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

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 y-a band and EEG power in the d, y, a and b 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.

Brain EEG activity correlates of chronic pain in persons with spinal cord injury: clinical implications

“…Consistent with both Sarnthein et al 3 and Boord et al, 4 and relative to individuals with SCI and no pain and healthy controls, individuals in our sample with SCI and chronic pain were found to have less alpha and more theta (although the theta finding was a nonsignificant trend, and was only observed for relative power). These patterns of activity do not appear related to sex or medication effects.…”

“…Boord et al 4 obtained similar results in a study comparing brain EEG activity in 16 individuals with SCI (8 with neuropathic pain and 8 without pain) and 16 matched healthy controls. The patients with SCI had a lower (that is, slower) peak band frequency than the healthy controls, but this difference was only statistically significant (in 12 of 14 electrode sites) for the SCI group with pain (see also Wydenkeller et al 5 ).…”

State-related electroencephalographic deviances in attention deficit hyperactivity disorder

“…The finding of less theta attenuation in ADHD following eye opening has to the best of our knowledge not been reported before. Modulation of EEG activity between eyes closed and eyes open conditions has been proposed to be an indicator of function of thalamocortical networks (Boord et al, 2008) resulting from cortical processing of visual input . This suggests that in the ADHD group, neuronal networks are impaired to adjust to the changes in input between eyes closed and eyes open states.…”

Spinal Cord Injury Immediately Changes the State of the Brain

“…Besides deafferentation of somatosensory structures, it is possible that spinal transection also directly affected the activity of brainstem structures and thalamic nuclei regulating cortical synchrony and arousal, contributing to the observed changes in cortical spontaneous activity (Moruzzi and Magoun, 1949;Lindvall et al, 1974;Hobson et al, 1975;Foote et al, 1980;Aston-Jones and Bloom, 1981a,b;Fox and Armstrong-James, 1986;Satoh and Fibiger, 1986;Hallanger et al, 1987;Steriade et al, 1990;Aguilar and Castro-Alamancos, 2005;Ren et al, 2009). Importantly, slower cortical activity after spinal cord injury has been previously observed with EEG recordings in patients (Tran et al, 2004;Boord et al, 2008), and both slower cortical activity (Wydenkeller et al, 2009) and long-term cortical reorganization (Wrigley et al, 2009) correlate with the emergence of neuropathic pain. From a translational perspective, it is thus tempting to suggest-with all the necessary caveats of comparing data from awake patients and anesthetized rats-that the immediate slowing of cortical spontaneous activity after spinal cord injury described here might have a pathophysiological role for long-term cortical reorganization and neuropathic pain.…”