Role of Autoimmunity and Infections in Tourette Syndrome

Abstract

Tourette's syndrome (TS) is characterized by the presence of both motor and vocal tics. The classically proposed autoimmunity model of TS is analogous to Sydenham's chorea. Per this model, tics and associated phenomena are thought to arise as a consequence of the immunological response to infections with group A beta hemolytic streptococci (GABHS). Antibodies directed against the streptococci are thought to cross-react with structures of the central nervous system, subsequently leading to damage to these structures, which eventually is thought to result in tics and associated features. Autoimmunity in TS may be triggered by infections. Relatively good evidence is available about a possible association of streptococcal infections with TS. The available evidence seems to suggest that patients with TS are more susceptible to infections. Most evidence points to more frequent streptococcal infections. Moreover animal studies have quite convincingly demonstrated that immunization with streptococcal antigens or transfer of antibodies evoked through immunization can indeed lead to tics. Also, there is also some indication about the possible involvement of non-streptococcal infections, including common viral infections, in exacerbations of tic disorders. Why would there be more frequent infections in patients with TS? Some studies have pointed to altered immune functioning as potential explanations, which might induce antineuronal autoantibodies. Animal models have quite convincingly pointed to the pathogenic relevance of infection-induced antineuronal antibodies. Obviously, standardization of assays in human sera should be next important steps to further our understanding of the role of antineuronal antibodies in TS. (PsycInfo Database Record (c) 2022 APA, all rights reserved)