Abstract
Traumata of the limbs which are accompanied by peripheral nerve lesions are commonly followed by painful peripheral states and trophic changes of the tissues [34,35,47]. These painful states are difficult to treat and sometimes even resistant to therapy. The neuronal mechanisms involved in the production and maintenance of the pathological pain states and trophic changes are unknown. They might comprise peripheral and central components: The peripheral component is produced by the complete or partial interruption of the continuity between target tissue (receptive structures of afferent fibers, autonomic effector organs) on one side and afferent and sympathetic efferent (postganglionic) fibers on the other side. This interruption may result in abnormal discharge patterns in the afferent and efferent neurones and in a change of retro- und anterograde axoplasmic flow. The central component being induced by this interruption is documented in dramatic changes of the peptide content of the substantia gelatinosa in the dorsal horn (such as depletion of endogenous phosphatase [31] and of substance P [30]), in changes of the receptive fields of dorsal horn neurones [11,12], and in a decline of primary afferent depolarization [50]. The present paper discusses results of our neurophysiological investigations of afferent and sympathetic efferent (postganglionic) fibers in a skin nerve (superficial peroneal nerve) of cat hind limbs which had been cut and ligated 6–245 days before the experiments so that neuromata had developed. These experimentally produced neuromata might be a pathophysiological model [51] for pain-producing neuromata occurring in humans after nerve trauma.
Published Version
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