Somatosensory evoked potentials in very preterm infants Bert J. Smit a, * , Bram W. Ongerboer de Visser b , Linda S. de Vries c , Friedo W. Dekker d , Joke H. Kok a a Department of Neonatology, Emma Children's Hospital Academic Medical Center, University of Amsterdam, H3N-148, P.O. Box 22700, 1100 DE Amsterdam, The Netherlands b Clinical Neurophysiology Unit of the Department of Neurology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands c Department of Neonatology, Wilhelmina Children's Hospital, University of Utrecht, Utrecht, The Netherlands d Department of Clinical Epidemiology and Biostatistics, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands Accepted 17 December 1999 Abstract Objective: Cross-sectional and longitudinal reference values of cortical N 1 peak latency of the median nerve SEP in very preterm infants. Methods: In infants in a placebo control group within an l-thyroxine supplementation trial, born at less than 30 weeks' gestation, cortical N 1 peak latency was measured at 2 weeks, at term and at 6 months corrected age. Cross-sectional N 1 latency values obtained in 50 infants and complete series of longitudinal values obtained in 15 infants were analyzed in relation to postmenstrual age (PMA). Results: Mean N 1 latency decreased from 66 ms at 2 weeks to 38 ms at term and 20 ms at 6 months corrected age. Possible confounding factors did not have any signi®cant effect on N 1 latency at 2 weeks or at term age except cranial ultrasound abnormalities at 2 weeks of age. Conclusions: Longitudinal N 1 latency values were consistent with cross-sectional N 1 latency values. The observed N 1 latency at term and at 6 months corrected age suggest that extrauterine maturation of the somatosensory pathway in infants born at less than 30 weeks' gestation is delayed by extrauterine life. q 2000 Elsevier Science Ireland Ltd. All rights reserved. Keywords: Electrophysiology; Evoked potentials; Preterm infant; Somatosensory; PMA, postmenstrual age; SEP, somatosensory evoked potentials 1. Introduction In recent years, median nerve somatosensory evoked potentials (SEPs) in newborns have received increased attention (De Vries et al., 1994; Mercuri et al., 1994; Majnemer and Rosenblatt, 1996; Taylor et al., 1996a). Until now, only few reference values of peak latencies of the ®rst cortical potential (N 1 ) in infants born at less than 30 weeks' gestation are available (Klimach and Cooke, 1988a; Taylor et al., 1996b). Moreover, the validity of median nerve SEPs as a prognostic test to predict neuro- developmental outcome especially in preterm infants is not yet fully established (De Vries et al., 1994; Mercuri et al., 1994; Majnemer and Rosenblatt, 1996; Taylor et al., 1996a; Ekert et al., 1997). To determine whether l-thyroxine supplementation improved neurodevelopmental outcome at the age of 2 years, we recently carried out a randomized, double-blind, placebo controlled trial in 200 very preterm infants, irre- spective of their clinical condition and thyroid hormone levels, who were born at less than 30 weeks' gestation (van Wassenaer et al., 1997; Smit et al., 1998a, 1999). In this trial, in addition to motor nerve conduction velocity measurements (Smit et al., 1998b) SEP recordings were obtained at 2 weeks, at term and at 6 months corrected age. The present paper describes cross-sectional and longitu- dinal reference values of the ®rst cortical peak latency (N 1 ) after stimulation of the median nerve based on data obtained in the placebo group. Because N 1 latency re¯ects the func- tional integrity of the somatosensory pathway in the nervous system, it can be abnormal due to intracerebral hemor- rhages, periventricular leucomalacia and ventriculomegaly. All of these conditions are not infrequently occurring in very preterm infants. Therefore, we examined all cranial ultrasound examinations of the infants during admission. Other possible confounding factors were also analyzed. Moreover, N 1 latency values were studied in relation to neurologic development at 2 years of age. Clinical Neurophysiology 111 (2000) 901±908 CLINPH 99542 1388-2457/00/$ - see front matter q 2000 Elsevier Science Ireland Ltd. All rights reserved. PII: S1388-2457(00)00245-5 www.elsevier.com/locate/clinph * Corresponding author. Tel.: 131-20-566-3956; fax: 131-20-696- 5099. E-mail address: b.j.smit@amc.uva.nl (B.J. Smit)