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