The purpose of this study was to determine if there are any correlations between carbamazepine serum levels of epileptic mothers during pregnancy and the brainstem auditory evoked potentials in their infants as an index of drug neurotoxicity in newborns exposed prenatally. We included 20 epileptic mothers with carbamazepine medication and their 20 otherwise healthy infants. The study was conducted from September 1, 1993, to December 15, 1999. Serum carbamazepine determinations were performed monthly by enzymatic immunoanalysis in the mothers, and the averages for each trimester during pregnancy were calculated. Brainstem auditory evoked potentials were performed at 10.2 +/- 4.6 weeks of postnatal life. Pearson's correlations were calculated between carbamazepine serum levels during pregnancy and waves and interwave intervals of brainstem auditory evoked potentials. Both examinations were performed without knowledge of the results of the other investigations. No alterations in the infants' brainstem auditory evoked potentials were evident, and carbamazepine determinations were within therapeutic levels. Significant Pearson's correlations between latencies of waves III and V and third trimester of carbamazepine serum concentration levels and I-V interwave intervals to third-trimester minimum serum levels of carbamazepine were found. The findings suggest that the higher carbamazepine levels in mothers are related to increased latencies in waves III and V and I-V interwave intervals in infants subclinically, which could be an early index of fetal neurotoxicity.

The purpose of this paper was to describe whether there are some relationships between amikacin serum levels and central conduction time in brainstem auditory evoked potentials (BAEP) within therapeutic range levels in newborns as index of drug toxicity in brainstem auditory centers in neonatally exposed infants. We performed a cross-sectional study to compare BAEP from 35 infants under amikacin administration and 24 control infants; both examinations were blinded to investigators. Bivariate and partial correlations were calculated between amikacin and BAEP measurements in treated infants. Amikacin determinations were within therapeutic levels. No clinical alterations in BAEP were found and no differences between amikacin-treated and control infants were found. Significant positive Pearson correlation between latency of I-III interwaves interval and amikacin Cmin serum levels was found and was present when calculations were controlled by partial correlations for gestational age at birth and Apgar score at 5 min. The findings suggest that increased amikacin levels in newborns are related to increased latencies in I-III interwave interval in infants, which may be an early index of brainstem effects of subclinical neurotoxicity of amikacin.