Inhibitory Control of Prepotent Eye Movements in ASD

Poster Presentation
Thursday, May 2, 2019: 5:30 PM-7:00 PM
Room: 710 (Palais des congres de Montreal)
S. E. Kelly1, L. M. Schmitt2, J. A. Sweeney3 and M. W. Mosconi4, (1)Clinical Child Psychology Program, Schiefelbusch Institute for Life Span Studies, Kansas Center for Autism Research and Training (KCART), University of Kansas, Lawrence, KS, (2)Psychiatry, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, (3)Division of Developmental Behavioral and Pediatrics, Cincinnati Children’s Hospital Medical Center, Cincinnati, OH, (4)Clinical Child Psychology Program, Schiefelbusch Institute for Life Span Studies, University of Kansas, Lawrence, KS
Background: Impairments in inhibitory control (IC), or the ability to suppress a dominant behavioral response, are common in individuals with autism spectrum disorder (ASD). Multiple psychological and neurophysiological processes contribute to successful IC, though the extent to which these distinct processes are affected in ASD is not known. We previously have documented that individuals with ASD show a reduced ability to proactively delay response onset during a manual motor stop-signal task which contributes to failures inhibiting contextually inappropriate responses. Relative to manual motor behaviors, eye movements are highly automated, more difficult to inhibit, and more closely linked to discrete neurophysiological processes. Characterizing IC of eye movements in ASD may provide key insights into spared and affected psychological and neurophysiological processes.

Objectives: To characterize oculomotor inhibitory control impairments in individuals with ASD.

Methods: Sixty individuals with ASD aged 5-29 years and 65 age- and gender-matched typically developing controls completed an oculomotor stop-signal task (i.e., countermanding). During this task, the majority of trials were GO trials, on which participants made rapid eye movements (i.e., saccades) toward peripheral targets (12 degrees to the left or right of center). The remaining trials were STOP trials, on which a stop signal appeared at variable intervals following the peripheral target (i.e., stop signal delays) to cue the participant to inhibit the saccade. Stopping accuracy (i.e., the percent of STOP trials successfully inhibited), estimated reaction time of the stopping process (SSRT), and reaction time slowing on GO trials (RT slowing) compared to a baseline RT task were examined.

Results: Individuals with ASD exhibited reduced stopping accuracy compared to controls, especially for rightward targets. Compared to controls, individuals with ASD also showed reduced RT slowing that was more severe for rightward targets. SSRT did not differ between groups. Across both groups, increased age was associated with higher stopping accuracy and RT slowing, and these effects did not differ as a function of group membership.

Conclusions: The results indicate that inhibitory control deficits in ASD reflect a reduced ability to strategically delay behavioral responses as evidenced by reduced RT slowing. These findings suggest that fronto-striatal pathways necessary for top-down proactive inhibitory control are compromised in ASD. Additionally, these impairments were found to be more severe when inhibiting rightward eye movements. Because rightward eye movements are controlled primarily by the left hemisphere, our findings suggest a lateralized deficit in communication between higher-level cognitive systems and motor control processes in individuals with ASD. Alternatively, as prior brain activation findings indicate that inhibitory control processes are right hemisphere dominant, our findings also may indicate inter-hemispheric communication impairments in ASD.