Despite strong evidence of the importance of hereditary factors in the etiology of Tourette's syndrome (TS), research findings have consistently pointed to a role of environmental influences. A recent line of research has suggested that tic disorders and associated behavioral disturbances, such as obsessive-compulsive disorder, might develop following streptococcal infection by the process of molecular mimicry, whereby antibodies directed against bacterial antigens cross-react with brain targets. Such investigations have given rise to the notion that there is a spectrum of childhood neurobehavioral disorders (termed pediatric autoimmune neuropsychiatric disorders associated with streptococcal infection [PANDAS]) that arise by postinfectious autoimmune mechanisms. This article reviews research results supporting the concept of PANDAS and discusses their limitations. Well-designed and adequately controlled studies are needed to determine whether there is a true etiologic relation between streptococcal infection and the onset or exacerbation of childhood neuropsychiatric disorders and whether the use of immune-modifying therapies for these conditions is rational.
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Roger Kurlan (1998) studied this question.
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