ArticleAlcohol, clinical & experimental research2023
Delayed cortical thinning in children and adolescents with prenatal alcohol exposure.
Article in Alcohol, clinical & experimental research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Neurodevelopmental impacts of unique postnatal adversity subgroups in children with prenatal alcohol exposure.Child neuropsychology : a journal on normal and abnormal development in childhood and adolescence · 2026Article
- Prenatal Adversities and Risk of Persistent Youth Psychopathology and Altered Cortical Thinning.JAMA psychiatry · 2026Article
- Persistent Alterations of Brain and Behavior in Children With Low Prenatal Alcohol Exposure.Biological psychiatry global open science · 2026Article
- Regional cerebellum volume anomalies and associated cognitive function in children with fetal alcohol spectrum disorders.Alcohol, clinical & experimental research · 2026Article
- Article
- Association of Adverse Prenatal Exposure Burden with Persistent Psychopathology and Accelerated Cortical Thinning in Youth.medRxiv : the preprint server for health sciences · 2025Article
- Control of precision grip in children with heavy prenatal alcohol exposure.Alcohol, clinical & experimental research · 2025Article
- Altered markers of brain metabolism and excitability are associated with executive functioning in young children exposed to alcohol in utero.Metabolic brain disease · 2024Article
- Association of in utero HIV exposure with child brain structure and language development: a South African birth cohort study.BMC medicine · 2024Article
- Sex and age effects on gray matter volume trajectories in young children with prenatal alcohol exposure.Frontiers in human neuroscience · 2024Article
- Proceedings of the 2022 annual meeting of the Fetal Alcohol Spectrum Disorders study group.Alcohol (Fayetteville, N.Y.) · 2023Article
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Authors and funding
12 authors.
Funding
Abstract
backgroundPrenatal alcohol exposure (PAE) is associated with abnormalities in cortical structure and maturation, including cortical thickness (CT), cortical volume, and surface area. This study provides a longitudinal context for the developmental trajectory and timing of abnormal cortical maturation in PAE.
methodsWe studied 35 children with PAE and 30 nonexposed typically developing children (Comparisons), aged 8-17 at enrollment, who were recruited from the University of Minnesota FASD Program. Participants were matched on age and sex. They underwent a formal evaluation of growth and dysmorphic facial features associated with PAE and completed cognitive testing. MRI data were collected on a Siemens Prisma 3T scanner. Two sessions, each including MRI scans and cognitive testing, were spaced approximately 15 months apart on average. Change in CT and performance on tests of executive function (EF) were examined.
resultsSignificant age-by-group (PAE vs. Comparison) linear interaction effects in CT were observed in the parietal, temporal, occipital, and insular cortices suggesting altered developmental trajectories in the PAE vs. Comparison groups. Results suggest a pattern of delayed cortical thinning in PAE, with the Comparison group showing more rapid thinning at younger ages and those with PAE showing accelerated thinning at older ages. Overall, children in the PAE group showed reduced cortical thinning across time relative to the Comparison participants. Symmetrized percent change (SPC) in CT in several regions was significantly correlated with EF performance at 15-month follow-up for the Comparison group but not the group with PAE.
conclusionsRegional differences were seen longitudinally in the trajectory and timing of CT change in children with PAE, suggesting delayed cortical maturation and an atypical pattern of development compared with typically developing individuals. In addition, exploratory correlation analyses of SPC and EF performance suggest the presence of atypical brain-behavior relationships in PAE. The findings highlight the potential role of altered developmental timing of cortical maturation in contributing to long-term functional impairment in PAE.
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