Cognitive Disengagement Syndrome (CDS) (Formerly Sluggish Cognitive Tempo), Autism, and Insomnia Symptoms in Childhood Predict CDS in Adolescence: A Longitudinal Population-Based Study.

Our study is the first using multiple variables to compare concurrent with longitudinal predictors of cognitive disengagement syndrome (CDS). The population-based sample comprised 376 youth (mean baseline age 8.7 and follow-up 16.4 years) rated by parents on the Pediatric Behavior Scale. The baseline CDS score was the strongest predictor of follow-up CDS. Baseline autism and insomnia symptoms also predicted follow-up CDS above and beyond baseline CDS. Autism, insomnia, inattention, somatic complaints, and excessive sleep were concurrently related to CDS at baseline and follow-up. Additionally, follow-up depression was associated with follow-up CDS, and baseline hyperactivity/impulsivity was negatively associated with baseline CDS. Oppositional defiant/conduct problems and anxiety were nonsignificant. Age, sex, race, and parent occupation were unrelated to CDS, and correlations between baseline CDS and 15 IQ, achievement, and neuropsychological test scores were nonsignificant. Results indicate childhood CDS is the strongest risk factor for adolescent CDS, followed by autism and insomnia symptoms.

Behavioral, neurocognitive, polysomnographic and cardiometabolic profiles associated with obstructive sleep apnea in adolescents with ADHD.

BACKGROUND: A high comorbidity between attention-deficit/hyperactivity disorder (ADHD) and obstructive sleep apnea (OSA) as well as similar impairments across neurobehavioral outcomes has been described in children. However, there is a paucity of research examining the comorbidity of these two disorders in adolescents. This study examined the association of OSA with sleep, neurobehavioral, and cardiometabolic outcomes in adolescents with ADHD from the general population. METHODS: 421 adolescents (16.9 ± 2.3 years, 53.9% male) underwent 9-hr polysomnography, neurobehavioral, and physical evaluation. ADHD was ascertained by a parent-or-self-report of a lifetime diagnosis/treatment of ADHD. OSA was defined as an apnea hypopnea index of ≥2 events/hour. Groups of controls (n = 208), OSA-alone (n = 115), ADHD-alone (n = 54), and ADHD+OSA (n = 44) were studied. Multivariable-adjusted general linear models tested group differences in PSG parameters, neurobehavioral, and cardiometabolic outcomes after controlling for sex, race/ethnicity, age, and/or body mass index percentile. RESULTS: The ADHD+OSA group had significantly longer sleep onset latency, shorter total sleep time, lower sleep efficiency, and higher percent of stage 1 sleep, as compared with all other groups, however, these differences were diminished by excluding adolescents on psychoactive medication. The ADHD-alone group showed significantly higher periodic limb movements than controls. The ADHD+OSA and ADHD-alone groups did not significantly differ on any measure of neurocognitive or behavioral functioning. The ADHD+OSA and OSA-alone groups showed significantly worse cardiometabolic and inflammatory biomarkers when compared to controls or the ADHD-alone, but did not significantly differ between each other. CONCLUSIONS: Adolescents with a diagnosis ADHD+OSA showed phenotypic risk factors for OSA (i.e., overweight/obesity, visceral adiposity, metabolic syndrome, and inflammation) but not worse neurobehavioral outcomes when compared with ADHD-alone. While comorbidity is possible, these data support that adolescents with a suspicion of ADHD should be screened for OSA, before a diagnosis is reached and psychoactive medication initiated.

Cross-Sectional Age Analysis of Sleep Problems in 2 to 17 Year Olds with ADHD Combined, ADHD Inattentive, or Autism.

