International Meeting for Autism Research: Electrophysiological Indices of Conflict Monitoring In Autism Spectrum Disorders

Electrophysiological Indices of Conflict Monitoring In Autism Spectrum Disorders

Thursday, May 12, 2011
Elizabeth Ballroom E-F and Lirenta Foyer Level 2 (Manchester Grand Hyatt)
2:00 PM
A. Clawson1, P. E. Clayson1, M. J. Larson1,2, O. Johnston3 and M. South1,2, (1)Psychology, Brigham Young University, Provo, UT, (2)Neuroscience, Brigham Young University, Provo, UT, (3)School of Accountancy, Brigham Young University, Provo, UT
Background: Children with autism spectrum disorders (ASD) often display deficits in cognitive control processes, potentially contributing to characteristic difficulties in monitoring and regulating behavior.  Studies examining the neural mechanisms underlying performance-monitoring components of cognitive control show that children with ASD have decreased neural activation and impaired response monitoring relative to controls (Henderson et al, 2006; South et al., 2010).  The N2, a stimulus-locked component of the event-related potential (ERP) putatively reflects conflict monitoring and the allocation of attention during conflict to increase behavioral control (Yeung & Cohen, 2006).  Thus, the N2 provides a physiological indicator of conflict monitoring processes and has direct implications for appropriate behavioral adjustment during social-emotional processing.  Examining such electrophysiological mechanisms in individuals with ASD may contribute to greater characterization across the spectrum and increase our understanding of the neural bases of behavioral abnormalities in ASD (Henderson et al, 2006).        

Objectives: The purpose of this study was to examine conflict monitoring processes in children with ASD relative to typically developing (TD) controls.  Specifically, we examined behavioral and electrophysiological correlates of the N2 during high-conflict and low-conflict trials.  We hypothesized that children with ASD would display an attenuated N2 relative to controls, indicating deficits in conflict monitoring processes.   

Methods:  High-density ERPs and behavioral data (error rates, reaction times [RTs]) were acquired while 17 children with ASD and 18 healthy controls completed a modified Eriksen flanker task. Groups were well matched for age, education, and IQ. The ADOS-G (total social communication score >7) and and SCQ (total score >15) were used to characterize ASD participants. Data were analyzed using a 2-Group (ASD, control) x 2-Congruency (congruent, incongruent) mixed model analysis of variance for ERP and behavioral data.

Results: Behaviorally, groups showed similar patterns of performance; both groups had longer RTs and higher error rates on high-conflict (incongruent) trials relative to low-conflict (congruent) trials. For N2 amplitude, the Group x Congruency interaction was significant. Controls demonstrated larger N2 amplitudes to high-conflict trials compared to low-conflict trials. Children with ASD showed no such differences between congruent and incongruent trials.

Conclusions: Results indicate disrupted neural reflections of conflict monitoring processes in children with ASD.  Uniform N2 amplitudes in children with ASD for high-conflict and low-conflict trials potentially indicate decreased attention to conflicting information.  Despite decreased N2 amplitudes relative to controls, behavioral data from children with ASD do not reflect greater conflict-based recruitment of cognitive control.  This mismatch between behavior and neural activation may indicate that children with ASD are unable to recognize conflict or unable to allocate cognitive control mechanisms to adapt their behavior relative to the presence of conflict.  Future research is necessary to accurately characterize and understand the behavioral implications of these deficits relative to diagnostic severity, anxiety, and personality.  

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