30538
Psychopathological Comorbidity in Children with Autism Spectrum Disorder: The Executive Function Mediator

Poster Presentation
Friday, May 3, 2019: 5:30 PM-7:00 PM
Room: 710 (Palais des congres de Montreal)
Q. Chen, B. Wan and Y. Jin, Sun Yat-sen University, Guangzhou, China
Background: Autism spectrum disorder (ASD) presents high prevalence of psychiatric disorders which worsen ASD core symptoms, and these disorders are associated with different components of executive function (EF). Previous studies articulate just one or two commodities in children with ASD. However, it is unclear which comorbidities are related to worsening ASD core symptoms in the system of various psychiatric disorders and the basis of the EF components remains unknown for these relationships.

Objectives: The study aimed to identify which psychiatric disorders worsen ASD core symptoms and examine the role of daily EF in comorbid psychopathology in children with ASD.

Methods: The present study analyzed 100 children with ASD (79 males, age: M=10.6 SD=1.6 years) and 180 typically developing (TD) children (94 males, age: M=10.4 SD=1.3 years). Achenbach’s Child Behavior Checklist (CBCL), Behavior Rating Inventory of Executive Function (BRIEF) and Social Responsiveness Scale (SRS) were applied for assessing parent-reported comorbid psychopathologies (affective disorder, anxiety disorder, somatic disorder, attention deficit/hyperactive disorder-ADHD, oppositional defiant disorder-ODD, conduct disorder-CD), EF (including two systems: behavioral regulation index, BRI; metacognition index, MI), and ASD core symptoms (social interaction and communication, SIC; repetitive restricted behaviors; RRB), respectively.

Results: The present study found that there were three psychopathological comorbidities (affective disorder, anxiety disorder, and ADHD) independently related to worsening ASD core symptoms, and observed full mediating effect of different EF systems in multivariate models. After controlling for the two other disorder domains, 1) affective disorder damaging SIC related to MI (indirect effect size=0.31, 95%CI= 0.11, 0.54); 2) anxiety disorder was mediated by BRI to worsen SIC (indirect effect size=0.42, 95%= 0.21, 0.69) and RRB (indirect effect size=0.42, 95%CI=0.21, 0.67); 3) ADHD was mediated by both EF systems (BRI, indirect effect size=0.26, 95%CI=0.09, 0.48; MI, indirect effect size=0.21, 95%CI=0.06, 0.40) to aggravate SIC and by BRI (indirect effect size=0.39, 95%CI=0.18, 0.65) to deteriorate RRB. In the meantime, the relationship between pathopsychological symptoms and the core symptoms of ASD was not full mediated by EF in TD children.

Conclusions: Our findings suggest that comorbid with affective disorder, anxiety disorder, and/or ADHD will worsen ASD core symptoms, in which association different EF components play a diverse mediating effect. Our study sheds light on the behavioral mechanism underlying to comorbid psychology in children with ASD.