Sleep problems are common in autism and ADHD. No study has compared sleep problems by age in 2 to 17 year olds with autism versus ADHD-Combined versus ADHD-Inattentive type. Mothers rated 1415 youth with autism and 1041 with ADHD on 10 Pediatric Behavior Scale sleep items. Nighttime sleep problems were most severe in autism, followed by ADHD-Combined, and then ADHD-Inattentive. Difficulty falling asleep, restless during sleep, and waking during the night were the most common problems. Adolescents slept more at night than other age groups, and youth who slept more at night were sleepier during the day. Sleep problems declined with age, but correlations were small. In adolescence, 63% with autism, 53% with ADHD-Combined, and 57% with ADHD-Inattentive had difficulty falling asleep. Given that the majority of children in all age groups had one or more sleep problem, developmentally appropriate interventions are needed to address sleep difficulties and limit their adverse effects.

Childhood high-frequency EEG activity during sleep is associated with incident insomnia symptoms in adolescence.

BACKGROUND: Insomnia has been associated in cross-sectional studies with increased beta (15-35 Hz) electroencephalogram (EEG) power during nonrapid eye movement (NREM) sleep, an index of cortical hyperarousal. However, it is unknown whether this cortical hyperarousal is present before individuals with insomnia develop the disorder. To fill this gap, we examined the association of childhood sleep high-frequency EEG activity with incident insomnia symptoms (i.e., absence of insomnia symptoms in childhood but presence in adolescence). METHODS: We studied a case-control subsample of 45 children (6-11 years) from the Penn State Child Cohort, a population-based random sample of 421 children, who were followed up after 8 years as adolescents (13-20 years). We examined low-beta (15-25 Hz) and high-beta (25-35 Hz) relative power at central EEG derivations during NREM sleep and, in secondary analyses, during sleep onset latency, sleep onset, and REM sleep. Incident insomnia symptoms were defined as the absence of parent-reported difficulty falling and/or staying asleep during childhood and a self-report of these insomnia symptoms during adolescence. RESULTS: Childhood high-beta power during NREM sleep was significantly increased in children who developed insomnia symptoms in adolescence (n = 25) as compared to normal sleeping controls (n = 20; p = .03). Multivariable-adjusted logistic regression models showed that increased childhood high-beta EEG power during NREM sleep was associated with a threefold increased odds (95% CI = 1.12-7.98) of incident insomnia symptoms in adolescence. No other significant relationships were observed for other sleep/wake states or EEG frequency bands. CONCLUSIONS: Increased childhood high-frequency EEG power during NREM sleep is associated with incident insomnia symptoms in adolescence. This study indicates that cortical hyperarousal during sleep may be a premorbid neurophysiological sign of insomnia, which may mediate the increased risk of psychiatric disorders associated with insomnia.

Increased inflammation from childhood to adolescence predicts sleep apnea in boys: A preliminary study.

While chronic systemic inflammation in obstructive sleep apnea (OSA) has been traditionally considered a consequence of intermittent hypoxia, several treatment studies targeting inflammation suggest that this process may precede the development of the disorder. A recent cross-sectional study in the Penn State Child Cohort (PSCC) revealed that inflammation largely mediates the association between visceral adiposity and OSA in adolescence. The purpose of this study was to examine for the first time whether, longitudinally, inflammation precedes OSA during this developmental period. A subsample of the PSCC with longitudinal sleep and inflammation data (n=51) was included in this study. Participants underwent 9-h polysomnography (22:00-7:00), physical exam, and fasting morning blood draw at both time points. Plasma C-reactive protein (CRP) was measured via ELISA. At follow-up, visceral, subcutaneous, and total fat area were assessed via dual X-ray absorptiometry. Sex differences in body composition emerged in adolescence, with boys having more visceral adiposity than girls. Longitudinal increases in waist circumference from childhood to adolescence were associated with increases in CRP (ΔCRP) and follow-up CRP in boys, but not girls. Furthermore, in boys, ΔCRP was associated with higher follow-up apnea/hypopnea index (AHI). When ΔCRP was entered into a model predicting follow-up AHI, Δwaist circumference was no longer significant, indicating that inflammation largely explains the association between increasing central obesity and OSA severity. These preliminary findings, in a longitudinal, non-clinical sample of children developing OSA, suggest that inflammation derived from visceral adipose tissue precedes the development of the disorder, suggesting a potential causal mechanism.

