Pain and Plasticity
Under normal conditions, pain is acute and protective, manifested as responsiveness to noxious stimuli. However, after tissue or nerve injury, pain becomes pathological and chronic, with increased responsiveness to noxious stimuli and even becoming responsive to innocuous stimuli. Pain hypersensitivity following intense nociceptive input or injuries results from neural plasticity that occurs both in the peripheral nervous system (e.g., primary sensory neurons), termed peripheral sensitization, and in the central nervous system (e.g., dorsal horn neurons), termed central sensitization. Activation of several intracellular signal pathways in nociceptive neurons leads to the induction and maintenance of both types of sensitization. Furthermore, activation of spinal glial cells following injuries can enhance and prolong central sensitization by producing inflammatory mediators centrally. © 2009 Elsevier Ltd All rights reserved.
