The specific aim of this research is to test the hypothesis that teratogenicity associated with carbamazepine (CBZ), in the form of growth retardation at birth and developmental delays after birth, is due to reactive metabolite exposure (specifically carbamazepine 10,11-epoxide, or CBZE). Synthesized CBZE is administered prenatally and the infant outcome is compared with control infant outcome. The results will give us a better understanding of the role of CBZE in clinical CBZ teratogenicity. This in turn could yield an index (CBZE plasma levels) for monitoring the potential risk to the fetus during CBZ therapy. Such monitoring strategies and subsequent prescription decisions can reduce the incidence of teratogenicity associated with CBZ therapy. To date, 21 infants have been born. Two of the infants born to dams that received CBZE during pregnancy were premature and not viable. All other infants have completed or are currently involved in follow-up measurements of growth parameters, motor development, and cognitive development. No problems have been encountered during the study. In fact, it has been noteworthy that although in past studies monkeys receiving carbamazepine (CBZ) have sometimes had to have medication discontinued due to signs of toxicity, only one monkey has shown signs of toxicity associated with the synthesized CBZE (in spite of matched blood plasma levels). In the previous studies the monkeys that required discontinuation of CBZ had relatively high parental CBZ and CBZE blood plasma levels. The results of the current study seem to indicate that CBZE alone may not be significantly toxic.