Prostaglandin D synthase (beta-trace) in healthy human sleep

STUDY OBJECTIVES: The prostaglandin D system plays an important role in animal sleep. In humans, alterations in the prostaglandin D system have been found in diseases exhibiting sleep disturbances as a prominent symptom, such as trypanosoma infection, systemic mastocytosis, bacterial meningitis, major depression, or obstructive sleep apnea. Assessment of this system's activity in relation to human physiologic sleep was the target of the present study. DESIGN: Serum concentrations of lipocalin-type prostaglandin D synthase (L-PGDS, former beta-trace), and plasma levels of the pineal hormone melatonin were measured in 20 healthy humans (10 women, 10 men; aged: 23.3 +/- 2.39 years) at 4-hour intervals over a period of 5 days and nights, which included physiologic sleep, rapid eye movement sleep deprivation, and total sleep deprivation. In addition, the serum L-PGDS and plasma melatonin levels of 6 subjects were determined under conditions of bright white (10,000 lux) or dark red light (< 50 lux) in a crossover design during total sleep deprivation. Nocturnal blood sampling was performed by a through-the-wall tube system. L-PGDS was measured by an automated immunonephelometric assay, and melatonin was analyzed by direct radioimmunoassay. RESULTS: Serum L-PGDS concentrations showed marked time-dependent changes with evening increases and the highest values at night (P < .0005). This nocturnal increase was suppressed during total sleep deprivation (P < .05), independent of external light conditions and melatonin secretion. Rapid eye movement sleep deprivation had no impact on circulating L-PGDS levels. CONCLUSIONS: The circadian L-PGDS pattern and its suppression by total sleep deprivation indicate an interaction of the prostaglandin D system and human sleep regulation. L-PGDS measurements may well provide new insights into physiologic and pathologic sleep regulation in humans.     

Early morning executive functioning during sleep deprivation is compromised by a PERIOD3 polymorphism

STUDY OBJECTIVES: To contrast the effects of total sleep deprivation (TSD) on executive and non-executive function in volunteers homozygous for either the short or long variant of a variable number tandem repeat polymorphism in PERIODS, which is a genetic marker for susceptibility to the negative effect of sleep loss on waking performance. DESIGN: Following two laboratory nights of baseline sleep, both groups underwent an approximately 40-hour constant routine, performing brief tests of executive, memory, attention, and motor function every 2 hours. SETTING: Clinical Research Centre. PARTICIPANTS: Fourteen PER3(4/4) (homozygotes for shorter variant of the gene) and 10 PER3(5/5) (homozygotes for longer variant) healthy, young adults (mean 25.0 +/- 1.0 years). INTERVENTIONS: Total sleep deprivation (approximately 40 hours) following baseline sleep. MEASUREMENTS AND RESULTS: Hormonal assays established that melatonin levels, which reflect circadian phase, reached their midpoint around 04:00 in both genotypes. Cognitive performance deteriorated across the night, and was similar for both genotypes throughout, except 2-4 h after the midpoint of the melatonin rhythm. Only at this time-point and only on tests of executive function (e.g., 3-back, paced visual serial addition task) did PER3(5/5) participants perform reliably worse. Covariance analyses controlling for genotype dependent differences in homeostatic sleep pressure derived from principal component analysis of baseline sleep latency, slow wave sleep and wake after sleep onset largely removed these early morning differences in executive function. CONCLUSIONS: This PER3 polymorphism differentially influences the effects of sleep deprivation on executive and non-executive function in the early morning. These effects appear to be mediated through homeostatic sleep pressure.     

Rhythm of melatonin excretion in obstructive sleep apnea syndrome

Melatonin is a pineal hormone that regulates sleep and wake status. Melatonin concentrations in blood serum were measured using radioisotope method in 33 males (age 48 +/- 10) with obstructive sleep apnea syndrome. The following melatonin concentrations were measured: 54 +/- 72 pg/ml (9 p.m.) 424 +/- 838 pg/ml (2 a.m.) and 307 +/- 534 pg/ml (6 a.m.). In patients with high peak melatonin concentration (> 200 pg/ml) as compared with the patients with low peak melatonin concentration (< 200 pg/ml) there were higher index of respiratory disorders during sleep (53 +/- 18 vs 38 +/- 20, p < 0.05) and lower minimal SaO2 during sleep apnea (52 +/- 17% vs 70 +/- 10%, p < 0.05); they were also more tired in the morning and were more sleepy during the day (Epworth sleepiness scale 17 +/- 6 vs 11 +/- 6, p < 0.01). In 66% of patients peak melatonin concentration was observed at 2 a.m. In 24% of patients peak melatonin secretion was prolonged to early morning hours. CONCLUSIONS: In most of patients there is peak melatonin excretion at 2 a.m. Patients with high apnea and hypopnea index and daytime sleepiness have high peak melatonin concentrations.     

