Rapport R L, Ojemann G A
Arch Neurol. 1975 Aug;32(8):539-48. doi: 10.1001/archneur.1975.00490500059007.
In chronic cobalt-induced experimental epilepsy in the cat, there are alterations in behavior, electroencephalograms, and brain sodium, potassium adenosine triphosphatase (Na,K ATPase) activity. The electrographic and enzymatic changes occur both in focus and homotopic cortex, and are time related. The onset of EEG paroxysms consistently precedes increases in Na,K ATPase activity, indicating that the enzymatic change is adaptive. Prophylactic treatment with phenytoin (formerly diphenylhydantoin) prevents these chronic alterations from developing, although some early changes do occur. After the drug is withdrawn following 28 days of therapy, treated animals still demonstrate no evidence of epileptiform discharges or changes in Na,K ATPase activity, although these changes persist in untreated cats. Given properly, phenytoin may prevent alterations in brain, which can result in the formation of a hyperexcitable population of cells. These data support the efficacy of early pharmacologic prophylaxis in posttraumatic epilepsy.
在猫的慢性钴诱导实验性癫痫中，行为、脑电图以及脑钠钾三磷酸腺苷酶（Na，K ATP酶）活性会发生改变。脑电图和酶活性的变化在病灶和同位皮层均会出现，且与时间相关。脑电图阵发性发作始终先于Na，K ATP酶活性的增加，这表明酶活性的变化是适应性的。苯妥英（以前称为二苯乙内酰脲）预防性治疗可防止这些慢性改变的发展，尽管确实会出现一些早期变化。在治疗28天后停药后，接受治疗的动物仍未显示出癫痫样放电或Na，K ATP酶活性变化的证据，尽管这些变化在未治疗的猫中持续存在。如果使用得当，苯妥英可能会预防脑部改变，而脑部改变可能会导致形成过度兴奋的细胞群。这些数据支持早期药物预防在创伤后癫痫中的疗效。
