Fetal Exposure to Maternal Depressive Symptoms Is Associated With Cortical Thickness in Late Childhood
College of Arts Humanities and Social Sciences, Psychology
Maternal depression is one of the most common prenatal complications. The consequences of fetal exposure to maternal depression are poorly understood. The aim of this study is to examine the association between fetal exposure to maternal depressive symptoms and cortical thickness in children 6–9 years old.
A prospective, longitudinal study of maternal depressive symptoms at 19, 25, and 31 weeks’ gestation was followed by acquisition of a structural magnetic resonance imaging scan in 81 children (age, 86.1 ± 9.9 months).
Significant (p < .01) cortical thinning in children primarily in the right frontal lobes was associated with exposure to prenatal maternal depression. The strongest association was at 25 weeks’ gestation; exposure to maternal depression at 25 gestational weeks was associated with cortical thinning in 19% of the whole cortex and 24% of the frontal lobes, primarily in the right superior, medial orbital, and frontal pole regions of the prefrontal cortex (p < .01). The significant association between prenatal maternal depression and child externalizing behavior (p < .05) was mediated by cortical thinning in prefrontal areas of the right hemisphere.
The pattern of cortical thinning in children exposed to prenatal maternal depression is similar to patterns in depressed patients and in individuals with risk for depression. Exposure to prenatal depression coupled with subsequent cortical thinning was associated with presence of externalizing behavior in preadolescent children and may be prodromal markers of risk for dysphoria. Vulnerability to prenatal influences at 25 gestational weeks may result from the enormous growth and dramatic structural changes in the nervous system.
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Sandman, Curt A, Buss, Claudia, Head, Kevin, & Davis, Elysia Poggi. (2015). Fetal Exposure to Maternal Depressive Symptoms Is Associated With Cortical Thickness in Late Childhood. Biological Psychiatry (1969), 77(4), 324-334. DOI: 10.1016/j.biopsych.2014.06.025.