) the vulnerability identified may underlie vulnerability to transient sleep disturbance associated with other sleep-disruptive factors.
346 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).
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: Evidence suggests that sedative-hypnotics, such as benzodiazepine site-specific agonists, may have a role in some cases, whereas atypical antipsychotics may be necessary in other cases, and the utility of melatonin as a hypnotic in this population appears equivocal.
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 found that mice lacking α1G T-type Ca2+ channels showed a loss of the thalamic delta waves and a reduction of sleep spindles, whereas slow (<1 Hz) rhythms were relatively intact, when compared with the wild-type during urethane anesthesia and non-rapid eye movement (NREM) sleep.
Abstract: T-type calcium channels have been implicated as a pacemaker for brain rhythms during sleep but their contribution to behavioral states of sleep has been relatively uncertain. Here, we found that mice lacking alpha1(G) T-type Ca(2+) channels showed a loss of the thalamic delta (1-4 Hz) waves and a reduction of sleep spindles (7-14 Hz), whereas slow ( 16 sec compared with the wild-type, whereas no difference was seen in BAs of <16 sec between the two genotypes. These results are consistent with the previous idea of the distinct nature of delta oscillations and sleep spindles from cortically generated slow waves. These results also suggest that the alpha1(G)-subunit of T-type calcium channels plays a critical role in the genesis of thalamocortical oscillations and contributes to the modulation of sleep states and the transition between NREM sleep and wake states.
TL;DR: It is proposed that the ‘CO2 reserve’ (i.e. the difference in PaCO2 between eupnoea and the apnoeic threshold (AT) is the key determinants of breathing instability in sleep and that chemoreceptor‐induced instability in respiratory motor output during sleep contributes significantly to the major clinical problem of cyclical obstructive sleep apNoea.
Abstract: Sleep unmasks a highly sensitive hypocapnia-induced apnoeic threshold, whereby apnoea is initiated by small transient reductions in arterial CO2 pressure (PaCO2) below eupnoea and respiratory rhythm is not restored until PaCO2 has risen significantly above eupnoeic levels. We propose that the ‘CO2 reserve’ (i.e. the difference in PaCO2 between eupnoea and the apnoeic threshold (AT)), when combined with ‘plant gain’ (or the ventilatory increase required for a given reduction in PaCO2) and ‘controller gain’ (ventilatory responsiveness to CO2 above eupnoea) are the key determinants of breathing instability in sleep. The CO2 reserve varies inversely with both plant gain and the slope of the ventilatory response to reduced CO2 below eupnoea; it is highly labile in non-random eye movement (NREM) sleep. With many types of increases or decreases in background ventilatory drive and PaCO2, the slope of the ventilatory response to reduced PaCO2 below eupnoea remains unchanged from control. Thus, the CO2 reserve varies inversely with plant gain, i.e. it is widened with hyperventilation and narrowed with hypoventilation, regardless of the stimulus and whether it acts primarily at the peripheral or central chemoreceptors. However, there are notable exceptions, such as hypoxia, heart failure, or increased pulmonary vascular pressures, which all increase the slope of the CO2 response below eupnoea and narrow the CO2 reserve despite an accompanying hyperventilation and reduced plant gain. Finally, we review growing evidence that chemoreceptor-induced instability in respiratory motor output during sleep contributes significantly to the major clinical problem of cyclical obstructive sleep apnoea.
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: 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: MSA patients, especially those with associated stridor, commonly display impaired breathing and abnormal control of respiratory and limb muscles during sleep, indicating a diffuse impairment of sleep homeostatic integration that should be included within the diagnostic features of MSA.
TL;DR: Increases in the intensity of REM sleep during the night of sleep following cognitive procedural/implicit task acquisition implicate REM sleep mechanisms in further off-line memory processing, and provide a biological marker of learning potential.
Abstract: Posttraining rapid eye movement (REM) sleep has been reported to be important for efficient memory consolidation. The present results demonstrate increases in the intensity of REM sleep during the night of sleep following cognitive procedural/implicit task acquisition. These REM increases manifest as increases in total number of rapid eye movements (REMs) and REM densities, whereas the actual time spent in REM sleep did not change. Further, the participants with the higher intelligence (IQ) scores showed superior task acquisition scores as well as larger posttraining increases in number of REMs and REM density. No other sleep state changes were observed. None of the pretraining baseline measures of REM sleep were correlated with either measured IQ or task performance. Posttraining increases in REM sleep intensity implicate REM sleep mechanisms in further off-line memory processing, and provide a biological marker of learning potential.
TL;DR: Extended sleep leads to substantial improvements in daytime alertness, reaction time, and mood in healthy young adults.
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: The magnetoencephalographic signal from three subjects before, during and after eye movements cued to a tone, self-paced, awake and during rapid eye movement (REM) sleep was recorded to construct a hypnogram.
Abstract: We recorded the magnetoencephalographic (MEG) signal from three subjects before, during and after eye movements cued to a tone, self-paced, awake and during rapid eye movement (REM) sleep. During sleep we recorded the MEG signal throughout the night together with electroencephalographic (EEG) and electromyographic (EMG) channels to construct a hypnogram. While awake, just prior to and during eye movements, the expected well time-locked physiological activations were imaged in pontine regions, with early 3 s priming. Activity in the frontal eye fields (FEF) was identified in the 300 ms before the saccade onset. Visual cortex activation occurred 200 ms after saccades. During REM, compared to the eyes closed awake condition, activity was higher in supplementary motor area (SMA) and lower in inferior parietal and precuneus cortex. Electro-occulographic (EOG) activity just prior to REM saccades correlated with bilateral pontine and FEF activity some 250-400 ms before REM saccade onset, which in turn was preceded 200 ms earlier by reciprocal activation of the pons and FEF. An orbitofrontal-amygdalo-parahippocampal-pontine sequence, possibly related to emotional activation during REM sleep, was identified in the last 100 ms leading to the REM saccade, but not linked to saccade initiation.
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: 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: 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.