Abstract
Fibromyalgia is characterized by chronic pain and a striking discrepancy between objective signs of tissue damage and severity of pain. Function and structural alterations in brain areas involved in pain processing may explain this feature. Previous case-control studies in fibromyalgia focused on acute pain processing using experimentally-evoked pain paradigms. Yet, these studies do not allow conclusions about chronic, stimulus-independent pain. Resting-state cerebral blood flow (rsCBF) acquired by arterial spin labelling (ASL) may be a more accurate marker for chronic pain. The objective was to integrate four different functional and structural neuroimaging markers to evaluate the neural correlate of chronic, stimulus-independent pain using a resting-state paradigm. In line with the pathophysiological concept of enhanced central pain processing we hypothesized that rsCBF is increased in fibromyalgia in areas involved in processing of acute pain. We performed an age matched case-control study of 32 female fibromyalgia patients and 32 pain-free controls and calculated group differences in rsCBF, resting state functional connectivity, grey matter volume and cortical thickness using whole-brain and region of interest analyses. We adjusted all analyses for depression and anxiety. As centrally acting drugs are likely to interfere with neuroimaging markers, we performed a subgroup analysis limited to patients not taking such drugs. We found no differences between cases and controls in rsCBF of the thalamus, the basal ganglia, the insula, the somatosensory cortex, the prefrontal cortex, the anterior cingulum and supplementary motor area as brain areas previously identified to be involved in acute processing in fibromyalgia. The results remained robust across all neuroimaging markers and when limiting the study population to patients not taking centrally acting drugs and matched controls. In conclusion, we found no evidence for functional or structural alterations in brain areas involved in acute pain processing in fibromyalgia that could reflect neural correlates of chronic stimulus-independent pain.
Highlights
Fibromyalgia is characterized by chronic and widespread pain with additional symptoms such as fatigue, sleep disturbance and cognitive dysfunctions [1,2,3]
Even though our main statistical approach was to perform voxel- and vertex-wise whole-brain analyses, we investigated several pre-specified cortical Regions of Interests (ROIs) likely to be involved in pain processing in fibromyalgia based on previous evidence for functional neuroimaging markers [8] and on atlases for structural markers [37, 38]
We found no differences in resting-state functional connectivity (rsFC) among areas associated with chronic pain in fibromyalgia in unadjusted or adjusted analyses after family wise error (FWE) correction
Summary
Fibromyalgia is characterized by chronic and widespread pain with additional symptoms such as fatigue, sleep disturbance and cognitive dysfunctions [1,2,3]. Brain areas identified to be involved in pain processing include subcortical regions such as thalamus and basal ganglia and the insula, somatosensory cortex, prefrontal cortex, anterior cingulum and supplementary motor area as cortical regions [8, 15, 16]. It remains a subject of debate whether these brain areas are mainly processing acute pain signals or whether they involved in chronic pain [8, 17]. Potential neuroimaging markers of chronic pain include resting-state cerebral blood flow (rsCBF) or functional connectivity on a functional level, as well as alterations of grey matter volume and cortical thickness on a structural level
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