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    • In conclusion a novel feature of

    2018-11-03

    In conclusion, a novel feature of the current study is the use of multi-method techniques, including daily diaries across 14days as well as dyadic order latrunculin scans. Our daily diary method to monitor how sleep-time changes day-by-day captures real life experience as it is lived (Bolger et al., 2003) and does not rely on retrospective accounts. To our knowledge, the current dyadic neural concordance analysis is the first empirical analytic approach to evaluate interpersonal neural connectivity beyond one single individual’s brain and link it to sleep patterns. Thus, the current multi-level approach significantly contributes to our understanding of adolescents’ sleep behavior with a robust and integrated perspective of brain-behavior associations. In sum, we provide the first empirical evidence to highlight the importance of dyadic concordance at both the behavioral and neural level in conferring benefits to adolescents’ sleep.
    Contributions
    Conflict of interest
    Acknowledgements This work was supported by the National Institute of Health (1R01DA039923). The funders had no role in study design, data collection, and analysis, decision to publish, or preparation of the manuscript.
    Introduction Autism spectrum disorder (ASD) and attention deficit hyperactivity disorder (ADHD) are two common childhood-onset disorders that show substantial behavioural and genetic overlap (Ronald et al., 2008). Impairments in executive function (EF), behaviours such as planning, online monitoring and working memory, characterise both children with ASD and ADHD, and may underlie some of the behavioural features of the disorders (Happé et al., 2006; Rommelse et al., 2011). Children with ASD often perform poorly on tasks requiring planning and mental flexibility, while children with ADHD consistently demonstrate difficulties inhibiting responses (Geurts et al., 2004; Happé et al., 2006). Event-related potentials (ERPs) which capture distinct underlying neural processes related to these functions, have demonstrated that ASD and ADHD can be dissociated on the basis of their neurophysiological responses during attentional (Tye et al., 2014a) and social cognitive tasks (Tye et al., 2013, 2014b). Specifically, children with ADHD symptoms (both ADHD and comorbid ASD and ADHD; ASD+ADHD) demonstrate impairment in response inhibition (reduced NoGo-P3 to non-targets) and attentional orienting (reduced Cue-P3 to cue/warning stimuli), while children with ASD (ASD and ASD+ADHD) show reduced conflict monitoring (reduced N2 enhancement from Go (target) to NoGo (non-target) trials; Tye et al., 2014a), on a cued Continuous Performance Task (CPT-OX). These findings indicate Cognate tRNAs impaired EF processes are distinct in ASD and ADHD, whereas children with co-occurring ASD+ADHD present as an additive co-occurrence with the unique deficits of both disorders. Still, little is known about the role of other co-occurring traits in moderating EF in ASD and ADHD and their overlap, particularly those that are associated with typical EF. The recent shift toward dimensional over categorical approaches in psychopathology (Cuthbert and Insel, 2013) emphasises the importance of a transdiagnostic approach, assessing traits rather than categorical disorders. Linking neurocognitive markers to dimensions will likely be more informative in terms of understanding the underlying mechanisms. There has been growing interest in the comorbidity demonstrated between psychopathic tendencies, anti-social behaviour and both ASD and ADHD (Colledge and Blair, 2001; Kadesjö and Gillberg, 2001; Simonoff et al., 2008; Leno et al., 2015). Children with ASD display increased antisocial and aggressive behaviour (Bauminger et al., 2010) and a quarter to a third of individuals have a co-occurring diagnosis of oppositional defiant disorder (ODD) and/or conduct disorder (CD; Simonoff et al., 2008; Kaat et al., 2013). These disruptive behaviours tend to have a highly stable and persistent course when left untreated and are associated with a higher rate of dysfunctional outcomes. Follow-up studies of children with ADHD indicate 21% meet criteria for antisocial personality disorder (ASPD) in young adulthood, with the severity of childhood conduct problems as a contributory factor (Fischer et al., 2002). Psychiatric comorbidity in ASD is a major factor contributing to violent offending (Woodbury-Smith et al., 2005; Newman and Ghaziuddin, 2008) and there are consistent associations between ASD traits and psychopathic traits (Soderstrom et al., 2005). A longitudinal study, however, suggested no risk for ASPD in adult patients with a childhood diagnosis of ASD (0%), but an increased risk for those with childhood-onset ADHD (30.9%) and ASD+ADHD (18.5%; Anckarsäter et al., 2006), although ASPD may be more common in pervasive developmental disorder-not otherwise specified (Hofvander et al., 2009). The pathophysiological mechanisms underlying the developmental trajectories to antisocial behaviour and psychopathic traits may be separable in ASD and ADHD.