Evening administration of melatonin and bright light: Interactions on the EEG during sleep and wakefulness

Both the pineal hormone melatonin and light exposure are considered to play a major role in the circadian regulation of sleep. In a placebo- controlled balanced cross-over design, we investigated the acute effects of exogenous melatonin (5 mg p.o. at 20.40 hours) with or without a 3-h bright light exposure (5000 lux from 21.00 hours–24.00 hours) on subjective sleepiness, internal sleep structure and EEG power density during sleep and wakefulness in healthy young men. The acute effects of melatonin, bright light and their interaction were measured on the first day (treatment day), possible circadian phase shifts were assessed on the post-treatment day. On the treatment day, the evening rise in subjective sleepiness was accelerated after melatonin and protracted during bright light exposure. These effects were also reflected in specific changes of EEG power density in the theta/alpha range during wakefulness. Melatonin shortened and bright light increased sleep latency. REMS latency was reduced after melatonin administration but bright light had no effect. Slow-wave sleep and slow-wave activity during the first non-rapid eye movement (NREMS) episode were suppressed after melatonin administration and rebounded in the second NREMS episode, independent of whether light was co-administered or not. Self rated sleep quality was better after melatonin administration whereas the awakening process was rated as more difficult after bright light. On the post-treatment day after evening bright light, the rise in sleepiness and the onset of sleep were delayed, independent of whether melatonin was co-administered or not. Thus, although acute bright light and melatonin administration affected subjective sleepiness, internal sleep structure and EEG power density during sleep and wakefulness in a additive manner, the phase shifting effect of a single evening bright light exposure could not be blocked by exogenous melatonin     

Challenging sleep homeostasis in narcolepsy-cataplexy: implications for non-REM and REM sleep regulation

STUDY OBJECTIVES: We recently proposed insufficient non-rapid eye movement sleep (NREMS) intensity to contribute to disturbed nocturnal sleep in patients with narcolepsy-cataplexy (NC). To test this hypothesis, we investigated the effect of physiologically intensified NREMS in recovery sleep following sleep deprivation. DESIGN: Nocturnal baseline and recovery sleep architecture, and the sleep electroencephalogram (EEG) before and after 40 hours of sustained wakefulness were compared between 6 drug-free patients with NC (age range: 19-37 years) and 6 individually matched, healthy control subjects (18-43 years). MEASUREMENTS: Sleep and sleep EEG power spectra (C3A2 derivation). The dynamics of the homeostatic Process S were estimated from the time course of slow-wave activity (SWA, spectral power within 0.75-4.5 Hz) across consecutive NREMS episodes. SETTINGS: Sleep research laboratory. RESULTS: In baseline, SWA decreased across consecutive NREMS episodes in patients with NC and control subjects. The build-up of SWA, however, was attenuated in NC in the second episode (P = 0.01) due to a higher number of short wake periods (P = 0.02). Prolonged wakefulness increased initial SWA in both groups (P = 0.003) and normalized the baseline differences between patients and control subjects in the time course of SWA in NREMS. The changed dynamics of SWA in the patients in recovery sleep when compared with baseline were associated with reduced numbers of intermittent wake periods in the first (P = 0.01) and second (P = 0.04) NREMS episodes. All patients, but no control subjects, showed a sleep-onset rapid eye movement period (SOREMP) in both baseline and recovery sleep. Sleep deprivation increased SOREMP duration (P = 0.03). CONCLUSIONS: Increased SWA after sleep deprivation indicates that sleep homeostasis is functional in NC. Increased NREMS intensity in recovery sleep postpones sleep fragmentation, supporting our concept that sleep fragmentation is directly related to insufficient NREMS intensity in NC. The persistence of SOREMP despite enhanced NREMS pressure suggests an abnormal interaction between NREMS and REMS regulatory processes.     

