Increased Sensitivity of the Circadian System to Light in Early/Mid-Puberty.

CONTEXT: Late adolescence is marked by a delay in sleep timing, which is partly driven by a delay shift of the circadian timing system. This study examined whether the sensitivity of the circadian system to light-the primary entraining stimulus to the circadian system-differs between pre- to mid-pubertal and late to postpubertal adolescents. OBJECTIVE: The study was designed to determine the influence of puberty on the sensitivity of the circadian system to light in humans. METHODS: Melatonin suppression to low and moderate light levels was assessed in 38 pre- to mid-pubertal (9.1-14.7 years) and 29 late to postpubertal (11.5-15.9 years) adolescents. They received 1 hour of four light levels on consecutive nights: approximately 0.1 (near-dark baseline condition), 15, 150, and 500 lux. One group received evening light beginning at 11:00 pm (n = 39); a second group received morning light beginning at 3:00 am (n = 28). Salivary melatonin was sampled every 30 minutes. Melatonin suppression for 15, 150, and 500 lux was calculated relative to unsuppressed baseline levels in the 0.1 lux setting, within individuals. RESULTS: The pre- to mid-pubertal group showed significantly greater melatonin suppression to 15 lux (9.2 ± 20.5%), 150 lux (26.0 ± 17.7%), and 500 lux (36.9 ± 11.4%) during evening light exposure compared to the late to postpubertal group (-5.3 ± 17.7%, 12.5 ± 17.3%, and 23.9 ± 21.7%, respectively; P < .05). No significant differences were seen between developmental groups in morning melatonin suppression. CONCLUSION: These results indicate support for a greater sensitivity to evening light in early pubertal children. The increased sensitivity to light in younger adolescents suggests that exposure to evening light could be particularly disruptive to sleep regulation for this group.

Sleepiness and Cognitive Performance among Younger and Older Adolescents across a 28-Hour Forced Desynchrony Protocol.

STUDY OBJECTIVES: Quantify the homeostatic and circadian effects on sleepiness and performance of adolescents. Examine age-related changes in homeostatic and circadian regulation of sleepiness and performance by comparing younger and older adolescent groups. DESIGN: Three-week laboratory study including 12 cycles of a 28-h forced desynchrony protocol. SETTING: Controlled laboratory environment with individual sleep and performance testing rooms and shared common areas. PARTICIPANTS: Twenty-seven healthy adolescents including 16 females. Ages ranged from 9.6-15.2 years and participants were split into younger (n = 14 ages 9-12) and older (n = 13 ages 13-15) groups based on median age split of 13.0 years. INTERVENTIONS: N/A. MEASUREMENTS AND RESULTS: Testing occurred every 2 h during scheduled wake periods. Measures included sleep latency during repeated nap opportunities and scores from a computerized neurobehavioral assessment battery including a 10-min psychomotor vigilance task, a digit symbol substitution task, and the Karolinska Sleepiness Scale. Significant main effects of circadian and homeostatic factors were observed, as well as several circadian and homeostatic interaction effects. Age group did not have a significant main effect on sleep and performance data. A significant interaction of circadian phase and age group was found for sleep latency, with younger adolescents showing greater circadian modulation than older teens during the circadian night. CONCLUSIONS: Adolescents demonstrated a similar pattern of response to forced desynchrony as reported for adults. Sleepiness and performance were affected by homeostatic and circadian factors, and age group did not interact with homoeostatic and circadian factors for subjective sleepiness and most performance metrics. Younger adolescents had a shorter latency to sleep onset than older during the circadian bin spanning 4 to 8 h after the onset of melatonin secretion.

A longitudinal assessment of sleep timing, circadian phase, and phase angle of entrainment across human adolescence.

