Autoantibodies and neuropathic pain

It is becoming apparent that autoantibodies contribute to neuropathic pain in a range of neurological conditions. In some cases, these autoantibodies clearly evoke injury (e.g., GBS or transverse myelitis); in others, they appear to directly regulate excitability of the sensory nervous system. There are immunotherapies that can reduce autoantibody levels, and confirmation that these autoantibodies are causal to pain will improve analgesic treatment strategies for these patients. For example, in patients with VGKCC-Ab, the effectiveness of immunotherapy in reducing pain has lessened the need for opioid treatment, resulting in a reprieve from the harmful side effects of narcotics and better pain management (Gadoth et al., 2017). An improved understanding of the prevalence of autoantibodies is needed and may provide an explanation for certain idiopathic pain conditions. Moreover, the work on autoantibodies can be used as a tool to provide insight into clinically relevant mechanisms controlling pain sensitivity in the more general context and help steer the future development of therapies to treat neuropathic pain.