Yuksel A, Senocak D, Sozuer D, Keskin G, Dirican A, Cenani A, Yalcin E
Department of Pediatric Neurology, Istanbul University, Cerrahpasa Faculty of Medicine, Turkey.
Childs Nerv Syst. 1995 Aug;11(8):474-7. doi: 10.1007/BF00334968.
Brainstem auditory evoked potentials (BAEPs) were recorded in 18 epileptic children receiving carbamazepine and 10 epileptic children receiving valproate. BAEPs were recorded before the administration of antiepileptic drugs (AEDs) and 13 months later during which the children received AEDs. Statistical analysis of peak latencies and interpeak intervals of waves I-III-V were made. Carbamazepine treatment resulted in prolongation of peak latencies of waves I-III-V and interpeak intervals I-III and I-V. Valproate monotherapy, on the other hand, caused no consistent changes on BAEP. On the basis of these results we suggest that chronic carbamazepine therapy exerts a suppressive influence on the auditory pathways, both peripherally at the level of the cochlea and/or auditory nerve, and centrally at the brainstem.
对18名接受卡马西平治疗的癫痫儿童和10名接受丙戊酸盐治疗的癫痫儿童进行了脑干听觉诱发电位(BAEP)记录。在给予抗癫痫药物(AEDs)之前以及之后13个月(在此期间儿童接受AEDs治疗)记录BAEP。对I-III-V波的峰潜伏期和峰间间期进行了统计分析。卡马西平治疗导致I-III-V波的峰潜伏期以及I-III和I-V峰间间期延长。另一方面,丙戊酸盐单药治疗未对BAEP产生一致的变化。基于这些结果,我们认为慢性卡马西平治疗对听觉通路有抑制作用,在耳蜗和/或听神经水平的外周以及脑干水平的中枢均有影响。