PubMed1993
Reflex sympathetic dystrophy is a progressive illness most often initiated by trauma to a nerve, plexus, or soft tissue. Its five components are pain, edema, autonomic dysfunction, movement disorder, and trophic changes. The illness evolves in stages that progress insidiously over time. The length of time a patient remains in a specific stage is unknown. In any stage of reflex sympathetic dystrophy, the symptom complex may be dissociated. Reflex sympathetic dystrophy occurs in one part of the body that seems to sensitize a patient so that a succeeding injury may initiate the process in the newly traumatized area. The length of time this sensitization lasts is unknown. Pain is the most disabling and the most difficult aspect of the illness to treat. At least in early stages the pain is sympathetically maintained, but with time becomes sympathetically independent. The alpha 1 adrenoreceptor appears to be the peripheral link that, when activated, sensitizes directly or indirectly C-nociceptor fibers. Dynamic mechanoallodynia is mediated by A beta low threshold mechanoreceptors, whereas static primary mechanical hyperalgesia may be mediated by sensitized C-nociceptors. A peripheral afferent C-nociceptor input appears to be necessary to alter the dorsal horn central processing mechanisms to allow for the expression of dynamic mechanoallodynia. This nociceptive barrage could be driven by the sympathetic efferent outflow or could be sympathetically independent. The response of immediate early response genes may change the neuropeptide concentration of the dorsal horn. Central sensitization mediated by excitatory amino acids, neuropeptides, and the N-methyl-D-aspartate receptor may be responsible for the severe pain seen in the later stages of the illness.