Drug Resistance in Epilepsy: Human Epilepsy

  1. Gregory Bock and
  2. Jamie A. Goode
  1. S. M. Sisodiya1,
  2. W.-R. Lin2,
  3. B. N. Harding3,
  4. M. V. Squier4 and
  5. M. Thom2

Published Online: 7 OCT 2008

DOI: 10.1002/0470846356.ch12

Mechanisms of Drug Resistance in Epilepsy: Novartis Foundation Symposium 243

Mechanisms of Drug Resistance in Epilepsy: Novartis Foundation Symposium 243

How to Cite

Sisodiya, S. M., Lin, W.-R., Harding, B. N., Squier, M. V. and Thom, M. (2002) Drug Resistance in Epilepsy: Human Epilepsy, in Mechanisms of Drug Resistance in Epilepsy: Novartis Foundation Symposium 243 (eds G. Bock and J. A. Goode), John Wiley & Sons, Ltd, Chichester, UK. doi: 10.1002/0470846356.ch12

Author Information

  1. 1

    Epilepsy Research Group, University Department of Clinical Neurology, University College London, Queen Square, London, UK

  2. 2

    Department of Neuropathology, Institute of Neurology, University College London, Queen Square, London, UK

  3. 3

    Department of Neuropathology, Institute of Child Health, University College London, Queen Square, London, UK

  4. 4

    Department of Neuropathology, Radcliffe Infirmary, Oxford, UK

Publication History

  1. Published Online: 7 OCT 2008
  2. Published Print: 25 MAR 2002

Book Series:

  1. Novartis Foundation Symposia

Book Series Editors:

  1. Novartis Foundation

ISBN Information

Print ISBN: 9780470841464

Online ISBN: 9780470846353

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Summary

The basis of drug resistance in human epilepsy is not understood. Parallels with resistance in cancer suggest that drug resistance proteins may have a role. To examine this possibility, we have studied human brain tissue containing pathologies capable of causing refractory epilepsy. Using immunohistochemistry for P glycoprotein (Pgp) and multidrug resistance-associated protein 1 (MRP1), we examined both pathological tissue and control tissue. We demonstrate expression of Pgp and MRP1 in glia from cases of malformation of cortical development studied both before and after the onset of epilepsy, as well as in cases of hippocampal sclerosis and dysembryoplastic neuroepithelial tumours. In one particular type of malformation, we also demonstrate that dysplastic neurons express MRP1. The pattern of immunolabelling suggests overexpression is concentrated particularly around vessels in most of the pathologies. The timing shows that expression may be constitutive in some pathologies. These findings suggest that drug resistance proteins may contribute to drug resistance in refractory epilepsy.