Chronic pain is a common occurrence in multiple sclerosis (MS) that severely affects quality of life, but the underlying brain mechanisms related to these symptoms are unknown. Previous electroencephalography studies have demonstrated a role of alpha-band and beta-band power in pain processing. However, how and where these brain signals change in MS-related chronic pain is unknown. Here, we used resting state magnetoencephalography to examine regional spectral power in the dynamic pain connectome—including areas of the ascending nociceptive pathway, default mode network (DMN), and the salience network (SN)—in patients with chronic MS pain and in healthy controls. Each patient was assessed for pain, neuropathic pain (NP), and pain interference with activities of daily living. We found that patients with MS exhibited an increase of alpha-band power and a decrease of beta-band power, most prominently in the thalamus and the posterior insula of the ascending nociceptive pathway and in the right temporoparietal junction of the SN. In addition, patients with mixed-NP exhibited slowing of alpha peak power within the thalamus and the posterior insula, and in the posterior cingulate cortex of the DMN. Finally, pain interference scores in patients with mixed-NP were strongly correlated with alpha and beta peak power in the thalamus and posterior insula. These novel findings reveal brain mechanisms of MS-related pain in the ascending nociceptive pathway, SN, and DMN, and that these spectral abnormalities reflect the impact of pain on quality of life measures.
Multiple sclerosis neuropathic pain is associated with alpha and beta spectral power abnormalities within the dynamic pain connectome, and these abnormalities are associated with pain interference.
aDivision of Brain, Imaging, and Behaviour-Systems Neuroscience, Krembil Brain Institute, Krembil Research Institute, Toronto Western Hospital, University Health Network, Toronto, ON, Canada
bInstitute of Medical Science, University of Toronto, Toronto, ON, Canada
cDivision of Neurology, Department of Medicine, St. Michael's Hospital, Toronto, ON, Canada
dDepartment of Medical Imaging, University of Toronto, Toronto, ON, Canada
eNeurosciences & Mental Health Program, The Hospital for Sick Children Research Institute, Toronto, ON, Canada
fDepartment of Surgery, University of Toronto, Toronto, ON, Canada
Corresponding author. Address: Division of Brain, Imaging, and Behaviour -Systems Neuroscience, Krembil Brain Institute, Krembil Research Institute, University Health Network, 399 Bathurst St, Room MP12-306, Toronto, ON M5T 2S8, Canada. Tel.: (416) 603-5662. E-mail address: email@example.com (K.D. Davis).
Sponsorships or competing interests that may be relevant to content are disclosed at the end of this article.
Received May 18, 2018
Accepted August 29, 2018