Attention deficit hyperactivity disorder (ADHD) is a common neurodevelopmental disorder in school-age children. Abnormal sensory–motor integration, such as concurrent visuomotor selection, is a prominent feature of ADHD. However, underlying pathophysiological substrates of impaired sensory–motor integration in childhood ADHD remain unclear. Identifying neural markers of cognitive impairment in children with ADHD is vital for the early assisted diagnosis and the selection of intervention targets.
We collected electroencephalography (EEG) signals from 70 children with ADHD and 65 matched typically developing (TD) children while performing a visual search task. Oscillation-based multivariate pattern decoding was used to investigate visuomotor coordination during spatial attention.
Compared with TD children, children with ADHD showed impairments in accuracy, response time, and response time variability. Multivariate machine learning revealed that the ADHD group showed deficits in alpha (visual-related) and beta (motor-related) power-based decoding accuracy, indicating the impaired sensory orienting and motor preparation. Importantly, children with ADHD exhibited a delay between alpha and beta decoding, suggesting a deficit of concurrent visuomotor coordination. However, this visuomotor asynchrony was absent in TD children. Furthermore, the degree of visuomotor asynchrony between alpha and beta decoding was predictive of behavioral impairments and symptom severity in children with ADHD.
These observations reveal that impaired concurrent visuomotor coordination might be a potential neural marker of impaired sensory–motor integration in children with ADHD, further advancing the understanding of cognitive deficits, and providing potential research directions for the early diagnosis and optimization of intervention in neurodevelopmental disorders.
Lower parental income is associated with more psychiatric disorders among offspring, but it is unclear if this association reflects effects of parental income (social causation) or shared risk factors (social selection). Prior research finds contradictory results, which may be due to age differences between the studied offspring.
Here, we studied psychiatric disorders in the entire Norwegian population aged 10 to 40 years between 2006 and 2018 (N = 2,468,503). By linking tax registries to administrative health registries, we described prevalence rates by age, sex, and parental income rank. Next, we grouped observations into age groups (adolescence, ages 10–20 years; early adulthood, 21–30 years; adulthood, 30–40 years) and applied kinship-based models with extended families of twins and siblings to decompose the parent–offspring correlation into phenotypic transmission, passive genetic transmission, and passive environmental transmission.
We found that lower parental income rank was associated with higher prevalence of nearly all psychiatric disorders, except for eating disorders, for both men and women at all ages from 10 to 40 years. Comparing the top with the bottom paternal income quartile, the prevalence ratio of any psychiatric disorder was 0.47 among 10-year-olds and decreased to 0.72 among 40-year-olds. The parent–offspring correlation was −.15 in adolescence, −.10 in early adulthood, and −.06 in adulthood. The kinship-based models indicated that phenotypic transmission could account for 39% of the parent–offspring correlation among adolescents (p < .001), but with no significant contribution in early adulthood (p = .181) or adulthood (p = .737). Passive genetic and environmental transmission contributed to the parent–offspring correlation in all age groups (all p's < .001).
Our findings are consistent with a significant role of social causation during adolescence, while social selection could fully explain the parent–offspring correlation in adulthood.
Anorexia nervosa (AN), often with an onset in adolescence, is a complex eating disorder characterized by distorted body image, fear of weight gain, and extreme food restriction, leading to severe underweight. Excessive goal pursuit and avoidance behaviors have been proposed as key factors in AN, which over time may become over-trained into habits.
This study investigated the behavioral and neural correlates of habit learning in AN with an experiment consisting of three consecutive phases: (1) training goal-directed behavior, (2) avoidance learning, and (3) a habit test. Forty-five acutely underweight adolescent female patients with AN and 45 age-matched healthy control participants underwent an fMRI scan.
No behavioral group differences were evident either during learning of avoidance habits or when testing habit strength. Importantly, however, the AN group showed both generally superior task performance and increased involvement of the frontoparietal brain regions during habit learning.
Collectively, our findings provide novel evidence suggesting that excessive goal pursuit may predominate in young AN in an avoidance learning context. Future research should examine if this tendency develops into habit learning over time and investigate the speed and strength of avoidance habit formation in adults with a longer history of AN to further elucidate the intricate dynamic between goal-directed and habitual processes in the disorder.
Over the past several years, increasingly younger children are being exposed to significant amounts of media, while at the same time parental monitoring of young children's media exposure is decreasing. Increasing media exposure in young children, including increased exposure to media with aggressive, violent, or otherwise inappropriate content, has potential adverse consequences for social, emotional, and neural development. Adverse effects are potentially greater in early childhood given the high neuroplasticity of this period. Despite this, very little research has rigorously examined potential detrimental consequences of exposure to excessive and/or inappropriate media during early childhood. The purpose of this article is to discuss potential adverse developmental effects of early childhood media exposure and to suggest directions for critically needed future research on these potential effects.
Persistent and/or distressing psychotic-like experiences (PLEs) during adolescence are associated with poorer subsequent psychiatric outcomes. Modifiable lifestyle factors (such as sleep quality or regular exercise) may improve mental health outcomes; however, it is unknown how lifestyle factors are linked to trajectories of PLEs.
Using data from the Adolescent Brain Cognitive Development Study (N = 10,075, age 9–10 years at baseline), we characterized trajectories of PLEs using latent growth mixture models assessed using the Prodromal Questionnaire-Brief Child Version. We examined trajectories of Total and Distress scores. We used multinomial logistic regressions to examine associations between baseline lifestyle behaviors (including self-reported screen time, physical activity and caffeine intake, and parent-reported sleep disturbances and recreational activities) and PLE trajectories.
