Jing-Jing Feng1, Wei-Ping Wang1, Shu-Juan Guo1, Zhi-Wei Liu2, Xiu Xu3. 1. Department of Child Health Care, Children's Hospital of Fudan University, Shanghai, China. 2. Department of Neonatology, International Peace Maternity & Child Hospital of the China Welfare Institute, Shanghai, China. 3. Department of Child Health Care, Children's Hospital of Fudan University, Shanghai, China. Electronic address: xiuxu2010@yahoo.cn.
Abstract
OBJECTIVE: To describe the development of flash visual evoked potentials (FVEPs) in preterm infants from 1 to 18 months and to determine if the maturation of FVEPs is similar to that of term infants. DESIGN: Longitudinal follow-up study. PARTICIPANTS: Twenty very low birth weight (VLBW) preterm infants, 42 low birth weight (LBW) preterm infants, and 41 term infants underwent FVEP recordings and neurodevelopmental examinations at 1, 3, 6, 9, 12, and 18 months of corrected and chronological ages. METHODS: The FVEP recordings were carried out with the VikingQuest-IV neuroelectrophysiological device (VikingQuest, Nicolet, WI), and neurodevelopmental assessments were made by the Development Screen Test and Bayley Scales of Infant Development, Second Edition. MAIN OUTCOME MEASURES: At 1, 3, 6, and 9 months of age, neurodevelopment was measured with the Mental Index and Developmental Quotient. At 12 and 18 months, neurodevelopment was assessed using the Mental Developmental Index and Psychomotor Developmental Index. Two FVEP values were analyzed: the P2 amplitude (peak to peak from the preceding N2 wave) and the latency of the P2 wave. RESULTS: There was no significant difference for age-dependent decreased pattern of FVEP P2 latency between preterm infants and the control group. This pattern consisted of a rapid decrease in the first 6 months of life, a gradual decline from 6 to 12 months of age, and a steady reduction from 12 to 18 months of age. The P2 latencies were prolonged significantly at all 6 recorded times in the VLBW group compared with the controls and showed a delay in the LBW group at 1 and 3 months of corrected age. The maturation of P2 latency in LBW infants is similar to that of the controls at 3 months of corrected age, but the maturation of P2 latency in VLBW children remained delayed when compared with the controls until 18 months of corrected age. CONCLUSIONS: Although the FVEP development pattern of preterm infants was similar to that of healthy full-term infants, the former had deficits in visual electrophysiologic maturation, especially for VLBW children.
OBJECTIVE: To describe the development of flash visual evoked potentials (FVEPs) in preterm infants from 1 to 18 months and to determine if the maturation of FVEPs is similar to that of term infants. DESIGN: Longitudinal follow-up study. PARTICIPANTS: Twenty very low birth weight (VLBW) preterm infants, 42 low birth weight (LBW) preterm infants, and 41 term infants underwent FVEP recordings and neurodevelopmental examinations at 1, 3, 6, 9, 12, and 18 months of corrected and chronological ages. METHODS: The FVEP recordings were carried out with the VikingQuest-IV neuroelectrophysiological device (VikingQuest, Nicolet, WI), and neurodevelopmental assessments were made by the Development Screen Test and Bayley Scales of Infant Development, Second Edition. MAIN OUTCOME MEASURES: At 1, 3, 6, and 9 months of age, neurodevelopment was measured with the Mental Index and Developmental Quotient. At 12 and 18 months, neurodevelopment was assessed using the Mental Developmental Index and Psychomotor Developmental Index. Two FVEP values were analyzed: the P2 amplitude (peak to peak from the preceding N2 wave) and the latency of the P2 wave. RESULTS: There was no significant difference for age-dependent decreased pattern of FVEP P2 latency between preterm infants and the control group. This pattern consisted of a rapid decrease in the first 6 months of life, a gradual decline from 6 to 12 months of age, and a steady reduction from 12 to 18 months of age. The P2 latencies were prolonged significantly at all 6 recorded times in the VLBW group compared with the controls and showed a delay in the LBW group at 1 and 3 months of corrected age. The maturation of P2 latency in LBW infants is similar to that of the controls at 3 months of corrected age, but the maturation of P2 latency in VLBW children remained delayed when compared with the controls until 18 months of corrected age. CONCLUSIONS: Although the FVEP development pattern of preterm infants was similar to that of healthy full-term infants, the former had deficits in visual electrophysiologic maturation, especially for VLBW children.