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Cortical miscommunication after prenatal exposure to alcohol

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Abstract

We report on the effects of prenatal alcohol exposure on resting-state brain activity as measured by magnetoencephalography (MEG). We studied 37 subjects diagnosed with fetal alcohol spectrum disorder in one of three categories: fetal alcohol syndrome, partial fetal alcohol syndrome, and alcohol-related neurodevelopmental disorder. For each subject, the MEG signal was recorded for 60 s during rest while subjects lay supine. Using time series analysis, we calculated the synchronous neural interactions for all pair-wise combinations of 248 MEG sensors resulting in 30,628 partial correlations for each subject. We found significant differences from control subjects in 6.19 % of the partial zero-lag crosscorrelations (synchronous neural interactions; Georgopoulos et al. in J Neural Eng 4:349–355, 2007), with these differences localized in the right posterior frontal, right parietal, and left parietal/posterior frontal regions. These results show that MEG can detect functional brain differences in the individuals affected by prenatal exposure to alcohol. Furthermore, these differences may serve as a biomarker for future studies linking symptoms and signs to specific brain areas. This may lead to new insights into the neuropathology of fetal alcohol spectrum disorders.

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Acknowledgments

This work was supported by the Department of Veterans Affairs, and the American Legion Brain Sciences Chair. R.R.V. was supported by a Fellowship form the Department of Pediatric Neurology, Charles University, 2nd Faculty of Medicine, University Hospital Motol, Prague, Czech Republic.

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Correspondence to Scott M. Lewis.

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The study protocol was approved by the Institutional Review Boards of the Minneapolis VA Medical Center and the University of Minnesota. The study was performed in accordance with the ethical standards outlined in the Declaration of Helsinki.

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Lewis, S.M., Vydrová, R.R., Leuthold, A.C. et al. Cortical miscommunication after prenatal exposure to alcohol. Exp Brain Res 234, 3347–3353 (2016). https://doi.org/10.1007/s00221-016-4732-3

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  • DOI: https://doi.org/10.1007/s00221-016-4732-3

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