Abstracts for poster presentation Disease entities (human): Myofascial pain and fibromyalgia| Volume 9, ISSUE 4, SUPPLEMENT 2, 14, April 2008

(155) Central μ-Opioid Receptor (MOR) availability covaries with mood state and pain in fibromyalgia

      Fibromyalgia (FM) is a chronic widespread pain condition that is often accompanied by comorbid negative mood states including stress and depression. Positron emission tomography (PET) studies have demonstrated alterations in central μ-opioid receptor (MOR) availability in fibromyalgia patients as well as patients diagnosed with major depressive disorder. However, the regulation of the endogenous opioid system in the experience of negative mood states and pain within the same individuals is less well understood. Using PET to label MORs, we examined the correlation between the availability of MORs in the brain and self reported mood and pain in 20 fibromyalgia patients (49.5 (13.2) yrs). Mood and pain were assessed by the Positive and Negative Affectivity Scale (PANAS) and the Short Form of the McGill Pain questionnaire respectively. Negative affect was positively correlated with MOR binding potential (BP; an in vivo measure of receptor availability) in anterior cingulate cortex (ACC: r=0.77;p<0.001), middle-posterior insula (r=0.67;p=0.001), hippocampus (r=0.67;p=0.001) and dorsolateral prefrontal cortex (r=0.75;p<0.001). Within these regions, clinical pain was positively correlated with MOR BP only in the ACC (r=0.58;p<0.01) and middle-posterior insula (r=0.56;p=0.01). Linear regression analyses demonstrated that MOR BP (availability) in the ACC was independently correlated with both negative affect (Beta 0.64; p<0.001) and pain (Beta 0.33; p=0.04). These data support a model in which reduced endogenous opioid release is associated with pain and negative affect in FM patients albeit in partially overlapping brain regions. Funding: Department of Army grant DAMD-17/002-0018. NIH/NCRR grant M01-RR000042, NIH/NCCAM grant R01 AT 001415 awarded to JKZ, and NIH/NCCAM K01 AT01111-01 awarded to REH.