Nocturnal sustained attention during sleep deprivation can be predicted by specific periods of subjective daytime alertness in normal young humans

In our 24-h society, nocturnal sleep-related accidents are common. Because all individuals are not equal in their responses to sleep loss, it is very important to identify predictors of vulnerability to sleep deprivation in normal subjects. We investigated the performance of a cognitive test of sustained attention, electroencephalogram theta/alpha power, subjective sleepiness, and two circadian markers (core temperature and melatonin) in 18 healthy men (nine morning types and nine evening types, 21.4 +/- 1.9 years) during a 36-h sleep deprivation in a constant routine protocol. Sleep need (self-reported) and baseline sleep structure were also investigated. Nighttime performance impairment was defined as the difference between the mean nocturnal number of lapses (00:00-07:30 [corrected] hours) and the mean diurnal number of lapses (07:30-20:30 hours) expressed as a percentage. Feeling fully alert in the morning just after awakening and/or sleepy in early afternoon were the only two factors (Multiple R > 0.80, > 60% of explained variance) which better predicted the decrease in performances of nocturnal operational tasks requiring sustained attention.     

The relation between polysomnography and subjective sleep and its dependence on age – poor sleep may become good sleep

Women complain more about sleep than men, but polysomnography (PSG) seems to suggest worse sleep in men. This raises the question of how women (or men) perceive objective (PSG) sleep. The present study sought to investigate the relation between morning subjective sleep quality and PSG variables in older and younger women. A representative sample of 251 women was analysed in age groups above and below 51.5 years (median). PSG was recorded at home during one night. Perceived poor sleep was related to short total sleep time (TST), long wake within total sleep time (WTSP), low sleep efficiency and a high number of awakenings. The older women showed lower TST and sleep efficiency and higher WTSP for a rating of good sleep than did the younger women. For these PSG variables the values for good sleep in the older group were similar to the values for poor sleep in the young group. It was concluded that women perceive different levels of sleep duration, sleep efficiency and wake after sleep onset relatively well, but that older women adjust their objective criteria for good sleep downwards. It was also concluded that age is an important factor in the relation between subjective and objective sleep.     

Hypoglycemia counterregulation during sleep

STUDY OBJECTIVES: In insulin-treated patients with diabetes, episodes of severe hypoglycemia often occur during sleep, which might reflect an altered counterregulation and reduced awareness. This study examined the influence of sleep on the counterregulatory response to hypoglycemia in healthy subjects. DESIGN: Subjects participated in two experimental conditions; statistical tests relied on within subject comparisons. SETTING: University hospital sleep laboratory. PARTICIPANTS: 15 healthy young men. INTERVENTIONS: Hypoglycemia (2.8 mmol/l) was induced for 45 min by insulin infusion once during sleep and once at the same time of night while being awake. MEASUREMENTS AND RESULTS: Counterregulatory hormone concentrations (epinephrine, norepinephrine, ACTH and cortisol) and sleep recordings were obtained. Differences in the hormonal responses to hypoglycemia between sleep and wake conditions remained non-significant, indicating that sleep does not exert a primary influence on the strength of counterregulation. However, the glycemic threshold for the onset of counterregulation was significantly changed during sleep: The average onset threshold for epinephrine and norepinephrine counterregulation was 3.3 +/- 0.1 mmol/l for the wake condition and 2.7 +/- 0.1 mmol/l for the sleep condition (P < 0.001). A decrease in sleep depth coincided with the onset of the counterregulatory response, with most subjects showing signs of awakening. CONCLUSIONS: During sleep, the organism is less sensitive to hypoglycemia. Hypoglycemia per se has an awakening effect.     

