Injury to the peripheral nerve can lead to paradoxical changes in functioning such that there is an ongoing dysesthesia and an altered processing such that low threshold stimuli are responded to in humans and animals as if they were painful. What are the mechanisms underlying these anomalous behaviors? The biological changes induced by nerve injury are complex. To attribute functional relevance to the many changes, systematic preclinical work using well-defined behavioral models of nerve injury has been undertaken. Such studies have provided support for the important role in nerve injury-evoked pain behavior for a number of channels and receptors in the injured nerve, the dorsal root ganglion of the injured nerve, and the dorsal horn. These changes and their effect upon behavior are the subject of this review.
Keywords: unmyelinated (c), mononeuropathies, nerve injury syndromes, complex regional pain syndrome, pro-inflammatory, growth factors, spinal cord, dorsal root ganglia (drg), chemotransduction, sodium channels
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