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Streptoccocus infection linked with Tourette's syndrome

BMJ 1998; 317 doi: (Published 04 July 1998) Cite this as: BMJ 1998;317:12
  1. Deborah Josefson
  1. San Francisco

    US researchers have uncovered evidence that Tourette's syndrome, a chronic debilitating neurological disorder, may have an immune mediated, infectious basis (Neurology 1998;50:1530-3).

    Tourette's syndrome is characterised by multiple involuntary motor and vocal tics. Additionally, copralalia, the involuntary utterance of obscenities, often shouted, may occur. Since familial clustering occurs, Tourette's is thought to be genetic in origin. An autosomal dominant mode of inheritance has been proposed, but only a small number of those who inherit a single copy of the gene ever develop the syndrome.

    Because of this discrepancy, Dr Harvey Singer and colleagues at the Johns Hopkins University School of Medicine in Baltimore, Maryland, concluded that other factors may be operating. “We think that antibodies made by the immune system in response to a bacterial infection may go on to attack brain nerve cells in a subset of children who develop Tourette's,” Dr Singer said.

    Streptococcus is suspected because there have been reports of the acute onset of Tourette's syndrome following streptococcal infections and worsening of tics in patients with Tourette's who have concurrent streptococcal infections. Moreover, another movement disorder, Sydenham's chorea, is associated with acute rheumatic fever, which has a streptococcal basis.

    The researchers tested their hypothesis by collecting blood samples from 41 children with Tourette's syndrome and 39 healthy children. The children had past evidence of streptococcal infection by serological studies.

    They then isolated antineuronal antibodies in the blood samples and tested them on basal ganglia tissue samples. The basal ganglia is an area of the brain involved in movement and is implicated in several movement disorders. Brain imaging studies had previously shown changes in the size and shape of the putamen (part of the basal ganglia) in patients with Tourette's syndrome. The new study found that patients with Tourette's had significantly higher levels of antineuronal antibodies directed against the putamen than did healthy controls. Similar levels of antibodies against two other parts of the basal ganglia—the globus pallidus and the caudate—were found in both groups of children.

    Although the latest study is intriguing, it falls short of proving a streptococcal link to Tourette's syndrome. Streptococcal infection is common in childhood, and evidence of a preceding infection cannot denote causation. Moreover, blood levels of antibodies were drawn only once during the study and a correlation of antibody expression with the severity of the symptoms was not done. The study also did not examine the effect of recent streptococcal infections on the exacerbation of symptoms.

    Dr Singer acknowledged these shortcomings and said that future studies will compare a group of patients with Tourette's syndrome who have had a recent streptococcal infection with those without evidence of recent infections and evaluate if such infection causes an exacerbation of the illness.

    In an accompanying editorial Dr Roger Kurlan of the University of Rochester School of Medicine in New York wrote: “Until such a link is confirmed, the routine testing of Tourette's patients for recent infection or for the presence of antineuronal antibodies, and a more widespread application of immune modifying therapies … does not appear to be justified.”

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