Somatosensory evoked potentials in neonates with primary congenital hypothyroidism during the first week of therapy.

At the present, the influence of intrauterine hypothyroidism on the fetus is estimated by bone age (BA). BA is also used as a predictor of later neuropsychologic development. The aim of this study was to investigate whether the neurophysiologic maturation of neonates with congenital hypothyroidism (CHT) is delayed at the start of therapy and, if so, whether this delay is comparable to that in BA. Twenty-seven infants with CHT were examined with median nerve somatosensory evoked potentials (SEP) before or within 1 wk after initiation of therapy. The effect of neonatal jaundice, a potential confounder of neonatal SEP, was also evaluated. Cervical (N13), first cephalic (N19), and second cephalic (N32) peak latencies were measured, as well as N13-N19 interval (central conduction time) and N13 latency divided by arm length. The SEP data of 103 normal infants were used as reference values. In the CHT newborns, a maturational delay was found for all SEP parameters. Preterm infants (n = 3) were conspicuously less affected than term patients. In term CHT infants, jaundice during the first postnatal week, but not late jaundice, had an additional adverse effect. SEP delay was not related to initial or actual T4 levels. BA delay exceeded SEP delay by several weeks. Our data suggest that the depressed T4 levels of the hypothyroid fetus and neonate affect the nervous tissue to a lesser degree than bone tissue and, further, that SEP is superior to BA as parameter for the evaluation of neurologic maturation of infants with CHT.