• R Staud.
• Division of Rheumatology and Clinical Immunology, University of Florida, Gainesville, FL 32610-0221, USA. staudr@ufl.edu
• Clin Exp Rheumatol. 2011 Nov 1;29(6 Suppl 69):S109-17.

AbstractFibromyalgia (FM) is a chronic musculoskeletal pain syndrome which is characterised by clinical pain as well as widespread hyperalgesia/allodynia to mechanical, thermal, electrical, and chemical stimuli. Lack of consistent tissue abnormalities in FM patients has more and more shifted the focus away from peripheral factors and towards central nervous system abnormalities including central sensitisation as well as aberrant pain facilitation and inhibition. Besides quantitative sensory testing, functional brain imaging has been increasingly utilised to characterise the abnormal pain processing of FM patients. Whereas initial work in FM patients identified abnormally increased pain-related brain activity within the thalamus, insula, anterior cingulate, S1, and prefrontal cortex (so-called 'pain matrix'), more recent research focused on altered 'connectivity' between multiple interconnected brain networks in these patients. Additionally, magnetic resonance spectroscopy studies demonstrated high concentration of the excitatory neurotransmitter glutamate in FM patients in pain-related brain areas which correlated not only with experimental but also with clinical pain ratings. Overall, functional brain imaging studies have provided compelling evidence for abnormal pain processing in FM, including brain activity that correlated with patients' augmented pain sensitivity (hyperalgesia/allodynia), temporal summation of pain, and prolonged pain aftersensations. Future imaging work needs to focus on identifying the neural correlates of FM patients' abnormal endogenous pain modulation which will likely not only shed more light on this important pain regulatory mechanism but may also provide useful information for future treatments of FM symptoms.

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