by : Uta Frith
Structural abnormalities in the brains of autistic individuals have turned up in anatomic studies and brain-imaging procedures. Both epidemiological and neuropsychological studies have demonstrated that autism is strongly correlated with mental retardation, which is itself clearly linked to physiological abnormality. This fact fits well with the idea that autism results from a distinct brain abnormality that is often part of more extensive damage. If the abnormality is pervasive, the mental retardation will be more severe, and the likelihood of damage to the critical brain system will increase. Conversely, it is possible for the critical system alone to be damaged. In such cases, autism is not accompanied by mental retardation.
Population studies carried out by Lorna Wing and her colleagues at the Medical Research Council’s Social Psychiatry Unit in London reveal that the different symptoms of autism do not occur together simply by coincidence. Three core features in particular—impairments in communication, imagination and socialization—form a distinct triad. The impairment in communication includes such diverse phenomena as muteness and delay in learning to talk, as well as problems in comprehending or using nonverbal body language. Other autistic individuals speak fluently but are overliteral in their understanding of language. The impairment in imagination appears in young autistic children as repetitive play with objects and in some autistic adults as an obsessive interest in facts. The impairment in socialization includes ineptness and inappropriate behavior in a wide range of reciprocal interactions, such as the ability to make and keep friends. Nevertheless, many autistic individuals prefer to have company and are eager to please.
The question is why these pairments, and only these, occur together. The challenge to psychological theorists
was clear: to search for a single cognitive component that would explain the deficits yet still allow for the abilities that autistic people display in certain aspects of interpersonal interactions. My colleagues at the Medical Research Council’s Cognitive Development Unit in London and I think we have identified just such a component. It is a cognitive mechanism of a highly complex and abstract nature that could be described in computational terms. As a shorthand, one can refer to this component by one of its main functions, namely, the ability to think about thoughts or to imagine another individual’s state of mind. We propose that this component is damaged in autism. Furthermore, we suggest that this mental component is innate and has a unique brain substrate. If it were possible to pinpoint that substrate—whether it is in fact an anatomical structure, a physiological system or a chemical pathway—one might be able to identify the biological origin of autism.
The power of this component in normal development becomes obvious very early. From the end of the first year onward, infants begin to participate in what has been called shared attention. For example, a normal child will point to something for no reason other than to share his interest in it with someone else. Autistic children do not show shared attention. Indeed, the absence of this behavior may well be one of the earliest signs of autism. When an autistic child points at an object, it is only because he wants it.
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