Mother, Father, and Teacher Agreement on Victimization and Bullying in Children With Psychiatric Disorders.

Bullying is a significant international problem, and parent-teacher agreement on identifying perpetrators and victims is poor in general population studies. The goal of our study is to assess informant discrepancies in children with mental health disorders. Parents and teachers completed the Pediatric Behavior Scale as part of a diagnostic evaluation for 1,723 children (ages 2-16 years) referred to a psychiatry clinic over the past 10 years. Mother and father bullying and victimization ratings on the Pediatric Behavior Scale were similar, but parent-teacher agreement was poor. Half of parents considered their child a victim, twice the percentage for teachers. Parents were 1.2 times more likely than teachers to perceive their child as a bully. Most parents reported their child was a victim or bully, whereas most teachers reported the children were neither. For both parents and teachers, victim and bully percentages for our psychiatric sample were twice as high as in general population studies. Clinicians should obtain information from multiple informants and consider that teacher report is likely to be lower than parent report.

Inflammation mediates the association between visceral adiposity and obstructive sleep apnea in adolescents.

Only a handful of studies, primarily in clinical samples, have reported an association between obesity, inflammation, and obstructive sleep apnea (OSA) in children and adolescents. No studies, however, have examined the pathogenetic link between visceral adiposity, systemic inflammation, and incident OSA in a large general population sample using objective measures of sleep and body fat. Adolescents (n = 392; mean age 17.0 ± 2.2 yr, 54.0% male) from the Penn State Child Cohort (PSCC) underwent 9-h overnight polysomnography; a DXA scan to assess body fat distribution; and a single fasting blood draw for the assessment of plasma interleukin-6 (IL-6), IL-6 soluble receptor (IL-6 sR), tumor necrosis factor alpha (TNFα), tumor necrosis factor receptor 1A (TNFR1), C-reactive protein (CRP), leptin, and adiponectin levels via ELISA. Visceral fat area was significantly elevated in moderate OSA (AHI ≥ 5), especially in boys. IL-6, CRP, and leptin were highest in adolescents with moderate OSA, even after adjusting for BMI percentile. Mediation analysis revealed that 42% of the association between visceral fat and OSA in adolescents was mediated by IL-6 (p = 0.03), while 82% of the association was mediated by CRP (p = 0.01). These data are consistent with the model of a feed-forward, vicious cycle, in which the release of proinflammatory cytokines by visceral adipocytes largely explains the association between central obesity and OSA; in turn, inflammation is also elevated in OSA independent of BMI. These findings, in a large, representative, non-clinical sample of young people, add to our understanding of the developmental pathogenesis of sleep apnea.

Insomnia and incident depression: role of objective sleep duration and natural history.

Longitudinal studies that have examined the association of insomnia with incident depression using objective sleep measures are very limited. The aim of this study was to examine the predictive role of the severity of insomnia for incident depression in a general population sample using psychometric and polysomnographic data. From a random, general population sample of 1741 individuals of the Penn State Adult Cohort, 1137 adults without depression were followed up with a structured telephone interview after 7.5 years. All subjects completed a full medical evaluation, 1-night polysomnogram and Multiphasic Minnesota Personality Inventory at baseline. The incidence of depression was 15%. Poor sleep (odds ratio = 1.5, P = 0.001) and insomnia (odds ratio = 1.9, P = 0.031) were significantly associated with incident depression. The odds of incident depression were highest (odds ratio = 2.2, P = 0.019) in insomnia with objective short sleep duration and independent of Multiphasic Minnesota Personality Inventory Ego Strength scores, an index of poor coping resources. The persistence of insomnia and worsening of poor sleep into insomnia significantly increased the odds of incident depression (odds ratios ranged from 1.8 to 6.3), whereas their full remission did not (odds ratio ranged from 1.2 to 1.8). Insomnia with short sleep duration is associated with incident depression independent of poor coping resources, whereas the association of insomnia with normal sleep duration with incident depression was mediated by poor coping resources. Persistence and worsening of poor sleep or insomnia, but not their full remission, are significant predictors of incident depression. These data suggest that there is a significant relationship between the severity of insomnia and incident depression.

