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THE CONTROVERSY OVER THE CLASSIFICATION OF GILLES DE LA TOURETTE'S SYNDROME, 1800-1995 HOWARD I. KUSHNER* and LOUISE S. KIESSLING** This paper examines the historical context for the classification of Gilles de la Tourette's syndrome as distinct from Sydenham's chorea. This separation , made most emphatically in the 1880s by the influential 19th-century neurologist Jean-Martin Charcot of the Salpêtrière hospital in Paris, was based upon observed differences in presenting symptoms. An alternative view, offered by avariety ofphysicians throughout the 19th century, focused on predisposing causes, rather than symptom manifestations. Those who emphasized an etiological perspective refused to accept Charcot's classificatory distinctions. Rather, these physicians insisted that Sydenham's chorea and Tourette's syndrome displayed a number of similarities that pointed to the conclusion that both were most likely variations ofa common neurobiological mechanism. This latter view is remarkably similar to our recent clinical findings. A number of obstacles, however, have made it difficult for many current researchers to rethink the possible etiological similarities between Tourette's syndrome and Sydenham's chorea. We believe that the reasons are as much historical as clinical, and that a historical perspective calls into question the diagnostic and clinical benefits of always viewing these disorders as distinct entities. In what follows, we focus on the history of the separation of Tourette's syndrome from chorea. We explore the extent to which this separation has been informed by the emphasis on the classification of childhood movement disorders by their symptoms, that is as syndromes, rather than by possible common underlying pathologies. Although we are personally inThis paper has been supported by Humanities, Science, & Technology Grant RH-21165, from the National Endowment for the Humanities. All translations from French are the authors '. *Department of History, San Diego State University, San Diego, CA 92182. **Department of Pediatrics, Brown University School of Medicine, Memorial Hospital of Rhode Island, Pawtucket, RI 02860.© 1995 by The University of Chicago. All rights reserved. 0031-5982/95/3804-0936$01.00 Perspectives in Biology and Medicine, 39, 3 · Spring 1996 409 volved in this research [1] , our purpose in this paper is not to make specific clinical claims. Rather, we point out the extent to which adherence to the classificatory boundaries established in the late 19th century has framed current clinical thinking, inhibiting consideration of alternative causal explanations (in the sense of predisposing co-factors) for childhood movement disorders and obsessive compulsive behaviors. The Possible Role of GABHS In 1956, Angelo Taranta and Gene H. Stollerman established the connection between the onset of Sydenham's chorea, a disorder in which the afflicted manifest a ceaseless occurrence of a wide variety of rapid, jerky, butwell-coordinated involuntary movements, and prior "rheumatological'' infections [2]. Taranta and Stollerman's conclusion, a connection which others had remarked on for more than a century and a half, was based on a prospective study that had followed a group of children admitted for convalescent treatment for acute rheumatic fever. All the children initially displayed a high elevation of antibacterial titers, namely anti-Group A betahemolytic streptococcus (GABHS). Later, when Sydenham's chorea appeared , only four of 10 children still had an elevated antistreptococcal titer. Thus, Taranta and Stollerman had documented the time-course and association between the prior throat infection and the late sequellea of a movement disorder. Subsequent studies have shown that anywhere from 20 to 40 percent of children with documented acute rheumatic fever eventually develop Sydenham's chorea. On the other hand, there is also a percentage of children who never show evidence of acute carditis but do present with Sydenham's chorea at any time up to nine months after a significant streptococcal infection. This later group, as Gunnar Husby and his colleagues demonstrated in 1976, may present only with a movement disorder [3, 4]. Husby's findings also had implicated the basic mechanisms of antigenantibody response. In this case, antibodies which were released to attack the invading GABHS also attacked similar sites on proteins (called epitopes) in the body's own cells—in the case of Sydenham's chorea, cells in the basal ganglia area of the brain. That both the bacteria and a human cell can...


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