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By Aaron T Beck; Gary Emery; Ruth L Greenberg

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Charman: The CHAT study won’t because we only targeted one domain of impairment: early social communication behaviours. Buitelaar: In the study I mentioned earlier, we have the opportunity to look at the distribution in the general population of the separate dimensions of social interaction skills/de¢cits, communication skills/de¢cits and other problems. We will also be able to look at whether these dimensions are relatively independent from each other in the general population; or, alternatively, whether de¢cits in social interaction, communication, language, etc.

What are the implications of these ¢ndings for our understanding of autism? Firstly, as apparently intact (or indeed perhaps also superior) behavioural performance may be mediated by unusual mechanisms, the distinctions between speci¢cally impaired and intact behaviours may sometimes be more apparent than real. Secondly, the ¢ndings raise the possibility that some de¢cits emerge only if potential compensatory brain pathways are also dysfunctional. Thirdly, autistic spectrum disorders in able individuals appear to be associated with quite widespread abnormal cortical organisation, raising the possibility that the neurobiological basis of supposedly speci¢c de¢cits and mental handicap may be more similar than previously supposed.

Secondly, there has been a particular focus on the speci¢city of primary de¢cits, especially with respect to preserved skills in individuals with autism, but also with respect to other disorders. Thirdly, these accounts are single mechanism explanations of a complex behavioural phenotype. Neurobiological models of autism have led to much less theoretically driven research. Historically, localizing anatomical accounts have been preferred, mainly because of the need to explain symptom speci¢city and the early assumption that mental handicap was simply a consequence of whatever process had damaged the critical systems.

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