Patients with Fibromyalgia Display Less Functional Connectivity in the Brain's Pain Inhibitory Network

Molecular Pain - Tập 8 - Trang 1744-8069-8-32 - 2012
Karin Jensen1,2, Rita Loitoile1,2, Eva Kosek3, Frank Petzke4, Serena Carville5, Peter Fransson3, Hanke Marcus6, Steven Williams7, Ernest Choy8, Yves Mainguy9, Olivier Vitton9, Richard H. Gracely10, Randy L. Gollub1,2, Martin Ingvar3, Jian Kong1,2
1Athinoula A. Martinos Center For Biomedical Imaging, Boston, USA
2Department of Psychiatry, Massachusetts General Hospital, Harvard Medical School, Boston, USA
3Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden
4Pain clinic, Centre for Anesthesiology, Emergency and Intensive care Medicine, University Medical Centre, Göttingen, Germany
5UK Age Research Forum, London, UK
6Department of Anesthesiology and Postoperative Intensive Care Medicine, University Hospital of Cologne, Cologne, Germany
7Centre for Neuroimaging Science, Institute of Psychiatry, King's College London, London, UK
8Department of Medicine, Cardiff University School of Medicine, Cardiff, UK
9Pierre Fabre Médicament, Labège, France
10Center for Neurosensory Disorders, University of North Carolina, Chapel Hill, USA

Tóm tắt

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<.001, two-tailed). During fMRI scanning, the rACC displayed significantly higher connectivity to the amygdala, hippocampus, and brainstem in healthy controls, compared to FM patients. There were no regions where FM patients showed higher rACC connectivity. Thalamus showed significantly higher connectivity to the orbitofrontal cortex in healthy controls but no regions showed higher thalamic connectivity in FM patients. 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.

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Molecular Pain

Tập 8

1744-8069-8-32

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