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Serum autoantibodies do not differentiate PANDAS and Tourette syndrome from controls

From the Departments of Neurology (Dr. Singer, Mr. Hong, Mr. Yoon, and Mr. Williams) and Pediatrics (Dr. Singer), Johns Hopkins University School of Medicine, Baltimore, MD.

Address correspondence and reprint requests to Dr. Harvey S. Singer, Division of Pediatric Neurology, Johns Hopkins Hospital, Jefferson Street Building 124, 600 North Wolfe Street, Baltimore, MD 21287-1000; e-mail: hsinger{at}jhmi.edu

Background: An autoimmune-mediated mechanism has been proposed for both pediatric autoimmune neuropsychiatric disorder associated with streptococcal infection (PANDAS) and Tourette syndrome (TS). Confirmatory evidence has, in part, been based on controversial findings of autoantibodies in the sera of children with these disorders.

Objective: To compare antineuronal antibody profiles in subjects with TS and PANDAS to age-matched controls.

Methods: Sera were obtained from 48 children with PANDAS, 46 with TS, and 43 age-matched controls. Serum autoantibodies were measured by use of ELISA and Western immunoblotting against a variety of epitopes, including human postmortem caudate, putamen, and prefrontal cortex (Brodmann area 10). Immunoreactivity was also measured against commercially available - and -enolase, aldolase C, and pyruvate kinase M1. Several assays were repeated after preabsorption of sera with M6 strain streptococci.

Results: Median ELISA optical density readings were similar among the groups. Western blot analyses showed complex staining patterns with no differences in any tissue region based on the number of bands, reactivity peaks at molecular weights 98, 60, 45, and 40 kDa, or total area under ScanPack (Biometra, Gottingen, Germany)–derived peaks. Immunoreactivity against four putative pathologic antigens did not differentiate the clinical groups. Repeat immunoblotting after serum preabsorption with streptococci showed no loss of reactivity. ELISA values exceeding a specified cutoff did not predict changes in binding to either brain epitopes or commercial antigens.

Conclusions: Results do not support the hypothesis that PANDAS and Tourette syndrome are secondary to antineuronal antibodies. Longitudinal studies are required to determine whether autoantibodies correlate with fluctuations in clinical activity.

Editorial, see page 1688

See also pages 1730 and 1802

This article was previously published in electronic format as an Expedited E-Pub on October 5, 2005, at www.neurology.org.

Supported by grants MH61940 and NS42240 from the National Institutes of Health.

Disclosure: The authors report no conflicts of interest.

Received April 4, 2005. Accepted in final form July 19, 2005.

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