During the last decade considerable advances have been made in clinical, epidemiologic, and biologic research of autism. Although there are still no definitive answers, and an effective treatment remains elusive, these advances have provided new and important clues about etiologies and mechanisms of this disorder. The etiologies of autism are all highly likely to be neurobiologic; prenatal and perinatal events provide neither a necessary nor sufficient explanation for autism.

Autism is one of the developmental disorders of brain function, not a disease. It is a syndrome defined by a characteristic set of behaviors which include (1) qualitative impairment in reciprocal social interaction, (2) qualitative impairment of verbal and nonverbal communication and imaginative activity, and (3) a markedly restricted repertoire of activities and interests. These tend to cluster together and are associated with a more or less predictable course. As is the case with all clinically defined syndromes such as dyslexia, epilepsy, or congestive heart failure, autism does not have a single etiology. Several etiologies are already known or suspected, and it is unlikely that a single pathophysiologic mechanism will account for all the cases. It is possible, however, that these different pathologies may impinge on a particular brain system of connected regions whose dysfunction is responsible for the common behavioral syndrome that links mildly and severely affected children.

Pediatricians are likely to be the first professionals consulted by parents concerned about their child's developmental achievement. Severely deficient or aberrant developmental lags are unlikely to be overooked, but the significance of more subtle abnormalities in toddlers and preschool children and of the differential diagnosis even in overt disorders of cerebral function is often less certain.

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