The Effect of Weekends and Clock Changes on the Sleep Patterns of Children with Autism: A Study of Historical Records

The aims were (1) to investigate differences by ethnicity and socioeconomic status (SES) in objective measures of sleep in children aged 7-9 years and (2) determine whether measures of sleep predict child achievement in reading or mathematics after controlling for ethnicity and SES. Four groups of parent-child dyads were recruited: Māori, low-SES schools (n = 18); Māori, high-SES schools (n = 17); New Zealand European, low-SES schools (n = 18); New Zealand European, high-SES schools (n = 17). Child sleep was measured by actigraphy. Parents and teachers reported child daytime sleepiness and behavior, and children completed a self-report of anxiety symptoms. Teachers also reported on child achievement in reading and mathematics. Children from low-SES schools went to bed later on school nights (F[1,68] = 12.150, P = .001) and woke later (F[1,68] = 15.978, P < .001) than children from high-SES schools but had similar sleep duration. There were no differences related to ethnicity. Children from low-SES schools were almost 3 times more likely to be below national standards for mathematics. Children not meeting academic standards in mathematics had a later sleep start time, lower sleep period efficiency, and a decreased total sleep time. However, when SES and sleep period efficiency were modeled together neither were found to significantly influence achievement in mathematics. In this study, SES influenced sleep timing but not the quality and quantity of sleep in 7- to 9-year-old children, and a significant independent effect of sleep efficiency on learning could not be demonstrated.

Sleep & attention profiles in children with Autism Spectrum Disorder

Disturbed sleep is a hallmark feature of posttraumatic stress disorder (PTSD). However, few studies have examined sleep objectively in individuals with PTSD compared to trauma-exposed controls. This study used wrist actigraphy to measure and compare sleep patterns in trauma-exposed Australian Vietnam veterans (VV) with and without PTSD. Trauma-exposed Australian VV with and without PTSD were recruited from the PTSD Initiative. VV wore wrist accelerometers over 14 days and completed daily sleep diaries. Sleep parameters were compared between groups including sleep latency (SL), time in bed (TIB), total sleep time (TST), wake after sleep onset (WASO), and movement index (MI). Night-to-night and overall within-individual variability were assessed by root mean squared successive differences and comparison of individual standard deviations. Correlations between sleep diary (self-reported) and wrist actigraphy (objective) variables were also assessed. A total of 40 male VV (20 with PTSD) participated in the study. We found no difference in sleep patterns determined by wrist actigraphy between groups with the exception of reduced SL in VV with PTSD (3.9 ± 0.9 versus 4.9 ± 1.4 minutes, P < .05). Overall within-individual variability was significantly greater in VV with PTSD for TIB, TST, WASO, and MI. Self-reported and objective TST and WASO were more strongly correlated in VV without PTSD than those with PTSD. Although there were no significant differences in sleep parameters, VV with PTSD had increased within-individual overall sleep variability and reduced correlation between self-reported and objective sleep parameters compared to trauma-exposed controls. Further evaluation of extended sleep patterns by actigraphy in VV with PTSD is warranted.

INTRODUCTION Autism Spectrum Disorder (ASD) is a neurodevelopmental disorder that often presents before the child enters the educational system and is characterized by developmental deficits with impairments in three main areas [1] personal, [2] social, and [3] academic or occupational functioning. The neurodevelopmental disorders represent a group of conditions with an onset early in the developmental period. Sleep disorders are commonly reported by parents of children with an ASD diagnosis with between 50% to 80% of parents reporting sleep problems with their children. Problems can be categorized into dyssomnias (problems falling and/or remaining asleep) and parasomnias (abnormal and/or unnatural movements, behaviors, emotions, perceptions, and dreams).

The present study aimed at further investigating trait aspects of sleep-related cognitive arousal and general cognitive arousal and their association with both objective and subjective sleep parameters in primary insomnia patients. A clinical sample of 182 primary insomnia patients and 54 healthy controls was investigated using 2 nights of polysomnography, subjective sleep variables, and a questionnaire on sleep-related and general cognitive arousal. Compared to healthy controls, primary insomnia patients showed both more sleep-related and general cognitive arousal. Furthermore, sleep-related cognitive arousal was closely associated with measures of sleep-onset and sleep-maintenance problems, while general cognitive arousal was not. Cognitive-behavioral treatment for insomnia might benefit from dedicating more effort to psychological interventions that are able to reduce sleep-related cognitive arousal.