Age-related changes in the time course of vigilant attention during 40 hours without sleep in men

STUDY OBJECTIVES: To examine whether vigilant attention and sleepiness develop differently during prolonged wakefulness in young and older men. DESIGN, SETTING, AND PARTICIPANTS: Psychomotor vigilance task (PVT) performance and subjective sleepiness were determined in 14 sessions at 3 hour intervals in healthy young (n = 12, mean age: 25.2 years, range: 21-31 years) and older (n = 11, mean age: 66.4 years, range: 61-70 years) men who were kept awake for 40 hours under continuous supervision in a sleep laboratory and on the morning after the recovery night. MEASUREMENTS AND RESULTS: PVT speed, response lapses and performance variability, and subjective sleepiness were analyzed. Sleep deprivation led to reversal of an age-related difference in PVT speed at the circadian trough of performance on the morning of the second day of prolonged wakefulness (Session x Age interaction: P < .0006). Beginning after 22 hours of wakefulness, the young men also produced more lapses (P < .004), showed higher performance instability (P < .0001), and felt sleepier (P < .03) than older men, especially during the morning after the night without sleep. CONCLUSIONS: Vigilant attention is more impaired after 1 night without sleep in young men than in older men, which has important implications for the prevention of accidents associated with the loss of sleep.     

Relationships among wake episode lengths, contiguous sleep episode lengths, and electroencephalographic delta waves in rats with suprachiasmatic nuclei lesions

The lengths of sleep and wake episodes during 2 consecutive days of recording were measured in five rats lacking circadian rhythms owing to lesions of the suprachiasmatic nuclei. Total sleep (TS) episode lengths and the amount of NREM sleep and paradoxical sleep (PS) within each episode were examined in relationship to the lengths of the immediately preceding and the immediately following wake episodes. As putative measures of sleep intensity, average and maximum delta wave (1-4 Hz) incidence and amplitude within NREM were also examined in relation to adjacent wake episode lengths. For sleep episodes longer than 50 min (78% of daily sleep), TS episode lengths and amount of NREM within these episodes showed significant positive correlations with both prior and subsequent wake episode lengths. PS durations within sleep episodes also showed significant positive correlations with subsequent wake episode lengths, but little correlation with prior wake episode lengths. The results suggest that in the absence of sleep-wake circadian rhythms, sleep time is subject to short-term homeostatic regulation. Amounts of PS within sleep episodes were highly correlated (r = 0.84) with amounts of NREM. NREM delta wave incidence and amplitude showed no significant relationships with the lengths of prior or subsequent wake episodes, suggesting that variations in sleep intensity may not play a prominent role in the short-term homeostatic regulation of ad lib sleep. Delta wave incidence and amplitude were also not correlated with the duration of NREM episodes, but incidence during wake was positively correlated with wake episode duration, suggesting that delta density during wake may be an electrophysiological indicator of the propensity to sleep.     

Diurnal preference, sleep habits, circadian sleep propensity and melatonin rhythm in healthy human subjects

After 24-h sleep deprivation, 33 healthy young subjects entered the 10/20 min ultra-short sleep–wake schedule for 26 h. Melatonin rhythm was hourly assessed simultaneously. Results indicated that morning preference was significantly correlated with habitual sleep onset (r=−0.41, P=0.04), habitual sleep offset (r=−0.52, P=0.002), melatonin peak time (r=−0.36, P=0.04), and sleep propensity onset time (r=−0.36, P=0.04). The intervals between habitual sleep mid-point and melatonin peak time and between habitual sleep mid-point and sleep propensity onset time were significantly longer in morning-preference subjects than in evening-preference subjects (P<0.05). These findings suggest that the variance of diurnal preference may be related to differences in phase relations between habitual sleep timing and the circadian pacemaker.     

The use of actigraphy for assessment of the development of sleep/wake patterns in infants during the first 12 months of life

Maturation of sleep/wake patterns is one of the most important physiological developments during the first year of life. In this study, we aimed to compare the use of actigraphy and parental sleep diaries (SD) for recording the development of sleep/wake patterns longitudinally in term infants in their own home environments over the first 12 months of life. Twenty healthy term infants (7F/13M) were studied for 3 days each month in their own homes over the first 12 months of life. Sleep/wake patterns were recorded using both SD and actigraphy (AW) (AW64, Mini Mitter Co. Inc., Sunriver, OR, USA). The development of sleep and wake was analysed over 24 h, during the day (08:00-20:00 hours) and during the night (20:00-08:00 hours). A total of 186 studies had complete data sets for both analysis methods. Overall, there was no difference between methods of measurement for determination of the total percentage of sleep or wake over 24 h, or for the total percentage of sleep or wake during the day. However, at night, AW scored less time asleep (73.3 +/- 0.9%) and more time awake (26.7 +/- 0.9%) compared with the SD (80.7 +/- 1.04% and 19 +/- 1.0%, respectively, P < 0.001). Mean percentage sleep during the day decreased from 51% at 1 month to 28% at 12 months with the 1-month values being significantly higher than all other ages, while mean percentage sleep at night was only different between 1 month and 11 and 12 months. In conclusion actigraphy provides a useful tool for assessing the development infant sleep.     

