Department of Neuroscience and Experimental Therapeutics, College of Medicine, Texas A&M Health Science Center, 8447 State Highway 47, MREB Building, Bryan, TX 77807, USA.
Horm Behav. 2013 Feb;63(2):254-66. doi: 10.1016/j.yhbeh.2012.04.016. Epub 2012 May 2.
This review describes the neuroendocrinological aspects of catamenial epilepsy, a menstrual cycle-related seizure disorder in women with epilepsy. Catamenial epilepsy is a multifaceted neuroendocrine condition in which seizures are clustered around specific points in the menstrual cycle, most often around perimenstrual or periovulatory period. Three types of catamenial seizures (perimenstrual, periovulatory and inadequate luteal) have been identified. The molecular pathophysiology of catamenial epilepsy remains unclear. Cyclical changes in the circulating levels of estrogens and progesterone (P) play a central role in the development of catamenial epilepsy. Endogenous neurosteroids such as allopregnanolone (AP) and allotetrahydrodeoxycorticosterone (THDOC) that modulate seizure susceptibility could play a critical role in catamenial epilepsy. In addition, plasticity in GABA-A receptor subunits could play a role in the enhanced seizure susceptibility in catamenial epilepsy. P-derived neurosteroids such as AP and THDOC potentiate synaptic GABA-A receptor function and also activate extrasynaptic GABA-A receptors in the hippocampus and thus may represent endogenous regulators of catamenial seizure susceptibility. Experimental studies have shown that neurosteroids confer greater seizure protection in animal models of catamenial epilepsy, especially without evident tolerance to their actions during chronic therapy. In the recently completed NIH-sponsored, placebo controlled phase 3 clinical trial, P therapy proved to be beneficial only in women with perimenstrual catamenial epilepsy but not in non-catamenial subjects. Neurosteroid analogs with favorable profile may be useful in the treatment of catamenial epilepsy.
这篇综述描述了月经性癫痫的神经内分泌方面，这是一种与女性癫痫相关的月经周期相关的癫痫发作障碍。月经性癫痫是一种多方面的神经内分泌疾病，其发作集中在月经周期的特定时间点，最常见的是围经期或围排卵期。已经确定了三种月经性发作（围经期、围排卵期和黄体不足）。月经性癫痫的分子病理生理学仍不清楚。雌激素和孕激素（P）的循环水平周期性变化在月经性癫痫的发生中起核心作用。调节癫痫易感性的内源性神经甾体如别孕烯醇酮（AP）和全四氢去氧皮质酮（THDOC）可能在月经性癫痫中起关键作用。此外，GABA-A 受体亚基的可塑性可能在月经性癫痫的增强癫痫易感性中起作用。P 衍生的神经甾体如 AP 和 THDOC 增强突触 GABA-A 受体功能，并且还在海马中激活 extrasynaptic GABA-A 受体，因此可能代表月经性癫痫易感性的内源性调节剂。实验研究表明，神经甾体在月经性癫痫的动物模型中提供了更大的癫痫保护作用，特别是在慢性治疗期间对其作用没有明显的耐受性。在最近完成的 NIH 赞助的、安慰剂对照的 3 期临床试验中，P 治疗仅对围经期月经性癫痫患者有益，而非月经性患者无益。具有良好特征的神经甾体类似物可能对月经性癫痫的治疗有用。
