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At least 19 recordsLinked to original sources
PubMed1995

Contribution of the circadian pacemaker and the sleep homeostat to sleep propensity, sleep structure, electroencephalographic slow waves, and sleep spindle activity in humans.

The role of the endogenous circadian pacemaker in the timing of the sleep-wake cycle and the regulation of the internal structure of sleep, including REM sleep, EEG slow-wave (0.75-4.5 Hz) and sleep spindle activity (12.75-15.0 Hz) was investigated. Eight men lived in an environment free of time cues for 33-36 d and were scheduled to a 28 hr rest-activity cycle so that sleep episodes (9.33 hr each) occurred at all phases of the endogenous circadian cycle and variations in wakefulness preceding sleep were minimized. The crest of the robust circadian rhythm of REM sleep, which was observed throughout the sleep episode, was positioned shortly after the minimum of the core body temperature rhythm. Furthermore, a sleep-dependent increase of REM sleep was present, which, interacting with the circadian modulation, resulted in highest values of REM sleep when the end of scheduled sleep episodes coincided with habitual wake-time. Slow-wave activity decreased and sleep spindle activity increased in the course of all sleep episodes. Slow-wave activity in non-REM sleep exhibited a low amplitude circadian modulation which did not parallel the circadian rhythm of sleep propensity. Sleep spindle activity showed a marked endogenous circadian rhythm; its crest coincident with the beginning of the habitual sleep episode. Analyses of the (nonadditive) interaction of the circadian and sleep-dependent components of sleep propensity and sleep structure revealed that the phase relation between the sleep-wake cycle and the circadian pacemaker during entrainment promotes the consolidation of sleep and wakefulness and facilitates the transitions between these vigilance states.

Adult↗
PubMed2000

Sleep latency and duration estimates among sleep disorder patients: variability as a function of sleep disorder diagnosis, sleep history, and psychological characteristics.

STUDY OBJECTIVES: Insomnia patients often report greater sleep disturbance than found via polysomnography; yet the specific patient factors related to such sleep time misperceptions are poorly understood. We sought to characterize the extent to which a diverse group of patients complaining of insomnia (n=104) misperceive overnight total sleep time and sleep latency, and to identify patient factors associated with these variations. DESIGN: Cross-sectional. SETTING: University based sleep disorders center. PATIENTS: Sleep disorder groups consisted of patients with psychophysiological insomnia (n=19), sleep state misperception (n=8), insomnia with depressive disorder (n=11), insomnia secondary to Axis I psychiatric disorder other than depression (n=21), periodic limb movement disorder (n=24), and obstructive sleep apnea (n=21). MEASUREMENT AND RESULTS: Patients completed a sleep history questionnaire and the MMPI, underwent overnight diagnostic polysomnographic assessment, and then estimated their total sleep time and sleep latency the subsequent morning. On average, patients overestimated sleep latency, but were equally likely to underestimate vs. overestimate total sleep time. Sleep time misperception was associated with longer periods of wakefulness following sleep onset, greater self-perceived sleep impairment, as well as several psychological dimensions. CONCLUSIONS: Patient factors, including sleep quality, perceptions of habitual sleep time, and current psychopathology, potentially influence sleep time estimation. Whereas psychological factors may lead to exaggeration of sleep disturbance among some patients, sleep quality itself may also influence the congruence between subjective and objective indices of sleep.

Adult↗
PubMed2002

The sleep of co-sleeping infants when they are not co-sleeping: evidence that co-sleeping is stressful.

