Neurophysiological Responses to Emotional Faces Discriminate Children with ASD and/or ADHD

Background:   Children with autism spectrum disorder (ASD) demonstrate characteristic deficits in processing facial information, particularly emotional expressions. There are high rates of clinical and behavioural overlap between ASD and attention deficit hyperactivity disorder (ADHD), and emotional impairment is also shown in ADHD. Pure and comorbid cases, however, have not been directly compared using event-related potentials (ERPs) that are able to measure distinct temporal stages in emotional processing. 

Objectives:  (1) To investigate the specificity of emotion processing abnormalities to ASD and ADHD and (2) to elucidate the neural basis of the common comorbidity between these two disorders.

Methods:  The N170 (an index of structural encoding) and N400 (an index of contextual processing) ERP components were measured during passive presentation of face stimuli with different emotional expressions (neutral, anger, fear, disgust, joy) to groups of ASD (n=19), ADHD (n=18), comorbid ASD+ADHD (n=29) and typically developing (TD) controls (n=26). 

Results: Subjects with ASD (ASD and ASD+ADHD) displayed reduced N170 amplitude across all stimuli, and reduced N170 amplitude for fearful versus neutral facial expressions, compared to children without ASD. Conversely, subjects with ADHD (ADHD and ASD+ADHD) demonstrated reduced modulation of N400 amplitude by fearful expressions at parietal sites and happy facial expressions at central sites, compared to subjects without ADHD. 

Conclusions: These findings indicate that while children with ASD demonstrate deficits at structural encoding stages of face processing (indexed by the N170), children with ADHD show impairments in contextual processing of emotion (indexed by the N400), which suggests a dissociation between disorders on the basis of distinct temporal stages of emotion processing. The comorbid ASD+ADHD group display the unique deficits of both disorders in early and late emotion processing, supporting the comorbid disorder as an additive condition rather than a separate disorder with distinct impairments. This supports the use of objective neural measurement of emotional function to delineate pathophysiological mechanisms and guide clinical assessment.