Stress-system activation in children with chronic pain: A focus for clinical intervention

2019 ◽  
Vol 25 (1) ◽  
pp. 78-97 ◽  
Author(s):  
Peter M McInnis ◽  
Taylor A Braund ◽  
Zhi Kai Chua ◽  
Kasia Kozlowska

Accumulating evidence indicates that psychological and neurophysiological processes interconnect and interact to activate the body’s stress system and to trigger and maintain functional somatic symptoms. This study used the Early Life Stress Questionnaire, Depression Anxiety Stress Scales and biological markers (heart rate, heart rate variability, skin conductance, C-reactive protein (CRP) titre, respiratory rate, and accuracy and reaction time in an emotion-face identification task), to examine childhood adversity, psychological distress and stress-system activation in 35 children and adolescents (23 girls and 12 boys, 9–17 years old) disabled by chronic pain (vs two groups of age- and sex-matched healthy controls). Patients reported more early-life stress ( U = 798.5, p = .026) and more psychological distress ( U = 978, p < .001). They showed activation of the autonomic system: elevated heart rate ( U = 862.5, p = .003), elevated electrodermal activity ( U = 804.5, p = .024) and lower heart rate variability in the time domain ( U = 380.5, p = .007) and frequency domain ( U = 409.5, p = .017). The group showed an upward shift of CRP titres (with 75th and 90th CRP percentiles of 4.5 and 10.5 mg/L, respectively), suggesting the activation of the immune–inflammatory system. Elevated CRP titres were associated with elevated heart rate ( p = .028). There were no differences in respiratory rate or in accuracy and reaction time in the emotion-face identification task. The results indicate that interventions for children and adolescents with chronic pain need a multidisciplinary mind–body approach that concurrently addresses psychological distress, physical impairment and stress-system dysregulation.

2020 ◽  
Vol 8 (10) ◽  
Author(s):  
Reiner Buchhorn

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.


2019 ◽  
Vol 374 (1785) ◽  
pp. 20190283 ◽  
Author(s):  
S. M. Géranton

Animal behaviours are affected not only by inherited genes but also by environmental experiences. For example, in both rats and humans, stressful early-life events such as being reared by an inattentive mother can leave a lasting trace and affect later stress response in adult life. This is owing to a chemical trace left on the chromatin attributed to so-called epigenetic mechanisms. Such an epigenetic trace often has consequences, sometimes long-lasting, on the functioning of our genes, thereby allowing individuals to rapidly adapt to a new environment. One gene under such epigenetic control is FKBP5 , the gene that encodes the protein FKPB51, a crucial regulator of the stress axis and a significant driver of chronic pain states. In this article, we will discuss the possibility that exposure to stress could drive the susceptibly to chronic pain via epigenetic modifications of genes within the stress axis such as FKBP5 . The possibility that such modifications, and therefore, the susceptibility to chronic pain, could be transmitted across generations in mammals and whether such mechanisms may be evolutionarily conserved across phyla will also be debated. This article is part of the Theo Murphy meeting issue ‘Evolution of mechanisms and behaviour important for pain’.


HORMONES ◽  
2018 ◽  
Vol 17 (4) ◽  
pp. 507-520 ◽  
Author(s):  
Agorastos Agorastos ◽  
Panagiota Pervanidou ◽  
George P. Chrousos ◽  
Gerasimos Kolaitis

2017 ◽  
Vol 149 (2) ◽  
pp. 79-83
Author(s):  
Takashi Nishinaka ◽  
Kazuo Nakamoto ◽  
Shogo Tokuyama

2020 ◽  
Vol 42 (1) ◽  
pp. 2-11
Author(s):  
Sabrina Salberg ◽  
Marissa Sgro ◽  
Rhys D. Brady ◽  
Melanie Noel ◽  
Richelle Mychasiuk

2020 ◽  
Vol 10 (3) ◽  
pp. 169 ◽  
Author(s):  
Panagiota Pervanidou ◽  
Gerasimos Makris ◽  
George Chrousos ◽  
Agorastos Agorastos

Traumatic stress exposure during critical periods of development may have essential and long-lasting effects on the physical and mental health of individuals. Two thirds of youth are exposed to potentially traumatic experiences by the age of 17, and approximately 5% of adolescents meet lifetime criteria for posttraumatic stress disorder (PTSD). The role of the stress system is the maintenance of homeostasis in the presence of real/perceived and acute/chronic stressors. Early-life stress (ELS) has an impact on neuronal brain networks involved in stress reactions, and could exert a programming effect on glucocorticoid signaling. Studies on pediatric PTSD reveal diverse neuroendocrine responses to adverse events and related long-term neuroendocrine and epigenetic alterations. Neuroendocrine, neuroimaging, and genetic studies in children with PTSD and ELS experiences are crucial in understanding risk and resilience factors, and also the natural history of PTSD.


2018 ◽  
Vol 9 (3) ◽  
pp. 344-350
Author(s):  
L. J. C. A. Smarius ◽  
T. G. A. Strieder ◽  
T. A. H. Doreleijers ◽  
T. G. M. Vrijkotte ◽  
S. R. de Rooij

AbstractEarly life stress has been shown to contribute to alterations in biobehavioral regulation. Whereas many different forms of childhood adversities have been studied in relation to cardiovascular outcomes, very little is known about potential associations between caregivers’ verbally aggressive behavior and heart rate and blood pressure in the child. This prospective study examined whether maternal verbally aggressive behavior in early infancy is associated with heart rate or blood pressure at age 5–6. In the Amsterdam Born Children and their Development study, a large prospective, population-based birth cohort, maternal verbally aggressive behavior was assessed by questionnaire in the 13th week after birth. The child’s blood pressure and heart rate were measured during rest at age 5–6 (n=2553 included). Maternal verbally aggressive behavior in infancy was associated with a higher systolic blood pressure (SBP) both in supine and sitting position after adjustment for sex, height and age (SBP supine B=1.01 mmHg; 95% CI [0.06; 1.95] and SPB sitting B=1.29 mmHg; 95% CI [0.12; 2.46]). Adjustment for potential confounding variables, such as other mother–infant dyad aspects, family hypertension and child’s BMI, only slightly attenuated the associations (SBP supine B=0.99 mmHg; 95% CI [0.06; 1.93] and SPB sitting B=1.11 mmHg; 95% CI [−0.06; 2.27]). Maternal verbally aggressive behavior was not associated with diastolic blood pressure or heart rate at age 5–6. Maternal verbally aggressive behavior might be an important early life stressor with negative impact on blood pressure later in life, which should be further investigated. Possible underlying mechanisms are discussed.


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