Atypical Processing of Gaze Cues and Faces Explains Comorbidity between Autism Spectrum Disorder (ASD) and Attention Deficit/Hyperactivity Disorder (ADHD)

Madeleine J Groom,Puja Kochhar,Marina Simeou,Elizabeth B Liddle,Antonia Hamilton,Chris Hollis

doi:10.1007/s10803-017-3078-4

Abstract

This study investigated the neurobiological basis of comorbidity between autism spectrum disorder (ASD) and attention deficit/hyperactivity disorder (ADHD). We compared children with ASD, ADHD or ADHD+ASD and typically developing controls (CTRL) on behavioural and electrophysiological correlates of gaze cue and face processing. We measured effects of ASD, ADHD and their interaction on the EDAN, an ERP marker of orienting visual attention towards a spatially cued location and the N170, a right-hemisphere lateralised ERP linked to face processing. We identified atypical gaze cue and face processing in children with ASD and ADHD+ASD compared with the ADHD and CTRL groups. The findings indicate a neurobiological basis for the presence of comorbid ASD symptoms in ADHD. Further research using larger samples is needed.

Highlights

Autism spectrum disorder (ASD) and attention deficit hyperactivity disorder (ADHD) are neurodevelopmental disorders that have significant, adverse effects on cognitive and socio-emotional development
We measured effects of ASD, ADHD and their interaction on the Early Directing Attention Negativity (EDAN), an event-related potentials (ERPs) marker of the orienting of visual attention towards a spatially cued location and the N170, a right-hemisphere lateralised ERP linked to face processing
We identified atypical gaze cue and face processing in children with ASD and ADHD+ASD, suggesting that these ERPs may Firstly, there was a significant EDAN effect for Chevron but not Gaze cues, replicating the findings of previous gaze cueing studies that have reported a lack of EDAN for gaze cues (Brignani et al 2009; Hietanen et al 2008; Holmes et al 2010)

Summary

Introduction

Autism spectrum disorder (ASD) and attention deficit hyperactivity disorder (ADHD) are neurodevelopmental disorders that have significant, adverse effects on cognitive and socio-emotional development. ASD symptoms are significantly higher in children with ADHD than in the general population (Kochhar et al 2011; Mulligan et al 2009). This diagnostic co-occurrence was formally recognised in the DSM-5 (American Psychiatric Association 2013) so that these diagnoses are no longer mutually exclusive. Despite this important change, still relatively little is known about the neurobiological basis of overlap between these conditions. Measuring cognitive markers of brain systems that are implicated in one or both conditions provides a useful tool for investigating the basis of comorbidity and may help distinguish between true overlap and ‘phenocopy’ (where the symptoms of one disorder mimic those of another, but arise from different pathways) (Rommelse et al 2011)

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