The Mediating Role of Executive Functioning in Problems Behaviors in Autism Spectrum Disorder

Background: Increased problem behaviors (such as lethargy and irritability) are commonly observed comorbidities in children with Autism Spectrum Disorder (ASD; Emerson, 1995). In the typically developing population, executive functioning (EF) deficits have been linked to problem behaviors (Hughes & Enor, 2008). It has been proposed that individuals with ASD have a different cognitive profile (Kenworthy et al., 2008). Additionally, prototypical EF deficits in ASD have been linked to alternate brain topographies (Voelbel et al., 2006), suggesting that individuals with ASD may demonstrate unique EF deficits which in turn may lead to increased problem behaviors. However, no studies have investigated the direct relationship between EF deficits, as assessed through validated, researcher administered measures, and problem behaviors.

Objectives: This study examines the relationship between EF, as measured by the NIH-Toolbox Cognition Battery (NIH-TCB), and problem behaviors, as measured by the Aberrant Behavior Checklist (ABC).

Methods: Children with ASD, ages 3-17, years and typically developing (TD) children matched on age are currently being recruited. Data from 143 children and adolescents with ASD (mean age = 9 years; SD= 4 years) and 92 TD controls (mean age = 8 years 5 months; SD = 3 years) is included in this preliminary analysis. TD children demonstrated a significantly higher intelligent quotient (IQ) as indexed via the Stanford-Binet Intelligence Test, Fifth Edition (SB-5; TD mean IQ = 111.6; ASD mean IQ = 91.93; p=.01); therefore, the analysis controlled for IQ. Parents completed the ABC. Four separate path analyses were conducted to test the following hypothesized mediation model: Diagnostic status -> mediator variable (cognitive inhibition and flexibility) -> outcome variable (lethargy or irritability). Both direct and indirect models were tested.

Results: For lethargy, the hypothesized model mediated by cognitive inhibition and direct paths were tested for differences. Both the indirect model (mediated by cognitive inhibition) and the direct model were significant (indirect: Beta= -0.53, p=0.06; direct: Beta= 7.66, p<0.01). However, the hypothesized model mediated by cognitive flexibility was non-significant (indirect: Beta= -0.05, p=0.18). In the case of irritability, the hypothesized model mediated by either cognitive flexibility or inhibition presented non-significant results (p=.40, p=.10, respectively).

Conclusions: These preliminary findings replicate previously observed pathways between cognitive inhibition and problem behaviors (lethargy) in children, while extending these findings to children with ASD using performance-based measures. These findings suggest that interventions targeting EF deficits in cognitive inhibition may also mediate lethargic problem behaviors. However, other problem behaviors such as irritability may not be mediated by EF in the ASD population.