We identified four trajectories of distress-related PLEs: No Distress (27%), Rapid Decreasing (17%), Gradual Decreasing (36%), and Persistent Elevated Distress (21%). Compared with the No Distress trajectory, individuals in the Persistent Elevated Distress trajectory spent more time using screens (adjusted Odds Ratio [OR] 2.27, 95% confidence interval [CI] 2.03–2.53), had higher caffeine intake (OR 1.62, 95% CI 1.28–2.04), greater sleep disturbance (OR 1.58, 95% CI 1.45–1.73), participated in fewer recreational activities (OR 0.75, 95% CI 0.68–0.83) and less frequent physical activity (OR 0.81, 95% CI 0.74–0.89). Greater screen time and sleep disturbances further distinguished the most severe group from all other trajectories. Findings were similar when examining total scores. Results remained statistically significant when we included established risk factors of psychosis in each model.
Lifestyle factors associate with trajectories of PLE-related distress, providing novel tools for intervention and risk prediction.
Mental health problems are elevated in adolescents with ADHD and/or autism. Emotion regulation deficits (ERD) have been hypothesised as a key driver of such difficulties. The Regulating Emotions – Strengthening Adolescent Resilience (RE-STAR) programme is examining an alternative pathway from neurodivergence to mental health problems, mediated by elevated emotional burden (EB) resulting from the interplay of increased exposure and an unusually intense emotional reaction to commonly upsetting events (CUEs). We present the development and application of the My Emotions in School Inventory (MESI), a self-report questionnaire co-produced with neurodivergent young people, focusing on EB in schools – a setting thought to be of particular significance in this regard.
The MESI, containing 25 school-related CUEs rated on their frequency and the intensity of negative emotions they induce, was completed by secondary school students meeting symptom cut-offs on clinically validated scales of ADHD (n = 100), autism (n = 104), ADHD + autism (n = 79) and neurotypical students (n = 452). Psychometric properties were examined. The ability of the MESI to discriminate adolescents with ADHD and/or autism from neurotypical adolescents, and to predict depression and anxiety, independently of ERD, was explored.
Adolescents in the ADHD and/or autism groups experienced higher CUE frequency and intensity of reaction than their neurotypical peers. Overall levels of EB, most robustly indexed by 24 MESI CUEs, were higher in the three neurodivergent groups, though they did not differ from each other. EB in the autism and ADHD groups was generated by distinctly different CUEs. EB and ERD each contributed independently to the prediction of higher depression or anxiety.
Our findings illustrate the potential value of the MESI as an instrument to measure the contribution of EB alongside ERD in relation to adolescent mental health risks in ADHD and/or autism. Future studies need to investigate its role longitudinally.
Emotional problems co-occur with difficulties in verbal and nonverbal cognitive ability, yet the pathways underlying their association remain poorly understood: It is unclear whether effects may be causal, and to what extent they may run from cognition to emotion, or vice versa.
Our preregistered analyses included 5,124 twin pairs from the Twins Early Development Study (TEDS). At ages 7, 9 and 12, emotional problems were assessed through the strengths and difficulties questionnaire, and cognition was assessed using task-based measures. Cross-lagged models examined the influence of cognition and subdomains of verbal and nonverbal abilities on emotional problems and vice versa, across development. Genetic cross-lagged models examined the effect of cognition on emotional problems and vice versa, after controlling for shared genetic and environmental influence.
Cross-lagged paths in both directions were observed between cognitive ability and emotional problems (from −0.11 to −0.05). Cross-lagged associations that persisted after accounting for common genetic and environmental influences were between nonverbal ability and emotional problems. Higher emotional problems at age 7 predicted lower nonverbal ability at age 9, with 22% of the phenotypic association remaining. This, in turn, predicted greater emotional problems at age 12, with 13% of the association remaining.
Genetic and environmental factors accounted for a large proportion of the cross-lagged associations. Emotional problems in early childhood could result in a cascade effect, leading to lower nonverbal cognition in middle childhood, which increases the risk of emotional problems in late childhood. These findings highlight the importance of age- and domain-specific interventions.
Children born preterm (<37 weeks' gestation) are at increased risk of mental health problems, and their mental health outcomes have not improved in the past decades. This study aims to (1) determine the degree of mental health resilience in preterm-born children; (2) identify modifiable factors at individual, parent–child, family, peer group, and neighbourhood levels associated with resilience; (3) explore differential effects of factors based on sex and contextual adversity.
Preterm-born children from the Bavarian Longitudinal Study (BLS; n = 574) born in Germany (1985–1986) and Millennium Cohort Study (MCS; n = 985) born in the UK (2000–2002) were assessed prospectively at 7 (MCS) or 8 (BLS) years. Resilience was defined as better-than-expected mental health outcomes, using a residuals approach. Potential promotive factors included (1) individual: self-regulation, perceived competence, cognition; (2) parent–child relationships; (3) family: home environment, interparental relationship, social support, sibling relationships; (4) peers: bullying, friendships; and (5) neighbourhood characteristics. Associations between promotive factors and resilience were tested using regression-based methods, with sex and contextual adversity (adverse life events, psychosocial stress, socioeconomic deprivation) as moderators and mediators.
The following factors were consistently (in both cohorts) associated with resilience: (1) individual: regulatory abilities, cognition; (2) parent–child: mother–child relationship; (3) family: authoritative and structured climate, interparental relationship; (4) peers: bullying. Regulatory abilities showed independent effect in both cohorts. Collectively, factors explained 30%–41% of the variance in resilience. Effects were similar across sex and contextual adversity, but promotive factors were less prevalent in boys and adverse contexts. Particularly in the UK, promotive resources were scarce amidst contextual adversity, which explained the lower resilience of children living in adversity.
This study identified modifiable factors such as child self-regulation, interparental relationships, and bullying that – if improved – have a high potential for improving mental health outcomes in preterm-born children.
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