Antistriatal Antibodies in Tourette Syndrome: Not a Simple Story
Abstract & Commentary
Source: Wendlandt JT, et al. J Neuroimmunol. 2001;119: 106-113.
Tourette syndrome (TS), the most common movement disorder in childhood, is a complex neuropsychiatric disorder. Recent suggestive evidence suggests the potential role of autoimmune mechanisms in TS (for review, see Trifiletti R, Packard AM. Child Adolesc Psychiatr Clin N Am. 1999;8:767). A prominent suggestive piece of data is the identification of a subset of patients with TS who appear to have symptoms triggered or at least temporally correlated to Group A beta-hemolytic streptococcal infection (the so-called PANDAS subgroup), similar to Sydenham’s chorea. Evidence has also included the finding of serum antibodies against human basal ganglia in patients with TS (Singer HS, et al. Neurology. 1998;50:1618-1624; Trifiletti R, et al. Ann Neurol. 1998;561), analogous to Sydenham’s chorea.
Wendlandt and colleagues extend these observations using powerful statistical techniques to assess the "difference" between serum antibodies directed against human brain and muscle antigens. They compared 20 children with long-standing TS (mean age at onset 6.6 years, mean age in study 10.7 years) to 21 children without such diagnosis, a diagnosis of obsessive-compulsive disorder, or attention deficit disorder with hyperactivity. The TS patients were not specifically selected or assessed with respect to potential streptococcal trigger, but patients with a prior diagnosis of Sydenham chorea were excluded. Wendlandt et al found that the "repertoire" of serum antibodies against human striatal antigens showed prominent and statistically significant differences between TS and controls. The "repertoire" involved many antigens, but was highly reproducible within a given patient. The antibody repertoire against human globus pallidus and human muscle did not show such differences. The technique did not identify "specific" bands which seem to be associated with TS, in contrast to prior studies that used simple visual analysis. (Singer HS, et al. Neurology. 1998;50:1618-1624; Trifiletti R, et al. Ann Neurol. 1998;561). This suggested that 83-, 60-, and 67-kilodalton targets may be prominent candidate autoantigens.
Commentary
This report is significant because it uses a rigorous and highly objective analysis of gel immunoblot data to demonstrate a consistent pattern of serum autoantibodies against human striatum in patients with TS. This adds further evidence that suggests the striatum is the target of a putative autoimmune response. It was disappointing that no one protein in a complex immunoblot pattern emerged as a dominant autoantigen that provides a clue to the pathophysiology of this condition. The likelihood of a simple serum-based immunological "test" for TS seems remote. —Rosario Trifiletti
Trifiletti, MD, PhD, Assistant Professor, Neurology and Pediatrics, New York Presbyterian Hospital-Cornell Campus, is Assistant Editor of Neurology Alert.
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