Fig. 2. Models representing the mechanism of sympathetically maintained pain (SMP). (A ) The original hypotheses proposed by William Roberts.3Roberts proposed that the sympathetic efferent activity was enhanced in SMP and that the ongoing pain in chronic SMP was mediated by activity in low-threshold, myelinated mechanoreceptors, the result of sympathetic efferent actions on myelinated, mechanoreceptor afferents or on afferent fibers ending in a neuroma. (B ) Revised hypotheses based on our studies and those of several other investigators. Subsequent studies indicate that the sympathetic outflow is not enhanced in SMP, but that α-adrenoceptors are enhanced on nociceptors and blood vessels in the periphery. The ongoing activity in nociceptors results in sensitization of wide-dynamic range neurons in the spinal cord. Activation of low-threshold mechanoreceptors converging on sensitized WDR cells results in allodynia (pain to normally innocuous stimuli). LTM = low-threshold mechanoreceptors; WDR = wide-dynamic range.