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.
The aim of the study was to investigate the relationship between affective state, pain, and coping in hospitalized women with rheumatoid arthritis, including both between- and within-person perspectives.
Participants were 95 female patients between 24 and 82 years of age (M = 50.91; SD = 13.80). For three consecutive days, they rated each night their state affect (positive and negative), pain level, and coping strategies (emotion-, problem- and meaning-focused ones). Relations among variables were tested with a multilevel approach with time included as a covariate.
Within-person meaning-focused coping suppressed the negative pain effect on emotional state, but only for positive affect (Sobel’s z = 2.07, p = .04). Moderators of the pain–affect relationship were between-person differences in pain level (B = −.23, SE = .08, t = −2.884, p = .004) and in meaning-focused coping (B = −.63, SE = .20, t = −2.097, p = .04). Specifically, suppression was significant only for patients who reported lower than sample average pain levels and for patients who reported lower than sample average use of meaning-focused strategies.
Findings indicated that meaning-focused coping can be a crucial strategy for keeping daily positive affect in the face of chronic pain and how this effect is modified by interindividual differences. Even if restricted to the specific context, it may inform an intervention for hospitalized women with rheumatoid arthritis.