scholarly journals Reduced sleep pressure in young children with autism

SLEEP ◽  
2019 ◽  
Vol 43 (6) ◽  
Author(s):  
Ayelet Arazi ◽  
Gal Meiri ◽  
Dor Danan ◽  
Analya Michaelovski ◽  
Hagit Flusser ◽  
...  

Abstract Study Objectives Sleep disturbances and insomnia are highly prevalent in children with Autism Spectrum Disorder (ASD). Sleep homeostasis, a fundamental mechanism of sleep regulation that generates pressure to sleep as a function of wakefulness, has not been studied in children with ASD so far, and its potential contribution to their sleep disturbances remains unknown. Here, we examined whether slow-wave activity (SWA), a measure that is indicative of sleep pressure, differs in children with ASD. Methods In this case-control study, we compared overnight electroencephalogram (EEG) recordings that were performed during Polysomnography (PSG) evaluations of 29 children with ASD and 23 typically developing children. Results Children with ASD exhibited significantly weaker SWA power, shallower SWA slopes, and a decreased proportion of slow-wave sleep in comparison to controls. This difference was largest during the first 2 hours following sleep onset and decreased gradually thereafter. Furthermore, SWA power of children with ASD was significantly negatively correlated with the time of their sleep onset in the lab and at home, as reported by parents. Conclusions These results suggest that children with ASD may have a dysregulation of sleep homeostasis that is manifested in reduced sleep pressure. The extent of this dysregulation in individual children was apparent in the amplitude of their SWA power, which was indicative of the severity of their individual sleep disturbances. We, therefore, suggest that disrupted homeostatic sleep regulation may contribute to sleep disturbances in children with ASD.

2019 ◽  
Author(s):  
Ayelet Arazi ◽  
Gal Meiri ◽  
Dor Danan ◽  
Analya Michaelovski ◽  
Hagit Flusser ◽  
...  

AbstractStudy ObjectivesSleep disturbances and insomnia are highly prevalent in children with Autism Spectrum Disorder (ASD). Sleep homeostasis, a fundamental mechanism of sleep regulation that generates pressure to sleep as a function of wakefulness, has not been studied in children with ASD so far, and its potential contribution to their sleep disturbances remains unknown. Here, we examined whether slow wave activity (SWA), a measure that is indicative of sleep pressure, differs in children with ASD.MethodsIn this case-control study, we compared overnight electroencephalogram (EEG) recordings that were performed during Polysomnography (PSG) evaluations of 29 children with ASD and 23 typically developing children.ResultsChildren with ASD exhibited significantly weaker SWA power, shallower SWA slopes, and a decreased proportion of slow wave sleep in comparison to controls. This difference was largest during the first two hours following sleep onset and decreased gradually thereafter. Furthermore, SWA power of children with ASD was significantly, negatively correlated with the time of their sleep onset in the lab and at home, as reported by parents.ConclusionsThese results suggest that children with ASD may have a dysregulation of sleep homeostasis that is manifested in reduced sleep pressure. The extent of this dysregulation in individual children was apparent in the amplitude of their SWA power, which was indicative of the severity of their individual sleep disturbances. We, therefore, suggest that disrupted homeostatic sleep regulation may contribute to sleep disturbances in children with ASD.Statement of significanceSleep disturbances are apparent in 40-80% of children with autism. Homeostatic sleep regulation, a mechanism that increases the pressure to sleep as a function of prior wakefulness, has not been studied in children with autism. Here, we compared Polysomnography exams of 29 children with autism and 23 matched controls. We found that children with autism exhibited reduced slow-wave-activity power and shallower slopes, particularly during the first two hours of sleep. This suggests that they develop less pressure to sleep. Furthermore, the reduction in slow-wave-activity was associated with the severity of sleep disturbances as observed in the laboratory and as reported by parents. We, therefore, suggest that disrupted homeostatic sleep regulation may contribute to sleep disturbances of children with autism.


2021 ◽  
Vol 11 ◽  
Author(s):  
Ying Wang ◽  
Jingjing Lin ◽  
Ying Zeng ◽  
Yanan Liu ◽  
Yamin Li ◽  
...  

Study Objectives: This study aims to identify the characteristic sleep disturbances that affect behavioral problems in children with autism spectrum disorder (ASD), providing a potential direction for sleep and behavioral intervention in ASD.Methods: The data of 513 children with ASD and 246 typically developing (TD) children aged between 2 and 5 years old were collected. The behavior performance of preschool children was assessed using the Child Behavior Checklist for 1.5–5.0 years old. The Children's Sleep Habits Questionnaire (CSHQ) was used to measure the sleep status of the children, and the Social Responsiveness Scale was used to measure the severity of disorder. Linear regression analysis was performed to examine the effects of sleep disturbances on behavioral problems, and independent-sample t-test was performed to compare the mean of the samples.Results: Compared to TD children, children with ASD had longer sleep onset delay and more night awakenings. The parasomnias score (a subscale of the CSHQ) was significantly associated with the internalizing (β = 0.113, P = 0.010), externalizing (β = 0.128, P = 0.006), and total problems (β = 0.143, P = 0.001) of children with ASD, while this association was not significant in TD children. “Bed wetting” and “restless and moves a lot” (two items in the CSHQ under parasomnia) significantly only affected the overall behavioral score in children with ASD (P < 0.05).Conclusion: Parasomnias, especially bed wetting and restlessness, are specifically associated with the behavioral problems of children with ASD rather than TD children.