Co-sleeping proponents consider the practice to be "natural" and a potential protection against sudden infant death syndrome (SIDS); others consider the practice of an infant sleeping in the parents' bed for prolonged periods at night to place an infant at risk for harm or death. For this study, co-sleeping was investigated from a different perspective, that is, as a significant early experience to investigate as it may have implications for the infant's development. The sleep of 101 normal, full-term infants was recorded nonintrusively in the home for 24 hr periods when they were 5 weeks and 6 months old. Infants were assigned to three groups: short-term co-sleepers, long-term co-sleepers, and non-co-sleepers. Their sleep states and wakefulness were compared at the two ages and over age. At 5 weeks and 6 months, the long-term co-sleeping infants differed significantly from the non-co-sleepers on a number of measures: At 5 weeks, they showed more quiet sleep and longer bouts of quiet sleep; and at 6 months, they also showed less active sleep, fewer arousals in active sleep, and less wakefulness. Each of these differences indicates a markedly lower arousal level in the long-term co-sleeping infants. This sleep pattern has been repeatedly found to be an indicator of stress. We infer that a major source of stress for these infants is the experience of sleep disturbance documented for infants when they were co-sleeping. Based on extensive evidence for long-term effects of early stress, we conclude that co-sleeping should have significant implications for infants' neurobehavioral development.

Arousal↗
PubMed2006

Sleep in overweight adolescents: shorter sleep, poorer sleep quality, sleepiness, and sleep-disordered breathing.

OBJECTIVE: To document the sleep of overweight adolescents and to explore the degree to which weight-related sleep pathology might account for diminished psychosocial outcome. METHODS: Sixty children aged 10-16.9 from a weight-management clinic were compared to 22 healthy controls using comprehensive actigraphic, polysomnographic, and parent- and self-report questionnaire assessments. RESULTS: Overweight participants averaged more symptoms of sleep-disordered breathing, later sleep onset, shorter sleep time, and more disrupted sleep than controls. Although the groups did not differ in self-reported sleep habits, multiple concerns were reported by parents of overweight participants, including daytime sleepiness, parasomnias, and inadequate sleep. Group differences in academic grades and depressive symptoms were at least partially accounted for by short sleep and daytime sleepiness. CONCLUSIONS: Excessive weight is associated with an increased risk of sleep problems. There is a need for further research in this area and for clinicians who work with overweight children to evaluate their sleep.

Adolescent↗
PubMed1987

Ultrashort sleep-wake cycle: timing of REM sleep. Evidence for sleep-dependent and sleep-independent components of the REM cycle.

This study investigated the temporal structure of REM sleep in three experiments utilizing the ultrashort 7-min sleep, 13-min waking cycle. The experiments were carried out for 24 or 36 h, with and without previous sleep deprivation, under two experimental conditions of instructing subjects to fall asleep or to resist sleep. Multiple REM episodes occurred in all three experiments in the two experimental conditions, particularly during the night period. The first nocturnal REM period appeared 5 h after the nocturnal sleep gate, of which 80-100 min were accounted for by non-REM (NREM) sleep. Thereafter, REM episodes occurred periodically, with a mean inter-REM interval of 86 min. Only 14 min of this interval consisted of NREM sleep. We believe that these results suggest that although the activation of the REM oscillator is dependent on a critical accumulation of NREM sleep, once activated, it continues to function during brief periods of waking.

Adult↗
PubMed2003

Obstructive sleep apnea in epilepsy patients: the Sleep Apnea scale of the Sleep Disorders Questionnaire (SA-SDQ) is a useful screening instrument for obstructive sleep apnea in a disease-specific population.

OBJECTIVE: To determine useful cutoffs on the Sleep Apnea scale of the Sleep Disorders Questionnaire (SA-SDQ) in an epilepsy population. BACKGROUND: Epilepsy and obstructive sleep apnea (OSA) frequently coexist, and treating OSA in epilepsy patients may reduce seizure frequency and improve daytime sleepiness. The SA-SDQ, a 12-item validated measure of sleep-related breathing disorders, may be a useful tool to screen epilepsy patients for OSA, although appropriate cutoff points have not been established in this population. Previously suggested SA-SDQ cutoff points for OSA in a non-epilepsy population were 32 for women and 36 for men. PATIENTS AND METHODS: One hundred twenty-five subjects with epilepsy undergoing polysomnography completed a survey about their sleep, including the 12-item SA-SDQ scale. Receiver-operating characteristics curves were constructed to determine optimal sensitivity and specificity. RESULTS: Sixty-nine of the 125 subjects (45%) had apnea-hypopnea indices greater than five, indicating OSA. The area under the curve was 0.744 for men and 0.788 for women. For men, an SA-SDQ score of 29 provided a sensitivity of 75% and a specificity of 65%. For women, an SA-SDQ score of 26 provided a sensitivity of 80% and a specificity of 67%. CONCLUSIONS: The SA-SDQ is a useful screening instrument for OSA in an epilepsy population. Our results indicate that the previously suggested cutoffs for OSA (36 for men and 32 for women) may be too high for this specific population. We suggest screening cutoffs of 29 for men and 26 for women.

