Brain processing of pain and expectancy of relief in fibromyalgia is modulated by catastrophizing

Abstract

Patients with fibromyalgia (FM) may demonstrate altered brain processing of cognitive and affective dimensions of pain, including the expectation of pain and its relief. Since catastrophizing levels are higher in FM patients than in healthy volunteers, we tested the hypothesis that catastrophizing modulates brain responses to pain, expectancy of pain and relief in FM patients. FMRI was performed on 31 FM patients (27 F; mean age = 44±11.9 SD) while 3 cuff pressure pain stimuli (46-74s) were delivered on the leg, calibrated to elicit a pain intensity rating of ∼50/100. Patients were trained to interpret visual cues 6-10s prior to pain onset (expectation of pain), and 6-12s prior to pain offset (expectation of relief). After each stimulus, subjects rated pain intensity (0-100). Catastrophizing was assessed using the Pain Catastrophizing Scale (PCS). The effect of catastrophizing on behavioral measures and brain response to pain and expectancy of pain and relief, were evaluated using regression analyses. Mean PCS scores were 23.4±13.6, with broad individual variability (Range= 0-46). PCS scores were negatively correlated with cuff pressure (r = -0.37, p<0.05) and positively correlated with the pain intensity ratings (r = 0.48, p<0.01). Whole brain voxelwise analyses revealed that PCS scores were positively correlated with 1) pain-evoked activation in medial thalamus and right fronto-insular cortex and 2) activations of the lateral temporal cortex (a core region of the Default Mode Network) during expectancy of relief. No PCS-related activations were observed during expectancy of pain. Our results reveal that catastrophizing has a modulatory effect on brain processing of experimental pain and expectancy of relief. These findings highlight the multifactorial nature of functional “central sensitization” disorders such as FM, and identify in catastrophizing a potential treatment target for therapy. This research was supported by NCCAM, NIH (R01-AT004714, P01-AT002048, P01-AT006663, R01-AT005280; R01-AG034982, R21-AR057920). Patients with fibromyalgia (FM) may demonstrate altered brain processing of cognitive and affective dimensions of pain, including the expectation of pain and its relief. Since catastrophizing levels are higher in FM patients than in healthy volunteers, we tested the hypothesis that catastrophizing modulates brain responses to pain, expectancy of pain and relief in FM patients. FMRI was performed on 31 FM patients (27 F; mean age = 44±11.9 SD) while 3 cuff pressure pain stimuli (46-74s) were delivered on the leg, calibrated to elicit a pain intensity rating of ∼50/100. Patients were trained to interpret visual cues 6-10s prior to pain onset (expectation of pain), and 6-12s prior to pain offset (expectation of relief). After each stimulus, subjects rated pain intensity (0-100). Catastrophizing was assessed using the Pain Catastrophizing Scale (PCS). The effect of catastrophizing on behavioral measures and brain response to pain and expectancy of pain and relief, were evaluated using regression analyses. Mean PCS scores were 23.4±13.6, with broad individual variability (Range= 0-46). PCS scores were negatively correlated with cuff pressure (r = -0.37, p<0.05) and positively correlated with the pain intensity ratings (r = 0.48, p<0.01). Whole brain voxelwise analyses revealed that PCS scores were positively correlated with 1) pain-evoked activation in medial thalamus and right fronto-insular cortex and 2) activations of the lateral temporal cortex (a core region of the Default Mode Network) during expectancy of relief. No PCS-related activations were observed during expectancy of pain. Our results reveal that catastrophizing has a modulatory effect on brain processing of experimental pain and expectancy of relief. These findings highlight the multifactorial nature of functional “central sensitization” disorders such as FM, and identify in catastrophizing a potential treatment target for therapy. This research was supported by NCCAM, NIH (R01-AT004714, P01-AT002048, P01-AT006663, R01-AT005280; R01-AG034982, R21-AR057920).