Abstract
Regional neuropathic pain syndromes above, at, or below the site of spinal damage arise after spinal cord injury (SCI) and are believed to entail distinct pathways; nevertheless, they may share shared defective glial systems. Neuropathic pain after SCI is caused by glial cells, ectopic firing of neurons endings and their intra- and extracellular signaling mechanisms. One such mechanism occurs when stimuli that were previously non-noxious become so after the injury. This will exhibit a symptom of allodynia. Another mechanism is the release of substances by glia, which keeps the sensitivity of dorsal horn neurons even in regions distant from the site of injury. Here, we review, the models and identifications of SCI-induced neuropathic pain (SCI-NP), the mechanisms of SCI-NP related to glia, and the treatments of SCI-NP.