MATERNAL RATINGS OF BULLYING AND VICTIMIZATION: DIFFERENCES IN FREQUENCIES BETWEEN PSYCHIATRIC DIAGNOSES IN A LARGE SAMPLE OF CHILDREN (.).

Little is known about psychiatric diagnoses that place children at risk for bullying and victimization. Mothers of 1,707 children 6-18 yr. rated their child as a bully and a victim (not at all, to very often a problem) on the Pediatric Behavior Scale. Children with psychiatric diagnoses were evaluated in an outpatient psychiatry clinic (M age = 9.2 yr., 68.4% male). Control children were community children not on psychotropic medication and with no neurodevelopmental disorder (M age = 8.7 yr., 43.5% male). Children with autism, intellectual disability, and ADHD-Combined type had higher victim and bully maternal ratings than children in the ADHD-Inattentive, depression, anxiety, eating disorder, and control groups. Eating disorder and controls were the only groups in which most children were not rated a victim or a bully. Comorbid oppositional defiant disorder accounted for the higher bully ratings for ADHD-Combined, autism, and intellectual disability. Victimization ratings did not differ between psychiatric groups. Except for eating disorders, victimization ratings were greater in all groups than in control children, suggesting that most psychiatric disorders place children at risk for victimization, as perceived by their mothers.

Insomnia symptoms, objective sleep duration and hypothalamic-pituitary-adrenal activity in children.

BACKGROUND: Insomnia symptoms are the most common parent-reported sleep complaints in children; however, little is known about the pathophysiology of childhood insomnia symptoms, including their association with hypothalamic-pituitary-adrenal (HPA) axis activation. The objective of this study is to examine the association between parent-reported insomnia symptoms, objective short sleep duration and cortisol levels in a population-based sample of school-aged children. DESIGN: A sample of 327 children from the Penn State Child Cohort (5-12 years old) underwent 9-h overnight polysomnography and provided evening and morning saliva samples to assay for cortisol. Objective short sleep duration was defined based on the median total sleep time (i.e., <7·7 h). Parent-reported insomnia symptoms of difficulty initiating and/or maintaining sleep were ascertained with the Pediatric Behavior Scale. RESULTS: Children with parent-reported insomnia symptoms and objective short sleep duration showed significantly increased evening (0·33±0·03 µg/dL) and morning (1·38±0·08 µg/dL) cortisol levels. In contrast, children with parent-reported insomnia symptoms and 'normal' sleep duration showed similar evening and morning cortisol levels (0·23±0·03 µg/dL and 1·13±0·08 µg/dL) compared with controls with 'normal' (0·28±0·02 µg/dL and 1·10±0·04 µg/dL) or short (0·28±0·02 µg/dL and 1·13±0·04 µg/dL) sleep duration. CONCLUSIONS: Our findings suggest that insomnia symptoms with short sleep duration in children may be related to 24-h basal or responsive physiological hyperarousal. Future studies should explore the association of insomnia symptoms with short sleep duration with physical and mental health morbidity.

Cognitive-emotional hyperarousal in the offspring of parents vulnerable to insomnia: a nuclear family study.

Cognitive-emotional hyperarousal is believed to be a predisposing factor for insomnia; however, there is limited information on the association of familial vulnerability to insomnia and cognitive-emotional hyperarousal. The aim of this study was to estimate the heritability of stress-related insomnia and examine whether parental vulnerability to stress-related insomnia is associated with cognitive-emotional hyperarousal in their offspring. We studied a volunteer sample of 135 nuclear families comprised of 270 middle-aged (51.5 ± 5.4 years) fathers and mothers and one of their biological offspring (n = 135, 20.2 ± 1.1 years). We measured vulnerability to stress-related insomnia (i.e. Ford Insomnia Response to Stress Test: FIRST), perceived stress, depression and anxiety in all participants, and arousability, presleep cognitive and somatic arousal, coping and personality in the offspring. We found a heritability estimate of 29% for FIRST scores. High FIRST parents had three to seven times the odds of having offspring highly vulnerable to stress-related insomnia. Offspring of high FIRST parents showed higher arousability, presleep cognitive arousal and emotion-oriented coping. Furthermore, high FIRST mothers contributed to offspring's higher anxiety and lower task-oriented coping, while high FIRST fathers contributed to offspring's higher presleep somatic arousal and conscientiousness. Vulnerability to stress-related insomnia is significantly heritable. Parents vulnerable to stress-related insomnia have offspring with cognitive-emotional hyperarousal who rely upon emotion-oriented coping. These data give support to the notion that arousability and maladaptive coping are key factors in the aetiology of insomnia.