2021 ◽  
Vol 8 ◽  
Author(s):  
Ho Wai Koo ◽  
Juriza Ismail ◽  
Wai Wai Yang ◽  
Syed Zulkifli Syed Zakaria

Introduction: Children with autism spectrum disorder (ASD) have a variety of co-morbid medical problems, including sleep disturbances. Prevalence of sleep disorders has been reported to be higher in this group as compared to the general population. Identifying sleep problems in children with ASD may help increase awareness and improve the overall quality of care for them. The aim of this study was to determine the prevalence of sleep problems and associated factors in a group of Malaysian children aged 6–16 years, with ASD.Method: This is a cross-sectional study at the Child Development Centre of UKM Medical Centre (UKM MC) on ASD children aged 6–16 years. Demographic data was obtained and the Sleep Disturbances Scale for Children (SDSC) questionnaire was completed by the main caregiver. Logistic regression analysis was used to determine factors related to higher total SDSC scores.Results: A total of 128 patients were recruited (111 boys) with a median age of 8 years 3 months (IQR: 2 years 10 months). Forty-seven (36.7%) of them obtained total SDSC scores in the pathological range with 19 (14.8%) scoring high for overall disturbances and 28 (21.9%) for at least one subtype of sleep disorders: 25 (19.5%) DIMS, 18 (14.1%) SBD, 10 (7.8%) DOES, 5 (3.9%) DOA, 6 (4.7%) SWTD, and 3 (2.3%) SHY. More than half of the children (57.8%) were reported to have sufficient sleep duration of 8–11 h, but longer sleep latency of at least 15 min (82.8%). Half of the ASD children also had co-morbidities in which one-third (34.4%) had attention-deficit hyperactivity disorder (ADHD). Using logistic regression analysis, four factors were significantly associated with higher total SDSC scores; female gender (p = 0.016), older age group (11–16 years old) (p = 0.039), shorter sleep length (p = 0.043), and longer sleep latency (p < 0.001).Conclusion: The prevalence of sleep disturbances is high among Malaysian children with ASD, especially DIMS. Female gender, older age group, shorter sleep length, and longer sleep latency were found to be associated with the sleep disturbances. Evaluation of sleep problems should form part of the comprehensive care of children with ASD.


Endocrinology ◽  
2011 ◽  
Vol 152 (3) ◽  
pp. 1193-1193
Author(s):  
Anne Caufriez ◽  
Rachel Leproult ◽  
Mireille L'Hermite-Balériaux ◽  
Myriam Kerkhofs ◽  
Georges Copinschi

Abstract Context: A number of neuroactive progesterone metabolites produce sedative-like effects. However, the effects of progesterone administration on sleep are not well characterized. Objective: To investigate the effects of a 3-wk progesterone administration on sleep architecture and multiple hormonal profiles. Subjects: Eight healthy postmenopausal women, 48–74 yr old, without sleep complaints or vasomotor symptoms. None was on hormone replacement therapy. They did not take any medication for ≥2 months. Design: Randomized, double-blind, placebo-controlled study. For 3 wk, subjects took daily at 2300 h a capsule of either 300 mg of progesterone or placebo. Sleep was polygraphically recorded during the last two nights, and blood samples were obtained at 15-min intervals for 24 h. Results: During the first night (no blood sampling), sleep was similar in both conditions. Under placebo, blood sampling procedure was associated with marked sleep disturbances, which were considerably reduced under progesterone treatment: mean duration of wake after sleep onset was 53% lower, slow-wave sleep duration almost 50% higher, and total slow-wave activity (reflecting duration and intensity of deep sleep) almost 45% higher under progesterone than under placebo (P ≤ 0.05). Nocturnal GH secretion was increased, and evening and nocturnal TSH levels were decreased under progesterone (P ≤ 0.05). Conclusions: Progesterone had no effect on undisturbed sleep but restored normal sleep when sleep was disturbed (while currently available hypnotics tend to inhibit deep sleep), acting as a “physiologic” regulator rather than as a hypnotic drug. Use of progesterone might provide novel therapeutic strategies for the treatment of sleep disturbances, in particular in aging where sleep is fragmented and of lower quality.