Age-related attenuation of the evening circadian arousal signal in humans

The human circadian pacemaker maintains timing and consolidation of sleep-wake behavior by opposing the build-up of homeostatic sleep pressure during the wake episode, particularly in the evening during the 'wake maintenance zone'. We tested whether age-related changes in sleep are a consequence of a weaker circadian arousal signal in the evening. Circadian rhythms and spectral components of the sleep EEG were investigated in 17 young (20-31 year) and 15 older (57-74 year) volunteers under constant posture conditions during a 40-h nap protocol (75/150 min sleep/wake schedule). Quantitative evidence for a weaker circadian arousal signal in aging arose from significantly more sleep occurring during the wake maintenance zone and higher subjective sleepiness ratings in the late afternoon and evening in the older group. In addition, we found a diminished melatonin secretion and a reduced circadian modulation of REM sleep together with less pronounced day-night differences in the lower alpha and spindle range of sleep EEG activity in the older group. Thus, our data indicate that age-related changes in sleep propensity are clearly related to a reduced circadian signal opposing the homeostatic drive for sleep.     

Age, performance and sleep deprivation

Young subjects are frequently involved in sleep-related accidents. They could be more affected than older drivers by sleep loss and therefore worsen their driving skills quicker, or have a different perception of their level of impairment. To test these hypotheses we studied variations of reaction time (RT), a fundamental prerequisite for safe performing, as measured by lapses, i.e. responses > or = 500 ms and self-assessment of performance and sleepiness after a night awake and after a night asleep in a balanced crossover design in young versus older healthy subjects. Ten young (20-25 years old) and 10 older volunteers (52-63 years old) were tested with and without 24 h of sleep deprivation. Without sleep deprivation, RTs were slower in older subjects than in the younger ones. However, after sleep deprivation, the RTs of young subjects increased while that of the older subjects remained almost unaffected. Sleepiness and self-perception of performance were equally affected in both age groups showing different perception of performance in the age groups. Our findings are discussed in terms of vulnerability to sleep-related accidents.     

Exploring the impact of experimental sleep restriction and sleep deprivation on subjectively perceived sleep parameters

We aimed to investigate the effect of increased sleep pressure and shortened sleep duration on subjective sleep perception in relation to electroencephalographic sleep measures. We analyzed the data from a study in which 14 healthy male volunteers had completed a baseline assessment with 8 hr time in bed, a sleep deprivation (40 hr of wakefulness) and a sleep restriction protocol with 5 hr time in bed during 7 nights. In this work, we assessed perception index, derived through dividing the subjectively perceived total sleep time, wake after sleep onset and sleep latency duration by the objectively measured one at each condition. We found that total sleep time was subjectively underestimated at baseline and shifted towards overestimation during sleep restriction and after deprivation. This change in accuracy of subjective estimates was not associated with any changes in sleep architecture or sleep depth. Wake after sleep onset was significantly underestimated only during sleep restriction. Sleep latency was always overestimated subjectively without any significant change in this misperception across conditions. When comparing accuracy of subjective and actimetry estimates, subjective estimates regarding total sleep time and wake after sleep onset deviated less from electroencephalography derived measures during sleep restriction and after deprivation. We conclude that self‐assessments and actimetry data of patients with chronic sleep restriction should be interpreted cautiously. The subjectively decreased perception of wake after sleep onset could lead to overestimated sleep efficiency in such individuals, whereas the underestimation of sleep time and overestimation of wake after sleep onset by actimetry could lead to further underestimated sleep duration.     

