The authors seek to highlight some of the recent advances in understanding the pharmacology and pathophysiology of sympathetically-maintained pain, and to develop alternate, and possibly more specific, diagnostic tests for this phenomenon. Mechanical hyperalgesia in sympathetically-maintained pain can be explained by central sensitization so that the activation of A-beta mechanoreceptors now causes pain. ⋯ The authors propose that an ongoing input from peripheral nociceptive afferents is necessary to maintain central sensitization. This nociceptive input may be due to an alpha-adrenoceptor mediated excitatory action of sympathetic efferents on sensory nerves that is independent of neurovascular transmission.
Department of Anesthesiology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
J Reconstr Microsurg. 1992 Jan 1;8(1):63-9.
AbstractThe authors seek to highlight some of the recent advances in understanding the pharmacology and pathophysiology of sympathetically-maintained pain, and to develop alternate, and possibly more specific, diagnostic tests for this phenomenon. Mechanical hyperalgesia in sympathetically-maintained pain can be explained by central sensitization so that the activation of A-beta mechanoreceptors now causes pain. The sensitization of central pain-signaling neurons is dynamic and reversible. The authors propose that an ongoing input from peripheral nociceptive afferents is necessary to maintain central sensitization. This nociceptive input may be due to an alpha-adrenoceptor mediated excitatory action of sympathetic efferents on sensory nerves that is independent of neurovascular transmission.