SLEEP ◽  
2021 ◽  
Author(s):  
Rackeb Tesfaye ◽  
Nicola Wright ◽  
Anat Zaidman-Zait ◽  
Rachael Bedford ◽  
Lonnie Zwaigenbaum ◽  
...  

Abstract Up to 80% of children with autism spectrum disorder (ASD) experience sleep disturbance. Poor sleep impairs executive functioning (EF), a lifelong difficulty in ASD. Evidence suggests EF difficulties in ASD are exacerbated by poor sleep. We examine whether early childhood sleep disturbances are associated with worsening EF trajectories in school-aged children with ASD. A subsample (n=217) from the Pathways in ASD longitudinal study was analyzed. The Children’s Sleep Habits Questionnaire captured sleep duration, onset, and night awakenings before age 5 (Mean=3.5years). Metacognition (MI) and Behavioral Regulation (BRI) indices, on the Teacher Behavior Rating Inventory of Executive Functioning, were used to measure cognitive and affective components of EF respectively at four time-points (7.8-11.8years). We applied latent growth curve models to examine associations between sleep and EF, accounting for relevant covariates, including school-age sleep (Mean=6.7years). Sleep traits had different age-related impacts on behavioral regulation, but not metacognition. Longer sleep onset at 3.5 years was associated with a worsening BRI difficulties slope (b=2.07, p<0.04), but conversely associated with lower BRI difficulties at 7.7 years (b=-4.14, p=0.04). A longer sleep onset at 6.7 years was related to higher BRI difficulties at 7.7 years (b=7.78, p<0.01). Longer sleep duration at 6.7 years was associated with higher BRI difficulties at age 7.7 (b=3.15, p=0.01), but subscale analyses revealed shorter sleep duration at age 6.7 was linked to a worsening inhibition slope (b=-0.60, p=0.01). Sleep onset is a robust early correlate of behavior regulation in children with ASD, whereas sleep duration is a later childhood correlate.


2019 ◽  
Vol 1 (4) ◽  
pp. 517-531 ◽  
Author(s):  
Christian Cajochen ◽  
Carolin Reichert ◽  
Micheline Maire ◽  
Luc J. M. Schlangen ◽  
Christina Schmidt ◽  
...  

We examined whether ambient lighting conditions during extended wakefulness modulate the homeostatic response to sleep loss as indexed by. slow wave sleep (SWS) and electroencephalographic (EEG) slow-wave activity (SWA) in healthy young and older volunteers. Thirty-eight young and older participants underwent 40 hours of extended wakefulness [i.e., sleep deprivation (SD)] once under dim light (DL: 8 lux, 2800 K), and once under either white light (WL: 250 lux, 2800 K) or blue-enriched white light (BL: 250 lux, 9000 K) exposure. Subjective sleepiness was assessed hourly and polysomnography was quantified during the baseline night prior to the 40-h SD and during the subsequent recovery night. Both the young and older participants responded with a higher homeostatic sleep response to 40-h SD after WL and BL than after DL. This was indexed by a significantly faster intra-night accumulation of SWS and a significantly higher response in relative EEG SWA during the recovery night after WL and BL than after DL for both age groups. No significant differences were observed between the WL and BL condition for these two particular SWS and SWA measures. Subjective sleepiness ratings during the 40-h SD were significantly reduced under both WL and BL compared to DL, but were not significantly associated with markers of sleep homeostasis in both age groups. Our data indicate that not only the duration of prior wakefulness, but also the experienced illuminance during wakefulness affects homeostatic sleep regulation in humans. Thus, working extended hours under low illuminance may negatively impact subsequent sleep intensity in humans.


Entropy ◽  
2021 ◽  
Vol 23 (4) ◽  
pp. 418
Author(s):  
Naoki Furutani ◽  
Tetsuya Takahashi ◽  
Nobushige Naito ◽  
Takafumi Maruishi ◽  
Yuko Yoshimura ◽  
...  

Recently, measuring the complexity of body movements during sleep has been proven as an objective biomarker of various psychiatric disorders. Although sleep problems are common in children with autism spectrum disorder (ASD) and might exacerbate ASD symptoms, their objectivity as a biomarker remains to be established. Therefore, details of body movement complexity during sleep as estimated by actigraphy were investigated in typically developing (TD) children and in children with ASD. Several complexity analyses were applied to raw and thresholded data of actigraphy from 17 TD children and 17 children with ASD. Determinism, irregularity and unpredictability, and long-range temporal correlation were examined respectively using the false nearest neighbor (FNN) algorithm, information-theoretic analyses, and detrended fluctuation analysis (DFA). Although the FNN algorithm did not reveal determinism in body movements, surrogate analyses identified the influence of nonlinear processes on the irregularity and long-range temporal correlation of body movements. Additionally, the irregularity and unpredictability of body movements measured by expanded sample entropy were significantly lower in ASD than in TD children up to two hours after sleep onset and at approximately six hours after sleep onset. This difference was found especially for the high-irregularity period. Through this study, we characterized details of the complexity of body movements during sleep and demonstrated the group difference of body movement complexity across TD children and children with ASD. Complexity analyses of body movements during sleep have provided valuable insights into sleep profiles. Body movement complexity might be useful as a biomarker for ASD.