Disorders of Excessive Somnolence↗
PubMed1987

Homeostatic changes in slow wave sleep during recovery sleep following restricted nocturnal sleep and partial slow wave sleep recovery during an afternoon nap.

There has been speculation and some evidence to suggest that certain fractions of sleep, notably, slow wave sleep (SWS), are under homeostatic control. In order to test this hypothesis, the sleep of eight subjects was terminated on four different occasions after 50% of their normal baseline SWS levels had been obtained. An afternoon nap then followed during which 100%, 50%, or 25% of the SWS debt was reclaimed. A fourth condition contained no afternoon nap. The change in SWS from baseline during subsequent recovery sleep was directly related to the outstanding SWS debt, thus demonstrating that SWS is under homeostatic control.

Adult↗
PubMed1994

REM-sleep timing is controlled homeostatically by accumulation of REM-sleep propensity in non-REM sleep.

Sleep structure in the rat was characterized during uninterrupted full-day recordings using an analytic procedure that identifies rapid eye movement (REM) sleep episodes based on REM-sleep-onset electroencephalograph phenomena, hence independently of REM-sleep duration. The data were used to determine whether REM-sleep timing is controlled homeostatically or by an oscillatory mechanism. The findings and conclusions are that 1) non-REM (NREM) sleep episode duration is positively correlated with prior REM-sleep episode duration, suggesting that REM-sleep expression is permissive of NREM sleep; 2) mean NREM-sleep episode duration decreases after repeated brief REM-sleep episodes (< 30 s), also suggesting that discharge of REM-sleep propensity is essential for NREM-sleep expression; 3) REM-sleep episode duration is independent of prior sleep history, suggesting that REM-sleep maintenance is controlled by factors other than accumulated REM-sleep propensity; 4) brief REM-sleep episodes occur progressively more frequently over the course of the NREM-sleep interval between sustained REM-sleep episodes (> 30 s), suggesting that REM-sleep propensity increases progressively within episodes of NREM sleep; and 5) the diurnal cycle of REM-sleep expression primarily reflects modulation in the efficiency of REM-sleep maintenance. These findings support the hypothesis that REM-sleep timing is controlled by accumulation of REM-sleep propensity during NREM sleep.

Animals↗
PubMed2003

The cumulative cost of additional wakefulness: dose-response effects on neurobehavioral functions and sleep physiology from chronic sleep restriction and total sleep deprivation.

