Effect of prenatal betamethasone/thyrotropin releasing hormone treatment on somatosensory evoked potentials in preterm newborns

Francis De Zegher*, Linda De Vries, Veronique Pierrat, Hans Daniels, Bernard Spitz, Paul Casaer, Hugo Devlieger, Ephrem Eggermont

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

12 Citations (Scopus)

Abstract

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 pre-natally 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 < 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.

Original languageEnglish
Pages (from-to)212-214
Number of pages3
JournalPediatric Research
Volume32
Issue number2
DOIs
Publication statusPublished - 1 Jan 1992
Externally publishedYes

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