Mechanism of neuropathic pain in an animal model of nerve trauma

Tactile allodynia develops on the hindpaw following transection of the L5 spinal nerve in rats. Logic says that partial denervation should blunt sensation, not augment it. Why, then, does this type of nerve injury trigger pain? Electrophysiological recordings were made from severed L5 nerve fibers. These revealed that the injured afferents rapidly became a source of spontaneous ectopic discharge. Most of the discharge originated in the soma of primary sensory neurons in the segmental dorsal root ganglion (DRG), and not at the nerve injury site. Moreover, the time of onset of the ectopic firing precisely matched the time of onset of the tactile allodynia. These data support the following mechanism: Axotomy triggers ectopic firing in the DRG which yields ongoing neuropathic paraesthesias and pain. In addition, it triggers spinal central sensitization, amplifying sensory signals arising from residual uninjured Ab touch afferents in the skin. Due to the central sensitization, light touch of the skin yields pain (tactile allodynia).