Molecular Pain (Apr 2012)

Patients with fibromyalgia display less functional connectivity in the brain’s pain inhibitory network

  • Jensen Karin B,
  • Loitoile Rita,
  • Kosek Eva,
  • Petzke Frank,
  • Carville Serena,
  • Fransson Peter,
  • Marcus Hanke,
  • Williams Steven CR,
  • Choy Ernest,
  • Mainguy Yves,
  • Vitton Olivier,
  • Gracely Richard H,
  • Gollub Randy,
  • Ingvar Martin,
  • Kong Jian

DOI
https://doi.org/10.1186/1744-8069-8-32
Journal volume & issue
Vol. 8, no. 1
p. 32

Abstract

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Abstract Background There is evidence for augmented processing of pain and impaired endogenous pain inhibition in Fibromyalgia syndrome (FM). In order to fully understand the mechanisms involved in FM pathology, there is a need for closer investigation of endogenous pain modulation. In the present study, we compared the functional connectivity of the descending pain inhibitory network in age-matched FM patients and healthy controls (HC). We performed functional magnetic resonance imaging (fMRI) in 42 subjects; 14 healthy and 28 age-matched FM patients (2 patients per HC), during randomly presented, subjectively calibrated pressure pain stimuli. A seed-based functional connectivity analysis of brain activity was performed. The seed coordinates were based on the findings from our previous study, comparing the fMRI signal during calibrated pressure pain in FM and HC: the rostral anterior cingulate cortex (rACC) and thalamus. Results FM patients required significantly less pressure (kPa) to reach calibrated pain at 50 mm on a 0–100 visual analogue scale (p Conclusion Patients with FM displayed less connectivity within the brain’s pain inhibitory network during calibrated pressure pain, compared to healthy controls. The present study provides brain-imaging evidence on how brain regions involved in homeostatic control of pain are less connected in FM patients. It is possible that the dysfunction of the descending pain modulatory network plays an important role in maintenance of FM pain and our results may translate into clinical implications by using the functional connectivity of the pain modulatory network as an objective measure of pain dysregulation.