The effects of carbamazepine (CBZ) on cognitive function were evaluated by using measurements of auditory event-related potentials (ERPs) and P300 latencies in 23 patients, aged 7 to 16 years, with benign childhood epilepsy and centrotemporal spikes (BCECT), at the Department of Pediatrics, Toyama Medical and Pharmaceutical University, Toyama, Japan. As the epilepsy was controlled at the initiation of therapy, and with increasing age, the P300 latency was at first shortened. During the course of therapy with CBZ, P300 latency was prolonged, and the age-corrected P300 latency showed a significant correlation with the serum CBZ level. The dose of CBZ ranged from 10-23 mg/kg/day (mean 15.8). The latency became shorter when CBZ was discontinued. [1]

COMMENT. The major positive component of auditory event-related potentials, at a latency of 300 msec (P300) for rare tones (2000 Hz), has been correlated with cognitive function. Abnormalities in ERPs in patients with epilepsy, and particularly prolongation of P300 latency, have been ascribed to the effects of the seizures and to antiepileptic drug therapy. Various epileptic syndromes have shown different degrees of abnormality in the ERPs. In this study, after a transient beneficial response, the cumulative effect of carbamazepine was associated with a chronic impairment of cognitive function, as measured by changes in auditory event-related potentials.

Studies of the effects of carbamazepine on auditory brainstem responses (ABR) in 21 epileptic patients examined at the Institute of Clinical and Experimental Neurology, Thilisi, Republic of Georgia, demonstrated prolongation of ABR peak latencies and interpeak intervals. In addition, CBZ was associated with increases in peak latencies of middle-latency responses and slow cortical potentials. CBZ has suppressive influences on central auditory structures and the acoustic nerve. [2]