Donald, KA, PhD 1; Fouche, JP, MSc2,3; Roos, A, PhD4 ; Koen, N, PhD3; Howells, FM, PhD3; Riley, EP, PhD5; Woods, RP, PhD6; Zar, HJ, PhD7; Narr, KL, PhD6; Stein, DJ, PhD8.
1: Division of Developmental Paediatrics, Department of Paediatrics and Child Health, Red Cross War Memorial Children’s Hospital and University of Cape Town, South Africa
2. Department of Human Biology, University of Cape Town and
Department of Psychiatry, Stellenbosch University, Cape Town, South Africa
3. Department of Psychiatry and Mental Health, University of Cape Town, Cape Town, South Africa
4. MRC Unit on Anxiety & Stress Disorders, UCT/Stellenbosch University, Cape Town, South Africa.
5. Department of Psychology, San Diego State University, San Diego, United States of America
6. Department of Neurology, University of California, Los Angeles, United States of America
7. Department of Paediatrics and Child Health and MRC Unit on Child & Adolescent Health, Red Cross War Memorial Children’s Hospital and University of Cape Town, Cape Town, South Africa
8. Department of Psychiatry and Mental Health and MRC Unit on Anxiety & Stress Disorders, University of Cape Town, Cape Town, South Africa
Alcohol use and alcohol use disorders contribute a significant proportion of the burden of disease in low, middle, and high-income countries. For neurodevelopmental disorders, studies have consistently shown that early intervention leads to better long-term outcomes. But early intervention is predicated on early detection and targeted interventions. Understanding the core areas of susceptibility to prenatal alcohol effects as they manifest in early life is key to developing strategies for early focused identification and interventions. Using multimodal imaging techniques in neonates prenatally exposed to alcohol, analysis revealed volume differences in global gray matter as well as in deep gray structures such as the amygdala and hippocampus, differences in the integrity of central white matter microstructure specifically in the superior longitudinal fasciculus, abnormal glutamate/glutamine concentrations in the parietal lobe as well as differences in the organisation of functional networks in the same group of infants. These alterations suggest prenatal alcohol exposure affects multiple biological processes that result in physical growth of the brain, quality and maturation of the connecting circuitry, neurotransmitter concentrations in the first weeks of life as well as functional connectivity, both within intrinsic networks as well as between hemispheres. The location of these results is remarkably consistent with an established theme in prenatal alcohol exposure studies of the importance of midline structures. We expect that the identification of alcohol effects on key midline structures in the infant brain may be an early marker for later functional cognitive and behavioral deficits. This highly sensitive approach may prove to be valuable in identifying affected children early as well as monitoring the effectiveness of interventions.