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The need for caution in considering the diagnostic utility of antibasal ganglia antibodies in movement disorders
  1. H S Singer,
  2. J J Hong,
  3. C A Rippel,
  4. C A Pardo
  1. Department of Neurology, Johns Hopkins University School of Medicine, Jefferson Street Building 124, 600 N Wolfe Street, Baltimore, MD, USA
  1. Correspondence to:
    Dr H S Singer
    Division of Pediatric Neurology, Johns Hopkins Hospital, Jefferson Street Building 124, 600 N Wolfe Street, Baltimore, MD 21287-1000, USA; hsingerjhmi.edu

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Commentary on the paper by Church et al (see page 611)

“Now this is not the end. It is not even the beginning of the end. But it is, perhaps, the end of the beginning.” (Sir Winston Churchill, Speech in November 1942)

In this issue, Church and colleagues discuss the possibility that immunological analyses of sera could serve as diagnostic markers for movement disorders associated with streptococcal infection.1 These investigators have been at the forefront of studies evaluating antibasal ganglia antibodies (ABGA) in a variety of proposed poststreptococcal movement conditions. These studies have great potential, given that identification of a specific immune mechanism could lead to insights into pathophysiological mechanisms as well as the development of new therapies. Nevertheless, based on ongoing studies in our laboratory, we feel compelled to raise concerns about the reproducibility of ABGA results, about methodology, and about the inability to confirm serum microinfusion induced alterations of rodent behaviour. As described in the quotation from the wise leader and historian Winston Churchill, we believe that whereas important initial steps have been taken, the final solution has not been reached. The goal of this commentary is not to criticise existing reports, but to identify disparities in data and to emphasise the need for additional testing, before implementing ABGA screening for children with movement disorders.

HYPOTHESIS AND REQUIREMENTS FOR CONFIRMATION

In susceptible individuals, antibodies produced against the group A β haemolytic streptococcus (GABHS) cross-react with epitopes on neurones located in the basal ganglia, through a process of molecular mimicry, and cause movement abnormalities (chorea, tics, other).

IAcceptance of the aforementioned poststreptococcal autoimmune hypothesis requires confirmation on two major levels: (1) epidemiological evidence showing a clear association between streptococcal infection and movement disorders; and (2) definitive evidence for an autoimmune mechanism. Since the focus of this commentary is on laboratory based approaches, …

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