Journal
JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY
Volume 55, Issue 7, Pages 802-810Publisher
WILEY
DOI: 10.1111/jcpp.12188
Keywords
Prematurity; temperament; infancy; neural development; motor inhibition
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Funding
- Israel Science Foundation [1518]
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Background Behavioral inhibition (BI), the tendency to withdraw or exhibit negative affect when experiencing stressful situations, is a major risk factor for the development of social anxiety. However, neonatal biologic origins of this progression are still unknown. Click here to enter text.This study aimed to extend frameworks of behavioral inhibition by exploring empirically the central role of neonatal brainstem electrophysiologic functions in the development of social disengagement and BI. Methods Sixty-six preterm neonates (means +/- SD: gestation age=33.1 +/- 1.22weeks, birth weight=1775+346.7g; 51% female) participated in a prospective longitudinal study. The infants were tested within the first 2weeks of postnatal life using an auditory brainstem-evoked response test. Based on the typicality of the major ABR wave latencies, waves I, III and V, neonates were divided into two groups (compromised, CBSF- with at least one component 1.5 SDs from the mean for the respective gestation age; normal, NBSF, with all components within 1.5 SD around the mean), and were enrolled in a prospective longitudinal follow-up study. This report extends previous work from 4m by testing responses to socioemotional challenges during the Separation-Reunion paradigm at 12m. Results Results show that infants with neonatal CBSF were more susceptible to be classified as BI at 12m (age corrected for prematurity) than infants with NBSF (66% vs. 40%, respectively). The most striking symptom in the CBSF group was a disability to initiate self-regulatory activities in response to a socioemotional challenge, resulting in frequent passivity/dependency (p<.001). Statistical regression analysis revealed that face-to-face gaze engagement at 4m moderates the risk related to neonatal CBSF for the emergence of BI at 12m, but did not overturn the emergence of BI. Conclusion Results support the hypothesis that neonatal brainstem dysfunction canalizes behavioral inhibition. These findings highlight, for the first time, the role of the early developing brainstem in later development of BI and in abilities to initiate self-regulatory behavior.
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