The aim of this descriptive analysis was to examine sleep timing, circadian phase, and phase angle of entrainment across adolescence in a longitudinal study design. Ninety-four adolescents participated; 38 (21 boys) were 9-10 years ("younger cohort") and 56 (30 boys) were 15-16 years ("older cohort") at the baseline assessment. Participants completed a baseline and then follow-up assessments approximately every six months for 2.5 years. At each assessment, participants wore a wrist actigraph for at least one week at home to measure self-selected sleep timing before salivary dim light melatonin onset (DLMO) phase - a marker of the circadian timing system - was measured in the laboratory. Weekday and weekend sleep onset and offset and weekend-weekday differences were derived from actigraphy. Phase angles were the time durations from DLMO to weekday sleep onset and offset times. Each cohort showed later sleep onset (weekend and weekday), later weekend sleep offset, and later DLMO with age. Weekday sleep offset shifted earlier with age in the younger cohort and later in the older cohort after age 17. Weekend-weekday sleep offset differences increased with age in the younger cohort and decreased in the older cohort after age 17. DLMO to sleep offset phase angle narrowed with age in the younger cohort and became broader in the older cohort. The older cohort had a wider sleep onset phase angle compared to the younger cohort; however, an age-related phase angle increase was seen in the younger cohort only. Individual differences were seen in these developmental trajectories. This descriptive study indicated that circadian phase and self-selected sleep delayed across adolescence, though school-day sleep offset advanced until no longer in high school, whereupon offset was later. Phase angle changes are described as an interaction of developmental changes in sleep regulation interacting with psychosocial factors (e.g., bedtime autonomy).

Patients' journeys to a narcolepsy diagnosis: a physician survey and retrospective chart review.

Narcolepsy is a lifelong disorder with potentially debilitating symptoms. Obtaining an accurate diagnosis often requires multiple tests and physician visits. This report describes results from an online, quantitative, company-sponsored survey in which physicians provided information from the charts of their patients with narcolepsy. Neurologists, pulmonologists, psychiatrists, and other specialists who were board certified in sleep medicine; had 2 to 30 years of clinical experience; and treated ≥ 5 narcolepsy patients per month were invited to complete ≤ 6 surveys using charts of patients who were treated for narcolepsy in the last 6 months. Data from 252 patients were collected from 77 physicians. Patients were predominantly male (55%), white (67%), and had a median age of 38 years (range: 12-83 years). Referral to the respondent physician was common, mainly from primary care physicians. The most common initial symptoms were excessive daytime sleepiness (91%), trouble staying awake during the day (44%), and trouble concentrating/functioning during the day (43%). Overall, initial symptoms were of at least moderate severity in 85% of patients. Most patients completed overnight polysomnography (83%), a Multiple Sleep Latency Test (76%), and/or the Epworth Sleepiness Scale (62%). The median time from patient-reported symptom onset to diagnosis was 22 months (range: 0-126 months); at least half saw ≥ 2 providers before being diagnosed; and 60% of patients had previously been misdiagnosed with other disorders, including depression (31%), insomnia (18%), and/or obstructive sleep apnea (13%). In this study, the journey to a narcolepsy diagnosis required evaluation by multiple physicians and took nearly 2 years in 50% of patients, and > 5 years in 18%. These data highlight the need for increased awareness of the signs and symptoms of narcolepsy.

Sleep patterns are associated with common illness in adolescents.

This prospective, field-based study examined the association between actigraphically measured total sleep time and incident illness including cold, flu, gastroenteritis and other common infectious diseases (e.g., strep throat) in adolescents during the course of a school semester. Participants were 56 adolescents ages 14-19 years (mean = 16.6, standard deviation = 1.2, 39% male) from five high schools in Rhode Island. Beginning in late January, adolescents wore actigraphs [mean 91 (19) days, range 16-112 days] and were assigned post-hoc to longer or shorter sleep groups based on median splits. Adolescents were interviewed weekly across as many as 16 weeks (modal number of interviews = 13) using a structured protocol that included 14 health event questions. Illness events and illness-related school absences were coded for 710 completed interviews, with 681 illness events and 90 school absences reported. Outcomes (illness bouts, illness duration and absences) were compared among sex, sleep and academic year groups using non-parametric regression. In a subset of 18 subjects, mean actigraphically estimated total sleep time six nights before matched illness/wellness events was compared using multivariate analysis of variance (manova). Longer sleepers and males reported fewer illness bouts; total sleep time effects were more apparent in males than females. A trend was found for shorter total sleep time before ill events. The present findings in this small naturalistic sample indicate that acute illnesses were more frequent in otherwise healthy adolescents with shorter sleep, and illness events were associated with less sleep during the previous week than comparable matched periods without illness.

Biphasic effects of alcohol as a function of circadian phase.

