Mercadé Cerdá J M
Servicio de Neurología, Hospital Carlos Haya, Málaga.
Neurologia. 1996 Dec;11 Suppl 4:93-9.
Great progress has been made in the development of antiepileptic drugs (AEDs) from their early empirical stage until the current scientifically-founded advancement based on our greater understanding of the genesis of epilepsy. Available AEDs decrease neuronal membrane excitability, acting on ion channels or synaptic receptors. The classic AEDs act on sodium channels (phenytoin and carbamazepine); increase GABA-A receptor-mediated inhibition (benzodiazepines and barbiturates); and on T-type Ca2+ channels (sodium valproate and ethosuximide). Many patients are resistant to these AEDs. The introduction of new drugs whose mechanisms of action are not well established has improved therapeutic prospects. Four promising new AEDs are now available in many countries. Vigabatrin is an irreversible inhibitor of GABA transaminase. Lamotrigine blocks Na+ channels, thereby inhibiting the presynaptic release of excitatory neurotransmitters. Gabapentin increases GABAergic inhibition and Felbamate acts on the NMDA receptor and Na+ channels. New techniques in molecular biology are likely to facilitate the design of better AEDs.
从早期的经验性阶段到基于我们对癫痫发病机制的更深入理解而取得的当前科学依据的进展，抗癫痫药物（AEDs）的发展已经取得了巨大进步。现有的抗癫痫药物通过作用于离子通道或突触受体来降低神经元膜兴奋性。经典的抗癫痫药物作用于钠通道（苯妥英和卡马西平）；增强GABA - A受体介导的抑制作用（苯二氮䓬类和巴比妥类）；以及作用于T型钙通道（丙戊酸钠和乙琥胺）。许多患者对这些抗癫痫药物耐药。作用机制尚未完全明确的新药的引入改善了治疗前景。现在许多国家都有四种有前景的新型抗癫痫药物。氨己烯酸是GABA转氨酶的不可逆抑制剂。拉莫三嗪阻断Na +通道，从而抑制兴奋性神经递质的突触前释放。加巴喷丁增强GABA能抑制作用，非氨酯作用于NMDA受体和Na +通道。分子生物学的新技术可能会促进更好的抗癫痫药物的设计。