Edward O. Bixler, PhD: from the Apollo project and chimpanzees to sleep epidemiology.

What an honor to write about Dr. Edward O. Bixler's contributions to the sleep field. In 1967, Dr. Bixler published a case report on a chimpanzee with implanted brain electrodes while working at an Air Force base in New Mexico. A few years later, in 1971, he published on the sleep effects of flurazepam in individuals with insomnia together with Dr. Anthony Kales, data that he had collected when the Sleep Research & Treatment Center (SRTC) was housed at the University of California Los Angeles. Dr. Bixler, a meticulous scientist, learned from Dr. Kales, a devoted clinician, to study "the whole patient, and all aspects of sleep," a legacy that continued when the SRTC moved to Penn State in Hershey. Indeed, Dr. Bixler's tenure at Penn State from 1971 until 2019 kept the science of the SRTC focused on that premise and helped translate scientific evidence into clinical care. He not only contributed early to the pharmacology of sleep and the effects of hypnotics, but he was also a pioneer in "sleep epidemiology." His "Prevalence of sleep disorders in the Los Angeles metropolitan area" study of 1979 was the first rigorous epidemiological study on sleep disturbances. Starting in 1990, he established the Penn State Adult Cohort to estimate the prevalence and natural history of sleep-disordered breathing and other sleep disorders in adults. Inspired by life-course epidemiology, he established in 2001 the Penn State Child Cohort to estimate the same phenomena in children. This Living Legend paper captures and highlights Dr. Bixler's enduring legacy to sleep science.

Short-term stability and night-to-night variability of sleep parameters in nightmares comorbid with chronic insomnia Disorder across multiple nights of polysomnography.

STUDY OBJECTIVES: The purpose of this study was to examine the degree of short-term stability of polysomnographic (PSG) measured sleep parameters and the overall differences between individuals with comorbid nightmares and insomnia compared to those with chronic insomnia disorder alone or good sleeping controls across four nights in the sleep lab. METHODS: A total of 142 good sleeping controls, 126 chronic insomnia alone, and 24 comorbid insomnia/nightmare participants underwent four consecutive nights of 8-hour PSG recordings. Outcomes included sleep continuity, architecture, and REM-related parameters across nights one through four. Intraclass correlation coefficients with mixed-effect variances and repeated-measure analysis of covariance were used, respectively, to determine short-term stability as well as between-participants and time-by-group interaction effects. RESULTS: Wake after sleep onset and stage 1 showed "poor stability" in the comorbid insomnia/nightmare group compared to "moderate stability" in the good sleeping controls and chronic insomnia alone group. Significant between-group effects (all ps < .05) showed that the comorbid insomnia/nightmare group took longer to fall asleep and had a greater first-night-effect in stage 1 compared to good sleeping controls and chronic insomnia alone group; in addition, the comorbid insomnia/nightmare and insomnia alone groups slept shorter, with fewer awakenings and REM periods, compared to the good sleeping controls. CONCLUSIONS: Nightmares are associated with abnormal sleep above and beyond REM disruption, as sleep continuity was the primary aspect in which poor stability and group differences emerged. The greater inability to fall asleep and instability of sleep fragmentation in those with comorbid insomnia/nightmares compared to chronic insomnia alone may be attributed to the impact of presleep anticipatory anxiety and nightmare-related distress itself. CLINICAL TRIAL INFORMATION: The data analyzed in this study does not come from any current or previous clinical trials. Therefore, there is no clinical trial information to report.