OBJECTIVES: To inform the debate over whether human sleep can be chronically reduced without consequences, we conducted a dose-response chronic sleep restriction experiment in which waking neurobehavioral and sleep physiological functions were monitored and compared to those for total sleep deprivation. DESIGN: The chronic sleep restriction experiment involved randomization to one of three sleep doses (4 h, 6 h, or 8 h time in bed per night), which were maintained for 14 consecutive days. The total sleep deprivation experiment involved 3 nights without sleep (0 h time in bed). Each study also involved 3 baseline (pre-deprivation) days and 3 recovery days. SETTING: Both experiments were conducted under standardized laboratory conditions with continuous behavioral, physiological and medical monitoring. PARTICIPANTS: A total of n = 48 healthy adults (ages 21-38) participated in the experiments. INTERVENTIONS: Noctumal sleep periods were restricted to 8 h, 6 h or 4 h per day for 14 days, or to 0 h for 3 days. All other sleep was prohibited. RESULTS: Chronic restriction of sleep periods to 4 h or 6 h per night over 14 consecutive days resulted in significant cumulative, dose-dependent deficits in cognitive performance on all tasks. Subjective sleepiness ratings showed an acute response to sleep restriction but only small further increases on subsequent days, and did not significantly differentiate the 6 h and 4 h conditions. Polysomnographic variables and delta power in the non-REM sleep EEG-a putative marker of sleep homeostasis--displayed an acute response to sleep restriction with negligible further changes across the 14 restricted nights. Comparison of chronic sleep restriction to total sleep deprivation showed that the latter resulted in disproportionately large waking neurobehavioral and sleep delta power responses relative to how much sleep was lost. A statistical model revealed that, regardless of the mode of sleep deprivation, lapses in behavioral alertness were near-linearly related to the cumulative duration of wakefulness in excess of 15.84 h (s.e. 0.73 h). CONCLUSIONS: Since chronic restriction of sleep to 6 h or less per night produced cognitive performance deficits equivalent to up to 2 nights of total sleep deprivation, it appears that even relatively moderate sleep restriction can seriously impair waking neurobehavioral functions in healthy adults. Sleepiness ratings suggest that subjects were largely unaware of these increasing cognitive deficits, which may explain why the impact of chronic sleep restriction on waking cognitive functions is often assumed to be benign. Physiological sleep responses to chronic restriction did not mirror waking neurobehavioral responses, but cumulative wakefulness in excess of a 15.84 h predicted performance lapses across all four experimental conditions. This suggests that sleep debt is perhaps best understood as resulting in additional wakefulness that has a neurobiological "cost" which accumulates over time.

Adult↗
PubMed2005

Manipulating REM sleep in older adults by selective REM sleep deprivation and physiological as well as pharmacological REM sleep augmentation methods.

Experimental approaches to manipulate REM sleep within the cognitive neuroscience of sleep are usually based on sleep deprivation paradigms and focus on younger adults. In the present study, a traditional selective REM sleep deprivation paradigm as well as two alternative manipulation paradigms targeting REM sleep augmentation were investigated in healthy older adults. The study sample consisted of 107 participants, male and female, between the ages of 60 and 82 years, who had been randomly assigned to five experimental groups. During the study night, a first group was deprived of REM sleep by selective REM sleep awakenings, while a second group was woken during stage 2 NREM sleep in matched frequency. Physiological REM sleep augmentation was realized by REM sleep rebound after selective REM sleep deprivation, pharmacological REM sleep augmentation by administering an acetylcholinesterase inhibitor in a double-blind, placebo-controlled design. Deprivation and augmentation paradigms manipulated REM sleep significantly, the former affecting more global measures such as REM sleep minutes and percentage, the latter more organizational aspects such as stage shifts to REM sleep, REM latency, REM density (only pharmacological augmentation) and phasic REM sleep duration. According to our findings, selective REM sleep deprivation seems to be an efficient method of REM sleep manipulation in healthy older adults. While physiological rebound-based and pharmacological cholinergic REM sleep augmentation methods both failed to affect global measures of REM sleep, their efficiency in manipulating organizational aspects of REM sleep extends the traditional scope of REM sleep manipulation methods within the cognitive neuroscience of sleep.

Aged↗
PubMed2002

Spontaneous sleep interruptions during extended nights. Relationships with NREM and REM sleep phases and effects on REM sleep regulation.

