Conversion of testosterone to estradiol Aromatase converts androstenedione to estrone Progesterone The major gonadal hormones: estrogen, progesterone, and testosterone, their levels vary greatly during the menstrual cycle, and this can trigger<unk> . These hormones are synthesized in various locations in the body, including the ovaries, adrenal gland, liver, subcutaneous fat, and brain. There is considerable research showing that these steroidal hormones are important in the pathophysiology of<unk> . Broadly defined, estrogen and its many forms are thought to be “proconvulsant,” whereas progesterone is thought to be “anticonvulsant” by virtue of its conversion to the neurosteroid allopregnanolone. Estrogen (estradiol, estrone, estriol) Estrogen can be found in the female body in various forms, all of which affect women with<unk> . Estrone (E1), estradiol (E2), and estriol (E3) are the three principal circulating estrogens in the body. These three forms influence neuronal excitability, but very little is known about their inter-hormone interactions, the relative concentrations and ratios of E1/E2/E3 and how that may influence the seizure frequency behavior in women with<unk> . In normally menstruating women, serum estradiol levels are typically present by day 10 of the menstrual cycle, and persist until ovulation. * Estrone’s main source is adipose tissue (subcutaneous fat), where it is formed by aromatization of androstenedione. Estrone is the major estrogen after menopause, and this hormone may be very influential in seizure control of the<unk>  woman if she is severely overweight or obese. * Estradiol represents the most prolific estrogen ligand receptor in the female body, particularly in non-pregnant females, and is a more effective activator of estrogen receptor function than estrone or estriol. Estradiol directly increases NMDA mediated receptors of glutamate activity at the neuronal membrane. Through this mechanism hippocampal pyramidal neurons CA1 are excited, and a repetitive firing response is induced. Dendritic spine density on CA1 hippocampal pyramidal cells is dependent upon estradiol levels, showing a direct correlation during normal fluctuations during the menstrual cycle. Estradiol has been shown to apply its effects on dendritic spine density of hippocampal cells by using a mechanism that requires activation of NMDA receptors. Furthermore, Herzog postulates that, “estradiol may thus further increase excitatory input to the CA1 neurons.” Through many animal models, as well as human-use of estrogen-based hormone replacement therapy, estrogens have been seen to increase the excitability of neurons, leading to a decreased seizure threshold. In female adult rat experimental trials, the limbic seizure threshold fluctuates inversely to estradiol levels during the estrous cycle. * Estriol is known to inhibit GABA and to promote kindling and epileptiform discharges. Estriol is only produced in significant quantities during pregnancy via placental aromatization of fetal androgen, however it can also be synthesized in smaller quantities (non-pregnancy) in the liver by hydroxylation of estrone. Progesterone Progesterone levels during the menstrual cycle. In general, progesterone administration is anticonvulsant, supported by experiments in laboratory animals, where injection of progesterone leads to a decrease in seizure threshold, or delay to the onset of seizures induced by convulsants. Similar to estrogen, progesterone receptors bind several molecules other than only progesterone. Progestogens are group of natural non-synthetic hormones, including progesterone, which binds to progesterone receptors. Other than progesterone, progestogens have several neuroactive metabolites, most notably allopregnanolone. Progesterone has been shown to lower the number of estrogen receptors, and thus act as an antagonist to estrogen actions. In trials, both progesterone and allopregnanolone administration have shown a neuroprotective effect on hippocampal neurons in seizure models induced by kainic acid.
Catamenial epilepsy
Rolandic epilepsy
Musicogenic epilepsy
Frontal lobe epilepsy
Childhood absence epilepsy
Northern epilepsy syndrome
Temporal lobe epilepsy
Progressive myoclonus epilepsy