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Neurobiology of neuropathic pain: mode of action of anticonvulsants

Authors

  • Anthony H. Dickenson PhD,

    Corresponding author
    1. Department of Pharmacology, University College London, London, UK
      Professor of Neuropharmacology, Department of Pharmacology, University College London, Gower Street, London WC1E 6BT UK. Tel: +44 171 419 3742; Fax: +44 171 380 7298; E-mail: anthony.dickenson@ucl.ac.uk
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  • Elizabeth A. Matthews,

    1. Department of Pharmacology, University College London, London, UK
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  • Rie Suzuki

    1. Department of Pharmacology, University College London, London, UK
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Professor of Neuropharmacology, Department of Pharmacology, University College London, Gower Street, London WC1E 6BT UK. Tel: +44 171 419 3742; Fax: +44 171 380 7298; E-mail: anthony.dickenson@ucl.ac.uk

Abstract

Anticonvulsants are widely used for the treatment of neuropathic pain. Here we review the evidence for a number of peripheral and central changes after nerve injury that may provide a basis for the mechanisms of action of anticonvulsant therapies. The roles of sodium channels, calcium channels, and central glutamate mechanisms are emphasized as the main targets for anticonvulsant drugs in neuropathic pain states. The focus of this article is on anticonvulsants; however, opioids and antidepressants can also be effective in increasing inhibitions to control of pain in a manner similar to that of the enhancement of γ-aminobutyric acid (GABA) function by antiepileptic drugs. A brief account of these approaches to neuropathic pain is also given. © 2002 European Federation of Chapters of the International Association for the Study of Pain

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