Journal
CLINICAL JOURNAL OF PAIN
Volume 33, Issue 3, Pages 215-221Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/AJP.0000000000000422
Keywords
cognitive behavioral therapy (CBT); insula; fibro-myalgia; fMRI; catastrophizing
Categories
Funding
- NIH [R01-AR064367]
- Arthritis Foundation
- American College of Rheumatology [P01-AT006663, R01-AT007550]
- National Center for Complementary and Integrative Health (NCCIH)
- National Institute of Biomedical Imaging and Bioengineering (NIBIB), National Institutes of Health
- KIOM [K16051]
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Objective(s): Fibromyalgia (FM) is a chronic, common pain disorder characterized by hyperalgesia. A key mechanism by which cognitive-behavioral therapy (CBT) fosters improvement in pain outcomes is via reductions in hyperalgesia and pain-related catastrophizing, a dysfunctional set of cognitive-emotional processes. However, the neural underpinnings of these CBT effects are unclear. Our aim was to assess CBT's effects on the brain circuitry underlying hyperalgesia in FM patients, and to explore the role of treatment-associated reduction in catastrophizing as a contributor to normalization of pain-relevant brain circuitry and clinical improvement. Methods: In total, 16 high-catastrophizing FM patients were enrolled in the study and randomized to 4 weeks of individual treatment with either CBT or a Fibromyalgia Education (control) condition. Resting state functional magnetic resonance imaging scans evaluated functional connectivity between key pain-processing brain regions at baseline and posttreatment. Clinical outcomes were assessed at baseline, posttreatment, and 6-month follow-up. Results: Catastrophizing correlated with increased resting state functional connectivity between S1 and anterior insula. The CBT group showed larger reductions (compared with the education group) in catastrophizing at posttreatment (P<0.05), and CBT produced significant reductions in both pain and catastrophizing at the 6-month follow-up (P<0.05). Patients in the CBT group also showed reduced resting state connectivity between S1 and anterior/medial insula at posttreatment; these reductions in resting state connectivity were associated with concurrent treatment-related reductions in catastrophizing. Discussion: The results add to the growing support for the clinically important associations between S1-insula connectivity, clinical pain, and catastrophizing, and suggest that CBT may, in part via reductions in catastrophizing, help to normalize pain-related brain responses in FM.
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