PLoS ONE (Jan 2012)

MEG can map short and long-term changes in brain activity following deep brain stimulation for chronic pain.

  • Hamid R Mohseni,
  • Penny P Smith,
  • Christine E Parsons,
  • Katherine S Young,
  • Jonathan A Hyam,
  • Alan Stein,
  • John F Stein,
  • Alexander L Green,
  • Tipu Z Aziz,
  • Morten L Kringelbach

DOI
https://doi.org/10.1371/journal.pone.0037993
Journal volume & issue
Vol. 7, no. 6
p. e37993

Abstract

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Deep brain stimulation (DBS) has been shown to be clinically effective for some forms of treatment-resistant chronic pain, but the precise mechanisms of action are not well understood. Here, we present an analysis of magnetoencephalography (MEG) data from a patient with whole-body chronic pain, in order to investigate changes in neural activity induced by DBS for pain relief over both short- and long-term. This patient is one of the few cases treated using DBS of the anterior cingulate cortex (ACC). We demonstrate that a novel method, null-beamforming, can be used to localise accurately brain activity despite the artefacts caused by the presence of DBS electrodes and stimulus pulses. The accuracy of our source localisation was verified by correlating the predicted DBS electrode positions with their actual positions. Using this beamforming method, we examined changes in whole-brain activity comparing pain relief achieved with deep brain stimulation (DBS ON) and compared with pain experienced with no stimulation (DBS OFF). We found significant changes in activity in pain-related regions including the pre-supplementary motor area, brainstem (periaqueductal gray) and dissociable parts of caudal and rostral ACC. In particular, when the patient reported experiencing pain, there was increased activity in different regions of ACC compared to when he experienced pain relief. We were also able to demonstrate long-term functional brain changes as a result of continuous DBS over one year, leading to specific changes in the activity in dissociable regions of caudal and rostral ACC. These results broaden our understanding of the underlying mechanisms of DBS in the human brain.