Chronic Stress, Cortisol Dysfunction, and Pain: A Psychoneuroendocrine Rationale for Stress Management in Pain Rehabilitation
Open accessAbstract
Pain is a primary symptom driving patients to seek physical therapy, and its attenuation commonly defines a successful outcome. A large body of evidence is dedicated to elucidating the relationship between chronic stress and pain; however, stress is rarely addressed in pain rehabilitation. A physiologic stress response may be evoked by fear or perceived threat to safety, status, or well-being and elicits the secretion of sympathetic catecholamines (epinephrine and norepinepherine) and neuroendocrine hormones (cortisol) to promote survival and motivate success. Cortisol is a potent anti-inflammatory that functions to mobilize glucose reserves for energy and modulate inflammation. Cortisol also may facilitate the consolidation of fear-based memories for future survival and avoidance of danger. Although short-term stress may be adaptive, maladaptive responses (eg, magnification, rumination, helplessness) to pain or non–pain-related stressors may intensify cortisol secretion and condition a sensitized physiologic stress response that is readily recruited. Ultimately, a prolonged or exaggerated stress response may perpetuate cortisol dysfunction, widespread inflammation, and pain. Stress may be unavoidable in life, and challenges are inherent to success; however, humans have the capability to modify what they perceive as stressful and how they respond to it. Exaggerated psychological responses (eg, catastrophizing) following maladaptive cognitive appraisals of potential stressors as threatening may exacerbate cortisol secretion and facilitate the consolidation of fear-based memories of pain or non–pain-related stressors; however, coping, cognitive reappraisal, or confrontation of stressors may minimize cortisol secretion and prevent chronic, recurrent pain. Given the parallel mechanisms underlying the physiologic effects of a maladaptive response to pain and non–pain-related stressors, physical therapists should consider screening for non–pain-related stress to facilitate treatment, prevent chronic disability, and improve quality of life.
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Excess cortisol may increase binding to mineralocorticoid receptors, which can produce a pro-inflammatory response.
“Additionally, excess cortisol may increase the binding to Mineralocorticoid Receptors that can produce a pro-inflammatory response [23,24].”
From Chronic Stress and Autoimmunity: The Role of HPA Axis and Cortisol Dysregulation (2025) · cites this paper as [24]
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- Authors
- Hannibal, K. E., & Bishop, M. D.
- Affiliations
- University of Florida (US)
- Corresponding author
- Hannibal, Kara E.
- ORCID
- Bishop, Mark D.
- Venue
- Physical Therapy
- Publisher
- Oxford University Press (OUP)
- Published
- 2014-12-01
- Volume
- 94
- Issue
- 12
- Pages
- 1816-1825
- ISSN
- 0031-9023 (ISSN-L)
- 1538-6724
- PMC
- PMC4263906
- OpenAlex
- W2104399350
- Cited by
- 729
- References
- 77
- Citations by year
- 2026: 75 · 2025: 141 · 2024: 93 · 2023: 97 · 2022: 75 · 2021: 74 · 2020: 70 · 2019: 36 · 2018: 25 · 2017: 17 · 2016: 13 · 2015: 10 · 2012: 1
- FWCI
- 6.55
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Physical Therapy (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Center for Complementary and Integrative Health (AT006334, R01AT006334)
- Topics
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Health Sciences › Medicine › Pharmacology › Musculoskeletal pain and rehabilitation
- Health Sciences › Medicine › Anesthesiology and Pain Medicine › Pain Management and Treatment
- Keywords
- chronic stress, pain, stress management, pain rehabilitation, fear-avoidance beliefs, pain catastrophizing, cognitive reappraisal, maladaptive stress response, inflammation, stress screening
- MeSH terms
- Adaptation, Psychological, Humans, Hydrocortisone, Hypothalamo-Hypophyseal System, Pain, Pituitary-Adrenal System, Stress, Physiological, Stress, Psychological
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