No abstract

Somatosensory evoked potentials (SEPs) were studied in jaundiced and normal neonates on the day the highest bilirubin values were reached, 2-3 days later, and at five weeks. During the first week three groups were formed according to peak bilirubin values: A: greater than or equal to 250 mumol/l (n = 20), B: 125-250 mumol/l (n = 6), C: less than 125 mumol/l or no jaundice (n = 19). At five weeks 10 infants of group A were reinvestigated, together with 17 controls. Cervical (N13) and scalp SEPs (N19) were recorded with a variable number of stimuli. The SEPs of group B and C did not differ from each other. In group A the N13 peak latencies were within the range of group C at the first investigation, but prolonged at the second and third. The cortical components were prolonged at the first investigation, improved but still prolonged at the second, while the N19 peak latency was still prolonged at the third investigation. The central conduction time (CCT) correlated positively with the bilirubin level. Since a rapid decrease in the N19 amplitude was found for all groups from 25 to 100 stimuli, recordings should be done with a low number of stimuli (less than 100). Our findings indicate that both the periferal and the central components of the SEPs in the neonatal period are delayed by jaundice and that full recovery is not obtained at five weeks. The non-invasive SEP technique can be used as a daily monitor of the effect of bilirubin on the CNS.

ABSTRACT. To assess the influence of treatment on the development of the somesthetic pathway in infants with congenital hypothyroidism receiving early treatment, median nerve somatosensory evoked potentials were measured during the 1st y of life.Twenty-nine infants were studied with six to seven somatosensory evoked potential tests per infant. The cervical latency (N13) divided by arm length and the first (N19) and second (N32) cephalic latencies as well as N13-N32 latency were measured. At diagnosis, all components showed a small but significant delay, which was not related to thyroxine (T4) levels before treatment. During treatment, T4 ranged from 50 to 290 nmol/L. At 12 mo, the cervical latency divided by arm length had normalized, whereas N19 and N13-N32 were more abnormal than at diagnosis. For N19, these abnormalities were related to a slow initial rise of T4 (1100 nmol/L after 1 wk of treatment) and the initial N19 values. Abnormal N13-N32 values were associated with high T4 values during treatment (>200 nmol/L) and the type of congenital hypothyroidism (partial or total deficiency in T4 production). Induction of therapy with I-triiodothyronine rather than I-thyroxine and the occurrence of low T4 values ( e l 0 0 nmol/L) after the 4th wk of therapy had no such effect. Our data suggest that, for normal CNS development, euthyroidism should be reached as soon as possible by adequate induction therapy. Thereafter, T4 supplementation should be strictly dosed, keeping the serum T4 values within narrow limits around the mean normal for age, because overtreatment, like initial undertreatment, may lead to CNS abnormalities at the end of the first year. (Pediatr Res 34: 73-78,1993) Abbreviations CHT, congenital hypothyroidism I-T4, levo-thyroxine 1-T3, levo-triiodothyronine I-T4/f, fast initial serum T4 rise on I-T4 induction I-T4/s, slow initial serum T4 rise on I-T4 induction PD, partial deficiency in T4 production TD, total deficiency in T4 production PMA, postmenstrual age SEP, somatosensory evoked potentials N13/AL, latency to first negative peak in cervical lead divided by arm length N19, latency to first negativity in cephalic lead N32, latency to second negativity in cephalic lead N60, latency to third negativity in cephalic lead P22, latency to first positivity after N19 T4>200, group with serum T4 >200 nmol/L on all occasions T 4~2 0 0 , group with serum T4 ~2 0 0 nmol/L on all occasions bl, slope for period T4 ~2 0 0 nmol/L b2, slope for period T4 >200 nmol/L The major objective of the national screening programs for CHT is the prevention of neurologic damage. On the whole, the results of the screening seem gratifying, but there are still unsatisfying aspects. Several studies (1-3) report CHT infants displaying minor neurologic dysfunctions and subnormal IQ at later age despite early diagnosis and treatment. Other studies report normal findings (4-6).Generally, the neurologic deficits are ascribed to perinatal thyroid hormone deficiency, because they were found to be related to very low initial T4 val...

ABSTRACT. 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. (Pediatr Res 30: 34-39, 1991)