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Botulinum Toxin for Focal Dystonia
  1. Nigel Hyman
  1. Department of Neurology, Radcliffe Infirmary, Woodstock Road, Oxford; E-mail: nigel.hyman{at}


It is a truth universally acknowledged that neurology outpatients are stimulating, challenging and varied. It is a truth less universally acknowledged that patients with severe epilepsy continue to have severe epilepsy, advanced Parkinson’s disease patients get worse, and patients with chronic daily headaches are untreatable. In contrast, patients who attend botulinum toxin clinics demonstrably improve with successive treatments. In addition, their complaints are unusual and fascinating – a perfect clinic for the general neurologist!


The primary action of botulinum toxin is to block acetylcholine release at the neuromuscular junction and so produce muscle weakness. However, the therapeutic effect is often greater than predicted, suggesting additional mechanisms. The drug is taken up preferentially by the most active nerve terminals and so the actively contracting muscle fibres are weakened while the strength in other fibres in the same muscle is preserved. Indeed patients commonly notice that

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