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Delayed cortical thinning in children and adolescents with prenatal alcohol exposure
Blake A Gimbel1, Donovan J Roediger1, Abigail M Ernst1
1Department of Psychiatry and Behavioral Sciences, University of Minnesota Twin Cities, Minneapolis, Minnesota, USA.
Insights
Prenatal alcohol exposure (PAE) alters brain development, leading to delayed cortical thinning and atypical brain-behavior relationships in children. These developmental changes may contribute to long-term functional impairments.
Area of Science:
- Neuroscience
- Developmental Neuroscience
- Neuroimaging
Background:
- Prenatal alcohol exposure (PAE) is linked to abnormal cortical development, affecting thickness, volume, and surface area.
- Understanding the longitudinal trajectory of these changes is crucial for identifying developmental timing disruptions.
Purpose of the Study:
- To examine the longitudinal developmental trajectory and timing of cortical maturation abnormalities in children with PAE.
- To investigate the relationship between cortical changes and executive function in children with PAE.
Main Methods:
- A longitudinal study of 35 children with PAE and 30 typically developing controls (aged 8-17).
- MRI scans and cognitive testing (executive function) were conducted approximately 15 months apart.
- Analysis focused on changes in cortical thickness (CT) and executive function (EF) performance.
Main Results:
- Significant age-by-group interactions in CT were found in multiple cortical regions, indicating altered developmental trajectories.
- Children with PAE exhibited delayed cortical thinning, with accelerated thinning occurring at older ages compared to controls.
- Reduced cortical thinning over time was observed in the PAE group, and altered brain-behavior relationships between cortical changes and EF were noted.
Conclusions:
- Longitudinal changes in CT trajectory and timing in PAE suggest delayed cortical maturation and atypical development.
- Atypical brain-behavior relationships between cortical development and executive function in PAE may contribute to functional impairments.
- Altered developmental timing of cortical maturation is a potential factor in long-term functional deficits associated with PAE.
Background:
Prenatal 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.
Methods:
We 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.
Results:
Significant 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.
Conclusions:
Regional 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.
