Repositorio Digital

Resumen en ingles

Objective—Fibromyalgia (FM) is a chronic functional pain syndrome characterized by widespread pain, significant pain catastrophizing, sympathovagal dysfunction, and amplified temporal summation for evoked pain. While several studies have found altered resting brain connectivity in FM, studies have not specifically probed the somatosensory system, and its role in both somatic and non-somatic FM symptomatology. Our objective was to evaluate resting primary somatosensory cortex (S1) connectivity, and explore how sustained, evoked deep-tissue pain modulates this connectivity.Methods—We acquired fMRI and electrocardiography data from FM patients and healthy controls (HC) during rest (REST) and sustained mechanical pressure pain (PAIN) over the lower leg. Functional connectivity associated with different S1 subregions was calculated, while S1leg (leg representation) connectivity was contrast between REST and PAIN, and correlated with clinically-relevant measures in FM. Results—At REST, FM showed decreased connectivity between multiple ipsilateral and cross-hemispheric S1 subregions, which was correlated with clinical pain severity. PAIN, compared to REST, produced increased S1legconnectivity to bilateral anterior insula in FM, but not in HC. Moreover, in FM, sustained pain-altered S1legconnectivity to anterior insula was correlated with clinical/behavioral pain measures and autonomic responses. Conclusion—Our study demonstrates that both somatic and non-somatic dysfunction in FM, including clinical pain, pain catastrophizing, autonomic dysfunction, and amplified temporal summation, are all closely linked with the degree to which evoked deep-tissue pain alters S1 connectivity to salience/affective pain processing regions. Additionally, diminished connectivity between S1 subregions at REST in FM may result from ongoing widespread clinical pain.