Dictionary of Biological Psychology
A developmental disorder characterized by impairments in social, imaginative and communicative functions, with restricted repetitive interests and activities. Qualitative impairments are evident by age three, although diagnosis often occurs much later. Since the manifestation of these impairments changes with age, and varies among individuals, autism is sometimes conceptualized as a spectrum. Prevalence is estimated at 4–10 per 10 000, according to the breadth of definition used. Males outnumber females by 3 to 1, and among high-functioning individuals by at least 5 to 1. The disorder is accompanied by general developmental delay/low INTELLIGENCE QUOTIENT (IQ) in perhaps three-quarters of cases, and by EPILEPSY in at least a third. These facts, among others, have argued against the PSYCHOGENIC view of autism as caused by ‘refrigerator parenting’, an outdated view now abandoned in favour of a biological explanation. Indeed, signs of social peculiarity in parents of children with autism may be results rather than causes of the child’s disorder, or may be signs of the ‘extended phenotype’ of autism, which appears to have a significant genetic component. Concordance rates for MONOZYGOTIC TWINS may be between 30 and 90%, according to the breadth of definition used, compared with a concordance for DIZYGOTIC TWINS of 0–10%. Siblings show a risk of autism at least 50 times that of the normal population. Current research appears to support a multiplicative multilocus model of inheritance. Obstetric complications, which are common in autism, are thought to be the result, rather than cause, of the child’s abnormalities.
The brain basis of autism is as yet unclear, with candidate regions including the CEREBELLUM, LIMBIC SYSTEM and FRONTAL LOBE being actively researched. In vivo and pathological anatomical studies, biochemical and electrophysiological investigations have provided some suggestive findings, but results have often remained unreplicated, and in many cases show abnormalities unlikely to be either specific or universal to autism.
Functional brain imaging investigations have only just begun and may prove useful. At present there is no specific drug treatment for autism but, in the absence of a ‘cure’, well-informed education and management achieves significant improvements.
More progress has been made in understanding the nature of the cognitive deficits in autism. A challenge here has been to explain why social, communication and imagination deficits should go together (often referred to as WING’S TRIAD, following epidemiological work by Wing and Gould which established this co-occurrence), and why other functions (for instance spatial skills, rote MEMORY) are often intact or even superior in autism. A currently influential hypothesis is that people with autism lack THEORY OF MIND—that is, they are unable to represent mental states (see METAREPRESENTATION), and fail to recognize the thoughts and feelings of those around them. Children with autism fail to show behaviours which require theory of mind (understanding deception, or keeping secrets for example), although other social abilities may be intact (such as attachment to parents). The earliest manifestation of this ‘mind-blindness’ may be a lack of pretend play, gaze following and joint attention at 18 months. The theory-of-mind account of autism has led to progress in early identification of autism, attempts to teach social insight, and FUNCTIONAL NEUROIMAGING of the regions normally involved in mental state attribution. Some people with autism, especially those with ASPERGER’S SYNDROME, who fall at the able end of the spectrum, do pass tests of theory of mind, though typically they are delayed by many years and appear to have developed alternative strategies for social insight.
Autism is characterized by a range of non-social symptoms which defy explanation in terms of theory of mind; motor stereotypies (see STEREOTYPY), obsessive interests, repetitive behaviours, savant skills (see IDIOT SAVANT), markedly uneven IQ sub-test profile, fragmented and anomalous perceptual experiences. Failures of inhibition, and a tendency to perseverate (see PERSEVERATION) as well as difficulties in planning and monitoring behaviour, have led to the suggestion that impaired EXECUTIVE FUNCTION (due perhaps to frontal lobe damage) might explain social and non-social handicaps in autism. The only current theory attempting to explain autistic skills and preserved abilities is the notion that people with autism have a different information processing style—referred to as weak ‘CENTRAL COHERENCE’—with a processing preference for parts over wholes, and an ability to process information piecemeal independent of context. Research on autism (theory of mind, executive functions and coherence) has had significant influence on current theories of normal cognition.
References
Bailey A., Phillips W. & Rutter M. (1996) Autism: towards an integration of clinical, genetic, neuropsychological, and neurobiological perspectives. Journal of Child Psychology and Psychiatry 37:89–126.
Happé, F. (1994) Autism: An Introduction to Psychological Theory, Harvard University Press: Cambridge MA.
FRANCESCA G.HAPPÉ
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