The causality between Electroencephalogram (EEG) and Central Neuropathic Pain (CNP), and the effectiveness of neuromodulation strategies on cortical excitability and CNP in patients with spinal cord injury

Spinal Cord Injury has primary consequences visible immediately upon injury and secondary consequence which develop some time after injury. One of the primary consequences of SCI is loss or impairment of sensory and motor functions. Related secondary consequences of the injury are Central Neuropathic Pain (CNP) and spasticity. Several studies have found that CNP can affect the cortical activity of the patient and long term CNP causes anatomical cortical changes. Therefore, early prediction and treatment of CNP could potentially prevent these changes and hopefully increase responsiveness to the treatment. Neurofeedback (NF) technique, which is a sub-category of biofeedback that uses brain waves as physiological parameters to be modulated, can be used to alter this change in cortical activity and treat CNP. The sensory motor cortex is the area of the brain responsible for voluntary control of movement and for cortical modulation of reflexes. NF provided from the sensory-motor area can therefore affect both CNP and voluntary and reflex movements. The aim of this PhD project was to explore the influence of neuromodulation strategies over the central cortex on the H reflex and CNP following SCI. It also aimed to investigate the causal relationship between the change in EEG activity and the transitional period from early symptoms of CNP to the chronic phase of CNP following SCI. The first study of this project was performed on able-bodied volunteers to explore the effect of the short-term neuromodulation strategies: NF, motor imagery (MI) and mental math (MM) of the sensory-motor rhythm (SMR) on the soleus H reflex. Results of the study showed that it is possible to achieve short-term modulation of the H reflex through short-term modulation of the SMR. Various mental tasks dominantly facilitate the H reflex irrespective of the direction of SMR modulation. The results of this study can be used to explain the effect of NF therapy on spasticity in SCI patient, for example. The second study analysed predictors of CNP in sub-acute SCI patients who have not yet developed physical symptoms of pain. It compared EEG signal between patients who did and did not develop pain within the first six months after EEG recording as well as patients with CNP and able bodied volunteers. This study demonstrated that changes in spontaneous and induced EEG can be both predictors and consequences of CNP following SCI. The third study explores the effectiveness of Neurofeedback (NF) on treatment of CNP in subacute SCI patients with CNP. The results of this study demonstrate that the NF treatment has a positive effect on the reduction of pain, at least over the period of the study. However, numerous factors, and in particular patients’ low prioritization of pain, indicate that early NF of CNP in SCI patients might not be a practical solution. The fourth study utilizes advanced methods of source analysis to define dynamic signatures of long standing CNP by using Measure Projection Analysis (MPA) for movement related cortical potential (MRCP). To separate the effect of long-term paralysis from the effect of long-term CNP, brain activity has been compared between three groups: able bodied volunteers, patients with chronic paraplegia (paralysis of lower limbs) with no pain and patients with chronic paraplegia and long standing CNP. This study showed that the movement related potential is dominantly influenced by paralysis while both CNP and paralysis affect the reafferentation component of the MRCP. Additionally, CNP influences cognitive processes in a manner that depends on the functional area of the cortex