The role of executive functions in social impairment in Autism Spectrum Disorder

Abstract

Autism Spectrum Disorder (ASD) is a neurodevelopmental disorder characterized by socio-communicative impairments. Executive dysfunction may explain some key characteristics of ASD, both social and nonsocial hallmarks. Limited research exists exploring the relations between executive function and social impairment in ASD and few studies have used a comparison control group. Thus, the objective of the present study was to investigate the relations between executive functioning using the Behavioral Rating Inventory of Executive Functioning (BRIEF), social impairment as measured by the Social Responsiveness Scale (SRS), and overall autistic symptomology as measured by the Autism Diagnostic Observation Schedule (ADOS) in children and adolescents with and without ASD. Seventy children and adolescents diagnosed with ASD and 71 typically developing controls were included in this study. Findings showed that behavioral regulation executive processes (i.e., inhibition, shifting, and emotional control) predicted social function in all children. However, metacognitive executive processes (i.e., initiation, working memory, planning, organization, and monitoring) predicted social function only in children with ASD and not in typically developing children. Our findings suggest a distinct metacognitive executive function-social symptom link in ASD that is not present in the typical population. Understanding components of executive functioning that contribute to the autistic symptomology, particularly in the socio-communicative domain, is crucial for developing effective interventions that target key executive processes as well as underlying behavioral symptoms.

Keywords:

• Autism Spectrum Disorder
• Executive function
• Social impairment
• Metacognition

The authors would like to thank Heather Leckey and Becky Baatjes for assistance with ADOS administration, and Rina Goukon, Jane Kouptsova, and Anjili Vara for their assistance with data collection.

No potential conflict of interest was reported by the author(s).

Additional information

Funding

Rachel Leung was supported through a studentship, fully or in part, by the Matching Funds Program, Hospital for Sick Children Foundation Student Scholarship Program. This work was supported by the Canadian Institutes of Health Research (Grant no. MOP-106582; Grant no. MOP-119541).