OBJECTIVES: There is no agreement in the literature as to whether sleep interruption causes rapid eye movement (REM) pressure to increase, and if so, whether this increase is expressed as shortened REM latency, increased REM density, or increased duration of REM sleep. The purpose of the present study was to examine the effect of different durations of spontaneous sleep interruptions on the regulation of REM sleep that occurs after return to sleep. METHODS: The occurrence of spontaneous periods of wakefulness and their effects on subsequent REM sleep periods were analysed in a total sample of 1189 sleep interruptions which occurred across 364 extended nights in 13 normal subjects. RESULTS: Compared with sleep interruptions that last less than 10 min, sleep interruptions that last longer than 10 min occur preferentially out of REM sleep. In both the short and long types of sleep interruptions, the duration of REM periods that ended in wakefulness were shorter than the duration of those that were not interrupted by wakefulness. REM densities of the REM periods that terminated in periods of wakefulness were higher than those of uninterrupted REM periods. The proportion of episodes of wakefulness following REM sleep that were long-lasting progressively increased over the course of the extended night period. The sleep episodes that followed the periods of wakefulness were characterised by a short REM latency. REM duration was increased in episodes that followed long sleep interruptions compared to those that followed short sleep interruptions. REM density did not appear to change significantly in the episodes that followed sleep interruption. CONCLUSIONS: REM sleep mechanisms appear to be the main force controlling sleep after a spontaneous sleep interruption, presumably because during the second half of the night, where more sleep interruptions occur, the pressure for non-rapid eye movement sleep is reduced and the circadian rhythm in REM sleep propensity reaches its peak. Processes promoting REM sleep at the end of the night are consistent with the Pittendrigh and Daan dual oscillator model of the circadian pacemaker.

Adult↗
PubMed1985

Platform sleep deprivation affects deep slow wave sleep in addition to REM sleep.

Rats were sleep deprived by the platform method to look for differential effects on light and deep slow wave sleep depending on platform size. Diameters of large and small platforms were 15 cm and 5.1 cm respectively. Sleep was recorded during a baseline light period (09.00-19.00 h), continuously during 48 h of sleep deprivation and during the first lights on recovery period (09.00-19.00 h). In both platform conditions REM sleep was virtually abolished during the first light period (hours 0-10 of sleep deprivation), while NREM sleep was reduced to approximately half of control values. During the second light period (hours 22-34 of sleep deprivation) REM sleep recovered somewhat in the large platform group. Light slow wave sleep (SWS-1) was comparable to baseline while deep slow wave sleep (SWS-2) was still significantly reduced. In the small platform group both SWS-2 and REM sleep was considerably reduced on day 2. Over the whole deprivation period there was an effect of platform size on SWS-1 (higher in the small platform group), and on SWS-2 and REM sleep (lower in the small platform group). During the 9 h light-time recovery sleep there was an REM sleep rebound in both groups. SWS-1 was reduced in both groups while SWS-2 was not significantly increased. The ratio SWS-2/SWS-1 was, however, significantly increased only in the small platform group recovery sleep. The results suggest that platform sleep deprivation deprives the animals of deep slow wave sleep in addition to REM sleep. This has implications for conclusions on REM sleep function based upon REM sleep deprivation.

Animals↗
PubMed2004

Melatonin advances the circadian timing of EEG sleep and directly facilitates sleep without altering its duration in extended sleep opportunities in humans.

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.

Adult↗
PubMed1997

Sleep-related myocardial ischemia and sleep structure in patients with obstructive sleep apnea and coronary heart disease.

