Patients with fibromyalgia display less functional connectivity in the brain’s pain inhibitory network
1 Department of Psychiatry, Massachusetts General Hospital, Harvard Medical School, Boston, USA
2 Athinoula A. Martinos Center for Biomedical Imaging, Boston, USA
3 Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden
4 Osher Center for Integrative Medicine, Karolinska Institutet, Stockholm, Sweden
5 Pain clinic, Centre for Anesthesiology, Emergency and Intensive care Medicine, University Medical Centre, Göttingen, Germany
6 UK Age Research Forum, London, UK
7 Department of Anesthesiology and Postoperative Intensive Care Medicine, University Hospital of Cologne, Cologne, Germany
8 Centre for Neuroimaging Science, Institute of Psychiatry, King’s College London, London, UK
9 Department of Medicine, Cardiff University School of Medicine, Cardiff, UK
10 Pierre Fabre Médicament, Labège, France
11 Center for Neurosensory Disorders, University of North Carolina, Chapel Hill, USA
Molecular Pain 2012, 8:32 doi:10.1186/1744-8069-8-32Published: 26 April 2012
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.
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.
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.