3. Neurosteroid Influences on Neuronal Excitability

The Menstrual Cycle and Catamenial Epilepsy as Dynamic Models

  1. Cynthia L. Harden MD Professor of Neurology2,
  2. Sanjeev V. Thomas MD, DM Professor of Neurology3 and
  3. Torbjörn Tomson MD, PhD Professor of Neurology and Epileptology4
  1. Doodipala Samba Reddy

Published Online: 24 JAN 2013

DOI: 10.1002/9781118531037.ch3

Epilepsy in Women

Epilepsy in Women

How to Cite

Reddy, D. S. (2013) Neurosteroid Influences on Neuronal Excitability, in Epilepsy in Women (eds C. L. Harden, S. V. Thomas and T. Tomson), John Wiley & Sons, Oxford. doi: 10.1002/9781118531037.ch3

Editor Information

  1. 2

    Chief, Division of Epilepsy and Electroencephalography, Hofstra North Shore-LIJ School of Medicine, Cushing Neuroscience Institutes, Brain and Spine Specialists, North Shore-Long Island Jewish Health System, Great Neck, New York, USA

  2. 3

    Department of Neurology, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Trivandrum, Kerala State, India

  3. 4

    Karolinska Institutet, Stockholm, Sweden

Author Information

  1. Department of Neuroscience and Experimental Therapeutics, College of Medicine, Texas A&M Health Science Center, Bryan, Texas, USA

Publication History

  1. Published Online: 24 JAN 2013
  2. Published Print: 11 MAR 2013

ISBN Information

Print ISBN: 9780470672679

Online ISBN: 9781118531037



  • allopregnanolone;
  • catamenial;
  • epilepsy;
  • GABA-A receptor;
  • neurosteroid


This chapter highlights the role of steroid hormones and neurosteroids in catamenial epilepsy. Catamenial epilepsy is the cyclical occurrence of seizure exacerbations during particular phases of the menstrual cycle in women with epilepsy. The molecular mechanisms underlying catamenial seizures are largely unknown. Ovarian cycle-related fluctuations in steroid hormones, especially progesterone-derived GABA-A receptor-modulating anticonvulsant neurosteroids such as allopregnanolone and allotetrahydrodeoxycorticosterone (THDOC), play a significant role in the pathophysiology of catamenial epilepsy. These neurosteroids enhances synaptic and extrasynaptic GABA-A receptor-mediated inhibition. We have investigated the possibility that plasticity of GABA-A receptor subunits could play a role in catamenial epilepsy. We have shown that neurosteroids confer greater seizure protection in animal models of catamenial epilepsy, which is consistent with the efficacy of progesterone in women with perimenstrual catamenial epilepsy. Synthetic neurosteroid analogs or TSPO ligands with favorable profile may show promise in the treatment of catamenial epilepsy.