The Neurobiology of Infant Attachment-Trauma and Disruption of Parent-Infant Interactions
Nimra Naeem1,2,3, Roseanna M Zanca2,3, Sylvie Weinstein1,3
1Department of Psychology, Center for Neuroscience, New York University, New York, NY, United States.
Insights
Early life adversity, particularly caregiver trauma, impacts infant brain development. Elevated stress hormones like corticosterone (CORT) in infancy can lead to subtle, yet significant, behavioral and emotional pathology later in life.
Area of Science:
- Neuroscience
- Developmental Psychology
- Psychopathology
Background:
- Early-life adversity disrupts brain development, leading to later maladaptive behaviors.
- The immediate impact of caregiver-infant trauma on development is not fully understood.
- Infant attachment occurs irrespective of care quality, even with trauma.
Purpose of the Study:
- Review infant trauma within attachment, focusing on animal research.
- Define mechanisms and translate findings for developmental child research.
- Understand the role of stress hormones in infant development and trauma.
Main Methods:
- Review of current clinical and animal literature on early-life adversity and attachment.
- Analysis of rodent neurobehavioral studies on stress hormone effects.
- Examination of corticosterone (CORT) elevations and their impact on the amygdala.
Main Results:
- Repeated trauma with attachment figures has subtle early effects, but acute stress reveals pathology.
- Infancy elevations in corticosterone (CORT), especially with the mother, target the amygdala and cause pathology.
- Altered infants appear stable at baseline but exhibit pathology under acute stress in emotion, social, and fear circuits.
Conclusions:
- Understanding stress hormone roles in typical and disrupted infant development is crucial.
- Elevated CORT during infancy can disrupt typical development, leading to pathology.
- Identifying early trauma effects and markers of later-life pathology requires comprehensive analysis of stress hormone impacts.
Abstract:
Current clinical literature and supporting animal literature have shown that repeated and profound early-life adversity, especially when experienced within the caregiver-infant dyad, disrupts the trajectory of brain development to induce later-life expression of maladaptive behavior and pathology. What is less well understood is the immediate impact of repeated adversity during early life with the caregiver, especially since attachment to the caregiver occurs regardless of the quality of care the infant received including experiences of trauma. The focus of the present manuscript is to review the current literature on infant trauma within attachment, with an emphasis on animal research to define mechanisms and translate developmental child research. Across species, the effects of repeated trauma with the attachment figure, are subtle in early life, but the presence of acute stress can uncover some pathology, as was highlighted by Bowlby and Ainsworth in the 1950s. Through rodent neurobehavioral literature we discuss the important role of repeated elevations in stress hormone corticosterone (CORT) in infancy, especially if paired with the mother (not when pups are alone) as targeting the amygdala and causal in infant pathology. We also show that following induced alterations, at baseline infants appear stable, although acute stress hormone elevation uncovers pathology in brain circuits important in emotion, social behavior, and fear. We suggest that a comprehensive understanding of the role of stress hormones during infant typical development and elevated CORT disruption of this typical development will provide insight into age-specific identification of trauma effects, as well as a better understanding of early markers of later-life pathology.
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