Sleep problems such as difficulties in sleep initiation, nighttime awakening, and shortened sleep time are often subjectively reported in children with autism spectrum disorder (ASD). However, results of objective studies have been mixed. Our goal was to evaluate the existing data from objective measures using a systematic approach to identify and describe the differences in sleep parameters by comparing total sleep time (TST), sleep latency (SL), and sleep efficiency (SE) in children with ASD with those of typically developing (TD) peers. Studies that used objective measures such as actigraphy or polysomnography (PSG) to describe the sleep parameters of TST, SL, and SE in children with ASD compared with children with TD were identified. A meta-analysis was performed for the 10 studies that met inclusion criteria with evaluation of differences in means using random effects models. A total of 343 children with ASD and 221 children with TD were included. Assessments for sources of heterogeneity and publication bias were undertaken. TST for children with ASD was on average 32.8 minutes less per day (95% confidence interval [CI]: 16.6-49.0 minutes) than their TD peers. Average SL was 10.9 minutes longer (95% CI: 6.7-15.0 minutes), and average SE was 1.9% less (95% CI: 0.7%-3.1%) than their TD peers. Notable heterogeneity was found within studies for TST, and mild heterogeneity was found for SE. Concurrent intellectual disability was a moderator of TST. Children with ASD and normal intelligence had a small and nonsignificant decrease in TST as compared with TD peers, whereas those with ASD and intellectual disability (ID) had a significant decrease in TST as compared with TD peers. The magnitude of the difference in mean SL and SE increased as compared with TD peers as age increased. Studies that used PSG and those that did not include children on medications were more likely to report mean decreases in SE. Children with ASD have small but measurable objective differences in their sleep parameters that are consistent with subjective reporting. Children with ASD have shorter TST, longer SL periods, and decreased SE as compared with TD peers. Concurrent ID, medication use, method of data collection, and age of subjects significantly moderated these results. The decrease in TST in children with ASD and normal intelligence was not significant as compared with TD peers, suggesting that ID may help explain the shortened TST in children with ASD.

The lifestyles change of children and adolescents during the COVID-19 pandemic due to antipandemic measures can affect their sleep health. Existing studies have used convenient samples and focused on the initial months of the pandemic, leaving a knowledge gap on changes in young people's sleep patterns under the "new normal" under COVID-19. As part of a territory-wide epidemiological study in Hong Kong, this cross-sectional study recruited primary and secondary school students by stratified random sampling. Sleep parameters were collected using the structured diagnostic interview for sleep patterns and disorders. We investigated the pandemic's effects on sleep parameters by comparing data of participants recruited pre-COVID and those recruited during COVID using multivariate regression, adjusting for age, sex, household income, seasonality, and presence of mental disorders, and the moderators and mediators of the effects. Between September 1, 2019 and June 2, 2021, 791 primary and 442 secondary school students were recruited and analyzed. Primary school and secondary school participants assessed before COVID had a longer sleep latency on school days (95% confidence interval [CI] = 1.0-5.2 minutes, adjusted P-value = .010; and 95% CI= 3.9-13.0 minutes, adjusted P-value = .004, respectively) and nonschool days (95% CI = 1.7-7.2 minutes, adjusted P-value = .005; 95% CI = 3.4-13.7 minutes, adjusted P-value = .014, respectively). Low household income was a moderator for later bedtime (adjusted P-value = .032) and later sleep onset (adjusted P-value = .043) during nonschool days among secondary school students. Changes associated with COVID have a widespread and enduring effect on the sleep health of school-aged students in Hong Kong. Household income plays a role in adolescent sleep health resilience, and the impact of antiepidemic measures on the health gaps of the youth should be considered. Chau SWH, Hussain S, Chan SSM, etal. A comparison of sleep-wake patterns among school-age children and adolescents in Hong Kong before and during the COVID-19 pandemic. J Clin Sleep Med. 2023;19(4):749-757.

