In a recent study published in Clinical Neurophysiology, paraplegic patients experiencing central neuropathic pain (CNP) were subjected to 20-40 neurofeedback sessions paired with limb movement imagination.1
Following neurofeedback/movement imagination, CNP-associated increases in cortical activity were reduced in paraplegic patients to levels of no pain individuals, highlighting the 2 main findings of this study: CNP affects cortical activity, which can be manipulated for pain relief.
In pilot experiments, researchers investigated mechanisms of neurofeedback training for CNP which affects about 40% of spinal cord injury (SCI) patients, as well as individuals with stroke, Parkinson’s disease and multiple sclerosis.2-5 As paraplegia-associated CNP displays specific cortical waves, scientists hypothesized that efficacy of patient training could be monitored with EEG recordings.
Other studies have found effects of CNP on resting-state EEG activity, and in particular, an increase in spectral power in the 2-25 Hz range, which includes delta (0-4 Hz), theta (4-8 Hz), alpha (8-12 Hz) and beta (12-40 Hz) waves, as well a shifting of the majority of the activity to the lower range of the spectrum.6
Here, paraplegic patients (n=5) at least 1 year post-SCI, pharmacologically treated for CNP for ≥ 6 months and with pain scores ≥5 on the Numerical Pain Rating Scale (with a range of 0 to 10, 10 being the highest), were compared with no pain paraplegic patients (n=10) and able-bodied subjects (n=10).
During neurofeedback, cortical activity was recorded using EEG, and conveyed to the patient on a computer monitor showing 3 bars: alpha power (center), theta and beta powers on each side, all 3 color- and size-coded. Instructions were given to “keep the bars green,” which indicated amplitude increase and decrease, for middle and side bars, respectively.
The most successful intervention –as assessed by largest reduction of CNP-associated theta bands- was achieved with motor imagination of feet. These changes were most noticeable in the frontal and parieto-occipital cortex.
Reduction in pain levels are directly visible on the EEG, which persisted for at least 1 month following neurofeedback treatment. “While there is no clear answer whether changes in EEG are a cause or a consequence of pain, a fact that modulation of resting state EEG through neurofeedback resulted in reduced pain indicate that ‘abnormal’ baseline EEG might precede pain,” write the authors.
“During the treatment [patients] learned the mental strategy and were capable of bringing themselves in a similar mental state even without a visual feedback,” add researchers. “It is therefore hard to say if reduced pain was a consequence of the neurofeedback therapy or it was a results of their independent practice at home. In the future it would be useful having a follow up of EEG measurement over a prolonged period of time, to assess whether changes in EEG still persist.”
- Hasan MA, Fraser M, Conway BA, Allan DB, Vučković A. Reversed cortical over-activity during movement imagination following neurofeedback treatment for central neuropathic pain. Clin Neurophysiol. 2016;127(9):3118-3127.
- Hassan MA, Fraser M, Conway BA, Allan DB, Vuckovic A. The mechanism of neurofeedback training for treatment of central neuropathic pain in paraplegia: a pilot study. BMC Neurol. 2015;15:200.
- Andersen G, Vestergaard K, Ingeman-nielsen M, Jensen TS. Incidence of central post-stroke pain. Pain. 1995;61(2):187-193.
- Santos-garcía D, Abella-corral J, Aneiros-díaz Á, Santos-canelles H, Llaneza-gonzález MA, Macías-arribi M. [Pain in Parkinson’s disease: prevalence, characteristics, associated factors, and relation with other non motor symptoms, quality of life, autonomy, and caregiver burden]. Rev Neurol. 2011;52(7):385-93.
- Osterberg A, Boivie J, Thuomas KA. Central pain in multiple sclerosis–prevalence and clinical characteristics. Eur J Pain. 2005;9(5):531-42.
- Sarnthein J, Stern J, Aufenberg C, Rousson V, Jeanmonod D. Increased EEG power and slowed dominant frequency in patients with neurogenic pain. Brain. 2006;129(Pt 1):55-64.