International Meeting for Autism Research (London, May 15-17, 2008): N2 and Response Inhibition in Children with High-Functioning Autism

N2 and Response Inhibition in Children with High-Functioning Autism

Friday, May 16, 2008
Champagne Terrace/Bordeaux (Novotel London West)
L. Mohapatra , University of Miami, University of Miami, Coral Gables, FL
C. Schwartz , University of Miami, Graduate Student
P. C. Mundy , UC Davis, Davis, CA
H. A. Henderson , Psychology, University of Miami, Coral Gables, FL
C. Burnette , Psychiatry and Kenedy Center, Vanderbilt University
A. P. Inge , University of Miami, Graduate Student, Coral Gables, FL
N. Zakha , University of Miami, Coral Gables, FL
Background: Discrepant findings on whether children with autism display response inhibition deficits may be partially due to the variety of behavioral tasks used to assess inhibition.  A more useful way of understanding early cognitive/attentional processess that influence inhibition may be to look at neurophysiological measures.  Specifically, the event related potential N2, a measurement of cognitive control or the effortful decision to inhibit a prepotent behavioral response, may be useful in understanding the discrepancy in response inhibition.

Objectives: In the current study we measured the N2 while high-functioning autistic children and age, IQ-matched control children performed a modified Flanker task.  We further examined the associations between N2 amplitude and latency and variations in social communication within the HFA sample.

Methods: Behavioral and electrophysiological data from a modified Flanker task were collected from 27 HFA (1 female) and 24 typically developing controls (1 female) ranging in age from 8- to 16-years.  Symptom severity was measured using the ASSQ, ADI, and SCQ.

Results: Regarding behavioral performance, HFA children committed more errors than control children after controlling for age and verbal IQ. Electrophysiological performance indicated marginal group differences in N2 amplitude after controlling for age.  However, a significant age-related decline in N2 amplitude was observed in the control but no in the HFA group.  In addition, greater N2 amplitude was correlated with lower scores on the SCQ for the HFA children.  There were no significant group differences in N2 latency.

Conclusions: Behavioral performance indicates that HFA children show impulsivity but not deficits in inhibition.  Electrophysiological N2 data, however, suggest that the development of neural processes associated with inhibition may not display the same age-related improvements as in control children.  Moreover, N2 in HFA children may be an indicator of stable differences in cognitive effort or control that are associated with social communication deficits.

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