Encoding of Self‐Referential Pain Catastrophizing in the Posterior Cingulate Cortex in Fibromyalgia. Issue 8 (22nd June 2018)

• Record Type: Journal Article
• Authors: Lee, Jeungchan; Protsenko, Ekaterina; Lazaridou, Asimina; Franceschelli, Olivia; Ellingsen, Dan‐Mikael; Mawla, Ishtiaq; Isenburg, Kylie; Berry, Michael P.; Galenkamp, Laura; Loggia, Marco L.; Wasan, Ajay D.; Edwards, Robert R.; Napadow, Vitaly
• Is Part Of: Arthritis & rheumatology. Volume 70:Issue 8(2018)
• Page Start: 1308
• Page End: 1318
• Publication Date: 2018-06-22
• Subjects: Arthritis -- Periodicals; Rheumatism -- Periodicals; 616.72
• DOI: 10.1002/art.40507
• Languages: English
• ISSNs: 2326-5191

Abstract

Abstract : Objective: Pain catastrophizing is a common feature of chronic pain, including fibromyalgia (FM), and is strongly associated with amplified pain severity and disability. While previous neuroimaging studies have focused on evoked pain response modulation by catastrophizing, the brain mechanisms supporting pain catastrophizing itself are unknown. We designed a functional magnetic resonance imaging (fMRI)–based pain catastrophizing task whereby patients with chronic pain engaged in catastrophizing‐related cognitions. We undertook this study to test our hypothesis that catastrophizing about clinical pain would be associated with amplified activation in nodes of the default mode network (DMN), which encode self‐referential cognition and show altered functioning in chronic pain. Methods: During fMRI, 31 FM patients reflected on how catastrophizing (CAT) statements (drawn from the Pain Catastrophizing Scale) impact their typical FM pain experience. Response to CAT statements was compared to response to matched neutral (NEU) statements. Results: During statement reflection, higher fMRI signal during CAT statements than during NEU statements was found in several DMN brain areas, including the ventral (posterior) and dorsal (anterior) posterior cingulate cortex (vPCC and dPCC, respectively). Patients' ratings of CAT statement applicability were correlated solely with activity in the vPCC, a main DMN hub supporting self‐referential cognition (r = 0.38, P < 0.05). Clinical pain severity was correlated solely with activity in the dPCC, a PCC subregion associated with cognitive control and sensorimotor processing (r = 0.38, P < 0.05). Conclusion: These findings provide evidence that the PCC encodes pain catastrophizing in FM and suggest distinct roles for different PCC subregions. Understanding the brain circuitry encoding pain catastrophizing in FM will prove to be important in identifying and evaluating the success of interventions targeting negative affect in chronic pain management.