STUDY OBJECTIVES: Patients with coronary heart disease (CHD) and obstructive sleep apnea may have an increased cardiac risk due to nocturnal myocardial ischemia triggered by apnea-associated oxygen desaturation. Sleep structure in patients with obstructive sleep apnea is fragmented by activation of the central nervous system (CNS) (arousal) due to obstructive apneas. Nocturnal myocardial ischemia may lead to activation of the CNS as well. PATIENTS: Fourteen patients with obstructive sleep apnea and CHD disease and seven patients suffering from obstructive sleep apnea without CHD were studied. Overnight sleep studies and simultaneous six-lead ECG recordings were performed. In addition, sleep studies and ECG recordings were performed with administration of a sustained-release nitrate in these patients in a double-blinded crossover design. RESULTS: Analysis of three nights' recordings revealed 144 episodes of nocturnal myocardial ischemia in six subjects. Five patients had underlying CHD and one patient exhibited diffuse wall defects of the coronary arteries; also, 85.4% of ischemic episodes were concomitant with apneas and oxygen desaturation > 3%, and 77.8% of ischemic episodes occurred during rapid eye movement (REM) sleep, although total amount of REM sleep was only 18% of total sleep time. Mean oxygen saturation was significantly lower (p < 0.05) during apnea-associated ischemic episodes than during nonapnea-associated ischemia (77.3% vs 93.1%). Nitrate administration did not reduce ischemic episodes. Sleep architecture (macrostructure) exhibited a reduction in sleep stages non-REM 3 and 4 and REM sleep. Comparing the microstructure of sleep (arousals) within episodes with and without ischemia but similar criteria like sleep stage, apnea activity, and oxygen saturation, we found significantly more (p < 0.01) and severe (p < 0.001) arousals during periods with myocardial ischemia than during control episodes. In addition, microstructure of sleep was disturbed by myocardial ischemia itself in absence of apneas. CONCLUSION: It is concluded that patients with CHD and obstructive sleep apnea are endangered by apnea-associated ischemia and that these ischemic episodes lead to activation of the CNS and additional fragmentation of sleep. Patients with nocturnal ischemia should be screened for underlying sleep apnea even if nitrate therapy fails.

Aged↗
PubMed1993

Circadian sleep regulation in the absence of light perception: chronic non-24-hour circadian rhythm sleep disorder in a blind man with a regular 24-hour sleep-wake schedule.

Sleep disturbances and the failure to entrain circadian rhythms to the 24-hour day have been reported in the majority of totally blind subjects. The present case study of a totally blind man with a well-documented recurring sleep disturbance was designed to investigate the mutual relationship between sleep and the circadian timing system. The 63-year-old subject, a high school teacher with a regular work schedule, had suffered from cyclically recurring insomnia for the past 28 years. Analysis of a sleep log that he had kept for the past 15 years suggested that his circadian rhythms were not entrained to the 24-hour day. During a 3-month inpatient study, the period of the endogenous circadian pacemaker was assessed by analysis of ambulatory core body temperature, urinary excretion and a series of estimates of the phase of core body temperature cycles and plasma cortisol levels during constant routines. All circadian markers revealed periods in the range of 24.22-24.27 hours, with no evidence for a modulation of the observed periods by the sleep-wake cycle. During this 3-month inpatient study, a complete cycle of the subject's sleep disturbance and remission was polysomnographically documented while the subject lived on a regular 24-hour schedule. Because the subject's circadian rhythms were free-running and his sleep times were fixed, sleep occurred at virtually all circadian phases. Analysis of sleep latency, REM sleep latency, sleep duration, wake in sleep episode and REM sleep during sleep episode revealed a strong modulation by circadian phase. These findings in this blind man suggest that: 1) the period of his cyclically recurring sleep disturbance is directly related to the nonentrained period of an endogenous circadian pacemaker that drives circadian variation in core body temperature, urinary excretion, plasma cortisol and sleep propensity; 2) both his sleep structure and the severity of his daily sleep disruption are directly related to circadian phase and 3) his circadian pacemaker, which has an endogenous period that deviates only 0.2-0.3 hours from 24 hours, cannot be entrained by periodic daily exposure to nonphotic time cues, including a very regular 24-hour sleep-wake schedule.

Blindness↗
PubMed2006

Sleep hygiene and actigraphically evaluated sleep characteristics in children with ADHD and chronic sleep onset insomnia.

