Distinct thalamocortical network dynamics are associated with the pathophysiology of chronic low back pain

Yiheng Tu, Zening Fu, Cuiping Mao, Maryam Falahpour, Randy L. Gollub, Joel Park, Georgia Wilson, Vitaly Napadow, Jessica Gerber, Suk-Tak Chan, Robert R. Edwards, Ted J. Kaptchuk, Thomas Liu, Vince Calhoun, Bruce Rosen and Jian Kong ()
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Yiheng Tu: Harvard Medical School
Zening Fu: Tri-Institutional Center for Translational Research in Neuroimaging and Data Science (TReNDS), Georgia State University, Georgia Institute of Technology, Emory University
Cuiping Mao: Harvard Medical School
Maryam Falahpour: University of California San Diego
Randy L. Gollub: Harvard Medical School
Joel Park: Harvard Medical School
Georgia Wilson: Harvard Medical School
Vitaly Napadow: Massachusetts General Hospital, Harvard Medical School
Jessica Gerber: Massachusetts General Hospital, Harvard Medical School
Suk-Tak Chan: Massachusetts General Hospital, Harvard Medical School
Robert R. Edwards: Harvard Medical School
Ted J. Kaptchuk: Harvard Medical School
Thomas Liu: University of California San Diego
Vince Calhoun: Tri-Institutional Center for Translational Research in Neuroimaging and Data Science (TReNDS), Georgia State University, Georgia Institute of Technology, Emory University
Bruce Rosen: Massachusetts General Hospital, Harvard Medical School
Jian Kong: Harvard Medical School

Nature Communications, 2020, vol. 11, issue 1, 1-12

Abstract: Abstract Thalamocortical dysrhythmia is a key pathology of chronic neuropathic pain, but few studies have investigated thalamocortical networks in chronic low back pain (cLBP) given its non-specific etiology and complexity. Using fMRI, we propose an analytical pipeline to identify abnormal thalamocortical network dynamics in cLBP patients and validate the findings in two independent cohorts. We first identify two reoccurring dynamic connectivity states and their associations with chronic and temporary pain. Further analyses show that cLBP patients have abnormal connectivity between the ventral lateral/posterolateral nucleus (VL/VPL) and postcentral gyrus (PoCG) and between the dorsal/ventral medial nucleus and insula in the less frequent connectivity state, and temporary pain exacerbation alters connectivity between the VL/VPL and PoCG and the default mode network in the more frequent connectivity state. These results extend current findings on thalamocortical dysfunction and dysrhythmia in chronic pain and demonstrate that cLBP pathophysiology and clinical pain intensity are associated with distinct thalamocortical network dynamics.

Date: 2020
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DOI: 10.1038/s41467-020-17788-z

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