Original Article

Spinal Cord (2008) 46, 118–123; doi:10.1038/sj.sc.3102077; published online 15 May 2007

Electroencephalographic slowing and reduced reactivity in neuropathic pain following spinal cord injury

P Boord1,2, P J Siddall3, Y Tran1, D Herbert1, J Middleton4 and A Craig1

  1. 1Department of Health Sciences, University of Technology Sydney, Broadway, New South Wales, Australia
  2. 2Brain Dynamics Centre, Westmead Millennium Institute, University of Sydney, Westmead Hospital, Westmead, New South Wales, Australia
  3. 3Pain Management Research Institute, University of Sydney, Royal North Shore Hospital, Sydney, New South Wales, Australia
  4. 4Moorong Spinal Unit & Rehabilitation Studies Unit, Faculty of Medicine, Royal Rehabilitation Centre Sydney, University of Sydney, Ryde, New South Wales, Australia

Correspondence: Dr P Boord, Brain Dynamics Centre, Westmead Millennium Institute, Acacia House, Westmead Hospital, Westmead, New South Wales 2042, Australia. E-mail: peter_boord@brainresource.com

Received 19 December 2006; Revised 8 March 2007; Accepted 1 April 2007; Published online 15 May 2007.

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Abstract

Study Design:

 

Brain wave activity in people with paraplegia, with and without neuropathic pain, was compared to brain wave activity in matched able-bodied controls.

Objectives:

 

To investigate whether spinal cord injury with neuropathic pain is associated with a slowing of brain wave activity.

Setting:

 

Australia.

Methods:

 

Electroencephalographic (EEG) data were collected in the eyes open (EO) and eyes closed (EC) states from 16 participants with paraplegia (eight with neuropathic pain and eight without pain) and matched able-bodied controls. Common EEG artefacts were removed using independent component analysis (ICA). Peak frequency in the thetaalpha band and EEG power in the delta, theta, alpha and beta frequency bands were compared between groups.

Results:

 

The results show significant slowing of the EEG in people with neuropathic pain, consistent with the presence of thalamocortical dysrhythmia (TCD). Furthermore, people with neuropathic spinal cord injury (SCI) pain had significantly reduced EEG spectral reactivity in response to increased or decreased sensory input flowing into the thalamocortical network, as modulated by the eyes open and eyes closed states.

Conclusion:

 

The results provide further evidence for alterations in brain electric activity that may underlie the development of neuropathic pain following SCI.

Keywords:

neuropathic pain, spinal cord injury, EEG, slowing, reactivity, thalamocortical dysrhythmia

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