Bouhassira D
INSERM U 161, Paris.
Cah Anesthesiol. 1994;42(6):689-97.
Animals studies have shown that peripheral nerve lesions can induce secondary changes in the dorsal horn of the spinal cord. Histological changes include degeneration of both primary afferent terminals (transganglionic degeneration) and second order neurones (transsynaptic degeneration). Secondary regeneration phenomena associated with changes in the topographical organization of central terminals of primary afferents have also been described. Neurochemical changes include a decrease of the spinal content of some peptides normally released by primary afferent terminals (substance P, CGRP...), and the synthesis of peptides which are not normally synthetized by dorsal root ganglia cells (galanin, VIP, neuropeptida Y...). Functional changes suggesting a sensitization of spinal neurones (increased spontaneous activities, expansion of receptive fields size) have been reported. Such a central sensitization might depend on a reduction of segmental inhibitory controls and/or intracellular changes induced by the activation of NMDA receptors by excitatory amino acids released by primary afferents. Such central changes might explain some of the features of spontaneous and/or evoked pains (allodynia/hyperalgesia) associated with peripheral neuropathies in humans.