Abstract

Stress reactivity is typically investigated in laboratory settings, which is inadequate for mothers in maternity settings. This study aimed at validating the Lausanne Infant Crying Stress Paradigm (LICSP) as a new psychosocial stress paradigm eliciting psychophysiological stress reactivity in early postpartum mothers (n = 52) and to compare stress reactivity in women at low (n = 28) vs. high risk (n = 24) of childbirth-related posttraumatic stress disorder (CB-PTSD). Stress reactivity was assessed at pre-, peri-, and post-stress levels through salivary cortisol, heart rate variability (high-frequency (HF) power, low-frequency (LF) power, and LF/HF ratio), and perceived stress via a visual analog scale. Significant time effects were observed for all stress reactivity outcomes in the total sample (all p < 0.01). When adjusting for perceived life threat for the infant during childbirth, high-risk mothers reported higher perceived stress (p < 0.001, d = 0.91) and had lower salivary cortisol release (p = 0.023, d = 0.53), lower LF/HF ratio (p < 0.001, d = 0.93), and marginally higher HF power (p = 0.07, d = 0.53) than low-risk women. In conclusion, the LICSP induces subjective stress and autonomic nervous system (ANS) reactivity in maternity settings. High-risk mothers showed higher perceived stress and altered ANS and hypothalamic–pituitary–adrenal reactivity when adjusting for infant life threat. Ultimately, the LICSP could stimulate (CB-)PTSD research.

Highlights

  • Changes in psychophysiological stress responses occurring during the early postpartum period after traumatic childbirth have not been investigated so far

  • These changes might play a significant role in the development of childbirth-related posttraumatic stress disorder (CB-Posttraumatic Stress DisorderPosttraumatic stress disorder (PTSD))

  • Results revealed that the Lausanne Infant Crying Stress Paradigm (LICSP) elicits autonomic nervous system (ANS) and subjective stress responses in women in the early postpartum period

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Summary

Introduction

Posttraumatic stress disorder (PTSD) may develop following a traumatic event, as defined by the PTSD stressor criterion of the Diagnostic and Statistical Manual of Mental Disorders, 5th ed. Four symptom clusters (criteria B–E of the DSM-5) characterize this disorder: intrusions, avoidance of trauma-related cues, negative cognitions and mood, and hyperarousal [1]. PTSD can be diagnosed one month following the traumatic stressor [1], even if an acute posttraumatic stress response can be observed in the meantime [2]. The question arises to understand why after having been exposed to a traumatic event, only some individuals develop PTSD symptoms [3]. According to psychobiological findings, altered stress reactivity, such as a dysregulation of the hypothalamic–pituitary– adrenal (HPA) axis or the autonomic nervous system (ANS), may play a major role in the development of PTSD [4,5]

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