Chronic Stress, Cortisol Dysfunction, and Pain: A Psychoneuroendocrine Rationale for Stress Management in Pain Rehabilitation

Abstract

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.

Associations of screen work with neck and upper extremity symptoms: a systematic review with meta-analysis

“…Increased muscle tension has also been suggested to arise from psychosocial and organisational work environment factors 13. An alternative explanation may be that psychosocial workplace stressors associated with screen work14 may be associated with a central sensitisation response in the body that can lead to musculoskeletal symptoms 15. To conclude, musculoskeletal risks associated with exposure to screen work can be physical or psychosocial, and may also interact with other aspects of work.…”

Mechanisms of Stress in Humans

“…Numerous studies have linked chronic stress to several health problems (e.g., Moffitt, 2013), including Parkinson's disease (in animal studies, e.g., Djamshidian & Lees, 2014;Sugama, et al, 2016), depression (e.g., Conway, Rutter & Brown, 2016;Gold, 2015;Swanson, Zeng, Weeks, & Colman, 2013) and pain (e.g., Hannibal & Bishop, 2014;Vachon-Presseau, 2013, Woda, Picard, & Dutheil, 2016. Stress was found to be associated with diminishing capacity to respond to reward (Admon, et al, 2013), declines in cognitive function (Vitaliano, et al, 2005) and disruptions in attentional control of the prefrontal cortex functions (Liston et al, 2009).…”

Natural cancer-killing activity of human granulocytes

“…The human body deals with acute stress with stress response or "fight-or-flight" response, in which stress hormones are released into the blood stream [33][34]. As a result, stress hormones stimulate energy utilization in the stress response organs, such as cardiac, pulmonary, muscular and sensory systems and inhibit energy metabolism in the non-response organs, such as digestive, renal and immunological systems [35][36][37]. Among stress hormones, cortisol, epinephrine, and norepinephrine are the quantitatively most important molecules released into blood stream [38,39].…”