The biological embedding of neonatal stress exposure: A conceptual model describing the mechanisms of stress‐induced neurodevelopmental impairment in preterm infants

Nist, Marliese Dion; Harrison, Tondi M.; Steward, Deborah K.

doi:10.1002/nur.21923

Cited by 45 publications

(52 citation statements)

References 106 publications

(156 reference statements)

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“…The model has been previously adapted for the study of preterm infant stress exposure and long‐term immune and hypothalamic pituitary adrenal axis functioning (Grunau et al, ). Using the ‘Biological Embedding of Childhood Adversity Model’ as the foundation, Nist, Harrison, and Steward () developed a conceptual model to describe the mediators of stress exposure and neurodevelopment in preterm infants. The Stress Neuro‐Immune Study will test the relationships among stress exposure, inflammation, and neurodevelopment, as theorized by the model.…”

Section: Introductionmentioning

confidence: 99%

Inflammatory mediators of stress exposure and neurodevelopment in very preterm infants: Protocol for the stress neuro‐immune study

Nist

Pickler

Steward

et al. 2019

Journal of Advanced Nursing

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Aims: (a) Determine relationships among stress exposure, inflammation, and neurodevelopment in very preterm infants and determine the mediated effect of inflammation on the relationship between stress exposure and neurodevelopment; (b) describe cytokine trajectories following birth and determine the effect of stress exposure on these trajectories; and (c) examine relationships between stress exposure and chronic stress responses in very preterm infants. Design: Non-experimental, repeated measures.Methods: Very preterm infants born 28-31 weeks post menstrual age will be enrolled. Cumulative stress exposure over the first 14 days of life will be measured using the Neonatal Infant Stressor Scale. Blood will be collected weekly for the quantification of cytokines. Neurodevelopment will be assessed using the Neurobehavioral Assessment of the Preterm Infant and hair for quantification of hair cortisol will be collected at 35 weeks post menstrual age. Multiple linear regression and conditional process analysis will be used to analyse the relationships among stress exposure, inflammation and neurodevelopment. Linear mixed models will be used to determine inflammatory trajectories over time. IRB approval for the study was Discussion: This study will determine the extent to which inflammation mediates the relationship between stress exposure and neurodevelopment. Interventions to attenuate inflammation in preterm infants may improve outcomes. Impact: Determining the potentially modifiable mediators of stress exposure and neurodevelopment in preterm infants is critical to improving long-term outcomes. K E Y W O R D S cytokines, inflammation, neonatal intensive care, neurodevelopment, nursing, preterm infant, repeated measures, stress | 2237 NIST eT al.

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Section: Introductionmentioning

confidence: 99%

Inflammatory mediators of stress exposure and neurodevelopment in very preterm infants: Protocol for the stress neuro‐immune study

Nist

Pickler

Steward

et al. 2019

Journal of Advanced Nursing

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“…More recently a conceptual model describing the mechanisms of stress-induced neurodevelopmental impairment in preterm infants has been published [20] . This concept is in good accordance with data published by Evans DJ et al in 2001 who showed that elevated norepinephrine levels are associated with adverse outcome in preterm infants [21].…”

Section: Hyothermia and Hrvmentioning

confidence: 99%

Early Life Stress, Growth and Neurodevelopment in Childhood

Buchhorn¹

2020

MRAJ

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Follow up studies of children with congenital heart disease, premature birth, small for gestational age syndrome and attention deficit hyperactivity disorder show significantly reduced 24-hours heart rate variability (HRV) that indicate autonomic dysfunction. The underlying pathophysiological process is of high clinical importance if autonomic dysfunction in these children is related to neurocognitive impairment, an enhanced cardiovascular risk, and a higher risk of short stature. Elevated norepinephrine levels, reduced HRV and MRI imaging indicate brain injury very early in life. We introduce the term autonomic imprinting to explain how early life stress have a lifelong imprinting effect on the autonomic nervous system. Many efforts are done for a careful management of infants in pediatric intensive care units. However, early life stress cannot be prevented if sympathetic activation is part of the underlying disease most of all due to congestive heart failure. We could demonstrate that beside a careful management, pharmacotherapy has a high impact on autonomic dysfunction in children with heart failure, attention deficit disorder and short stature. Moreover, online HRV monitoring is a complete noninvasive tool to monitor early life stress if it uses the data from routine heart rate monitoring. HRV online monitoring on the pediatric intensive care unit and Holter ECG monitoring in a daily life setting are clinical routine in our department for each pharmacotherapy affecting the autonomic nervous system. In the same time as monitoring of early life stress becomes clinically routine, the situation of children will improve if we realize which interventions increase early life stress or improve its detrimental damages in longtime follow up.

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“…The importance of pediatric-focused research cannot be overstated. Early experiences (including prenatal) of infants and children serve as the foundation for health and wellness throughout the life course (Bates et al, 2017, Nist, Harrison, Steward, 2019Shonkoff et al, 2012). That is, when infants and children are exposed to prenatal insults, toxic stress, poverty, maltreatment, or other social, economic, and experiential adversities, biological embedding of stress-induced physiologic responses results in neurodevelopmental problems and learning disorders, highrisk behaviors, and subsequent chronic physical and mental illness.…”

Section: Introductionmentioning

confidence: 99%