Poor sleep is associated with poorer physical performance and greater functional limitations in older women

STUDY OBJECTIVES: This study examined the association between disturbed sleep and poorer daytime function in older women. DESIGN: Observational study. PARTICIPANTS: 2,889 women, mean age 83.5 years, participating in the 2002-2004 examination of the Study of Osteoporotic Fractures. INTERVENTIONS: N/A. MEASUREMENTS AND RESULTS: Participants wore actigraphs for an average +/- SD of 4.1 +/- 0.83 24-hour periods. Actigraphy measured sleep variables were total sleep time and hours awake after sleep onset during the night and daytime napping behavior. Neuromuscular performance measurements included gait speed, chair stands, and grip strength. Functional limitations were assessed as self-reported difficulty with one or more of 6 instrumental activities of daily living (IADL). In fully adjusted, multivariable models, women who slept <6 hours per night walked 3.5% slower than those who slept 6.0-6.8 hours. Those who slept > or =7.5 hours took 4.1% longer to complete 5 chair stands than those who slept 6.8-7.5 hours. With higher wake after sleep onset (> or =1.6 hours compared to <0.7 hours) gait speed was 9.1% slower; it took 7.6% longer to complete 5 chair stands, and odds of functional limitation were 1.8 (95% CI: 1.4, 2.4) higher. Women with 1.0-1.8 hours of daytime sleep had higher odds (1.4 [95% CI: 1.1, 1.8]) of a functional limitation than those with <0.5 hours. Sleep variables did not appear to be associated with grip strength. CONCLUSIONS: Objectively measured poorer sleep was associated with worse physical function. Future research is needed to identify the underlying mechanisms for the association between poor sleep and functional decline.     

The effects of rapid eye movement sleep deprivation during late pregnancy on newborns' sleep

Sleep deprivation during pregnancy is an emerging concern, as it can adversely affect the development of the offspring brain. This study was conducted to evaluate the effects of deprivation of rapid eye movement (REM) sleep during the third term of pregnancy on the sleep–wake profiles of neonates in the Wistar rat model. Sleep–wake patterns were assessed through electrophysiological measures and behavioural observations during postnatal days 1–21 on pups born to REM sleep‐deprived dams and control rats. Pups of REM sleep‐deprived dams had active sleep that was not only markedly higher in percentage during all the days studied, but also had reduced latency during later postnatal days 15–21. Quiet sleep and wake periods were lower. These factors, along with less frequent but longer sleep–wake cycles, indicated maturational delay in the sleep–wake neural networks. The disruption of time‐bound growth of sleep–wake neural networks was substantiated further by the decreased slope of survival plots in the sleep bouts. Examination of altered sleep–wake patterns during early development may provide crucial information concerning deranged neural development in the offspring. This is the first report, to our knowledge, to show that maternal sleep deprivation during pregnancy can delay and impair the development of sleep–wake profile in the offspring.     

Eszopiclone Improves Overnight Polysomnography and Continuous Positive Airway Pressure Titration: A Prospective, Randomized, Placebo-Controlled Trial

STUDY OBJECTIVES: To assess whether premedication with eszopiclone would improve sleep duration and continuity during polysomnography, thereby improving the quality of diagnostic and CPAP titration studies. DESIGN: Prospective, double-blinded, placebo-controlled trial SETTING: Academic, multidisciplinary sleep center. PATIENTS: 226 adult subjects undergoing polysomnography for suspected sleep disordered breathing; 113 received eszopiclone and 113 received placebo. INTERVENTIONS: Subjects received eszopiclone 3 mg or matching placebo before polysomnography. We compared sleep latency, efficiency, total sleep time, and apnea-hypopnea index between these groups. We also compared rates of inadequate studies, defined as insufficient sleep time (< 120 min or sleep efficiency < or = 70%) or incomplete CPAP titrations (> or = 5 events/h on the highest CPAP or complete intolerance). MEASUREMENTS AND RESULTS: Eszopiclone premedication significantly improved a number of measured variables. Eszopiclone reduced sleep latency (21.7 +/- 27.1 vs. 32.6 +/- 38.2 min, P = 0.014), improved sleep efficiency (87.6% +/- 10.8% vs. 78.1% +/- 15.6%, P < 0.001), reduced wake after sleep onset (39.2 +/- 31.9 vs. 64.5 +/- 45.4 min, P <0.001) and prolonged sleep time (346.5 +/- 53.1 vs. 312.2 +/- 64.2 min, P < 0.001). Sleep efficiencies < or = 70% were more common with placebo than medication (21.2% vs. 7.1%, P = 0.004). Eszopiclone facilitated improved CPAP titrations with fewer residual events (5.7 +/- 10.3 vs. 11.9 +/- 19.6, P = 0.02) and fewer incomplete titrations (31.1% vs. 48.0%, P = 0.04). Poor quality studies (46.0% vs. 26.5%, P = 0.004) were more common with placebo than with eszopiclone. There was a trend for more non-usable studies with placebo (7.1% vs. 2.7%, P = 0.22). Side effects were uncommon and did not differ between groups. CONCLUSION: Pretreatment with eszopiclone improves the quality of polysomnography and CPAP titration and decreases the need to repeat studies. Given the ever-growing demand for polysomnography and the need to improve efficiency, the routine use of nonbenzodiazepines as premedication for polysomnography should be considered.     

