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Neurological dilemma |
1 Clinical Research Fellow Department of Neurological and Psychiatric Sciences, University of Bari, Bari, Italy
2 Senior Scientist Department of Neuroinflammation, Institute of Neurology, University College London, London, UK
3 Professor of Neurology Institute of Cell and Molecular Science, Queen Mary University London, Head of Department, Department of Neurology, Barts and the London NHS Trust, London, UK
Correspondence to:
Correspondence to:
Dr G Giovannoni
Department of Neurology, Barts and the London NHS Trust, The Royal London Hospital, Whitechapel, London E1 1BB, UK; g.giovannoni@ion.ucl.ac.uk
| The first 150 words of the full text of this article appear below. |
In the last decade there has been controversy over the existence and clinical significance of autoantibodies that react with the basal ganglia, referred to as antibasal ganglia antibodies (ABGAs) (some investigators have referred to them as anti-neuronal antibodies). The spectrum of disorders associated with ABGAs has recently been widened to include several neuropsychiatric syndromes; in common is their association with recent streptococcal infection, which suggests that these syndromes are due to an aberrant immune response triggered by streptococcal infection. Like other emerging diseases it will take time to establish causation, if any, and for these disorders to be accepted as real disease entities. Because they may turn out to have a considerable clinical impact, they clearly need to be better understood, as does ABGA testing in clinical practice.
WHAT ARE ABGAS?
ABGAs are autoantibodies that cross-react with human brain tissue, with the highest binding specificity against extracts from the caudate and putamen.1 They
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