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19 p., 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.

11 p., Objective.Fibromyalgia (FM) is a chronic func-tional pain syndrome characterized by widespread pain,significant pain catastrophizing, sympathovagal dysfunc-tion, and amplified temporal summation for evoked pain.While several studies have demonstrated altered restingbrain connectivity in FM, studies have not specificallyprobed the somatosensory system and its role in bothsomatic and nonsomatic FM symptoms. Our objective wasto evaluate resting primary somatosensory cortex (S1) con-nectivity and to explore how sustained, evoked deep tissuepain modulates this connectivity.Methods.We acquired functional magnetic reso-nance imaging and electrocardiography data on FMpatients and healthy controls during rest (the rest phase)and during sustained mechanical pressure–induced painover the lower leg (the pain phase). Functional connectiv-ity associated with different S1 subregions was calculated,while S1legconnectivity (representation of the leg in theprimary somatosensory cortex) was contrasted betweenthe rest phase and the pain phase and was correlated withclinically relevant measures in FM.Results.During the rest phase, FM patientsshowed decreased connectivity between multiple ipsilat-eral and cross-hemispheric S1 subregions, which wascorrelated with clinical pain severity. Compared to therest phase, the pain phase produced increased S1legconnectivity to the bilateral anterior insula in FMpatients, but not in healthy controls. Moreover, in FMpatients, sustained pain–altered S1legconnectivity tothe anterior insula was correlated with clinical/behavioral pain measures and autonomic responses.Conclusion.Our study demonstrates that bothsomatic and nonsomatic dysfunction in FM, includingclinical pain, pain catastrophizing, autonomic dysfunction,and amplified temporal summation, are closely linkedwith the degree to which evoked deep tissue pain alters S1 connectivity to salience/affective pain-processing regions. Additionally, diminished connectivity between S1 subregions during the rest phase in FM may result from ongoing widespread clinical pain.

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 demonstrated altered resting brain connectivity in FM, studies have not specifically probed the somatosensory system and its role in both somatic and nonsomatic FM symptoms. Our objective was to evaluate resting primary somatosensory cortex (S1) connectivity and to explore how sustained, evoked deep tissue pain modulates this connectivity.We acquired functional magnetic resonance imaging and electrocardiography data on FM patients and healthy controls during rest (the rest phase) and during sustained mechanical pressure-induced pain over the lower leg (the pain phase). Functional connectivity associated with different S1 subregions was calculated, while S1(leg) connectivity (representation of the leg in the primary somatosensory cortex) was contrasted between the rest phase and the pain phase and was correlated with clinically relevant measures in FM.During the rest phase, FM patients showed decreased connectivity between multiple ipsilateral and cross-hemispheric S1 subregions, which was correlated with clinical pain severity. Compared to the rest phase, the pain phase produced increased S1(leg) connectivity to the bilateral anterior insula in FM patients, but not in healthy controls. Moreover, in FM patients, sustained pain-altered S1(leg) connectivity to the anterior insula was correlated with clinical/behavioral pain measures and autonomic responses.Our study demonstrates that both somatic and nonsomatic dysfunction in FM, including clinical pain, pain catastrophizing, autonomic dysfunction, and amplified temporal summation, are 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 during the rest phase in FM may result from ongoing widespread clinical pain.