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.