Circadian misalignment impacts the association of visceral adiposity with metabolic syndrome in adolescents.

STUDY OBJECTIVES: Although insufficient sleep is a risk factor for metabolic syndrome (MetS), the circadian timing of sleep (CTS) is also involved in cardiac and metabolic regulation. We examined whether delays and deviations in the sleep midpoint (SM), a measure of CTS, modify the association between visceral adipose tissue (VAT) and MetS in adolescents. METHODS: We evaluated 277 adolescents (median 16 years) who had at least 5 nights of at-home actigraphy (ACT), in-lab polysomnography (PSG), dual-energy X-ray absorptiometry (DXA) scan, and MetS score data. Sleep midpoint (SM), sleep irregularity (SI), and social jetlag (SJL) were examined as effect modifiers of the association between VAT and MetS, including waist circumference, blood pressure, insulin resistance, triglycerides, and cholesterol. Linear regression models adjusted for demographics, ACT-sleep duration, ACT-sleep variability, and PSG-apnea-hypopnea index. RESULTS: The association between VAT and MetS was significantly stronger (p-values for interactions < 0.001) among adolescents with a schooldays SM later than 4:00 (2.66 [0.30] points increase in MetS score), a SI higher than 1 hour (2.49 [0.30]) or a SJL greater than 1.5 hours (2.15 [0.36]), than in those with an earlier SM (<3:00; 1.76 [0.28]), lower SI (<30 minutes; 0.98 [0.70]), or optimal SJL (<30 minutes; 1.08 [0.45]). CONCLUSIONS: A delayed sleep phase, an irregular sleep-wake cycle, and greater social jetlag on schooldays identified adolescents in whom VAT had a stronger association with MetS. Circadian misalignment is a risk factor that enhances the impact of visceral obesity on cardiometabolic morbidity and should be a target of preventative strategies in adolescents.

Racial/ethnic disparities in the trajectories of insomnia symptoms from childhood to young adulthood.

STUDY OBJECTIVES: To examine differences in the longitudinal prevalence of childhood insomnia symptoms across black/African American, Hispanic/Latinx, and non-Hispanic white groups. METHODS: Participants were 519 children from the Penn State Child Cohort (baseline [V1] from 2000-2005) who were followed up 8 years later as adolescents (V2) and 15 years later as young adults (S3). Mean age at S3 was 24.1 ±â€…2.7 years. Approximately, 76.5% identified as non-Hispanic white, 12.9% as black/African American, 7.1% as Hispanic/Latinx, and 3.5% as "other" race/ethnicity. Insomnia symptoms were defined as parent-reported (childhood) or self-reported (adolescence and young adulthood) moderate-to-severe difficulties initiating/maintaining sleep. Longitudinal trajectories of insomnia symptoms were identified across three-time points and the odds of each trajectory were compared between racial/ethnic groups, adjusting for sex, age, overweight, sleep apnea, periodic limb movements, psychiatric/behavioral disorders, and psychotropic medication use. RESULTS: Black/African Americans compared to non-Hispanic whites were at significantly higher odds of having a childhood-onset persistent trajectory through young adulthood (OR = 2.58, 95% CI [1.29, 5.14]), while Hispanics/Latinx were at nonsignificantly higher odds to have the same trajectory (OR = 1.81, 95% CI [0.77, 4.25]). No significant racial/ethnic differences were observed for remitted and waxing-and-waning trajectories since childhood or incident/new-onset trajectories in young adulthood. CONCLUSIONS: The results indicate that disparities in insomnia symptoms among black/African American and, to a lesser extent, Hispanic/Latinx groups start early in childhood and persist into young adulthood. Identifying and intervening upon upstream determinants of racial/ethnic insomnia disparities are warranted to directly address these disparities and to prevent their adverse health sequelae. CLINICAL TRIAL INFORMATION: N/A; Not a clinical trial.

Agreement between mother, father, and teacher ratings of cognitive disengagement syndrome (sluggish cognitive tempo) in children with autism and children with ADHD.

