It is now recognized that a number of cognitive, behavioral, and mental health outcomes across the lifespan can be traced to fetal development. Although the direct mediation is unknown, the substantial variance in fetal growth, most commonly indexed by birth weight, may affect lifespan brain development. We investigated effects of normal variance in birth weight on MRI-derived measures of brain development in 628 healthy children, adolescents, and young adults in the large-scale multicenter Pediatric Imaging, Neurocognition, and Genetics study. This heterogeneous sample was recruited through geographically dispersed sites in the United States. The influence of birth weight on cortical thickness, surface area, and striatal and total brain volumes was investigated, controlling for variance in age, sex, household income, and genetic ancestry factors. Birth weight was found to exert robust positive effects on regional cortical surface area in multiple regions as well as total brain and caudate volumes. These effects were continuous across birth weight ranges and ages and were not confined to subsets of the sample. The findings show that (i) aspects of later child and adolescent brain development are influenced at birth and (ii) relatively small differences in birth weight across groups and conditions typically compared in neuropsychiatric research (e.g., Attention Deficit Hyperactivity Disorder, schizophrenia, and personality disorders) may influence group differences observed in brain parameters of interest at a later stage in life. These findings should serve to increase our attention to early influences.
BackgroundA growing body of evidence links socioeconomic status (SES) to children's brain structure. Few studies, however, have specifically investigated relations of SES to white matter structure. Further, although several studies have demonstrated that family SES is related to development of brain areas that support executive functions (EF), less is known about the role that white matter structure plays in the relation of SES to EF. One possibility is that white matter differences may partially explain SES disparities in EF (i.e., a mediating relationship). Alternatively, SES may differentially shape brain‐behavior relations such that the relation of white matter structure to EF may differ as a function of SES (i.e., a moderating relationship).MethodIn a diverse sample of 1082 children and adolescents aged 3–21 years, we examined socioeconomic disparities in white matter macrostructure and microstructure. We further investigated relations between family SES, children's white matter volume and integrity in tracts supporting EF, and performance on EF tasks.ResultsSocioeconomic status was associated with fractional anisotropy (FA) and volume in multiple white matter tracts. Additionally, family income moderated the relation between white matter structure and cognitive flexibility. Specifically, across multiple tracts of interest, lower FA or lower volume was associated with reduced cognitive flexibility among children from lower income families. In contrast, children from higher income families showed preserved cognitive flexibility in the face of low white matter FA or volume. SES factors did not mediate or moderate links between white matter and either working memory or inhibitory control.ConclusionsThis work adds to a growing body of literature suggesting that the socioeconomic contexts in which children develop not only shape cognitive functioning and its underlying neurobiology, but may also shape the relations between brain and behavior.
Automated surface-based MRI morphometry equipped with machine learning showed robust performance across cohorts from different centers and scanners. The proposed method may be a valuable tool to improve FCD detection in presurgical evaluation for patients with pharmacoresistant epilepsy.
Knowing the maturational schedule of typical brain development is critical to our ability to identify deviations from it; such deviations have been related to cognitive performance and even developmental disorders. Chronological age can be predicted from brain images with considerable accuracy, but with limited spatial specificity, particularly in the case of the cerebral cortex. Methods using multi-modal data have shown the greatest accuracy, but have made limited use of cortical measures. Methods using complex measures derived from voxels throughout the brain have also shown great accuracy, but are difficult to interpret in terms of cortical development. Measures based on cortical surfaces have yielded less accurate predictions, suggesting that perhaps cortical maturation is less strongly related to chronological age than is maturation of deep white matter or subcortical structures. We question this suggestion. We show that a simple metric based on the white/gray contrast at the inner border of the cortex is a good predictor of chronological age. We demonstrate this in two large datasets: the NIH Pediatric Data, with 832 scans of typically developing children, adolescents, and young adults; and the Pediatric Imaging, Neurocognition, and Genetics data, with 760 scans of individuals in a similar age-range. Further, our usage of an elastic net penalized linear regression model reveals the brain regions which contribute most to age-prediction. Moreover, we show that the residuals of age-prediction based on this white/gray contrast metric are not merely random errors, but are strongly related to IQ, suggesting that this metric is sensitive to aspects of brain development that reflect cognitive performance.
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