Abstract
Causalgia is caused by nervous system lesions. Here, we present recently accumulating data about the contribution of the dorsal root ganglion neurons spared from direct injury to the pathomechanisms of causalgia. The phenotypic changes in the spared neurons are similar with those in the neurons in peripheral inflammation models, as opposed to those in the directly injured neurons. Electrophysiological changes also favor the contribution of the spared neurons. On the other hand, the injured A-fiber neurons also can cause sensitization of the secondary neurons in dorsal column nucleus, and modulate nociceptive input to the thalamus. These attractive targets of study will give us new approaches for understanding the abnormal pain.