STUDY OBJECTIVES: To assess how alcohol affects multiple sleep latency tests (MSLT) and subjective measures of stimulation/sedation when alcohol is given at different circadian phases. PARTICIPANTS: Twenty-seven healthy young adults (age 21-26 yr) were studied. DESIGN: Double-blind placebo and alcohol (vodka tonic targeting 0.05 g% concentration) beverages were each administered three times during the 20-h forced desynchrony protocol. Sleep latency tests and Biphasic Effects of Alcohol Scale (BAES) were administered on each forced desynchrony day. The outcome variables for this study include sleep onset latency (SOL) and stimulation and sedation value (from the BAES). Each outcome variable was associated with the ascending or descending limb of the breath alcohol concentration (BrAC) curve and assigned a circadian phase within a 90° bin. MEASUREMENTS AND RESULTS: BrAC confirmed targeted maximal levels. Only outcome variables associated with the ascending and descending limb of the alcohol curve were analyzed for this article. Alcohol administered at a circadian time associated with greatest sleepiness showed longer SOL compared with placebo when measured on the ascending limb of the BrAC curve. We also found longer SOL with alcohol on the ascending limb of the BrAC curve in a circadian bin that favors greatest alertness. We observed shorter SOLs on the descending limb of the BrAC curve, but with no circadian phase interaction. The subjective data were partially consistent with the objective data. CONCLUSIONS: The physiologic findings in this study support the biphasic stimulating and sedating properties of alcohol, but limit the effect to specific circadian times.

Adolescence and parental history of alcoholism: insights from the sleep EEG.

BACKGROUND: Disrupted sleep is a common complaint of individuals with alcohol use disorder and in abstinent alcoholics. Furthermore, among recovering alcoholics, poor sleep predicts relapse to drinking. Whether disrupted sleep in these populations results from prolonged alcohol use or precedes the onset of drinking is not known. The aim of this study was to examine the sleep electroencephalogram (EEG) in alcohol-naïve, parental history positive (PH+), and negative (PH-) boys and girls. METHODS: All-night sleep EEG recordings in 2 longitudinal cohorts (child and teen) followed at 1.5 to 3 year intervals were analyzed. The child and teen participants were 9/10 and 15/16 years old at the initial assessment, respectively. Parental history status was classified by Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV) criteria applied to structured interviews (DIS-IV) resulting in 14 PH- and 10 PH+ children and 14 PH- and 10 PH+ teens. Sleep data were visually scored in 30-second epochs using standard criteria. Power spectra were calculated for EEG derivations C3/A2, C4/A1, O2/A1, O1/A2 for nonrapid eye movement (NREM) and rapid eye movement (REM) sleep. RESULTS: We found no difference between PH+ and PH- individuals in either cohort for any visually scored sleep stage variable. Spectral power declined in both cohorts across assessments for NREM and REM sleep in all derivations and across frequencies independent of parental history status. With regard to parental history, NREM sleep EEG power was lower for the delta band in PH+ teens at both assessments for the central derivations. Furthermore, power in the sigma band for the right occipital derivation in both NREM and REM sleep was lower in PH+ children only at the initial assessment. CONCLUSIONS: We found no gross signs of sleep disruption as a function of parental history. Modest differences in spectral EEG power between PH+ and PH- children and teens indicate that a marker of parental alcohol history may be detectable in teens at risk for problem drinking.

Human puberty: salivary melatonin profiles in constant conditions.

This analysis examined the relative contributions of sex, age, body mass index (BMI), and puberty (Tanner) stage on salivary melatonin amplitude. Sixty-nine children and adolescents (30 females; 9.6-17.8 years) were examined for Tanner stage. Serial salivary melatonin samples were collected in controlled conditions, from which these melatonin amplitude measures were derived: area under the curve (AUC) and maximum value (MAX). AUC declined with advancing Tanner stage. This melatonin decline was similar between boys and girls, but girls secreted more melatonin compared to boys. Tanner stage and sex explained AUC variability, but age and BMI did not; similar results emerged for MAX. These results indicate that puberty stage may either mediate the decline of melatonin, or the decrease in melatonin amplitude may be an indicator of pubertal progression. These findings also indicate that the melatonin decline during puberty is not entirely accounted for by body mass or by age.

Evening alcohol suppresses salivary melatonin in young adults.

