Abstract
One of the brain signatures of the central neuropathic pain (CNP) is the theta band over-activity of wider cortical structures, during imagination of movement. The objective of the study was to investigate whether this over-activity is reversible following the neurofeedback treatment of CNP. Five paraplegic patients with pain in their legs underwent from twenty to forty neurofeedback sessions that significantly reduced their pain. In order to assess their dynamic cortical activity they were asked to imagine movements of all limbs a week before the first and a week after the last neurofeedback session. Using time-frequency analysis we compared EEG activity during imagination of movement before and after the therapy and further compared it with EEG signals of ten paraplegic patients with no pain and a control group of ten able-bodied people. Neurofeedback treatment resulted in reduced CNP and a wide spread reduction of cortical activity during imagination of movement. The reduction was significant in the alpha and beta band but was largest in the theta band. As a result cortical activity became similar to the activity of other two groups with no pain. Reduction of CNP is accompanied by reduced cortical over-activity during movement imagination. Understanding causes and consequences mechanism through which CNP affects cortical activity.
Highlights
Central neuropathic pain (CNP) is a frequent secondary consequence of spinal cord injury (SCI), affecting about 40% of patients (Siddall et al, 2003)
We show a difference in cortical responses in PWP before and after therapy (PWP_after – PWP_before) in the form of a time– frequency response for individual electrodes and in a form of eventrelated synchronization (ERS)/event related desynchronization (ERD) scalp maps
In this paper we demonstrate that prolonged neurofeedback treatment that leads to longer term reduction of pain results in decreased activity of sensory-motor cortex, bringing it closer to the activity seen in able bodied people and in spinal cord injured patients with no pain (Stern et al, 2006; Wrigley et al, 2009; Vuckovic et al, 2014)
Summary
Central neuropathic pain (CNP) is a frequent secondary consequence of spinal cord injury (SCI), affecting about 40% of patients (Siddall et al, 2003). CNP is caused by an injury to the. Neuroimaging studies have demonstrated changes in the resting state brain activity in the presence of CNP, which is reflected in increased thalamo-cortical coherence in the theta band (Stern et al, 2006; Sarnthein and Jeanmonod, 2008), as well as increased resting state EEG power and a dominant alpha frequency shift towards lower frequencies (Stern et al, 2006; Sarnthein et al, 2006; Boord et al, 2008; Jensen et al, 2013a; Vuckovic et al, 2014).
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