“…It has been reported that any pathology in the spinal cord may cause hyperexcitability in the dorsal horn. [25,26] This might occur through dysregulation of glutamate release, uptake and receptor expression, [25,[27][28][29] dendritic spine remodeling, [30,31] loss of local inhibitory (GABAergic) tone, [32][33][34][35][36] descending (particularly serotonergic) inhibitory input to spinal nociceptive circuitry, [28,39,40] or increased expression of calcium channel subunit. [39] Within a few months of spinal cord injury, NADPH-diphosphorase abnormality is seen in the nucleus cunaetus, nucleus gracilis, and spinal trigeminal tract of rats.…”