The study objective was to determine the acute effects of a moderate evening dose of alcohol on salivary melatonin levels in humans with stable prior sleep-wake histories and in a controlled environment. Twenty-nine adults (nine males) ages 21 to 25 (M=22.6, SD=1.2) yrs adhered to a 10-day at-home stabilized sleep schedule followed by three in-lab adaptation, placebo, and alcohol (order counterbalanced) study nights. Alcohol (vodka: 0.54 g/kg for men and 0.49 g/kg for women) or placebo beverage was consumed over 30 min, ending 1 h before stabilized bedtime. At 140 and 190 min after alcohol administration, melatonin level was reduced by 15% and 19%, respectively, in comparison to placebo. The findings indicate that a moderate dose of alcohol in the evening suppressed melatonin in young adults.

The association between children's sleep disruption and salivary interleukin-6.

We explored relations between children's sleep and levels of salivary interleukin-6 (IL-6). Children were healthy boys (n = 28) and girls (n = 36) who ranged in age between 8 and 9 years. Through actigraphy, the amount and quality of children's sleep was examined objectively in their homes for 1 week. Children also rated their Morningness/Eveningness predisposition and subjective sleepiness, and parents reported on their children's Sleep Disordered Breathing and Sleepiness. Children provided saliva samples before and after a series of cognitive/social tasks (an intelligence test, listening to a marital argument, and performing a star-tracing task), which were later assayed for IL-6. Children with higher salivary IL-6 levels reported increased Eveningness predispositions and their parents reported higher levels of Sleep Disordered Breathing. Furthermore, lower levels of sleepiness, longer sleep amount, and better quality sleep in children were each predictive of increased IL-6 reactivity from pre- to post-task conditions. The findings illustrate (for the first time to our knowledge) that sleep disruptions in otherwise healthy and normally developing children may be associated with individual differences in levels of IL-6 in saliva.

Effects of a moderate evening alcohol dose. I: sleepiness.

BACKGROUND: Few studies examining alcohol's effects consider prior sleep/wake history and circadian timing. We examined introspective and physiological sleepiness on nights with and without moderate alcohol consumption in well-rested young adults at a known circadian phase. METHODS: Twenty-nine adults (males=9), ages 21 to 25 years (M=22.6, SD=1.2), spent 1 week on an at-home stabilized sleep schedule (8.5 or 9 hours), followed by 3 in-lab nights: adaptation, placebo, and alcohol. Alcohol (vodka; 0.54 g/kg for men; 0.49 g/kg for women) or placebo beverage was consumed over 30 minutes ending 1 hour before stabilized bedtime. In addition to baseline, 3 sleep latency tests (SLTs) occurred after alcohol/placebo ingestion (15, 16.5, and 18 hours after waking). Stanford Sleepiness Scales (SSS) and Visual Analog Scales (VAS) of sleepiness were completed before each SLT and approximately every 30 minutes. The Biphasic Alcohol Effects Scale (BAES) was administered a total of 4 times (baseline, 5, 60, and 90 minutes postalcohol/placebo). Subjects' circadian phase was determined from melatonin levels in saliva samples taken at approximately 30-minute intervals. RESULTS: All sleepiness and sedation measures increased with time awake. Only SSS and BAES sedation measures showed higher levels of sleepiness and sedation after alcohol compared with placebo. The mean circadian phase was the same for assessments at both conditions. CONCLUSIONS: Alcohol did not increase physiological sleepiness compared with placebo nor was residual sedation evident under these conditions. We conclude that the effects on sleepiness of a moderate dose of alcohol are masked when sleep-wake homeostatic and circadian timing influences promote high levels of sleepiness.

Effects of a moderate evening alcohol dose. II: performance.

BACKGROUND: This second of a pair of papers investigates the effects of a moderate dose of alcohol and staying up late on driving simulation performance and simple visual reaction time (RT) at a known circadian phase in well-rested young adults. METHODS: Twenty-nine adults (9 males), ages 21 to 25 years, spent 1 week on an at-home stabilization schedule of 8.5 to 9 hours, followed by 3 nonconsecutive nights in-lab: adaptation, placebo, and alcohol. Performance task practice occurred on 3 occasions before the study. Alcohol (vodka; 0.54 g/kg men; 0.49 g/kg women mixed with tonic) was consumed over 30 minutes ending 1 hour before normal bedtime; the same quantity of beverage was given on placebo. Driving simulation (with drive-only and dual-task drive and subtract components) and psychomotor vigilance task (PVT) testing occurred before and after alcohol/placebo ingestion. Breath alcohol concentration (BrAC) readings were taken before all test sessions. Saliva samples were taken approximately every 30 minutes to determine circadian phase. RESULTS: Driving simulation and PVT variables significantly deteriorated with increasing time awake. Driving simulator lane variability was worse with alcohol compared with placebo at 15.5 hours awake. No PVT variable showed an effect of alcohol. CONCLUSIONS: Driving simulation performance deteriorated with extended waking and with alcohol; driving was most impaired at the peak alcohol level. The PVT, less complex than the driving simulation, did not show effects of alcohol, a finding consistent with previous literature that disruptive effects of low alcohol concentrations increase with task complexity. Overall, simulated driving performance is significantly impaired late at night when even a moderate dose of alcohol is consumed.

