TY - JOUR
T1 - Association of catastrophizing with interleukin-6 responses to acute pain
AU - Edwards, Robert R.
AU - Kronfli, Tarek
AU - Haythornthwaite, Jennifer A.
AU - Smith, Michael T.
AU - McGuire, Lynanne
AU - Page, Gayle G.
N1 - Funding Information:
This work was supported by NIH Grant K23 AR051315 (to R.R.E.), by awards from the American College of Rheumatology (to R.R.E.) and Arthritis Foundation (to R.R.E.), as well as the Johns Hopkins General Clinical Research Center (M01-RR002719). Thanks to Monika Haack for her extremely helpful comments and feedback. No authors have any conflict of interest regarding this work.
PY - 2008/11/15
Y1 - 2008/11/15
N2 - Catastrophizing exerts its deleterious effects on pain via multiple pathways, and some researchers have reported that high levels of catastrophizing are associated with enhanced physiological reactivity to painful stimulation. In this project, 42 generally healthy adults underwent a series of psychophysical pain testing procedures assessing responses to noxious mechanical, heat, and cold stimuli. Pain catastrophizing cognitions were assessed prior to and then immediately after the various pain induction procedures. Blood samples were taken at baseline and then at several time points from the end of the procedures to 1 h post-testing. Samples were assayed for serum levels of cortisol and interleukin-6 (IL-6). Both cortisol and IL-6 increased from baseline during the post-testing period (p's < .05), with cortisol returning to baseline by 1 h post-testing and IL-6 remaining elevated. Pain catastrophizing, measured immediately after the pain procedures, was unrelated to cortisol reactivity, but was strongly related to IL-6 reactivity (p < .01), with higher levels of catastrophizing predicting greater IL-6 reactivity. In multivariate analyses, the relationship between catastrophizing and IL-6 reactivity was independent of pain ratings. Collectively, these findings suggest that cognitive and emotional responses during the experience of pain can shape pro-inflammatory immune system responses to noxious stimulation. This pathway may represent one important mechanism by which catastrophizing and other psychosocial factors shape the experience of both acute and chronic pain in a variety of settings.
AB - Catastrophizing exerts its deleterious effects on pain via multiple pathways, and some researchers have reported that high levels of catastrophizing are associated with enhanced physiological reactivity to painful stimulation. In this project, 42 generally healthy adults underwent a series of psychophysical pain testing procedures assessing responses to noxious mechanical, heat, and cold stimuli. Pain catastrophizing cognitions were assessed prior to and then immediately after the various pain induction procedures. Blood samples were taken at baseline and then at several time points from the end of the procedures to 1 h post-testing. Samples were assayed for serum levels of cortisol and interleukin-6 (IL-6). Both cortisol and IL-6 increased from baseline during the post-testing period (p's < .05), with cortisol returning to baseline by 1 h post-testing and IL-6 remaining elevated. Pain catastrophizing, measured immediately after the pain procedures, was unrelated to cortisol reactivity, but was strongly related to IL-6 reactivity (p < .01), with higher levels of catastrophizing predicting greater IL-6 reactivity. In multivariate analyses, the relationship between catastrophizing and IL-6 reactivity was independent of pain ratings. Collectively, these findings suggest that cognitive and emotional responses during the experience of pain can shape pro-inflammatory immune system responses to noxious stimulation. This pathway may represent one important mechanism by which catastrophizing and other psychosocial factors shape the experience of both acute and chronic pain in a variety of settings.
KW - Catastrophizing
KW - Cortisol
KW - Experimental pain
KW - Interleukin-6
KW - Pro-inflammatory
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U2 - 10.1016/j.pain.2008.07.024
DO - 10.1016/j.pain.2008.07.024
M3 - Article
C2 - 18778895
AN - SCOPUS:54249087012
SN - 0304-3959
VL - 140
SP - 135
EP - 144
JO - Pain
JF - Pain
IS - 1
ER -