International Meeting for Autism Research (London, May 15-17, 2008): AMELIORATING INHIBITORY CONTROL ABILITIES IN ASD

AMELIORATING INHIBITORY CONTROL ABILITIES IN ASD

Friday, May 16, 2008
Champagne Terrace/Bordeaux (Novotel London West)
H. M. Geurts , Psychonomics, University of Amsterdam, Amsterdam, Netherlands
Background: For treatment purposes it is crucial to disentangle in what circumstances people with ASD encounter difficulties. The executive dysfunctions (ExDys) account of ASD has resulted in numerous studies delineating the precise types of ExDys that people with ASD encounter. However, hardly any study has focused on ways to reduce or overcome these difficulties.

Objectives: To disentangle how deficient processes that lead to the observed deficits in inhibitory control in ASD can be ameliorated.

Methods: In the first experiment 22 boys with ASD, 22 boys with ADHD and 32 typically developing boys (TD) matched on age (8 to 13 years) participated. An Eriksen Flanker task was applied as this inhibitory control task measures the ability to suppress irrelevant information. The task is applied in a neutral and a motivational situation. In the motivational situation, participants were told that they were competing with peers. In the other experiments 18 children with HFA and 22 TD children matched on age, FSIQ, and gender participated. Two Go/NoGo paradigms were applied, one with neutral stimuli and one with emotional stimuli. The stimuli were presented with varying presentation rates to manipulate arousal level of the children. 
Results: 1) All groups benefited from motivation: The boys were faster and made fewer errors when they were competing with peers. However, this was mainly due to the improvement in performance in the children with ADHD. The children with ASD still had difficulties with the task. 2) Children with HFA only encounter inhibition deficits when information is presented very fast and consists of emotional stimuli.

Conclusions: The findings will be discussed in terms of the ExDys account of ASD. However, the ExDys account is not sufficient to explain the pattern of results and alternative explanations will be put forward. Moreover, we will stress the clinical implications of our findings.

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