In the present study we investigated sleep hygiene and actigraphically evaluated sleep in 74 medication-naïve children, aged 6-12 years, with rigorously diagnosed attention-deficit/hyperactivity disorder (ADHD) and chronic sleep onset insomnia (ADHD-SOI) and 23 ADHD controls without insomnia (ADHD-noSOI). Between-group differences were analysed for lights out (sleep log), actigraphically evaluated sleep onset, sleep latency, total sleep duration, actual sleep time and sleep hygiene as measured with the Children's Sleep Hygiene Scale. We found a significant difference (P < 0.001) in mean (+/-SD) sleep onset between the ADHD-SOI group (21:49 +/- 0:56 h) and ADHD-noSOI groups (20:41 +/- 0:45 h). Sleep latency was significantly (P < 0.001) longer in ADHD-SOI (00:53 +/- 0:25 h) compared to ADHD-noSOI (00:26 +/- 0:25 h). The difference in total sleep duration between ADHD-SOI (9:42 +/- 0:44 h) and ADHD-noSOI (10:09 +/- 0:43 h) was not significantly different (P = 0.18). The group difference in actual sleep time was also not significant (8:43 +/- 0:52 h in ADHD-SOI versus 9:13 +/- 1:16 h; P = 0.40). There was no significant difference (P = 0.17) in mean (+/-SD) total sleep hygiene score between the ADHD-SOI (56.4 +/- 10.5) and ADHD-noSOI groups (53.0 +/- 10.6). We conclude that there were differences in sleep onset and sleep latency in ADHD children with chronic SOI and those without insomnia; however, sleep hygiene practices were similar and did not relate to sleep characteristics.

Age of Onset↗
PubMed1990

Effect of partial sleep deprivation on sleep stages and EEG power spectra: evidence for non-REM and REM sleep homeostasis.

The effect of repeated partial sleep deprivation on sleep stages and sleep EEG parameters was investigated in young subjects. After 2 baseline nights (B1, B2) of 7.5 h, sleep was restricted for 2 nights (D1, D2) to the first 4 h of the habitual bedtime period. Two recovery nights (R1, R2) with 7.5 h sleep followed. During the deprivation nights, stages 1 and 2 and REM sleep were reduced, while slow wave sleep (SWS; stages 3 and 4) was not significantly affected. However, the time integral of EEG power density in the range of 0.75-4.5 Hz (slow wave energy) was reduced. In the recovery period, SWS showed an enhancement in R1, and REM sleep showed a rebound in R1 and R2. An increase of REM sleep in the early part of the sleep period was evident in R1. Sleep latency was reduced in D2, R1 and R2. In accordance with the 2-process model of sleep regulation, EEG power density in non-REM sleep in the range of 0.75-4.5 Hz (slow wave activity) was only slightly higher in D2 and R1 than in baseline. An enhancement of slow wave activity in REM sleep was present in D2. Power density in the frequency range of 13-16 Hz was reduced in non-REM sleep (R1), SWS (R2) and stage 2 (R1). The results show (1) that the moderate reduction of slow wave energy in the deprivation nights induces only a minor enhancement of slow wave activity during recovery sleep; and (2) that a REM sleep deficit gives rise to an immediate rebound when 'slow wave pressure' is low.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2006

Comparison of the sleep pattern throughout a protocol of chronic sleep restriction induced by two methods of paradoxical sleep deprivation.

The purpose of the present study was to evaluate the sleep homeostasis of rats submitted to a protocol of chronic sleep restriction by two methods and to evaluate the sleep characteristics during the recovery period. The sleep restriction protocol was accomplished by sleep depriving rats for 18 h everyday for 21 days, using the single platform method (SPM) or the modified multiple platform method (MMPM) of paradoxical sleep (PS) deprivation. Rats were allowed to sleep for 6 h (from 10:00 to 16:00; starting 3 h after lights on) in their individual home-cages, during which their sleep was recorded. At the end of the sleep restriction protocol, rats were recorded in their home-cages for 4 days, where they could sleep freely. Both methods used to induce chronic sleep restriction were effective, in sofar as they resulted in augmented sleep time during the 6h-sleep period, with very few bouts of wakening. Although comparison between the methods did not reveal differences, sleep restriction under MMPM produced a more consistent daily rebound, mainly of paradoxical sleep, with longer episodes. These results showed distinct sleep recovery patterns, suggesting a possible role of the waking experiences (i.e. immobilization stress, social interaction) acting on sleep consolidation.

Animals↗