Use of opioid analgesics for management of chronic nonmalignant pain has become common, yet there are presently no well-validated predictors of optimal opioid analgesic efficacy. We examined whether psychosocial factors (eg, depressive symptoms) predicted changes in spontaneous low back pain after administration of opioid analgesics, and whether endogenous opioid (EO) function mediated these relationships. Participants with chronic low back pain but who were not chronic opioid users (N = 89) underwent assessment of low back pain intensity pre- and post-drug in 3 (counterbalanced) conditions: (1) placebo, (2) intravenous naloxone, and (3) intravenous morphine. Comparison of placebo condition changes in back pain intensity to those under naloxone and morphine provided indexes of EO function and opioid analgesic responses, respectively. Results showed that (1) most psychosocial variables were related significantly and positively to morphine analgesic responses for low back pain, (2) depressive symptoms, trait anxiety, pain catastrophizing, and pain disability were related negatively to EO function, and (3) EO function was related negatively to morphine analgesic responses for low back pain. Bootstrapped mediation analyses showed that links between morphine analgesic responses and depressive symptoms, trait anxiety, pain catastrophizing, and perceived disability were partially mediated by EO function. Results suggest that psychosocial factors predict elevated analgesic responses to opioid-based medications, and may serve as markers to identify individuals who benefit most from opioid therapy. Results also suggest that people with greater depressive symptoms, trait anxiety, pain catastrophizing, and perceived disability may have deficits in EO function, which may predict enhanced response to opioid analgesics.
Individuals with elevated depressive symptoms, pain catastrophizing, and perceived disability may have deficient endogenous opioid function, which may predict enhanced response to opioid analgesics.
aDepartment of Behavioral Sciences, Rush University Medical Center, Chicago, IL USA
bDepartment of Anesthesiology, Vanderbilt University School of Medicine, Vanderbilt, TN, USA
cDepartment of Psychology, Ohio University, Athens, OH, USA
Corresponding author. Address: Department of Behavioral Sciences, Rush University Medical Center, 1645 W. Jackson Blvd, Chicago, IL 60612, USA. Tel.: 312 942 0379. E-mail address: John_burns@rush.edu (J.W. Burns).
Sponsorships or competing interests that may be relevant to content are disclosed at the end of this article.
Received October 28, 2015
Received in revised form August 31, 2016
Accepted November 10, 2016