The effects on brainstem auditory evoked potentials (BAEPs) of carbamazepine in 18 and of valproate in 10 epileptic children were determined after 13 months of therapy at Istanbul University, Turkey. Blood levels were therapeutic and not associated with side effects. The peak latencies of waves I, II, and V, and interpeak intervals I-III and I-V were significantly prolonged following carbamazepine. Valproate monotherapy caused similar changes in BAEP but prolongation was not significant nor consistent. Carbamazepine suppresses auditory pathways peripherally, at the cochlea and/or auditory nerve and centrally, at the brainstem. [1]

COMMENT. Similar findings have been reported in 21 epileptic patients treated with carbamazepine and studied at the Institute of Clinical and Experimental Neurology, Thilisi, Republic of Georgia. (Japaridze G et al. 1993; see Ped Neur Briefs January 1994). Carbamazepine suppressed both central auditory structures and the acoustic nerve. Chronic impairment of cognitive function, as measured by changes in auditory event-related potentials, was also reported in 23 patients treated with carbamazepine at Toyama Medical University, Japan (Naganuma Y et al, 1994; see Ped Neur Briefs Ian 1994).