Neuropathic pain and pain interference are linked to alpha-band slowing and reduced beta-band magnetoencephalography activity within the dynamic pain connectome in patients with multiple sclerosis

Abstract

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.

Hyperexcitability of Cortical Oscillations in Patients with Somatoform Pain Disorder: A Resting-State EEG Study

“…This hypothesis was further supported by the positive correlation between resting-state alpha oscillation power and somatization severity across the SPD patients, where somatization severity and somatosensory amplification are closely linked [53, 54]. Although the observed increased alpha oscillation among SPD patients was consistent with findings from many chronic pain studies [17, 19, 43, 55], it was in contrast with experimental pain studies [12, 13, 56] showing the negative correlation between prestimulus alpha oscillation and subsequent pain perception. This could be arising from the differences between experimental pain (well controlled with limited duration and specified location) and clinical pain (long lasting and widespread, with pain interference such as sleep interference), particularly considering the absence of organic pathology involved in the maintenance of chronic pain suffered by SPD patients.…”

“…An increase of the oscillation at alpha band frequency has ever been reported in chronic pain patients [17, 43]. For example, among patients with multiple sclerosis, Kim et al observed an increase of alpha oscillation power within several nodes of the salience network and ascending nociceptive pathway [17], which was interpreted as a result of overflowing sensory information due to a reduced sensory gating. The increased alpha oscillation has also been identified among migraine patients, suggesting an overintegration of sensory information in these patients [48].…”

“…Well consistent with these results, SPD patients had increased alpha oscillations with maximal distribution over the parietal region, as confirmed by both electrode-level spectral power density and source-level eLORETA cortical current density. Considering the functional role of alpha oscillations in local inhibition and sensory gating [17, 51, 52], the increased alpha oscillations in SPD patients could be reflecting the attenuated sensory information gating and excessive integration of pain-related information, thus appeared as somatosensory amplification in these patients. This hypothesis was further supported by the positive correlation between resting-state alpha oscillation power and somatization severity across the SPD patients, where somatization severity and somatosensory amplification are closely linked [53, 54].…”

“…While alterations of resting-state cortical oscillations have been reported for many types of chronic pain patients, the obtained results were not fully consistent. The increased resting-state alpha oscillation in patients with multiple sclerosis has been associated with attention deficit and attenuated sensory gating [16, 17], the enhanced alpha oscillation in patients with neuropathic pain has been interpreted as cognitive dysfunction [18, 19], and the positive correlation between pain duration and alpha oscillation power among patients with chronic back pain led to the speculation for the role of alpha oscillations in pain chronification [20]. In contrast, some studies also reported the decrease of alpha oscillation power among patients with chronic low back pain [21] and patients with chronic pain after spinal cord injury [22], which has been interpreted as a dysfunction of cortical inhibition and the functional comorbidity of drowsiness among these patients.…”

Differentiating trait pain from state pain: a window into brain mechanisms underlying how we experience and cope with pain

“…This concept has been developed in other fields such as cognition and aging, 17 and we have discussed this in relation to acute 34 and chronic pain. 4,23,35…”