• Stephen Bruehl, Ok Y Chung, and Melissa Chont.
• Department of Anesthesiology, Vanderbilt University School of Medicine, 701 Medical Arts Building, 1211 Twenty-First Avenue South, Nashville, TN 37212, USA. Stephen.Bruehl@vanderbilt.edu
• Pain. 2010 Jan 1;148(1):167-71.

AbstractThis 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 [4]. 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.Copyright 2009 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.

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