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.
Auditory brainstem responses (ABRs), middle-latency responses (MLRs), and slow cortical potentials (SCPs) have been recorded in patients with partial epilepsy previously untreated by anticonvulsants. Peak latencies, interpeak intervals, and amplitudes were estimated and the mean group values were compared with the respective data in age- and gender-matched healthy individuals. Neither ABRs nor MLRs in the patients differed significantly from those in the control group. Conversely, the SCP characteristics demonstrated regular differences: the P2 peak latency in the patients was prolonged and both the P1N1 and N1P2 amplitudes were increased. Considering the mechanisms of the ABR and MLR, it has been suggested that the specific structures of central auditory pathway up to the primary cortex do not play any essential role in the pathogenesis of partial epilepsy. Furthermore, it is speculated that the SCP-generating cortical areas, being primarily of non-specific qualities, are intimately involved in the mechanisms of epilepsy.
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