Change in brain oscillations as a mechanism of mindfulness-meditation, cognitive therapy, and mindfulness-based cognitive therapy for chronic low back pain.

Psychological treatments for chronic low back pain (CLBP) can alter brain activity, as measured by electroencephalography (EEG). In adults with CLBP who completed cognitive therapy, mindfulness meditation, or mindfulness-based cognitive therapy, there were significant reductions in theta and alpha power in the left frontal region and in beta power across all five brain regions examined. Reduced beta power in the central region was linked to lower pain intensity only for mindfulness-based cognitive therapy. These changes suggest that all three treatments lowered cortical arousal, indicating a shared neurophysiological effect.

Study at a glance

Abstract

OBJECTIVE Psychological treatments for chronic low back pain (CLBP) are effective. However, limited research has investigated their neurophysiological mechanisms. This study examined electroencephalography- (EEG-) assessed brain oscillation changes as potential mechanisms of cognitive therapy (CT), mindfulness-meditation (MM), and mindfulness-based cognitive therapy (MBCT) for CLBP. The a priori bandwidths of interest were changes in theta, alpha and beta power, measured at pre- and post-treatment. DESIGN A secondary analysis of a clinical trial. SETTING University of Queensland Psychology Clinic. SUBJECTS Adults (N = 57) with CLBP who completed pre- and post-treatment EEG and pain outcome assessments. METHODS EEG data were examined for five regions of interest (ROIs); the primary outcome was pain intensity. RESULTS A significant reduction in theta (p=.015) and alpha (p=.006) power in the left frontal ROI across all treatments was found, although change in theta and alpha power in this region was not differentially associated with outcome across treatments. There were significant reductions in beta power in all five ROIs across all treatments (ps≤.013). Beta power reduction in the central ROI showed a significant association with reduced pain intensity in MBCT only (p=.028). Changes in other regions were not statistically significant. CONCLUSIONS These findings provide support for the capacity of psychological CLBP treatments to induce changes in brain activity. The reduced beta power in all five ROIs indicated that all three treatments engendered a state of lowered cortical arousal. The growing body of research in this area could potentially inform novel directions towards remedying central nervous system abnormalities associated with CLBP.