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Published on: August 5, 2017
Longitudinal effects of prenatal alcohol exposure on visual neurodevelopment over infancy
Emma T Margolis1, Lauren Davel2, Niall J Bourke3
1Department of Psychology, Northeastern University.
Insights
First trimester prenatal alcohol exposure impacts infant visual development. Binge drinking specifically altered visual-evoked potential timing, suggesting early alcohol exposure disrupts neurodevelopmental trajectories.
Area of Science:
- Neuroscience
- Developmental Psychology
- Public Health
Background:
- Prenatal alcohol exposure (PAE) globally affects over 59 million individuals, impacting neurodevelopment.
- Previous research often used limited dichotomous categorizations of alcohol and substance use.
- A continuous measurement of PAE, including timing, dose, and patterns, is needed to understand specific impacts.
Purpose of the Study:
- To investigate the specific effects of prenatal alcohol exposure on early human neurodevelopment.
- To characterize the relationship between first-trimester alcohol exposure, including binge drinking, and visual neurodevelopment in infancy.
- To explore the association between visual-evoked potential (VEP) latencies and myelination in infants with PAE.
Main Methods:
- Longitudinal cohort study in Cape Town, South Africa, measuring PAE continuously.
- High-density electroencephalography (EEG) during a visual-evoked potential (VEP) task in infants aged 8–52 weeks.
- Magnetic resonance imaging (MRI) T1w/T2w ratios used to assess myelination in a subsample.
Main Results:
- First-trimester alcohol exposure altered P1 VEP component timing in the first six months postnatally.
- First-trimester binge drinking exposure was associated with longer P1 VEP latencies, with increasing age related to shorter latencies.
- Decreased myelination (lower MRI T1w/T2w ratios) in the primary visual cortex was linked to longer P1 VEP latencies.
Conclusions:
- First-trimester alcohol exposure may disrupt visual neurodevelopmental timing in early infancy.
- Both prenatal alcohol exposure and postnatal myelination appear to independently influence VEP latency during infancy.
- Continuous measurement of PAE provides nuanced insights into its neurodevelopmental consequences.
Abstract:
Prenatal alcohol exposure (PAE) affects neurodevelopment in over 59 million individuals globally. Prior studies using dichotomous categorization of alcohol use and comorbid substance exposures provide limited knowledge of how prenatal alcohol specifically impacts early human neurodevelopment. In this longitudinal cohort study from Cape Town, South Africa, PAE is measured continuously-characterizing timing, dose, and drinking patterns (i.e., binge drinking). High-density electroencephalography (EEG) during a visual-evoked potential (VEP) task was collected from infants aged 8 to 52 weeks with prenatal exposure exclusively to alcohol and matched on sociodemographic factors to infants with no substance exposure in utero. First trimester alcohol exposure related to altered timing of the P1 VEP component over the first 6 months postnatally, and first trimester binge drinking exposure altered timing of the P1 VEP components such that increased exposure was associated with longer VEP latencies while increasing age was related to shorter VEP latencies (n = 108). These results suggest alcohol exposure in the first trimester may alter visual neurodevelopmental timing in early infancy. Exploratory individual-difference analysis across infants with and without PAE tested the relation between VEP latencies and myelination for a subsample of infants with usable magnetic resonance imaging (MRI) T1w and T2w scans collected at the same time point as EEG (n = 47). Decreased MRI T1w/T2w ratios (an indicator of myelin) in the primary visual cortex (n = 47) were linked to longer P1 VEP latencies. Results from these two sets of analyses suggest that prenatal alcohol and postnatal myelination may both separately impact VEP latency over infancy. (PsycInfo Database Record (c) 2024 APA, all rights reserved).
