Jeungchan Lee #,1,2, Asimina Lazaridou #,3, Myrella Paschali 3, Marco L Loggia 1,4, Michael P Berry 1, Dan-Mikael Ellingsen 5,6, Kylie Isenburg 1, Alessandra Anzolin 1,2, Arvina Grahl 1,2, Ajay D Wasan 7, Vitaly Napadow #,1,2, Robert R Edwards #,3
1Department of Radiology, Athinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA, 02129, USA.
2Discovery Center for Recovery from Chronic Pain, Physical Medicine and Rehabilitation, Spaulding Rehabilitation Hospital, Harvard Medical School, Charlestown, MA, 02129, USA.
3Department of Anesthesiology, Perioperative & Pain Medicine, Brigham & Women's Hospital, Harvard Medical School, Boston, MA, 02115, USA.
4Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA, 02129, USA.
5Department of School of Health Sciences, Kristiania University College, Oslo, Norway.
6Department of Physics and Computational Radiology, Division of Radiology and Nuclear Medicine, Oslo University Hospital, Oslo, Norway.
7Department of Anesthesiology and Perioperative Medicine, Center for Innovation in Pain Care, University of Pittsburgh, Pittsburgh, PA, 15261, USA.
CORRESPONDING AUTHOR : Jeungchan Lee PhD
Objective: Fibromyalgia (FM) is characterized by pervasive pain-related symptomatology and high levels of negative affect. Mind-body treatments such as cognitive-behavioral therapy (CBT) appear to foster improvement in FM via reductions in pain-related catastrophizing, a set of negative, pain-amplifying cognitive and emotional processes. However, the neural underpinnings of CBT's catastrophizing-reducing effects remain uncertain. This randomized, controlled, mechanistic trial was designed to assess CBT's effects on pain catastrophizing and its underlying brain circuitry.
Methods: Of 114 enrolled participants, 98 underwent a baseline neuroimaging assessment and were randomized to 8 weeks of individual CBT or a matched fibromyalgia education control condition (EDU).
Results: Compared with EDU, CBT produced larger decreases in pain catastrophizing at post-treatment (P < 0.05), and larger reductions in pain interference and symptom impact. Decreases in pain catastrophizing played a significant role in mediating those functional improvements in the CBT group. At baseline, brain functional connectivity between ventral posterior cingulate cortex (vPCC), a key node of the default mode network, and somatomotor and salience network regions was increased during catastrophizing thoughts. Following CBT, vPCC connectivity to somatomotor and salience network areas was reduced.
Conclusion: Our results suggest clinically important and CBT-specific associations between somatosensory/motor- and salience-processing brain regions and the default mode network in chronic pain. These patterns of connectivity may contribute to individual differences (and treatment-related changes) in somatic self-awareness. CBT appears to provide clinical benefits at least partially by reducing pain-related catastrophizing and producing adaptive alterations in default mode network functional connectivity.