Sleep problems are a common consequence of multiple sclerosis; however, there is limited evidence regarding the agreement between device-measured and self-reported sleep parameters in adults with multiple sclerosis. The present study examined the agreement between self-reported and device-measured parameters of sleep quality in a sample of adults with multiple sclerosis. Participants (n = 49) completed a 7-day sleep diary and wore a wrist-worn ActiGraph GT3×+ (ActiGraph Corp., Pensecola, FL) for seven consecutive nights to quantify self-reported and device-measured sleep parameters, respectively. There was a significant discrepancy between self-reported and device-measured parameters of total time in bed (mean difference = 19.8 [51.3] min), sleep onset latency (mean difference = 22.2 [19.5] min), and frequency of awakenings during the night (mean difference = 12.8 [6.8]). Intraclass correlation estimates indicated poor agreement between methods on most parameters, except for total time in bed (intraclass correlation = 0.80). Bland-Altman plots suggested that total time in bed and total sleep time had acceptable levels of agreement and linear regression analyses indicated that sleep onset latency (F = 113.91, B = -1.34, P < .001), number of awakenings (F = 543.34, B = 1.85, P < .001), and sleep efficiency (F = 18.39, B = -0.77, P < .001) had significant proportional bias. Our results draw attention to the discrepancies between sleep parameter measurements and highlight the importance of including both self-report and device-measured outcomes for a complete and accurate representation of sleep in adults with multiple sclerosis. Cederberg KLJ, Mathison BG, Schuetz ML, Motl RW. Discrepancies between self-reported and device-measured sleep parameters in adults with multiple sclerosis. J Clin Sleep Med. 2022;18(2):415-421.

Circadian rhythmicity plays a crucial role in regulating sleep timing and continuity, but it may be altered in people with insomnia. This study tested whether dim-light melatonin onset (DLMO) timing is associated with sleep difficulties in insomnia. In total, 128 people diagnosed with insomnia disorder were recruited. Participants completed daily sleep diaries and wore an actigraph for up to 14 days before the laboratory visit to estimate mean sleep continuity (e.g., sleep latency, sleep duration) and sleep timing (sleep onset time and wake time from diaries, bedtime from diaries and actigraphy). After a sleep study, participants underwent salivary melatonin collection to estimate DLMO on the following night. Regressions and analyses of variances on tertile groups tested associations between DLMO (clock times and phase angle differences between DLMO and sleep timing) and sleep continuity and timing. There were associations between DLMO and sleep timing, r(s) = 0.27-0.37, but not with sleep continuity. The phase angle between sleep onset time and DLMO was associated with sleep latency, sleep duration, and sleep efficiency, r(s) = -0.32 to 0.41. Participants with a longer phase angle between DLMO and sleep onset time (> 3 h; i.e., greater delays) had longer sleep latencies (Mean diff = 43.21 min, SE = 12.99, p = 0.004) and shorter sleep durations (Mean diff = -65.66 min, SE = 20.75, p = 0.006) than participants with a shorter phase angle (< 2 h). Other phase angles (DLMO and mid-sleep, wake time) were not consistently associated with sleep continuity. Melatonin onset timing is associated with sleep timing in insomnia disorder. Larger phase angle differences between sleep onset and DLMO are linked to poorer sleep continuity. These findings highlight the importance of considering circadian alignment and its impact on sleep in understanding the pathophysiology of insomnia and in developing targeted treatment interventions.

