Original ArticlesEffects of Prenatal Substance Exposure: Altered Maturation of Visual Evoked Potentials
Introduction
Neurophysiologic studies are used to document electrographic patterns that correlate with maturation and electroencephalographic (EEG)-sleep organization of the developing brain 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15. EEG sleep patterns and evoked potential testing may also reflect neurophysiologic dysfunction associated with a variety of medical problems, including maternal diabetes, toxemia, chromosomal defects, asphyxia, untreated hypothyroidism, seizures, and drug addiction 16, 17, 18, 19, 20, 21, 22, 23, 24, 25. These neurophysiologic abnormalities may be present in asymptomatic neonates who later develop neurobehavioral difficulties during childhood 14, 19, 22, 26.
Although there has been considerable research on the effects of maternal alcohol or marijuana use during pregnancy on the offspring’s physical and morphologic development 27, 28, 29, 30, few studies have assessed neurophysiologic development. Several investigations have reported disturbances in sleep or EEG patterns in children with prenatal alcohol exposure, including disrupted sleep architecture and continuity, altered power spectral values, and disruptions in behavioral state and arousal 31, 32, 33, 34, 35, 36, 37. One study has reported delayed maturation of visual evoked potentials (VEPs) during early infancy in children with prenatal alcohol exposure [37].
These studies differ with respect to the measurement of prenatal substance use. Some studies have used retrospective reporting over the entire pregnancy, whereas others have not controlled adequately for confounding variables related to substance use 31, 32, 33, 36, 37. To measure prenatal substance use more accurately, our research group used a more frequent and temporally fixed interview schedule 38, 39.
In previous publications, using data from two large cohorts of women, we have described the effects of prenatal substance use on a variety of outcomes, including neonatal EEG-sleep organization 30, 34, 35, 40, 41, 42, 43, 44, 45, 46. We now report VEP findings from birth through 18 months of age using a different cohort of infants.
Section snippets
Study Design
The sample for this investigation was a cohort of women and their infants participating in a longitudinal study of substance use during pregnancy at a large university-affiliated obstetric hospital. Written consent was obtained for both mothers and infants according to the guidelines established by the University’s Institutional Review Board for Biomedical Research and by the Research Review and Human Experimentation Committee of Magee-Womens Hospital.
Previous publications from this project 30,
Results
Table 2, Table 3 list the means, standard deviations, and ranges of the latencies of the N 1, P1, and N2 waves, as well as the amplitudes of the N1-P1 wave, at birth 1, 4, 8, and 18 months obtained by binocular flash and pattern VEP testing, respectively. The results of the regression analyses referenced to substance use are presented in Table 4, Table 5, Table 6, respectively. In general, changes in the latency responses for the N1, N2, and P1 waves and N1-P1 amplitudes depended on the
Discussion
These data demonstrate that changes occur in the VEPs of children prenatally exposed to moderate levels of alcohol, marijuana, tobacco, or other illicit drugs. Maternal alcohol use in the first trimester predicted increased N1 and P1 latencies at month 1, and then a reversed pattern of decreased latencies at 18 months. Increased N2 latencies and increased amplitude (N1-P1) were also related to alcohol exposure during the last trimesters of pregnancy. By contrast, prolonged N1 and P1 latencies
Acknowledgements
This study was supported by National Institute on Alcohol Abuse and Alcoholism: “Effect of Alcohol Use During Pregnancy” (AA06390), N. Day, PI; “Prenatal Alcohol Effects on Brain Maturation” (AA08528), M. Scher, PI; National Institute on Drug Addiction: “Marijuana Use During Pregnancy: A Longitudinal Study” (DA03873), N. Day, PI; National Institute on Neurological Disorders and Stroke: “Ontogeny of EEG Sleep in Healthy Premature Neonates” (NS01110), M. Scher, PI; “EEG-Sleep in the Healthy
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