ABSTRACT
Gonadal and adrenal steroids have a pivotal role in a wide range of behavioral phenomena such as sexual behavior and aggression, impregnation, pregnancy, birth, maternal behavior, anxiety, sleep, coordination of the neuroendocrine response to stress, and adaptation to environmental challenges. They play a key role in the regulation of cell development, conservation of body sodium and carbohydrate metabolism, and so forth. The failure of any or several of these functions may be sufficient to contribute to epilepsy. By the same token, many of them might be conceived of as being a part of an endogenous machinery directed at stabilizing brain reactivity. Among the more celebrated examples are the proconvulsant potency of estrogens, as well as certain anticonvulsive influences of progesterone and deoxycorticosterone metabolites that were long reproduced in experimental animals (Heuser, Ling, & Buchwald, 1965; Michael, 1965; Timiras, 1969; Woodbury, 1952; Woolley & Timiras, 1962a, 1962b). There are numerous indications of a cyclic exacerbation of adverse emotional disturbances, somatic discomfort, and seizures in females known as catamenial epilepsy (New-mark & Penry, 1980; Schechter, chapter 7, this volume). The enhanced photo-sensitivity and episodes of petit mal epilepsy also are occasionally subject to catamenial exacerbations (Newmark & Penry, 1979), thereby suggesting the contribution of the ovarian steroids (Rosciszewska, Buntner, Guz, & Zawisza, 1986). Yet, until very recently, no firm conclusion could be drawn regarding the nature of these effects.
