Clinical noteChronic pain-related changes in endogenous opioid analgesia: A case reportBruehl, Stephen*; Chung, Ok Y.; Chont, MelissaAuthor Information Department of Anesthesiology, Vanderbilt University School of Medicine, Nashville, TN, USA *Corresponding author. Address: Vanderbilt University Medical Center, 701 Medical Arts Building, 1211 Twenty-First Avenue South, Nashville, TN 37212, USA. Tel.: +1 615 936 1821; fax: +1 615 936 8983. E-mail address:Stephen.Bruehl@vanderbilt.edu Submitted July 14, 2008; revised August 18, 2009; accepted September 22, 2009. Pain: January 2010 - Volume 148 - Issue 1 - p 167-171 doi: 10.1016/j.pain.2009.09.025 Buy Metrics Abstract This case report presents data regarding endogenous opioid analgesia in a healthy female subject prior to developing chronic pain, and again 4 and 13 months following onset of chronic daily back pain. At each assessment period, the subject underwent identical protocols involving two sessions one week apart with randomized double-blind crossover administration of saline placebo and naloxone, an opioid antagonist. Each session included a 5-min anger recall interview, followed by finger pressure and ischemic acute pain tasks. Increases in acute pain ratings induced by opioid blockade were interpreted as reflecting endogenous opioid analgesia. When the subject was healthy and pain-free, naloxone produced a mean overall 16% decrease in pain ratings relative to placebo. However, 4 months after onset of chronic pain, a mean naloxone-induced increase of 22% in pain ratings over placebo was observed, consistent with presence of endogenous opioid analgesia. The mean magnitude of this opioid blockade effect for the finger pressure task exceeded the 99% confidence interval for the healthy control population based on a previous study using a similar opioid blockade protocol . At 13-month follow-up, naloxone produced a mean 45% decrease in acute pain ratings compared to placebo, arguing against presence of endogenous opioid analgesia. Although results must be interpreted cautiously, findings are consistent with the hypothesis that chronic pain may initially be associated with upregulation of endogenous opioid analgesic systems which then may become dysfunctional over time. © 2010 Lippincott Williams & Wilkins, Inc.