Neurocognitive Strategies Supporting Behavioral Response Inhibition in ASD

Background:  Executive dysfunctions, including deficits in behavioral response inhibition, have been repeatedly documented in ASD.  A reduced ability to voluntarily inhibit prepotent eye movements has been shown to be related to the severity of patients’ repetitive behaviors.  We recently demonstrated that the ability to inhibit an unwanted or inappropriate behavior is enhanced by strategically delaying the onset of that behavior.  Both behavioral response inhibition and these strategic biases in response timing are supported by frontostriatal brain systems.  Assessments of behavioral response inhibition and strategic biases in response timing are therefore important for characterizing patterns of frontostriatal dysfunctions in ASD and the neurocognitive bases of repetitive behaviors.

Objectives:  To characterize behavioral response inhibition deficits and underlying neurocognitive strategies in individuals with ASD using oculomotor and manual stop signal tasks.

Methods:  Sixty-nine individuals with ASD and 56 healthy controls matched on age (range 6-38 years), gender, and nonverbal IQ were administered manual motor and oculomotor stop-signal tasks (SST).  Participants were instructed to either press a button (manual version) or make a saccade (oculomotor version) when a peripheral target appeared ('GO' trials), or inhibit these responses when a central stop signal appeared at varying times following the appearance of the peripheral cue (‘STOP’ trials).  GO and STOP trials were interleaved.  Oculomotor and manual motor baseline reaction time (RT) tasks consisting only GO trials were administered to assess adaptive RT slowing during the SST GO trials.  The Autism Diagnostic Interview-Revised (ADI-R) was used to assess social-communication deficits and repetitive behaviors.

Results:  Subjects showed increased RTs for both oculomotor and manual motor SSTs relative to baseline, indicating that they strategically delayed their responses when STOP trials were interleaved with GO trials.  Greater RT slowing during the SSTs was associated with increased accuracy on STOP trials.  During both SSTs, participants with ASD made more STOP trial commission errors than healthy controls, and they did not slow their reaction times as much as controls.  Response inhibition performance was similar across tasks in healthy controls, but performances on the SSTs were not related in subjects with ASD.  Increased STOP trial error rates and reduced RT slowing relative to baseline during the manual SST each were related to higher-order repetitive behaviors in ASD.

Conclusions: Individuals with ASD show deficits inhibiting prepotent behavioral responses that involve failures to strategically delay their responses in the context of uncertainty.  Importantly, both increased error rates and reduced strategic slowing each appear to contribute to higher-order repetitive behaviors in ASD, including compulsive and ritualistic behaviors and circumscribed interests.  Behavioral response inhibition is supported by discrete frontostriatal circuits, including medial prefrontal cortices that are involved in strategically delaying response onset during conditions in which caution and speed must be dynamically balanced.  Thus, our current findings suggest that pharmacological treatments targeting frontostriatal circuits, and cognitively mediated therapies targeting top down behavioral control, each may be useful for reducing higher-order repetitive behaviors in ASD.