Poster #14 - Multiple measures of prenatal distress are associated with hippocampal functional connectivity in human neonates

• In Event: 3-106 - Poster Session 11
  In Poster Session: PS 11 Section - Biological Processes: Neuroscience and Genetics

Integrative Statement

Maternal prenatal distress—typically assessed as depression, anxiety, or stress—is a risk factor for children’s future psychiatric disorders including autism, ADHD, depression, and substance use. Data suggest that prenatal exposure to maternal distress is associated with altered brain development of children and adolescents. Consistently, the hippocampus has been shown to be vulnerable to high levels of maternal distress across preclinical and human studies. More recently, the effects of prenatal maternal distress on offspring brain development have been highlighted to be identifiable as early as the fetal to infancy periods. Nevertheless, distress is multifaceted. Previous studies typically have relied on a single assessment approach. The goal of the current study is to determine whether various types of maternal prenatal distress affect neonatal functional connectivity in similar or unique ways.

Forty-five young pregnant women at high risk for life distress, aged 14 to 19, were recruited from Columbia University Medical Center. They received routine prenatal care and had no major health problems. At 34-37 weeks of gestation, the women provided self-report psychological stress assessment including the Perceived Stress Scale (PSS), Reynolds Adolescent Depression Scale (RADS), and Prenatal Distress Questionnaire (PDQ). For the neonates, resting-state functional MRI data were acquired on a GE Signa 3T scanner. Standard seed connectivity from the right and left hippocampus was performed. Prenatal distress measures were correlated with connectivity while controlling for postmenstrual age (PMA) at scan and sex. All results are at p<0.05, corrected for multiple comparisons.

All neonates were appropriate for gestational age (birth weight: 3206.9±461.3 g, gestational at birth: 39.3±1.3 weeks) and were scanned at 42.4±1.6 weeks postmenstrual age. The majority of participants were male (68.8%). With higher levels of maternal scores on the PSS, neonates exhibited weaker connectivity between the left hippocampus and dorsal anterior cingulate cortex (dACC), between the right hippocampus and the dACC, and between the right hippocampus and the mid cingulate cortex (MCC), and stronger connectivity between the right hippocampus and left fusiform gyrus. With higher levels of maternal scores on the RADS, neonates exhibited weaker connectivity between the left hippocampus and posterior cingulate cortex (PCC) and between the right hippocampus and precuneus. With higher levels of maternal scores on the PDQ, neonates exhibited stronger connectivity between the left hippocampus and right superior temporal sulcus (STS).

Using multiple measures of prenatal maternal distress, we demonstrate mainly weaker functional connectivity between the hippocampus and several cortical regions in the neonatal brain. We show associations between perceived stress and hippocampal – dACC/MCC connectivity; between depressive symptoms and hippocampal – PCC/precuneus connectivity; and between pregnancy distress and hippocampal – STS connectivity. These connectivity patterns suggest functional differences that are unique to the type of prenatal maternal distress. The current study highlights the importance of considering multiple facets of distress. Future studies are necessary to examine these hippocampal connectivity patterns to toddler outcomes, as they will establish the corresponding behavioral phenotypes in early life that may contribute to risk for future psychiatric symptoms and an intergenerational transmission of familial pattern of affect dysregulation.

Authors

• Dustin Scheinost, Yale University
  Presenting Author

• Marisa N Spann, Columbia University, College of Physicians and Surgeons
  Non-Presenting Author

• Bradley S Peterson, Institute for the Developing Mind, Children’s Hospital Los Angeles & Keck School of Medicine, University of South California
  Non-Presenting Author

• Catherine Monk, Columbia University
  Non-Presenting Author