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J Neurol Neurosurg Psychiatry 2002;73:121-125 doi:10.1136/jnnp.73.2.121
  • Paper

Reproductive dysfunction in women with epilepsy: recommendations for evaluation and management

  1. J Bauer1,
  2. J I T Isojärvi2,
  3. A G Herzog3,
  4. M Reuber4,
  5. D Polson5,
  6. E Taubøll6,
  7. P Genton7,
  8. H van der Ven8,
  9. B Roesing8,
  10. G J Luef9,
  11. C A Galimberti10,
  12. J van Parys11,
  13. D Flügel12,
  14. A Bergmann13,
  15. C E Elger1
  1. 1Department of Epileptology, University of Bonn, Bonn, Germany
  2. 2Department of Neurology, University of Oulu, Finland
  3. 3Harvard Neuroendocrine Unit, Beth Israel Deaconess Medical Center, Boston, Massachusetts, USA
  4. 4Department of Neurology, Leeds Teaching Hospitals, Leeds, UK
  5. 5Department of Gynaecology, Hope Hospital, Manchester, UK
  6. 6Department of Neurology, Rikshospitalet, University of Oslo, Oslo, Norway
  7. 7Centre Saint Paul, Marseille, France
  8. 8Department of Gynaecological Endocrinology, University of Bonn, Bonn, Germany
  9. 9Department of Neurology, University of Innsbruck, Innsbruck, Austria
  10. 10Epilepsy Centre, Neurological Institute “C Mondino” Foundation, Pavia, Italy
  11. 11Epilepsiecentre Kempenhaeghe, Heeze, The Netherlands
  12. 12Department of Neurology, University of Regensburg, Regensburg, Germany
  13. 13Neurologist, Neuburg/Donau, Germany
  1. Correspondence to:
 Dr J Bauer, Universitätsklinikum Bonn, Klinik für Epileptologie, Sigmund Freud Str 25, D-53105 Bonn, Germany;
 juergen.bauer{at}ukb.uni-bonn.de
  • Received 28 November 2001
  • Accepted 28 March 2002
  • Revised 15 March 2002

Abstract

Background: Epilepsy is commonly associated with reproductive endocrine disorders. These include polycystic ovary syndrome (PCOS), isolated components of this syndrome such as polycystic ovaries, hyperandrogenaemia, hypothalamic amenorrhoea, and functional hyperprolactinaemia.

Objective: To summarise the currently known relations between epilepsy and reproductive endocrine disorders.

Methods: A review of clinical experience and published reports.

Results: The most likely explanations for endocrine disorders related to epilepsy or antiepileptic drugs are: (1) a direct influence of the epileptogenic lesion, epilepsy, or antiepileptic drugs on the endocrine control centres in the brain; (2) the effects of antiepileptic drugs on peripheral endocrine glands; (3) the effects of antiepileptic drugs on the metabolism of hormones and binding proteins; and (4) secondary endocrine complications of antiepileptic drug related weight changes or changes of insulin sensitivity. Regular monitoring of reproductive function at visits is recommended, including questioning about menstrual disorders, fertility, weight, hirsutism, and galactorrhoea. Particular attention should be paid to patients on valproate and obese patients or those experiencing significant weight gain. Single abnormal laboratory or imaging findings without symptoms may not constitute a clinically relevant endocrine disorder. However, patients with these kinds of abnormalities should be monitored to detect the possible development of a symptomatic disorder associated with, for example, menstrual disorders or fertility problems.

Conclusions: If a reproductive endocrine disorder is found, antiepileptic drug treatment should be reviewed to ensure that it is correct for the particular seizure type and that it is not contributing to the endocrine problem. The possible benefits of a change in treatment must be balanced against seizure control and the cumulative side effect of alternative agents.

Footnotes

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