摘要: New animal models of peripheral nerve injury have facilitated our understanding neuropathic pain mechanisms. Nerve increases expression and redistribution newly discovered sodium channels from sensory neuron somata to the site; accumulation at both loci contributes spontaneous ectopic discharge. Large myelinated neurons begin express nociceptive substances, their central terminals sprout into regions dorsal horn. Descending facilitation brain stem horn also in setting injury. These other mechanisms drive various pathologic states sensitization associated with distinct clinical symptoms, such as touch-evoked pain.