No indication of a rise in rsCBF in the brain areas involved in pain processing was noted as opposed to the assumption that rsCBF is increased in fibromyalgia in regions of the brain involved in pain processing. 

This case-control study used structural and functional neuroimaging markers, i.e. resting-state cerebral blood flow (rsCBF), grey matter volume (GMV), rs functional connectivity (rsFC), and cortical thickness (CoTh) to estimate its association with chronic, stimulus-independent neuropathic pain via a resting-state hypothesis.

Overall, 32 female fibromyalgia people and 32 pain-free controls were included in this multimodal neuroimaging study. Inter-group differences in neuroimaging markers were evaluated with the use of whole-brain and region of interest analyses. All the analyses for anxiety and depression were adjusted. A subgroup analysis restricted to patients not taking the central-acting drugs was executed.

No differences in rsCBF of brain regions (somatosensory and prefrontal cortex, thalamus, basal ganglia, insula, anterior cingulate cortex, and supplementary motor area) were found to be involved in the processing of acute pain in fibromyalgia patients amongst both the groups.

The findings demonstrated robustness across all structural and functional neuroimaging markers and were limited to people using central-acting drugs and matched controls. Also, the markers of structural and functional neuroimaging were not able to map stimulus-independent neuropathic pain.

No evidence underlying the functional or structural modifications in brain regions responsible for acute pain processing in fibromyalgia people was noted that can indicate neural correlates of chronic stimulus-independent pain.