A transcranial magnetic stimulation paired-pulse paradigm was used to determine that cortical excitability was less during the late luteal phase than in the early follicular phase in a woman with epilepsy who had premenstrual seizure exacerbation. The data are consistent with the possibility that a reduction in GABA-mediated cortical inhibitory activity may be responsible. The administration of progesterone, a reproductive steroid with potent GABAergic metabolites, during the luteal phase restored cortical excitability to normal range.