Sleep, circadian rhythms, and delayed phase in adolescence.

Sleep/wake timing shifts later in young humans during the second decade of life. In this review we describe sleep/wake patterns, changes in these patterns across adolescence, and evidence for the role of environmental, psychosocial, and biological factors underlying these changes. A two-process model incorporating circadian (Process C) and sleep/wake homeostatic (Process S) components is outlined. This model may help us to understand how developmental changes translate to shifted sleep/wake patterns. Delayed sleep phase syndrome (DSPS), which has a typical onset during the second decade of life, may be an extreme manifestation of homeostatic and circadian changes in adolescence. We describe symptoms, prevalence, and possible etiology of DSPS, as well as treatment approaches in adolescents.

Child emotional insecurity and academic achievement: the role of sleep disruptions.

The authors examined children's sleep as an intervening variable in the connection between emotional insecurity in the family and academic achievement. The role of ethnicity (African American and European American) and socioeconomic status (SES) in moderating the examined relations was assessed. One hundred sixty-six children (8- and 9-year-olds) reported their emotional insecurity, and the quantity and quality of children's sleep were examined through actigraphy and self-report. Decreased amount and quality of sleep were intervening variables in the relations between insecurity in the marital relationship and children's achievement. The effects of disrupted sleep on achievement were more pronounced for both African American children and children of lower SES. Results highlight the importance of the contemporaneous examinations of family and sleep functioning in the prediction of child outcomes.

Actigraphy.

Actigraphy is a methodology for recording and analyzing activity (movement) from small, computerized devices worn on the body. Published reports on the reliability and validity of actigraph measures, although not comprehensive, generally indicate that sleep estimated by scoring algorithms is relatively consistent with PSG-scored sleep for normal individuals across the lifespan and for some patient groups. Accuracy is often greatly decreased when sleep is disordered or disrupted. Although actigraphy maybe suitable for documenting and evaluating some sleep disorders, its role in clinical diagnosis is limited. Actigraphy is a useful methodology for investigating group differences, sleep-pattern variations over time, and the effects of behavioral or treatment interventions. Controlling artifacts is extremely important, and using some form of daily log is essential for documenting events. The recording period should be long enough to provide reliable measures and to capture important variations across time.

Marital conflict and disruption of children's sleep.

Marital conflict was examined as a predictor of the quality and quantity of sleep in a sample of healthy 8- to 9-year-olds. Parents and children reported on marital conflict, the quantity and quality of children's sleep were examined through an actigraph worn for 7 consecutive nights, and child sleepiness was derived from child and mother reports. Increased marital conflict was associated with disruptions in the quantity and quality of children's sleep as well as subjective sleepiness, even after controlling for child age, ethnic group membership, socioeconomic status, sex, and body mass index. The results support the sensitization hypothesis in that exposure to marital conflict may influence an important facet of children's biological regulation, namely sleep.

Estimating dim light melatonin onset (DLMO) phase in adolescents using summer or school-year sleep/wake schedules.

