About this srcd poster session

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Panel information
Panel 3. Biological Processes: Psychophysiology

Abstract

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The autonomic nervous system (ANS) develops during the perinatal period, maintains homeostasis, and is susceptible to environmental input. As suggested in the RDoC framework, alterations in ANS function may contribute to the development of nonoptimal socioemotional/behavioral outcomes. Prenatal cocaine exposure (PCE) may disrupt ANS function, is often used in tandem with other substances, and is associated with maternal childhood maltreatment. These risks may also affect offspring ANS function via non-optimal parenting and postnatal adversity. We tested two hypothesized models (one for parasympathetic and one for sympathetic response) that included maternal childhood maltreatment and prenatal substance exposure as predictors of non-optimal autonomic regulation during rest and in response to frustration at early school-age via autonomic regulation in infancy; chronicity of harsh parenting from infancy to preschool age; and cumulative postnatal adversities from birth to early school-age.

216 families (51% girls, 72% Black) were recruited at delivery (115 cocaine-exposed, 101 non-exposed), with repeated postnatal assessments between birth and early school-age (Mchild age=5.51 years, SD=0.37). Multimethod assessments were used to measure prenatal substance use and cocaine group status (maternal/child urine assays at delivery, maternal hair assays, and maternal calendar-based interviews). A composite of emotional, physical, and sexual abuse subscales from the Childhood Trauma Questionnaire reflected maternal childhood maltreatment. Harsh parenting was measured during mother-child free play coded using a global 5-point scale (higher scores=less harsh parenting). Cumulative postnatal adversity included maternal psychological distress, caregiver instability, violence exposure, and maternal postnatal substance use from birth to early school-age. Child autonomic reactivity and regulation were indexed via respiratory sinus arrhythmia (RSA) reflecting parasympathetic functioning and skin conductance (SCL) reflecting sympathetic functioning at early school-age while watching affectively neutral video (baseline) followed by a frustration task (see Table 1 for descriptive statistics).

Structural equation modeling indicated that the hypothesized models fit the data well (Figures 1A and 1B). PCE was associated with lower baseline RSA in infancy and harsh parenting from infancy to preschool age. Maternal childhood maltreatment was marginally associated with higher infant baseline RSA which was marginally associated with early school-age baseline RSA. In addition, maternal childhood maltreatment and prenatal tobacco and alcohol exposure were associated with higher postnatal adversity. Higher postnatal adversity predicted lower baseline SCL and SCL during a frustration task.

Findings provide further evidence that PCE is associated with alterations in infant ANS function. Specifically, lower baseline RSA may reflect parasympathetic nervous system wear and tear, leading to less available physiological resources for responding to stress. Further, findings support intergenerational transmission of risk from maternal childhood maltreatment directly to infant ANS function and to child ANS function via increased cumulative environmental risk. Specifically, lower baseline SCL and SCL reactivity may reflect a more passive response to stress, likely due to chronicity of stress and wear and tear of the sympathetic nervous system over time. Interestingly, maternal childhood abuse predicted higher infant baseline RSA. Both higher and lower baseline RSA have been characterized as non-optimal within the literature, with baseline RSA positively associated with environmental risk susceptibility.

Author information

Author	Role
Olivia Bell, The Pennsylvania State University	Presenting author
Madison Kelm, The Pennsylvania State University	Non-presenting author
Pamela Schuetze, SUNY Buffalo State University	Non-presenting author
Rina D. Eiden, The Pennsylvania State University	Non-presenting author

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