No studies have analyzed differences between mother, father, and teacher ratings of cognitive disengagement syndrome (CDS; formerly sluggish cognitive tempo). The sample included 1,115 children with autism and/or attention-deficit/hyperactivity disorder (ADHD) 4-16 years of age who were rated by mothers on the Pediatric Behavior Scale. Subsets of these children were also rated by fathers and/or teachers, resulting in 896 mother/father, 964 mother/teacher, and 745 father/teacher dyads. The CDS factor comprised four items assessing the core features of CDS: cognitive disengagement (in a fog/confused and stares/preoccupied/in own world) and hypoactivity (sluggish/slow moving/low energy and drowsy/sleepy/not alert). Overall, 37% of teachers, 22% of mothers, and 16% of fathers rated the children as significantly elevated on CDS symptoms. Teacher scores were significantly higher than mother scores, whose scores exceeded those of fathers. Agreement on whether a child had CDS was fair-moderate for mothers and fathers but poor for parents and teachers. Findings of more severe CDS teacher than parent ratings are in marked contrast to the opposite pattern found in studies of anxiety, depression, ADHD, oppositional behavior, conduct problems, autism, bullying, and victimization. Children may display fewer behavior problems at school than at home, and parents may be more aware of their child's internal state than teachers. However, teachers may be more aware of the cognitive component of CDS that might interfere with functioning in the classroom more so than at home. Cognitive demands in school may reveal and intensify CDS symptoms. Findings highlight the importance of multi-informant ratings in research and clinical practice. (PsycInfo Database Record (c) 2023 APA, all rights reserved).

Comparison of the Cognitive Disengagement and Hypoactivity Components of Sluggish Cognitive Tempo in Autism, ADHD, and Population-Based Samples of Children.

An international Sluggish Cognitive Tempo (SCT) Work Group proposed a new term for SCT, "cognitive disengagement syndrome," that more accurately describes the syndrome than does SCT. According to the Work Group, symptoms of SCT represent a cognitive dimension (cognitive disengagement) and a motor dimension (hypoactivity). Our study determined (1) if distinct factors representing cognitive disengagement and hypoactivity emerged when SCT items were factor analyzed and (2) the degree of differences in cognitive disengagement and hypoactivity within diagnostic groups. Mothers rated 1,177 children with autism, 725 with ADHD-Combined, and 307 with ADHD-Inattentive (4-17 years) and 665 elementary school children (6-12 years) on the Pediatric Behavior Scale (PBS). SCT prevalence rates were autism 32%, ADHD-Inattentive 27%, ADHD-Combined 18%, and elementary school students 7%. Factor analysis of the SCT items yielded two factors reflecting cognitive disengagement (in a fog/confused and stares/preoccupied/in own world) and hypoactivity (sluggish/slow moving/low energy, drowsy/sleepy/not alert, and tires easily) in all diagnostic groups. Cognitive disengagement prevalence rates and scores were significantly higher than hypoactivity in the autism and ADHD-C groups and in the autism and ADHD-C subgroups of children with SCT (but not in the ADHD-I and elementary school total groups and SCT subgroups). Our findings factor analyzing five SCT items support two SCT subfactors: cognitive disengagement and hypoactivity.

Sluggish cognitive tempo: Association with neuropsychological test scores, motor incoordination, and dysgraphia in elementary school children.

