Pain catastrophizing is prominent in chronic pain conditions such as fibromyalgia, and has been proposed to contribute to the development of pain widespreadness. However, the brain mechanisms responsible for this association are unknown. We hypothesized that increased resting Salience Network (SLN) connectivity to nodes of the Default Mode Network (DMN), representing previously reported pain-linked cross-network enmeshment, would be associated with increased pain catastrophizing and widespreadness across body sites.We applied functional Magnetic Resonance Imaging (fMRI) and digital pain drawings (free-hand drawing over a body outline, analyzed using conventional software for multivoxel fMRI analysis) to investigate precisely-quantified measures of pain widespreadness and the associations between pain catastrophizing (Pain Catastrophizing Scale, PCS), resting brain network connectivity (Dual-regression Independent Component Analysis, 6-minute multiband accelerated fMRI), and pain widespreadness in fibromyalgia patients (N=79).Fibromyalgia patients reported pain in multiple body areas (most frequently the spinal region, from the lower back to the neck), with moderately high pain widespreadness (mean±SD: 26.1±24.1 percent of total body area), and high PCS scores (27.0±21.9, scale range: 0-52), which were positively correlated (r=0.26,p=0.02). A whole-brain regression analysis focused on SLN connectivity indicated that pain widespreadness was also positively associated with SLN connectivity to the Posterior Cingulate Cortex (PCC), a key node of the DMN. Moreover, we found that SLN-PCC connectivity statistically mediated the association between pain catastrophizing and pain widespreadness (p=0.01).In conclusion, we identified a putative brain mechanism underpinning the association between greater pain catastrophizing and a larger spatial extent of body pain in fibromyalgia, implicating a role for brain SLN-DMN cross-network enmeshment in mediating this association.

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