The impact of anxiety and catastrophizing on interleukin-6 responses to acute painful stress
Authors Lazaridou A, Martel MO, Cahalan CM, Cornelius MC, Franceschelli O, Campbell CM, Haythornthwaite JA, Smith M, Riley J, Edwards RR
Received 30 July 2017
Accepted for publication 4 October 2017
Published 28 March 2018 Volume 2018:11 Pages 637—647
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 4
Editor who approved publication: Dr E Alfonso Romero-Sandoval
Asimina Lazaridou,1 Marc O Martel,1 Christine M Cahalan,1 Marise C Cornelius,1 Olivia Franceschelli,1 Claudia M Campbell,2 Jennifer A Haythornthwaite,2 Michael Smith,2 Joseph Riley,3 Robert R Edwards1
1Department of Anesthesiology, Harvard Medical School, Brigham & Women’s Hospital, Boston, MA, USA; 2Department of Psychiatry and Behavioral Sciences, School of Medicine, Johns Hopkins University, Baltimore, MD, USA; 3Department of Community Dentistry and Behavioral Science, College of Dentistry, University of Florida, Gainesville, FL, USA
Objective: To examine the influence of anxiety and pain-related catastrophizing on the time course of acute interleukin-6 (IL-6) responses to standardized noxious stimulation among patients with chronic pain.
Methods: Data were collected from 48 participants in the following demographically matched groups: patients with chronic pain (n=36) and healthy controls (n=12). Participants underwent a series of Quantitative Sensory Testing (QST) procedures assessing responses to mechanical and thermal stimuli during two separate visits, in a randomized order. One visit consisted of standard, moderately painful QST procedures, while the other visit involved nonpainful analogs to these testing procedures. Blood samples were taken at baseline, and then for up to 2 hours after QST in order to study the time course of IL-6 responses.
Results: Results of multilevel analyses revealed that IL-6 responses increased across assessment time points in both visits (p<0.001). While patients with chronic pain and healthy controls did not differ in the magnitude of IL-6 responses, psychological factors influenced IL-6 trajectories only in the chronic pain group. Among patients, increases in catastrophizing over the course of the QST session were associated with elevated IL-6 responses only during the painful QST session (p<0.05). When controlling for anxiety, results indicated that the main multilevel model among patients remained significant (p<0.05).
Conclusion: Under specific conditions (eg, application of a painful stressor), catastrophizing may be associated with amplified proinflammatory responses in patients with persistent pain. These findings suggest that psychosocial interventions that reduce negative pain-related cognitions may benefit patients’ inflammatory profiles.
Keywords: anxiety, catastrophizing, chronic pain, interleukin-6
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