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The Journal of Neuroscience, September 12, 2007, 27(37):10000-10006; doi:10.1523/JNEUROSCI.2849-07.2007

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Neurobiology of Disease
Decreased Central µ-Opioid Receptor Availability in Fibromyalgia

Richard E. Harris,¹ Daniel J. Clauw,¹ David J. Scott,² Samuel A. McLean,³ Richard H. Gracely,¹ and Jon-Kar Zubieta^2,4

¹Department of Internal Medicine, ²Department of Psychiatry and Molecular and Behavioral Neuroscience Institute, and Departments of ³Emergency Medicine and ⁴Radiology, The University of Michigan, Ann Arbor, Michigan 48109

Correspondence should be addressed to Dr. Richard E. Harris, Chronic Pain and Fatigue Research Center, 24 Frank Lloyd Wright Drive, P.O. Box 385, Lobby M, Ann Arbor, MI 48106. Email: reharris{at}med.umich.edu

The underlying neurophysiology of acute pain is fairly well characterized, whereas the central mechanisms operative in chronic pain states are less well understood. Fibromyalgia (FM), a common chronic pain condition characterized by widespread pain, is thought to originate largely from altered central neurotransmission. We compare a sample of 17 FM patients and 17 age- and sex-matched healthy controls, using µ-opioid receptor (MOR) positron emission tomography. We demonstrate that FM patients display reduced MOR binding potential (BP) within several regions known to play a role in pain modulation, including the nucleus accumbens, the amygdala, and the dorsal cingulate. MOR BP in the accumbens of FM patients was negatively correlated with affective pain ratings. Moreover, MOR BP throughout the cingulate and the striatum was also negatively correlated with the relative amount of affective pain (McGill, affective score/sensory score) within these patients. These findings indicate altered endogenous opioid analgesic activity in FM and suggest a possible reason for why exogenous opiates appear to have reduced efficacy in this population.

Key words: fibromyalgia; opioid; pain; chronic; positron emission tomography; µ

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Received May 7, 2007; revised Aug. 1, 2007; accepted Aug. 2, 2007.

Correspondence should be addressed to Dr. Richard E. Harris, Chronic Pain and Fatigue Research Center, 24 Frank Lloyd Wright Drive, P.O. Box 385, Lobby M, Ann Arbor, MI 48106. Email: reharris{at}med.umich.edu

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