Debilitating neuropathic pain occurs in 40-70% of people who suffer from spinal cord injury (SCI). It is unknown why, with similar injuries, one person will develop neuropathic pain while another will not. There are no distinguishing characteristics to identify who will develop neuropathic pain. The objective of this research is to develop a biomarker signature prognostic of SCI-induced neuropathic pain. The ultimate goal is to identify new non-addictive treatments for its prevention. R61 Phase Specific Aim 1: To identify autoantibodies (ab) in plasma samples from acute SCI patients to CNS autoantigens and determine the relationship between ab levels to the development of NP. R61 Phase Specific Aim 2: To identify the autoantibody combination with maximal prognostic accuracy for the development of NP at 6 months after SCI. R33 Phase Specific Aim 3: Develop and optimize an assay to simultaneously measure several autoantibodies (to be determined during R61) and independently validate the prognostic efficacy for NP using plasma samples collected prospectively. The research will use banked and prospectively enrolled samples from SCI patients and healthy controls. Subjects' pain phenotypes will be carefully characterized. Techniques capitalizing on antibody-antigen binding will be used to optimize an autoantibody biomarker signature predictive of neuropathic pain. Establishing a panel will refine the prognostic value of these autoantibodies as biomarkers in order to detect those who are vulnerable to developing neuropathic pain with high reliability and may be used to facilitate the future development of non-addictive pain therapeutics.
Chronic neuropathic pain is a debilitating condition that occurs in 10% of the general population and in 40-70% of those with spinal cord injury. This research aims to identify a biomarker signature with high sensitivity and specificity that is prognostic of neuropathic pain after spinal cord injury. The research would contribute knowledge about the relationship between autoantibodies and neuropathic pain, and the application of this knowledge may pave the way for clinical studies utilizing non-opioid therapeutics aimed at reducing plasma autoantibody levels in order to hinder the development of neuropathic pain.
