title: Fetal glucocorticoid exposure is associated with preadolescent brain development.
abstract: BACKGROUND
  Glucocorticoids play a critical role in normative regulation of fetal brain development. Exposure to excessive levels may have detrimental consequences and disrupt maturational processes. This may especially be true when synthetic glucocorticoids are administered during the fetal period, as they are to women in preterm labor. This study investigated the consequences for brain development and affective problems of fetal exposure to synthetic glucocorticoids.
  
  
  METHODS
  Brain development and affective problems were evaluated in 54 children (56% female), aged 6 to 10, who were full term at birth. Children were recruited into two groups: those with and without fetal exposure to synthetic glucocorticoids. Structural magnetic resonance imaging scans were acquired and cortical thickness was determined. Child affective problems were assessed using the Child Behavior Checklist.
  
  
  RESULTS
  Children in the fetal glucocorticoid exposure group showed significant and bilateral cortical thinning. The largest group differences were in the rostral anterior cingulate cortex (rACC). More than 30% of the rACC was thinner among children with fetal glucocorticoid exposure. Furthermore, children with more affective problems had a thinner left rACC.
  
  
  CONCLUSIONS
  Fetal exposure to synthetic glucocorticoids has neurologic consequences that persist for at least 6 to 10 years. Children with fetal glucocorticoid exposure had a thinner cortex primarily in the rACC. Our data indicating that the rACC is associated with affective problems in conjunction with evidence that this region is involved in affective disorders raise the possibility that glucocorticoid-associated neurologic changes increase vulnerability to mental health problems.
authors.affiliation: Department of Psychology, University of Denver, Denver, Colorado; Departments of Psychiatry and Human Behavior, University of California Irvine, Orange, California. Electronic address: Elysia.Davis@du.edu.
authors.forename: Elysia Poggi
authors.initials: EP
authors.lastname: Davis
authors.forename: Curt A
authors.initials: CA
authors.lastname: Sandman
authors.forename: Claudia
authors.initials: C
authors.lastname: Buss
authors.forename: Deborah A
authors.initials: DA
authors.lastname: Wing
authors.forename: Kevin
authors.initials: K
authors.lastname: Head
mesh_terms: D000328:Adult; D001284:Atrophy; D001921:Brain / Q000187:drug effects* / Q000254:growth & development* / Q000473:pathology; D016022:Case-Control Studies; D002648:Child; D005260:Female; D005938:Glucocorticoids / Q000009:adverse effects*; D006801:Humans; D008297:Male; D019964:Mood Disorders / Q000473:pathology / Q000523:psychology; D059906:Neuroimaging; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000139:chemically induced / Q000473:pathology* / Q000523:psychology*
chemical_list: D005938:Glucocorticoids
keywords: Development; MRI; fetal programming; glucocorticoid; prenatal; stress