Abstract
Autism Spectrum Disorder (ASD) is a developmental disorder characterized by social-communication difficulties as well as restricted and repetitive behaviour and interests (APA, 2013). One model of ASD considers amygdala dysfunction as a central factor in the disorder (Adolphs et al. 2001) accounting for impaired social perception (e.g. facial expressions) in this population (Walsh et al., 2016; Harms et al., 2010). This hypothesis predicts impairments to be limited to negative emotions. Indeed, multiple studies have reported supporting evidence for this (Poljac et al., 2013; Farran, 2011; Ashwin et al. 2006), though results based on 50 studies on this topic have generally been mixed (Uljarevic et al., 2013). Methodological choices such as use of emotional labeling or expression-matching tasks and assessments of accuracy or reaction times may explain the inconsistency across study results. Previous methods used confound emotion processing with physical stimulus properties and run the risk of ceiling effects, potentially masking group differences. Here we used a two-interval forced choice psychophysical paradigm that allowed us to assess performance across expressions while maintaining the inherent difficulty of the task to measure discrimination thresholds for three expressions (anger, happiness, and sadness) in a group of adults with ASD (n=30) and controls (n=30) matched on IQ. We assessed social competence using the Multidimensional Social Competence Scale (MSCS) (Yager & Iarocci, 2013) and autism symptoms with the Autism Spectrum Quotient (AQ). Participants with ASD were significantly impaired in all expressions tested, including happiness. Our results show a strong association with expression performance and the Empathic Concern (EC) sub-scale and the total social competence score of the MSCS. These findings indicate that social competence is associated with impaired facial emotion processing ability in adults with ASD; affecting positive and negative expressions alike and not specific to negative emotions as postulated in the amygdala theory of ASD.
Meeting abstract presented at VSS 2017