PERIPHERAL AND CENTRAL-NERVOUS-SYSTEM MECHANISMS OF SYMPATHETIC RELATED PAIN

Pathophysiological processes initiated by tissue and nerve damage contribute actively to chronic pain by injecting abnormal discharge into the nervous system. The abnormal firing may trigger pain in two ways. First, ectopic discharge carried in nociceptors evokes pain directly. Second, nociceptive input can generate and maintain a special state in the spinal cord, termed ''central sensitization,'' under which input entering along otherwise intact afferents, including low threshold afferents, is amplified and can contribute to pain. Abnormal afferent discharge in peripheral nerves may be exacerbated by activity in sympathetic efferent fibres. This is paradoxical as post-ganglionic sympathetic neurons normally function purely as efferent (motor) elements. However, under certain circumstances, they can become coupled to sensory afferents in such a way that their activity drives afferents. Such ''sympathetic-sensory coupling'' is probably a major cause of RSD and related sympathetic dependent chronic pain states. The coupling appears to be mediated by noradrenaline released from the sympathetic efferent ending which acts on alpha-adrenoreceptors on injured, hyperexcitable afferents. Sympathetic-sensory coupling occurs at the nerve injury site as well as at the level of the sensory cell soma in the DRG, and in the peripheral target tissue.