In addition to causing the loss of voluntary sensory and motor function, spinal cord injury (SCI) often creates a state of central neuropathic pain. Rats given SCI display increases in the activated form of transcription factors ERK 1/2, p38 MAPK, and CREB in the spinal cord, which correspond to allodynia in a model of neuropathic pain. The current study was designed to determine if lidocaine had an effect on the development of neuropathic pain in response to SCI.

Male Sprague Dawley rats were anesthetized and then received a L5-L6 spinal nerve ligation (neuropathic rats). The levels of intracellular cell-signaling protein, ERK 1/2 and CREB were then assessed by western blot analysis of samples collected from a sham operated (control) group, a neuropathic pain and normal saline (NP + NS) group, and a neuropathic pain and 5% lidocaine (NP + Lido) group.

The increased levels of ERK 1/2 and CREB protein that were observed in the neuropathic pain model were reduced by continuous infusion of 5% lidocaine.

The current results suggest that lidocaine therapy may be an effective method of preventing and treating central neuropathic pain following SCI, and that these effects may occur via the reduced expression of ERK 1/2 and CREB in the intracellular cell-signaling pathway.