Cut-out and Keep Guide...Nerve Injury and Pain

Pain resulting from direct damage to the peripheral or central nervous system is a different creature than from any other process. Nerve injury can arise from many causes (Table 1) and results in a rapid and specific cascade of events leading to unique cellular, molecular, and microanatomic changes. In brief, nerve injury causes ectopic signaling from both the site of the injury (neuroma) and the dorsal root ganglion (DRG). This results in altered connectivity in the DRG and the dorsal horn of the spinal cord (via sprouting of afferents and postganglionic sympathetics), altered spinal excitability via loss of inhibitory control, and activation of non-neuronal (immunomodulating, glial) cells. Gene expression changes to neurons can make this condition permanent. As a result of these changes, patients can experience “maladaptive pain”, which may take various facets including protracted pain, hyperalgesia (exaggerated response to a noxious stimulus), allodynia (pain evoked from a non-noxious stimulus), spontaneous pain, dysesthesias (pain in conjunction with other sensations such as tingling or itch), pain distant from the original site of injury, and pain associated with sympathetic signs (Complex Regional Pain Syndrome).