RESUMO
PIP: Young epileptic women frequently question their physicians concerning appropriate contraception for them, the effects of pregnancy on epilepsy, and the effects of the disease on the fetus. In 1/2 of cases the frequency of epileptic crises is unaffected by pregnancy, in 1/4 it is augmented and in 1/4 it is decreased. An increase in crises may be caused by psychological factors or by changing the treatment to avoid injuring the fetus. Recent studies show that the plasma level of the medications tends to decline during pregnancy and to increase postpartum. During the past decade several cases of pregnancy in young women taking oral contraceptives (OCs) and antiepileptic drugs have been observed. The inactivation of OCs, which occurs with all antiepileptics except sodium valproate and the benzodiazepines, appears to be due to a mechanism of enzymatic induction. Most cases of pregnancy were in women using sequential pills with 50 mcg or less of ethinyl estradiol. (EE) Sodium valproate can be prescribed for women with primary epilepsy, but in cases of incompletely controlled epilepsy or those requiring various drugs, it is better not to modify a successful regimen. Another method of contraception such as the IUD can be prescribed, or possibly a higher dose formulation of OC can be selected. The vascular risk of a stronger dose of contraceptive steroids should be weighed, but it may be that the process of enzymatic induction maintains a level of EE comparable to that of the minipill. If combined OCs are used, the appearance of metrorrhagia should be noted and the temperature shift should be recorded for the 1st months of treatment to guard against possible failure to inhibit ovulation. The teratogenic risk of antiepileptic medications has not been entirely evaluated, but diphenylhydantoines have been shown experimentally to cause malformations in monkeys. Statistics indicate a doubled risk of malformation in the children of epileptic mothers treated during pregnancy. All antiepileptic drugs were found to be involved. In a personal series of 170 babies of treated epileptic mothers, there were 4 malformations and 1 fatal neonatal hemorrhage. It would be reasonable to assume that malformations result from the interaction of genetic factors related to the severity of the disease, maternal age at pregnancy, and medication used. The role of the anticonvulsants may possibly be explained by their effect on nucleic acid metabolism or by deficiencies of folic acid and vitamin K, which in turn may play a role in neonatal hemorrhage. In case of pregnancy, the patient should be reassured about the small risk of malformation. The smallest possible doses and, if possible, single drugs should be used. Injections of vitamin K for the mother before delivery and for the infant may prevent coagulation problems. The infant may have withdrawal symptoms for which replacement medication may be prescribed for a few weeks. Breastfeeding does not appear to be contraindicated.^ieng
