How is chronic pain related to sympathetic dysfunction and autonomic dysreflexia following spinal cord injury

摘要: Autonomic dysreflexia (AD) and neuropathic pain occur after severe injury to higher levels of the spinal cord. Mechanisms underlying these problems have rarely been integrated in proposed models cord (SCI). Several parallels suggest significant overlap mechanisms, although relationships between sympathetic function (dysregulated AD) nociceptive pain) are complex. One general mechanism likely be shared is central sensitization – enhanced responsiveness synaptic reorganization circuits that mediate reflexes or process relay pain-related information brain. Another sensory input caused by extensive alterations primary neurons. Both AD SCI-induced associated with sprouting peptidergic nociceptors might increase involved SCI pain. In addition, numerous become hyperexcitable, hypersensitive chemicals inflammation, spontaneously active, greatly amplifying sensitized circuits. As discussed aid a preliminary functional model, effects mutually reinforcing each other, consequences interruption descending excitatory inhibitory influences on circuits, inflammation DRGs, activity fibers within DRGs promotes local spontaneous This model suggests interventions selectively targeting hyperactivity C-nociceptors useful for treating chronic high SCI.