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Neurocognitive Deficits Underlying Insistence On Sameness in Autism Spectrum Disorders (ASD)

Friday, 3 May 2013: 16:30
Meeting Room 3 (Kursaal Centre)
M. W. Mosconi1, M. E. Ragozzino2, L. M. Schmitt1, E. H. Cook3 and J. A. Sweeney4, (1)University of Texas Southwestern Medical Center, Dallas, TX, (2)University of Illinois at Chicago, Chicago, IL, (3)Psychiatry, University of Illinos at Chicago, Chicago, IL, (4)Center for Autism and Developmental Disabilities, UT Southwestern Medical Center, Dallas, TX
Background:  Individuals with Autism Spectrum Disorder (ASD) frequently show a rigid adherence to a rule or routine, or an Insistence on Sameness (IS).  The neurocognitive alterations that underlie IS behaviors are not well understood.  We have recently shown that individuals with ASD often fail to inhibit prepotent responses, suggesting dysfunction of frontostriatal brain systems that may limit affected individuals’ ability to interrupt behavioral routines.

Objectives:  To determine whether individuals show inhibitory control deficits on a novel stop-signal task, and to examine the relationship of stopping errors and clinically-rated IS behaviors.

Methods:  Forty-five individuals with ASD and 40 healthy controls matched on age (range 6-38 years) and Performance IQ were administered manual motor and oculomotor stop-signal tasks (SST) and baseline measures of reaction time.  During the SST, subjects 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 following the appearance of the peripheral cue (‘STOP’ trials).  We examined subjects' reaction times during both baseline and SST GO trials, as well as the rate at which they failed STOP trials (i.e., they pressed a button or looked towards the peripheral target).

Results:  Subjects with ASD made more STOP trial errors than healthy controls during manual motor and oculomotor SST (p’s<.05).  For individuals with ASD, increased STOP trial error rates were related to increased rates of IS behaviors (p<.05). STOP trial error rates also were associated with the degree to which subjects slowed their reaction times from baseline to task GO trials, such that increased slowing was associated with fewer STOP trial errors (p<.01).  Subjects with ASD did not slow their reaction times as much as controls (p<.05).  Increased age was associated with fewer STOP trial errors and increased slowing of reaction times in healthy controls (p’s<.01), but not in subjects with ASD.  

Conclusions:  These results indicate that individuals with ASD show inhibitory control deficits that are associated with the severity of their IS behaviors. From a neurocognitive perspective, IS appears to reflect, at least in part, a reduced ability to suppress unwanted or context inappropriate responses.  This impairment involves a failure to strategically slow behavioral reaction times in order to optimize the capacity to stop these responses when cued.  Inhibiting unwanted behaviors involves frontostriatal suppression of the motor pathways that support volitional action.  The application of strategic timing biases during SST performance has been shown to recruit medial prefrontal cortices including supplementary motor cortex and supplementary eye fields.  Our findings suggest that the development of frontostriatal and medial prefrontal brain systems underlying response inhibition may be disrupted during childhood and adolescence in ASD. Future treatments targeting the biological mechanisms underlying these behaviors therefore may be able to continue advancing behavioral abilities through adolescence and early adulthood even after early emerging impairments have been established in affected individuals.

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