Linking prenatal maternal distress and infant neural noise to problem behavior in toddlerhood

• In Event: Prenatal Distress and Neurobehavior in Infancy and Early Childhood: Testing Putative Biological Mechanisms

Abstract

A mother’s distress while pregnant may contribute to behavior problems in her young child (van den Bergh et al., 2017). The neuronal mechanisms underlying this association, however, remain opaque. One potential mechanism may be “noisy” neuronal communication in infants’ brains. The aperiodic (1/f-like) exponent of neural power spectra is considered a putative marker of neural noise. A small aperiodic exponent—equivalent to a flatter power spectrum—indicates more asynchronous neuronal spiking relative to an oscillatory regime, possibly due to increases in the excitation/inhibition ratio in the brain (Gao et al., 2017). While a moderate level of noise is thought to facilitate synchronization between developing neural networks, low levels of neural noise may contribute to internalizing disorders, as relevant neural networks become overcoupled as a result of reinforcement (e.g., rumination) and then strengthened via Hebbian learning mechanisms (Voytek & Knight, 2015). Though provocative, these hypotheses have not been tested in early childhood, when problem behavior may first become apparent. In this study, we test the hypothesis that infants of mothers who experienced more distress while pregnant would exhibit less neural noise and more problematic behavior.

Pregnant women (N = 162, Mage = 29.0, 27% Hispanic) reported on their mental health and recent experiences of stress (Table 1). An exploratory factor analysis (maximum likelihood, promax rotation) identified two underlying latent constructs: one reflected general distress and another reflected pregnancy-specific distress (Table 1). When infants were age 7 months, their aperiodic exponents were estimated from infant electroencephalogram data (n = 85) via FOOOF (Haller et al., 2018). Mothers reported on infants’ internalizing, externalizing, and dysregulated behavior at 18 months using the ITSEA (Carter & Briggs, 2005). Missing data were handled using FIML.

A path model showed that high neural noise (a small aperiodic exponent) at 7 months predicted high internalizing problems at 18 months (β = -.28, p = .02) but not externalizing behavior or dysregulation (ps > .82). We found that the association with internalizing problems was driven by a link between neural noise and the inhibition to novelty subscale. Neural noise was not associated with either maternal distress factor (ps > .50). Maternal distress predicted infant externalizing behavior (β = .34, p = .01) and dysregulation (β = .29, p = .03) at 18 months, but not internalizing behavior (β = .20, p = .13).

Contrary to our expectations, these results suggest that high levels of neural noise in the first year of life was related to risk for internalizing behaviors in toddlerhood, chiefly inhibition to novelty. Although not associated with infants’ neural noise, maternal distress did predict infants’ externalizing and dysregulated behaviors at 18 months, lending additional support for the intergenerational transmission of psychopathology risk. Follow-up analyses will examine whether maternal distress postnatally, as well as the stability of maternal distress across the perinatal period, are associated with individual differences in infant neural noise and problem behavior.

Authors

• Brendan Dale Ostlund, Pennsylvania State University, University Park
  Presenting Author

• Lee Raby, University of Utah
  Non-Presenting Author

• Lauren Williams, University of California, San Diego
  Non-Presenting Author

• Sheila E Crowell, University of Utah
  Non-Presenting Author

• Liz Conradt, Duke University
  Non-Presenting Author

• Trafton Drew, University of Utah
  Non-Presenting Author