Antiseizure drugs (ASDs) prevent the occurrence of seizures; there is no evidence that they have disease-modifying properties. In the more than 160 years that orally administered ASDs have been available for epilepsy therapy, most agents entering clinical practice were either discovered serendipitously or with the use of animal seizure models. The ASDs originating from these approaches act on brain excitability mechanisms to interfere with the generation and spread of epileptic hyperexcitability, but they do not address the specific defects that are pathogenic in the epilepsies for which they are prescribed, which in most cases are not well understood. There are four broad classes of such ASD mechanisms: (1) modulation of voltage-gated sodium channels (e.g. phenytoin, carbamazepine, lamotrigine), voltage-gated calcium channels (e.g. ethosuximide), and voltage-gated potassium channels [e.g. retigabine (ezogabine)]; (2) enhancement of GABA-mediated inhibitory neurotransmission (e.g. benzodiazepines, tiagabine, vigabatrin); (3) attenuation of glutamate-mediated excitatory neurotransmission (e.g. perampanel); and (4) modulation of neurotransmitter release via a presynaptic action (e.g. levetiracetam, brivaracetam, gabapentin, pregabalin). In the past two decades there has been great progress in identifying the pathophysiological mechanisms of many genetic epilepsies. Given this new understanding, attempts are being made to engineer specific small molecule, antisense and gene therapies that functionally reverse or structurally correct pathogenic defects in epilepsy syndromes. In the near future, these new therapies will begin a paradigm shift in the treatment of some rare genetic epilepsy syndromes, but targeted therapies will remain elusive for the vast majority of epilepsies until their causes are identified.

中文翻译：

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当前使用的抗癫痫药的作用机理。

抗癫痫药（ASD）可防止癫痫发作的发生；没有证据表明它们具有改善疾病的特性。在口服给药的ASD用于癫痫治疗已有160多年的历史中，大多数进入临床实践的药物都是偶然发现的，或者是通过动物癫痫发作模型发现的。源自这些方法的ASD会作用于大脑兴奋性机制，以干扰癫痫性高兴奋性的产生和传播，但它们并未解决处方的癫痫病中的致病性特定缺陷，在大多数情况下，人们尚不了解。此类ASD机制分为四大类：（1）电压门控钠通道（例如苯妥英，卡马西平，拉莫三嗪），电压门控钙通道（例如ethosuximide）的调节，和电压门控钾通道[例如，瑞替加滨（ezogabine）]；（2）增强GABA介导的抑制性神经传递（例如苯并二氮杂，替加滨，维加巴特林）；（3）谷氨酸介导的兴奋性神经传递的减弱（如perampanel）；（4）通过突触前作用调节神经递质的释放（例如左乙拉西坦，布立西坦，加巴喷丁，普瑞巴林）。在过去的二十年中，在鉴定许多遗传性癫痫的病理生理机制方面取得了巨大进展。有了这种新的认识，人们正在尝试工程化特定的小分子，反义和基因疗法，这些疗法可以在功能上逆转或在结构上纠正癫痫综合征的致病性缺陷。在不远的将来，