The Pharmaceutical Journal
Vol 268 No 7193 p487-492
13 April 2002

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High disability rate in children born to women treated for epilepsy confirmed

A new study that assesses the long-term consequences of intrauterine drug exposure for children born to mothers with epilepsy shows that the malformation rate in children exposed to epilepsy treatment is 13.8 per cent, a figure comparable with results of other studies. As well as having higher rates of malformation, the study shows that children exposed to antiepileptics have an increased risk of developmental delay.

Researchers followed the development of children born to 149 mothers being treated for epilepsy. The mothers had 293 children whose health and neurological development were assessed. Of these, 38 had not been exposed to epilepsy treatment in utero. After excluding cases with a family history of developmental delay, the researchers found that developmental delay occurred in 19 per cent of exposed children compared with 3 per cent of their non-exposed siblings. Monotherapy with carbamazepine, valproate and phenytoin or polytherapy were all associated with a higher frequency of developmental delay. Those exposed to phenobarbitone monotherapy were not at higher risk.

Drug withdrawal symptoms were most likely to occur in children exposed to polytherapy (30 per cent) and least likely to occur in those exposed to phenobarbitone monotherapy (13 per cent). The influence of drug dosage was not apparent in children exposed to monotherapy except for carbamazepine. Children who had developmental delay were exposed to higher doses of this drug than children with normal development (mean daily dose 683mg, compared with 462mg, P=0.032).

The researchers note that the group of children with major malformations and the group with developmental delay do not fully coincide. "The risk of either major malformation or developmental delay is therefore higher than the risk of either alone," they say.

They conclude that women with epilepsy need to be given better information before pregnancy (Journal of Medical Genetics 2002;39:251).