Japaridze G, Kvernadze D, Geladze T, Kevanishvili Z
Institute of Clinical and Experimental Neurology, Tbilisi, Republic of Georgia.
Epilepsia. 1993 Nov-Dec;34(6):1105-9. doi: 10.1111/j.1528-1157.1993.tb02141.x.
Auditory brainstem responses, middle-latency responses, and slow cortical potentials (ABRs, MLRs, SCPs) were recorded in 21 epileptic patients before and during treatment with carbamazepine (CBZ). The peak-latencies, interpeak intervals, and amplitudes were estimated and evaluated statistically. CBZ monotherapy resulted in prolongation of peak latencies of ABR waves I, III, and V as well as of interpeak intervals I-III and I-V. A significant increase in the peak-latencies of MLR components Na, Pa, and Nb and of interpeak intervals V-Pa and Na-Nb was also observed along with the systematic NaPa amplitude reduction. CBZ also prolonged the peak-latencies of SCP components P1 and N1. Based on the obtained results, we suggest that CBZ exerts suppressive influences both on modally specific (lemniscal) and modally nonspecific (extralemniscal) auditory structures.
在21例癫痫患者服用卡马西平（CBZ）治疗前和治疗期间记录了听觉脑干反应、中潜伏期反应和慢皮层电位（ABR、MLR、SCP）。对其峰潜伏期、峰间间期和波幅进行了测量并进行统计学评估。单一使用CBZ治疗导致ABR波I、III和V的峰潜伏期以及I-III和I-V峰间间期延长。还观察到MLR成分Na、Pa和Nb的峰潜伏期以及V-Pa和Na-Nb峰间间期显著增加，同时NaPa波幅系统性降低。CBZ还延长了SCP成分P1和N1的峰潜伏期。基于所获结果，我们认为CBZ对模态特异性（lemniscal）和模态非特异性（extralemniscal）听觉结构均有抑制作用。
