Journal Home
Search for

Volume 11, Issue 2, Pages 186-194 (February 2010)


View previous. 13 of 17 View next.

Pain Catastrophizing and Salivary Cortisol Responses to Laboratory Pain Testing in Temporomandibular Disorder and Healthy Participants

Phillip J. Quartana, Luis F. Buenaver, Robert R. Edwards, Brendan. Klick, Jennifer A. Haythornthwaite, Michael T. SmithCorresponding Author Informationemail address

Received 18 March 2009; received in revised form 6 July 2009; accepted 11 July 2009. published online 23 October 2009.

Abstract 

Pain catastrophizing is an important variable in the context of acute and chronic pain. The neurophysiological correlates of pain catastrophizing, however, have not been rigorously evaluated. We examined the relationship between trait-pain catastrophizing and morning salivary cortisol levels before and following a 45-minute laboratory pain-testing session in healthy, pain-free (n = 22), and temporomandibular disorder (TMD) participants (n = 39). We also examined whether TMD patients evidenced generalized hyperalgesia and hypercortisolism. Pain catastrophizing was associated with a flattened morning salivary cortisol profile in the context of pain testing, irrespective of pain status. Cortisol profiles did not differ between healthy and TMD participants. TMD was associated with mechanical hyperalgesia only at the masseter. These data are the first to show an association between pain catastrophizing and elevated salivary cortisol profiles in the context of standardized experimental pain testing. These findings in both healthy individuals and those with chronic orofacial pain suggest that aberrant adrenocortical responses to pain may serve as a neurophysiologic pathway by which pain catastrophizing enhances vulnerability for development of chronic pain and maintains and/or exaggerates existing pain and associated morbidity.

Perspective

Neurophysiological mechanisms by which pain catastrophizing is related to acute and chronic pain recently have come under empirical study. Understanding of these mechanisms has the unique potential to shed light on key central-nervous-system factors that mediate catastrophizing-pain relations and therapeutic benefits associated with changes in catastrophizing and related cognitive processes.

 Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, Maryland

 Department of Anesthesiology, Perioperative Medicine, Brigham & Women's Hospital/Harvard Medical School, Boston, Massachusetts

Corresponding Author InformationAddress reprint requests to Michael T. Smith, PhD, Associate Professor, Department of Psychiatry & Behavioral Sciences, Johns Hopkins University School of Medicine, 5510 Nathan Shock Drive, Suite 100, Baltimore, MD 21224.

 Supported by Grants K23NS047168 from the National Institute of Neurological Disorder and Stroke (MTS), R01AR054871 from the National Institute of Arthritis and Musculoskeletal and Skin Diseases (MTS), the Johns Hopkins General Clinical Research Center(M01-RR002719), R24AT004641 from the National Center for Complementary and Alternative Medicine (JAH), and postdoctoral fellowship Grant T32MH75884 from the National Institute of Mental Health.

PII: S1526-5900(09)00653-1

doi:10.1016/j.jpain.2009.07.008


View previous. 13 of 17 View next.