Ramirez J A, Mendell J R, Warmolts J R, Griggs R C
Ann Neurol. 1986 Feb;19(2):162-7. doi: 10.1002/ana.410190209.
Phenytoin has been implicated as a causative agent in peripheral neuropathy, although structural changes in nerve have not been characterized. A 47-year-old man was seen with clinical and electrophysiological signs of peripheral neuropathy after 30 years of phenytoin administration. Despite a modest dose of phenytoin (300 mg/day) blood levels were 31 to 38 micrograms/ml. A sural nerve biopsy showed a loss of large myelinated nerve fibers and a nonrandom clustered distribution of segmental demyelination and remyelination. The latter findings were accompanied by axonal shrinkage. Sixteen months after phenytoin was stopped, the patient's clinical and electrophysiological findings reflected improvement. These data indicate that long-term phenytoin administration can cause a reversible neuropathy characterized by axonal shrinkage and secondary demyelination.
苯妥英已被认为是周围神经病变的致病因素，尽管神经的结构变化尚未明确。一名47岁男性在服用苯妥英30年后出现了周围神经病变的临床和电生理体征。尽管苯妥英剂量适中（300毫克/天），但其血药浓度为31至38微克/毫升。腓肠神经活检显示有大量有髓神经纤维缺失，节段性脱髓鞘和再髓鞘化呈非随机的簇状分布。后一发现伴有轴突萎缩。停用苯妥英16个月后，患者的临床和电生理表现有所改善。这些数据表明，长期服用苯妥英可导致一种以轴突萎缩和继发性脱髓鞘为特征的可逆性神经病变。