2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Jing Wen ◽  
Ting Yang ◽  
Jiang Zhu ◽  
Min Guo ◽  
Xi Lai ◽  
...  

Abstract Background Vitamin A deficiency (VAD) and sleep disturbances have been reported in children with autism spectrum disorder (ASD). The influence of vitamin A (VA) levels on sleep regulation and sleep disturbances in ASD has garnered concern. The present study aimed to characterize the association of VA levels with sleep disturbances in children with ASD. Methods This cross-sectional study compared children with ASD (n = 856) to typically developing children (TDC; n = 316). We used the Children’s Sleep Habits Questionnaire to assess sleep disturbances, Childhood Autism Rating Scale to evaluate the severity of autism symptoms, and Autism Behavior Checklist and Social Responsiveness Scale to assess autism behaviors. Serum VA levels were estimated using high-performance liquid chromatography. Multivariable linear regression and two-way analysis of variance were performed to investigate if VAD was related to sleep disturbances in children with ASD. Results Children with ASD had lower serum VA levels and a higher prevalence of sleep disturbances than TDC did. The incidence of VAD in ASD children with sleep disturbances was higher, and the symptoms more severe than those without sleep disturbances and TDC. Interestingly, the interaction between VAD and sleep disturbances was associated with the severity of autism symptoms. Conclusion VAD and sleep disturbances are associated with the core symptoms of ASD in children. Regular monitoring of sleep and VA levels may be beneficial for children with ASD. Trial registration Chinese Clinical Trial Registry, registration number: ChiCTR-ROC-14005442, registration date: December 9th 2014.


2020 ◽  
Vol 9 (6) ◽  
pp. 1978
Author(s):  
Enise Yavuz-Kodat ◽  
Eve Reynaud ◽  
Marie-Maude Geoffray ◽  
Nadège Limousin ◽  
Patricia Franco ◽  
...  

Sleep disorders are among the most common comorbidities in children with Autism Spectrum Disorder (ASD), and subjectively defined sleep disturbances have been related to ASD symptom severity. However, no study has investigated the differential impact of objectively measured sleep and circadian rhythm disturbances on behavioral difficulties in this population. Fifty-two children with ASD aged 3–10 years underwent assessments of sleep and circadian rest–activity rhythms objectively with actigraphy and subjectively with the Children’s Sleep Habits Questionnaire. Behavioral difficulties were assessed using the ABC-C. Group comparison analyses were used to compare sleep and circadian rhythm parameters of children with higher and lower behavioral difficulties and dominance analysis to rank predictors and address multicollinearity. Children with high irritability had a shorter continuous sleep period compared to those with lower irritability (−60 min, p = 0.04), as well as those with high stereotypic behaviors compared to children with less stereotypies (−75 min, p = 0.006). Objective circadian and sleep disturbances accounted together for, respectively, 17%, 18% and 36% of the variance in social withdrawal, irritability and stereotypic behaviors. The identification of both sleep and circadian rhythm disturbances as explanatory factors for behavioral difficulties warrants their inclusion in the existing behavioral management strategies for children with ASD.


1998 ◽  
Vol 275 (1) ◽  
pp. R148-R157 ◽  
Author(s):  
Marcos G. Frank ◽  
Roger Morrissette ◽  
H. Craig Heller

This investigation represents the first systematic study of sleep homeostasis in developing mammals that spans the preweaning and postweaning periods. Neonatal rats from 12 to 24 days of postnatal life ( P12– P24) were anesthetized with Metofane (methoxyflurane) and implanted with miniaturized electroencephalographic (EEG) and electromyographic electrodes. After 48 h of recovery, neonatal rats were sleep deprived for 3 h by either gentle handling or forced locomotion. We find that 3-h sleep deprivation produces dramatically different compensatory responses at different stages of postnatal development. In striking contrast to adult rats, sleep deprivation does not increase slow-wave sleep EEG delta (0.5–4.0 Hz) activity in rats younger than P24. However, P12– P20rats do show evidence of sleep regulation because they show compensatory increases in sleep time and sleep continuity during recovery. In P12 rats, ∼90% of total slow wave sleep time lost during the sleep-deprivation period was recovered during subsequent sleep. A similar recovery of active sleep time was observed in P20– P24rats. These findings suggest not only that sleep is regulated in neonatal rats but that the accumulation and/or discharge of sleep need changes dramatically between the third and fourth postnatal weeks.


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