Sleep tendency during extended wakefulness: insights into adolescent sleep regulation and behavior

Sleep tendency (latency to sleep onset) was examined during extended waking in prepubertal and mature adolescents to determine whether sleep pressure is lower near bedtime in the latter group. Participants were nine prepubertal (pubertal stage Tanner 1, mean age 11.1 years, SD+/-1.3 years, five males) and 11 pubertally mature adolescents (Tanner 5, 13.9+/-1.2 years, three males). They spent 10 nights at home on an identical fixed 10-h sleep schedule followed by a 36-h constant routine with sleep latency tests at 2-h intervals using standard polysomnography. Saliva was collected to assess dim-light melatonin onset (DLMO) phase. DLMO was earlier in the Tanner 1 (mean clock time=20:33 hours, SD=49 min) than Tanner 5 group (21:29 hours+/-42 min). Sleep latency compared at a 'critical period' spanning 12.5 (20:30 hours clock time) to 18.5 h (02:30 hours) after waking did not differ at 20:30 hours, but was shorter for the Tanner 1 group at 22:30 hours (Tanner 1=9.2+/-6.3 min; Tanner 5=15.7+/-5.8 min), 00:30 hours (Tanner 1=3.6+/-1.7 min; Tanner 5=9.0+/-6.4 min), and 02:30 hours (Tanner 1=2.0+/-1.7 min; Tanner 5=4.3+/-3.2 min; trend). These differences were apparent controlling for circadian phase by partial correlation. Sleep tendency after 14.5, 16.5, and 18.5 h awake was lower in mature versus prepubertal adolescents, supporting our hypothesis that a developmental change of intrinsic sleep-wake regulation may provide physiologically mediated 'permission' for later bedtimes in older adolescents.     

Age-Related Reduction in Daytime Sleep Propensity and Nocturnal Slow Wave Sleep

Objective:

To investigate whether age-related and experimental reductions in SWS and sleep continuity are associated with increased daytime sleep propensity.

Methods:

Assessment of daytime sleep propensity under baseline conditions and following experimental disruption of SWS. Healthy young (20-30 y, n = 44), middle-aged (40-55 y, n = 35) and older (66-83 y, n = 31) men and women, completed a 2-way parallel group study. After an 8-h baseline sleep episode, subjects were randomized to 2 nights with selective SWS disruption by acoustic stimuli, or without disruption, followed by 1 recovery night. Objective and subjective sleep propensity were assessed using the Multiple Sleep Latency Test (MSLT) and the Karolinska Sleepiness Scale (KSS).

Findings:

During baseline sleep, SWS decreased (P < 0.001) and the number of awakenings increased (P < 0.001) across the 3 age groups. During the baseline day, MSLT values increased across the three age groups (P < 0.0001) with mean values of 8.7min (SD: 4.5), 11.7 (5.1) and 14.2 (4.1) in the young, middle-aged, and older adults, respectively. KSS values were 3.7 (1.0), 3.2 (0.9), and 3.4 (0.6) (age-group: P = 0.031). Two nights of SWS disruption led to a reduction in MSLT and increase in KSS in all 3 age groups (SWS disruption vs. control: P < 0.05 in all cases).

Conclusions:

Healthy aging is associated with a reduction in daytime sleep propensity, sleep continuity, and SWS. In contrast, experimental disruption of SWS leads to an increase in daytime sleep propensity. The age-related decline in SWS and reduction in daytime sleep propensity may reflect a lessening in homeostatic sleep requirement. Healthy older adults without sleep disorders can expect to be less sleepy during the daytime than young adults.

Citation:

Dijk DJ; Groeger JA; Stanley N; Deacon S. Age-related reduction in daytime sleep propensity and nocturnal slow wave sleep. SLEEP 2010;33(2):211-223.