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Dysfunctional stress responses in chronic pain.
Alain Woda1, Pascale Picard2, Frédéric Dutheil3
1Dental faculty, EA 3847, CROC, 11 Boulevard Charles-de-Gaulle, Clermont-Ferrand, France; University Hospital of Clermont-Ferrand (CHU), Odontology department, Clermont-Ferrand, France.
Psychoneuroendocrinology
|June 6, 2016
Summary
Chronic stress response deregulation, involving the HPA axis, neuroactive steroids, and autonomic nervous system, is a common factor in pain and dysfunction. Genetic and immune factors also influence individual stress vulnerability and chronic conditions.
Area of Science:
- Neuroscience
- Immunology
- Endocrinology
Background:
- Chronic pain and dysfunction often share overlapping mechanisms.
- The adaptive response to stress is crucial for maintaining homeostasis.
- Dysregulation of stress response systems can lead to chronic conditions.
Purpose of the Study:
- To review the modes of chronic stress response deregulation.
- To identify common factors underlying dysfunctional and chronic pain conditions.
- To explore the roles of the hypothalamo-pituitary-adrenal axis, neuroactive steroids, autonomic nervous system, immune system, and genetics in stress response.
Main Methods:
- Literature review of studies on stress response pathways.
- Analysis of hypothalamo-pituitary-adrenal axis functions (basal levels, reactivity).
- Examination of neuroactive steroid synthesis and function (DHEA, DHEA-S, progesterone).
- Review of autonomic nervous system activity (sympathetic, parasympathetic).
- Investigation of immune system modulation (Th1/Th2 balance, cytokines).
- Exploration of genetic influences (polymorphisms, epigenetics).
Main Results:
- Hypothalamo-pituitary-adrenal axis dysfunction presents as hyper- or hypocortisolism and altered reactivity.
- Neuroactive steroids (e.g., DHEA, progesterone) synthesized locally can influence symptom localization and neurodegeneration.
- Autonomic nervous system dysfunction includes altered sympathetic and parasympathetic activity.
- Immune system deregulation involves shifts in the Th1/Th2 balance, impacting inflammation.
- Genetic factors, including polymorphisms and epigenetics, contribute to individual stress vulnerability.
Conclusions:
- Chronic deregulation of stress response systems is a unifying factor in various dysfunctional and pain conditions.
- Multiple systems, including the HPA axis, neuroactive steroids, autonomic nervous system, and immune/genetic factors, interact in stress response.
- Understanding these complex interactions is key to developing targeted therapies for chronic conditions.
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