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Background: Children with autism spectrum disorder (ASD) often have co-occurring symptoms of attention-deficit/ hyperactivity disorder (ADHD) and/or anxiety. It is unclear whether these disorders arise from shared or distinct developmental pathways. We explored this question by testing the specificity of early-life (infant and toddler) predictors of mid-childhood ADHD and anxiety symptoms compared to ASD symptoms. Methods: Infants (n = 104) at high and low familial risk for ASD took part in research assessments at 7, 14, 24 and 38 months, and 7 years of age. Symptoms of ASD, ADHD and anxiety were measured by parent report at age 7. Activity levels and inhibitory control, also measured by parent report, in infancy and toddlerhood were used as early-life predictors of ADHD symptoms. Fearfulness and shyness measured in infancy and toddlerhood were used as early-life predictors of anxiety symptoms. Correlations and path analysis models tested associations between early-life predictors and midchildhood ADHD and anxiety symptoms compared to mid-childhood ASD symptoms, and the influence of controlling for ASD symptoms on those associations. Results: Increased activity levels and poor inhibitory control were correlated with ADHD symptoms and not ASD or anxiety; these associations were unchanged in path models controlling for risk-group and ASD symptoms. Increased fearfulness and shyness were correlated with anxiety symptoms, but also ASD symptoms. When controlling for risk-group in path analysis, the association between shyness and anxiety became nonsignificant, and when further controlling for ASD symptoms the association between fearfulness and anxiety became marginal. Conclusions: The specificity of early-life predictors to ADHD symptoms suggests early developmental pathways to ADHD might be distinct from ASD. The overlap in early-life predictors of anxiety and ASD suggests that these disorders are difficult to differentiate early in life, which could reflect the presence of common developmental pathways or convergence in early behavioural manifestations of these disorders.

Objective: The diagnosis of autism spectrum disorder (ASD) has been found to be remarkably stable but few studies have followed children not initially diagnosed with ASD beyond age 3 to examine late or delayed diagnoses. The current study used a prospective familial-risk design to identify children who had undergone multiple comprehensive assessments in preschool and were determined to be ASD-negative, only to meet criteria for ASD when tested in middle childhood. Method: Data were pooled across three research teams studying later-born siblings of children with ASD. Fourteen children met inclusion criteria for the Late Diagnosed group and were compared to a large sample of high- and low-risk siblings from the same sites who had ASD or typical development (TD) outcomes at age 3. Results: As a group, the Late Diagnosed children scored between the TD and ASD groups on most measures administered at age 3 and differed significantly from the ASD group on most measures. However, there was significant heterogeneity among the Late Diagnosed cases. Seven showed very little evidence of ASD in preschool, while seven demonstrated subtle, subthreshold symptomatology. Conclusion: Some children with ASD may present with a subtle phenotype early in life or show a prolonged time course of symptom development. This emphasizes the need for screening and surveillance schedules that extend past 36 months and continued evaluation of any child who presents with atypical early development and/or high-risk status. The findings also shed light on reasons why the mean age of ASD diagnosis remains over 4 years.

Almost 20% of infants with an older sibling with autism spectrum disorder (ASD) exhibit ASD themselves by age 3 years. The longer‐term outcomes of high‐risk infants are less clear. We examined symptoms of ASD, attention‐deficit/hyperactivity disorder (ADHD) and anxiety, language, IQ, and adaptive behaviour at age 7 years in high‐ and low‐risk children prospectively studied since the first year of life. Clinical outcomes were compared between high‐risk children who met diagnostic criteria for ASD at age 7 (HR‐ASD‐7 group, n = 15), high‐risk children without ASD (HR‐Non‐ASD‐7 group, n = 24), and low‐risk control children (LR group, n = 37). Diagnostic stability between age 3 and 7 years was moderate, with five children who did not meet diagnostic criteria for ASD at age 3 years being assigned the diagnosis at age 7, and three children showing the opposite pattern. The HR‐ASD‐7 group showed elevated ADHD and anxiety symptoms and had lower adaptive behaviour scores than LR controls. The HR‐Non‐ASD‐7 group had higher repetitive behaviour, lower adaptive functioning and elevated scores on one anxiety subscale (Separation Anxiety) compared to LR controls, but evidence for subclinical ASD symptoms (the broader autism phenotype, BAP) was limited in the group as a whole, although we identified a subgroup with elevated ASD traits. The difficulties experienced by high‐risk siblings at school‐age extend beyond ASD symptoms. The pattern of difficulties exhibited by the HR‐ASD‐7 group may inform our understanding of developmental trajectories of co‐occurring psychopathology in ASD. Autism Res 2017, 10: 546–557. © The Authors Autism Research published by Wiley Periodicals, Inc. on behalf of International Society for Autism Research

Altered power of resting-state neurophysiological activity has been associated with autism spectrum disorder (ASD) and attention-deficit/hyperactivity disorder (ADHD), which commonly co-occur. We compared resting-state neurophysiological power in children with ASD, ADHD, co-occurring ASD + ADHD, and typically developing controls. Children with ASD (ASD/ASD + ADHD) showed reduced theta and alpha power compared to children without ASD (controls/ADHD). Children with ADHD (ADHD/ASD + ADHD) displayed decreased delta power compared to children without ADHD (ASD/controls). Children with ASD + ADHD largely presented as an additive co-occurrence with deficits of both disorders, although reduced theta compared to ADHD-only and reduced delta compared to controls suggested some unique markers. Identifying specific neurophysiological profiles in ASD and ADHD may assist in characterising more homogeneous subgroups to inform treatment approaches and aetiological investigations.

Impaired habit-learning has been proposed to underlie the tic symptoms of Tourette syndrome (TS). However, accounts differ in terms of how habit-learning is altered in TS, with some authors proposing habit formation is impaired due to a deficient 'chunking' mechanism, and others proposing habit-learning is overactive and tics reflect hyperlearned behaviours. Attention-deficit/hyperactivity disorder (ADHD) frequently co-occurs with TS and is known to affect cognitive function in young people with co-occurring TS and ADHD (TS + ADHD). It is unclear, however, how co-occurring ADHD symptoms affect habit-learning in TS. In this study, we investigated whether young people with TS would show deficient or hyperactive habit-learning, and assessed the effects of co-occurring ADHD symptoms on habit-learning in TS. Participants aged 9-17 years with TS (n = 18), TS + ADHD (n = 17), ADHD (n = 13), and typical development (n = 20) completed a motor sequence learning task to assess habit-learning. We used a 2 (TS-yes, TS-no) × 2 (ADHD-yes, ADHD-no) factorial analysis to test the effects of TS, ADHD, and their interaction on accuracy and reaction time indices of sequence learning. TS was associated with intact sequence learning, but a tendency for difficulty transitioning from sequenced to non-sequenced performance was suggestive of hyper-learning. ADHD was associated with significantly poorer accuracy during acquisition of the sequence, indicative of impaired habit-learning. There were no interactions between the TS and ADHD factors, indicating young people with TS + ADHD showed both TS- and ADHD-related atypicalities in habit-learning.

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