The pathophysiology of peripheral neuropathic pain--abnormal peripheral input and abnormal central processing.
A review is given on the pathogenesis of peripheral neuropathic pain. Central neuropathic pain resulting from damage of the spinal cord or brain is not covered. The following conclusions are proposed. At the time of peripheral injury, an abnormal injury discharge may be sufficient to produce long term changes in the excitability of the spinal cord and/or an excitotoxic death of dorsal horn neurons. These acute changes might set the scene for the maintenance of sensory disorders both as a result of an ongoing ectopic input, which might persistently induce a state of central sensitization and for a structural reorganization of the synaptic connections of the dorsal horn. The implications of these findings is that it may be possible to prevent some of the long term consequences of nerve damage, that the treatment at the time of injury may need to be quite different for that required later, and finally that treatment directed only at the periphery may be insufficient to eliminate the sensory disturbance of chronic neuropathic pain.
Woolf
C J
CJ
Department of Anatomy and Developmental Biology, University College London, U.K.
D016923:Cell Death; D005260:Female; D006801:Humans; D008297:Male; D009413:Nerve Fibers, Myelinated; D009434:Neural Pathways; D009619:Nociceptors / Q000502:physiology; D010146:Pain / Q000517:prevention & control*; D010525:Peripheral Nerves / Q000503:physiopathology*; D010523:Peripheral Nervous System Diseases / Q000517:prevention & control*; D011494:Protein Kinases / Q000378:metabolism; D016194:Receptors, N-Methyl-D-Aspartate / Q000378:metabolism; D015290:Second Messenger Systems / Q000502:physiology
D016194:Receptors, N-Methyl-D-Aspartate; D011494:Protein Kinases