STUDY OBJECTIVES: This analysis examined associations between the salivary dim light melatonin onset (DLMO) phase and self-selected sleep/ wake schedules in groups of children and adolescents during summer vacation and during the school year to determine the degree to which sleep/wake patterns can estimate salivary DLMO phase. DESIGN AND SETTING: Participants slept at home on self-selected schedules for 5 consecutive nights and reported their bedtime and wake-up time via daily telephone messages. Salivary melatonin was sampled in the laboratory on one evening every 30 minutes in dim light (< 50 lux) to determine DLMO phase. Within group bivariate regressions between sleep pattern measures (bedtime, wake-up time, and midsleep time) and DLMO phase were computed. PARTICIPANTS: One group, ages 9 to 17 years (mean age = 12.5, SD = 2.3 years, 74 males, 75 females) contributed 149 DLMO phase and sleep/wake pattern measures while on a school year schedule ("school group"). A separate group, ages 9 to 16 years (mean age = 13.1, SD = 1.3 years, 30 males, 29 females) contributed 59 DLMO phase and sleep/wake pattern measures while on a summer schedule ("summer group"). RESULTS: Bedtime, midsleep time, and wake-up time were positively correlated with DLMO phase in both groups. Although all correlation coefficients for the summer group were statistically greater compared to the school group, the regression equations predicted DLMO phase within +/- 1 hour of the measured DLMO phase in approximately 80% for both groups. CONCLUSIONS: DLMO phase can be estimated using self-selected sleep/wake patterns during the school year or summer vacation in healthy children and adolescents.

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.

Experimental restriction of sleep opportunity in children: effects on teacher ratings.

STUDY OBJECTIVE: To determine the effects of experimental restriction of sleep opportunity on teacher ratings of academic performance and behavior in healthy normal children. DESIGN: Home-based, within-subjects design in which participants followed 3 week-long sleep schedules-Baseline (self-selected), Optimized, and Restricted-while attending school, with order of conditions counter-balanced (Optimized and Restricted). PARTICIPANTS: Seventy-four children (39 boys; aged 6 to 12 years, mean = 10) screened for medical and psychological health. MEASUREMENTS AND RESULTS: Teachers masked to assigned hours of sleep completed paper-and-pencil questionnaires at the end of each study condition. Questionnaire items were selected from several published measures. Summary scores included Academic Problems, Hyperactive-Impulsive Behaviors, Internalizing, Oppositional-Aggressive, Sleepiness, Total Attention Problems, and Mean Severity of Attention Problems. Main effects of sleep condition were found forAcademic Problems, Sleepiness, Total Attention Problems, and Mean Severity of Attention Problems. Restricting sleep increased ratings of Academic Problems (medium effect) relative to both Baseline (P < .01, eta(p)2 = .11) and Optimized (P < .05, eta(p)2 = .10) conditions and increased the Mean Severity of Attention Problems (medium effect) relative to Baseline (P < .01, eta(p)2 = .12). CONCLUSIONS: These findings provide experimental support for widely held beliefs about the importance of sufficient time-in-bed for academic functioning in children. Reducing sleep opportunity had a direct effect on academic performance, as rated by teachers, even among healthy students with no history of behavioral problems or academic difficulty. Findings also support insufficient sleep as a direct source of variability in the manifestation of attention problems but not hyperactivity.

Sleep/wake patterns derived from activity monitoring and maternal report for healthy 1- to 5-year-old children.

STUDY OBJECTIVES: To describe behavioral sleep/wake patterns of young children from actigraphy and mothers' reports, assess age-group and sex differences, describe daytime napping, and investigate the impact of family demographic variables on sleep-wake measures. DESIGN: Cross-sectional sample of children wore actigraphs for 1 week; mothers kept concurrent diaries. SETTING: Children studied in their homes. PARTICIPANTS: 169 normal healthy children in 7 age groups (12, 18, 24, 30, 36, 48, and 60 months old); 84 boys and 85 girls. INTERVENTIONS: N/A. MEASUREMENTS AND RESULTS: Nocturnal sleep/wake measures estimated from activity recordings using a validated algorithm; mothers' reports of nocturnal sleep/wake patterns and daytime naps obtained from concurrent diaries. Bedtimes and sleep start times were earliest and time in bed and sleep period times were longest for 12-month-old children. Rise time, sleep end time, and nocturnal sleep minutes did not differ across age groups. Actigraphic estimates indicated that children aged 1 to 5 years slept an average of 8.7 hours at night. Actigraph-based nocturnal wake minutes and wake bouts were higher than maternal diary reports for all age groups. Daytime naps decreased monotonically across age groups and accounted for most of the difference in 24-hour total sleep over age groups. Children in families with lower socioeconomic status had later rise times, longer time in bed, more nocturnal wake minutes and bouts, and more night-to-night variability in bedtime and sleep period time. Children with longer naps slept less at night. CONCLUSIONS: Individual differences in sleep/wake measures reflect characteristics of children, parents, or parent-child interactions.