Background: Life adversities, such as neighborhood disadvantage and lower household incomes, are associated with well-established impairments on language development, which predict academic difficulties throughout school. These language delays are observable by age 2, but it remains unclear if adversities experienced in utero affect neurological underpinnings of language development before delays emerge. Of interest are 3 white matter tracts implicated in early language skills: the corpus callosum (CC), inferior fronto-occipital fasciculus (IFOF), and uncinate (Unc).

Methods: A longitudinal cohort of 160 term-born (>36 weeks gestation) neonates were recruited from the eLABE study at Washington University, which oversampled St. Louis families exposed to poverty. Structural equation modeling was used to create 2 latent constructs of prenatal adversity. The first, “social disadvantage”, aggregates neighborhood disadvantage, family income, insurance status, maternal education, and diet. The second, “maternal psychosocial stress”, models maternal depression, stress, life adversities, and perceived discrimination. At birth, diffusion MRI data were collected, and parameters for white matter tract development were created using probabilistic tractography in FSL. In-person follow-up at age 2 evaluated child language skills. To assess the independent and interactive effects of prenatal adversities and neonatal white matter microstructure on language skills, stepwise linear regression models were conducted after adjustment for child sex, gestational age, and postmenstrual age at scan. 


Results: Prenatal social disadvantage (p=.00) and maternal psychosocial stress (p=.00) predicted significantly lower language scores by age 2. However, in a joint model, only the effects due to social disadvantage remained significant. Lower CC fractional anisotropy predicted significantly lower language scores (p=.02) independently of social disadvantage (p=.00). IFOF and Unc were not predictive of language ( p > .05). To examine the relationship between CC maturation and social disadvantage, a moderation analysis was conducted after dichotomizing families’ income into above and below 200% the federal poverty line (FPL), as most federal assistance programs use this value as a threshold for benefit eligibility. The interaction term was not significant (p= .11), but upon plotting results by income group, the slope for infants above 200% FPL was somewhat stronger. 

Conclusion: This study suggests that prenatal adversity, particularly social disadvantage, and immature CC myelination are strong predictors of language delays by age 2. These data can be used as empirical evidence to advocate for increased funding of federal assistance programs that benefit pregnant people (ex., WIC) and downstream fetal brain development. By continuing to explore the relationship between prenatal adversities on fetal brain development and emerging language skills, future studies will continue to identify specific neurological markers of early language development to allow clinicians to intervene before delays emerge.

The Effects of Prenatal Adversity and Neonatal White Matter Microstructure on Child Language Skills at Age 2

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