Research on the relationship between sluggish cognitive tempo (SCT) and scores on neuropsychological tests (such as those measuring processing speed and reaction time) is inconclusive, and the association between SCT and motor incoordination and dysgraphia has not been objectively investigated. Mothers of 413 elementary school children (6-12 years of age) rated their children on the Pediatric Behavior Scale (PBS), which yields psychological problem scores, including SCT. Children were administered an extensive battery of neuropsychological tests assessing processing and performance speed, working memory, immediate and delayed recall, sustained attention, response inhibition, cognitive flexibility, fine motor manipulative skill, verbal fluency and retrieval, set shifting, and interference control, as well as intelligence and reading and math achievement. Only three of the 19 correlations between SCT and neuropsychological scores were significant, and all involved graphomotor tests (two timed and one untimed). In regression analysis, the strongest independent predictor of SCT was the maternal PBS incoordination factor score, followed by ratings of autism, inattention, and depression. Neuropsychological test scores did not contribute significantly more to predicting SCT. Among the incoordination PBS factor items, clumsy and draws or writes poorly were significant SCT predictors. Our novel and unexpected findings showed that motor incoordination was a stronger correlate of SCT than other variables assessed in our study, including those previously linked with SCT. Future SCT research needs to include measures of incoordination and dysgraphia in order to replicate and expand upon the current findings. Our results suggest that SCT traits are not reliably measured by currently available neuropsychological tests.

Circadian Misalignment Impacts the Association of Visceral Adiposity With Elevated Blood Pressure in Adolescents.

BACKGROUND: Although insufficient sleep has been shown to contribute to obesity-related elevated blood pressure, the circadian timing of sleep has emerged as a novel risk factor. We hypothesized that deviations in sleep midpoint, a measure of circadian timing of sleep, modify the association between visceral adiposity and elevated blood pressure in adolescents. METHODS: We studied 303 subjects from the Penn State Child Cohort (16.2±2.2 years; 47.5% female; 21.5% racial/ethnic minority). Actigraphy-measured sleep duration, midpoint, variability, and regularity were calculated across a 7-night period. Visceral adipose tissue (VAT) was measured with dual-energy X-ray absorptiometry. Systolic blood pressure (SBP) and diastolic blood pressure levels were measured in the seated position. Multivariable linear regression models tested sleep midpoint and its regularity as effect modifiers of VAT on SBP/diastolic blood pressure levels, while adjusting for demographic and sleep covariables. These associations were also examined as a function of being in-school or on-break. RESULTS: Significant interactions were found between VAT and sleep irregularity, but not sleep midpoint, on SBP (P interaction=0.007) and diastolic blood pressure (P interaction=0.022). Additionally, significant interactions were found between VAT and schooldays sleep midpoint on SBP (P interaction=0.026) and diastolic blood pressure (P interaction=0.043), whereas significant interactions were found between VAT and on-break weekdays sleep irregularity on SBP (P interaction=0.034). CONCLUSIONS: A delayed and an irregular sleep midpoint during school and during free-days, respectively, increase the impact of VAT on elevated blood pressure in adolescents. These data suggest that deviations in the circadian timing of sleep contribute to the increased cardiovascular sequelae associated with obesity and that its distinct metrics require measurement under different entrainment conditions in adolescents.

Pediatric sleep: current knowledge, gaps, and opportunities for the future.

This White Paper addresses the current gaps in knowledge, as well as opportunities for future studies in pediatric sleep. The Sleep Research Society's Pipeline Development Committee assembled a panel of experts tasked to provide information to those interested in learning more about the field of pediatric sleep, including trainees. We cover the scope of pediatric sleep, including epidemiological studies and the development of sleep and circadian rhythms in early childhood and adolescence. Additionally, we discuss current knowledge of insufficient sleep and circadian disruption, addressing the neuropsychological impact (affective functioning) and cardiometabolic consequences. A significant portion of this White Paper explores pediatric sleep disorders (including circadian rhythm disorders, insomnia, restless leg and periodic limb movement disorder, narcolepsy, and sleep apnea), as well as sleep and neurodevelopment disorders (e.g. autism and attention deficit hyperactivity disorder). Finally, we end with a discussion on sleep and public health policy. Although we have made strides in our knowledge of pediatric sleep, it is imperative that we address the gaps to the best of our knowledge and the pitfalls of our methodologies. For example, more work needs to be done to assess pediatric sleep using objective methodologies (i.e. actigraphy and polysomnography), to explore sleep disparities, to improve accessibility to evidence-based treatments, and to identify potential risks and protective markers of disorders in children. Expanding trainee exposure to pediatric sleep and elucidating future directions for study will significantly improve the future of the field.