The maternal administration of betamethasone and thyrotropin releasing hormone (TRH) to accelerate the maturation of the fetus is an increasingly adopted strategy to prevent neonatal morbidity in preterm infants. The effect of this prenatal treatment on the neural maturation of the infant was assessed by measuring somatosensory evoked potentials (SEP) in preterm infants (gestational age 29-36 wk) on the 1st postnatal day, at the age of 1 wk, and before discharge. The N1 latency values of the SEP obtained in 14 infants who were exposed prenatally to betamethasone/TRH were compared with the N1 latencies measured in 12 control infants. On the 1st postnatal day, the N1 latencies in the betamethasone/TRH-treated infants were strikingly shorter (p less than 0.01) than in the controls. However, at the age of 1 wk and at discharge, the N1 latency values of both groups were similar. In conclusion, the present study provides the first solid evidence for the concept that the prenatal exposure to betamethasone/TRH accelerates the SEP-assessed neural maturation of the human fetus, that this prenatal acceleration is followed by a compensatory relative deceleration during the early neonatal period, and that the subsequent SEP-assessed neural maturation proceeds at a normal velocity.