BackgroundSleep difficulties are common in patients with anorexia nervosa (AN), but objective assessments have mostly been performed in hospital and laboratory settings. We aimed to identify differences in sleep patterns between patients with AN and healthy controls (HC) in their free-living environments, and potential associations between sleep patterns and clinical symptoms in patients with AN.MethodsThis cross-sectional study analyzed 20 patients with AN prior to them starting outpatient treatment and 23 HC. Sleep patterns were measured objectively using an accelerometer (Philips Actiwatch 2) for 7 consecutive days. Average sleep onset, sleep offset, total sleep time, sleep efficiency, wake after sleep onset (WASO) and mid-sleep awakenings lasting ≥ 5 min were compared between patients with AN and HC using nonparametric statistical analyses. Associations of sleep patterns with body mass index, eating-disorder symptoms, eating-disorder-associated impairment, and symptoms of depression were assessed in the patient group.ResultsCompared with HC, patients with AN had shorter WASO [median (interquartile range(IQR)): 33 vs. 42 min], but a longer average duration of mid-sleep awakenings lasting ≥ 5 min [median (IQR): 9 vs. 6 min, p = 0.006] and had more nights with no sleep (six nights in four patients with AN vs. zero nights in HC). There were no differences between patients with AN and HC regarding other sleep parameters and no significant correlations between sleep patterns and clinical parameters in patients with AN. However, HC presented a Intraindividual variability pattern that was closer to a normal distribution, whereas patients with AN tended to either have very regular or large variability in sleep onset time (AN; n = 7 < 25th percentile and n = 8 > 75th percentile vs. HC; n = 4 < 25 percentile and n = 3 > 75th percentile) during the week of sleep recordings.ConclusionPatients with AN seem to spend more time awake during the night and have more nights without sleep than do HC, even though their average weekly sleep duration did not differ from that in HC. The intraindividual variability in sleep pattern seems to be an important parameter that should be assessed when studying sleep in patients with AN.Trial registration ClinicalTroals.gov. Identifier: NCT02745067. Registered: April 20, 2016.

This study compared the sleep pattern between children with autism spectrum disorders and children with typical development using a matched case-control design (matched age, gender, and body mass index). Significant differences were found in night-time sleep duration (total amount of sleep at night), sleep efficiency (percentage of time spent asleep), sleep-onset latency (length of time that it takes to transit from awake to asleep), and wake after sleep onset (total amount of time spent awake after defined sleep onset). Findings showed that children with autism spectrum disorder had poorer sleep quality than children with typical development. Mechanisms underlying the differences should be further explored in order to develop an effective treatment intervention.

The aim of this study was to investigate melatonin-related findings in autism spectrum disorders (ASD), including autistic disorder, Asperger syndrome, Rett syndrome, and pervasive developmental disorders, not otherwise specified. Comprehensive searches were conducted in the PubMed, Google Scholar, CINAHL, EMBASE, Scopus, and ERIC databases from their inception to October 2010. Two reviewers independently assessed 35 studies that met the inclusion criteria. Of these, meta-analysis was performed on five randomized double-blind, placebo-controlled studies, and the quality of these trials was assessed using the Downs and Black checklist. Nine studies measured melatonin or melatonin metabolites in ASD and all reported at least one abnormality, including an abnormal melatonin circadian rhythm in four studies, below average physiological levels of melatonin and/or melatonin derivates in seven studies, and a positive correlation between these levels and autistic behaviors in four studies. Five studies reported gene abnormalities that could contribute to decreased melatonin production or adversely affect melatonin receptor function in a small percentage of children with ASD. Six studies reported improved daytime behavior with melatonin use. Eighteen studies on melatonin treatment in ASD were identified; these studies reported improvements in sleep duration, sleep onset latency, and night-time awakenings. Five of these studies were randomized double-blind, placebo-controlled crossover studies; two of the studies contained blended samples of children with ASD and other developmental disorders, but only data for children with ASD were used in the meta-analysis. The meta-analysis found significant improvements with large effect sizes in sleep duration (73 min compared with baseline, Hedge's g 1.97 [95% confidence interval {CI} CI 1.10-2.84], Glass's Δ 1.54 [95% CI 0.64-2.44]; 44 min compared with placebo, Hedge's g 1.07 [95% CI 0.49-1.65], Glass's Δ 0.93 [95% CI 0.33-1.53]) and sleep onset latency (66 min compared with baseline, Hedge's g-2.42 [95% CI -1.67 to -3.17], Glass's Δ-2.18 [95% CI -1.58 to -2.76]; 39 min compared with placebo, Hedge's g-2.46 [95% CI -1.96 to -2.98], Glass's Δ-1.28 [95% CI -0.67 to -1.89]) but not in night-time awakenings. The effect size varied significantly across studies but funnel plots did not indicate publication bias. The reported side effects of melatonin were minimal to none. Some studies were affected by limitations, including small sample sizes and variability in the protocols that measured changes in sleep parameters. Melatonin administration in ASD is associated with improved sleep parameters, better daytime behavior, and minimal side effects. Additional studies of melatonin would be helpful to confirm and expand on these findings.

