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Published on: August 5, 2017
Central white matter integrity alterations in 2-3-year-old children following prenatal alcohol exposure
Annerine Roos1, Catherine J Wedderburn2, Jean-Paul Fouche3
1SAMRC Unit on Risk and Resilience in Mental Disorders, Department of Psychiatry, Stellenbosch University, South Africa; Department of Pediatrics and Child Health, University of Cape Town, South Africa; Neuroscience Institute, University of Cape Town, South Africa.
Insights
Prenatal alcohol exposure (PAE) alters white matter integrity in toddlers, affecting brain stem, limbic, and association tracts. Prenatal tobacco exposure amplifies these effects, particularly in motor function pathways.
Area of Science:
- Neuroscience
- Developmental Biology
- Radiology
Background:
- Prenatal alcohol exposure (PAE) is a significant, preventable risk to neurodevelopment.
- Limited evidence exists on PAE's specific impact on toddler brain development.
- This study addresses the knowledge gap regarding PAE's effects on white matter integrity in young children.
Purpose of the Study:
- To investigate the impact of prenatal alcohol exposure on brain white matter integrity in 2-3-year-old children.
- To compare white matter parameters between children with PAE and unexposed controls.
- To explore the influence of maternal tobacco smoking on these differences.
Main Methods:
- Diffusion MRI was performed on 83 children (30-37 months old) from a birth cohort.
- Tract-based Spatial Statistics (TBSS) was used to analyze white matter parameters.
- Children with PAE (n=25) were compared to unexposed controls (n=58).
Main Results:
- Children with PAE exhibited altered fractional anisotropy, radial diffusivity, and axial diffusivity in multiple brain tracts.
- Significant reductions in fractional anisotropy were observed in the uncinate fasciculus.
- Lower diffusivity was noted in the fornix stria terminalis and corticospinal tract in the PAE group.
- A significant interaction between PAE and prenatal tobacco exposure was found, impacting the corticospinal tract.
Conclusions:
- Altered white matter microstructural integrity in toddlers with PAE indicates persistent effects from early life exposure.
- Findings suggest PAE impacts brain development beyond the neonatal period.
- Prenatal tobacco exposure exacerbates PAE's effects on white matter, particularly in motor pathways.
Background:
Prenatal alcohol exposure (PAE) remains a potentially preventable, but pervasive risk factor to neurodevelopment. Yet, evidence is lacking on the impact of alcohol on brain development in toddlers. This study aimed to investigate the impact of PAE on brain white matter integrity in 2-3-year-old children.
Methods:
Children (n = 83, 30-37 months old) of the Drakenstein Child Health Study birth cohort, underwent diffusion MRI on a 3 T Siemens scanner during natural sleep. Parameters were extracted in children with PAE (n = 25, 56 % boys) and unexposed controls (n = 58, 62 % boys) using Tract-based Spatial Statistics, and compared by group. The contribution of maternal tobacco smoking to white matter differences was also explored.
Results:
Children with PAE had altered fractional anisotropy, radial diffusivity and axial diffusivity in brain stem, limbic and association tracts compared to unexposed controls. Notably lower fractional anisotropy was found in the uncinate fasciculus, and lower mean and radial diffusivity were found in the fornix stria terminalis and corticospinal tract (FDR corrected p < 0.05). There was a significant interaction effect of PAE and prenatal tobacco exposure which lowered mean, radial and axial diffusivity in the corticospinal tract significantly in the PAE group but not controls.
Conclusion:
Widespread altered white matter microstructural integrity at 2-3 years of age is consistent with findings in neonates in the same and other cohorts, indicating persistence of effects of PAE through early life. Findings also highlight that prenatal tobacco exposure impacts the association of PAE on white matter alterations, amplifying effects in tracts underlying motor function.

