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首页> 外文期刊>CNS drug reviews >Ethosuximide: from bench to bedside.
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Ethosuximide: from bench to bedside.

机译：乙草胺：从长凳到床头。

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Ethosuximide, 2-ethyl-2-methylsuccinimide, has been used extensively for "petit mal" seizures and it is a valuable agent in studies of absence epilepsy. In the treatment of epilepsy, ethosuximide has a narrow therapeutic profile. It is the drug of choice in the monotherapy or combination therapy of children with generalized absence (petit mal) epilepsy. Commonly observed side effects of ethosuximide are dose dependent and involve the gastrointestinal tract and central nervous system. Ethosuximide has been associated with a wide variety of idiosyncratic reactions and with hematopoietic adverse effects. Typical absence seizures are generated as a result of complex interactions between the thalamus and the cerebral cortex. This thalamocortical circuitry is under the control of several specific inhibitory and excitatory systems arising from the forebrain and brainstem. Corticothalamic rhythms are believed to be involved in the generation of spike-and-wave discharges that are the characteristic electroencephalographic signs of absence seizures. The spontaneous pacemaker oscillatory activity of thalamocortical circuitry involves low threshold T-type Ca2+ currents in the thalamus, and ethosuximide is presumed to reduce these low threshold T-type Ca2+ currents in thalamic neurons. Ethosuximide also decreases the persistent Na+ and Ca2+ -activated K+ currents in thalamic and layer V cortical pyramidal neurons. In addition, there is evidence that in a genetic absence epilepsy rat model ethosuximide reduces cortical gamma-aminobutyric acid (GABA) levels. Also, elevated glutamate levels in the primary motor cortex of rats with absence epilepsy (but not in normal animals) are reduced by ethosuximide.
机译：乙乙酰亚胺，2-乙基-2-甲基琥珀酰亚胺，已被广泛用于“小发作”，在无癫痫研究中它是一种有价值的药物。在癫痫的治疗中，乙琥胺的治疗范围狭窄。在患有广泛性失神（小发作）癫痫的儿童的单一疗法或联合疗法中，它是选择的药物。普遍观察到的乙氧嘧啶副作用是剂量依赖性的，并涉及胃肠道和中枢神经系统。乙乙酰亚胺与多种特异反应和造血不良反应有关。丘脑和大脑皮层之间复杂的相互作用会导致典型的失神发作。丘脑皮质回路在由前脑和脑干引起的几种特定的抑制性和兴奋性系统的控制下。皮层丘脑节律被认为与尖峰和波放电的产生有关，而尖峰和波放电是失神发作的特征性脑电信号。丘脑皮质电路的自发性起搏器振荡活动涉及丘脑中的低阈值T型Ca2 +电流，而乙巯乙酰亚胺被认为可降低丘脑神经元中的这些低阈值T型Ca2 +电流。依索舒米特还降低丘脑和V层皮质锥体神经元中持久的Na +和Ca2 +激活的K +电流。此外，有证据表明，在遗传性癫痫大鼠模型中，乙琥胺可降低皮质γ-氨基丁酸（GABA）水平。同样，乙氧嘧啶可减少无癫痫病大鼠的原发性运动皮层中谷氨酸水平的升高（但在正常动物中则不会）。

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