UHNM NHS TRUSTAims• Sleep is extremely important to support children’s development both physically and mentally.• Establishing good sleep patterns can help children to meet their full potential.• A good night’s...

Melatonin is an endogenous neurohormone produced predominantly in the pineal gland. Recent studies have implicated abnormalities in melatonin physiology and the circadian rhythm in individuals with autism spectrum disorders (ASD). These physiological abnormalities include lower nighttime melatonin or melatonin metabolite concentrations in ASD compared to controls. These abnormalities in melatonin concentrations may be directly attributed to variations in melatonin pathway physiology as both functional and genetic variations in this pathway have been reported in children with ASD. Four studies have observed a correlation between abnormal melatonin concentrations and the severity of autistic behaviors. Twenty clinical studies have reported improvements in sleep parameters with exogenous melatonin supplementation in ASD, including longer sleep duration, less nighttime awakenings and quicker sleep onset. A recent meta-analysis of five randomized, double-blind, placebo-controlled crossover trials examining exogenous melatonin supplementation in ASD reported significant improvements with large effect sizes in total sleep duration and sleep onset latency compared to both baseline and placebo. Six studies reported that the nighttime administration of exogenous melatonin was associated with better daytime behaviors. Four studies reported improvements with exogenous melatonin supplementation when other sleep medications had previously failed. Adverse effects of melatonin were minimal to none in the twenty treatment studies. These studies indicate that the administration of exogenous melatonin for abnormal sleep parameters in ASD is evidence-based. Further studies examining optimal effective dosing and timing of dosing are warranted.

Physical inactivity and sleep disorders are health-related concerns of youth with autism spectrum disorder (ASD) that can persist from childhood and exacerbate core symptoms. However, evidence on group differences in accelerometer-assessed physical activity and sleep parameters among youth with and without ASD is inconclusive and age-specific effects remain unclear. To synthesize evidence on group differences in accelerometer-assessed physical activity and sleep parameters and examine the moderating effects of age between children and adolescents with and without ASD. American Psychological Association PsychInfo, CINAHL Ultimate, ERIC, MEDLINE, SPORTDiscus with Full Text, and Web of Science from inception to February 2023. Two independent reviewers screened articles for observational research comparing accelerometer-assessed physical activity levels and sleep parameters in children and adolescents with and without ASD. After developing a standardized form, relevant data were extracted. Quality was assessed using the McMaster Critical Review Form and rated based on sample, measurement, and analyses. The Preferring Reporting Items for Systematic Reviews and Meta-Analyses guideline was followed. The primary outcomes were actigraphy-measured MVPA, sleep latency, sleep efficiency, total sleep time, and wake after sleep onset. Data were pooled using a random-effects model. Hedges g was used to express the effect size index. Meta-regression on age was also performed to investigate the potential moderating effects. Collectively, 1757 studies were initially identified. Among 104 articles that were assessed, 28 were included, comprising moderate-to-vigorous physical activity (MVPA), 4 sleep parameters, and 73 independent effect sizes. A total of 28 studies were included in analysis, comprising 805 children and adolescents with ASD and 1573 without ASD (age range, 5.1-16.9 years). Compared with peers without ASD, children and adolescents with ASD had a small-to-moderate difference in MVPA (g = -0.450; 95% CI, -0.622 to -0.277), total sleep time (g = -0.332; 95% CI, -0.574 to -0.090), sleep efficiency (g = -0.424; 95% CI, -0.645 to -0.203), and a moderate difference in sleep latency (g = 0.514; 95% CI, 0.351 to 0.677) measured by actigraphy. Children and adolescents with ASD experienced an age-related decline in moderate-to-vigorous physical activity (β = -0.049 [95% CI, -0.097 to -0.001]; P = .045), indicating that younger children with ASD showed a smaller difference in MVPA compared with their peers without ASD. Moderating effects of age on sleep parameters were not significant. The findings of this meta-analysis suggested that children and adolescents with ASD had lower MVPA and worse sleep than peers without ASD, and the difference in MVPA varied with age. These findings reinforce the need for public health initiatives aimed at reducing these group disparities.