Spinal cord injuries (SCIs) result in a devastating loss of function below the level of the lesion in which there are variable motor recoveries. In the majority of cases, chronic central neuropathic pain (CCNP) syndromes develop several months to years after injury. Unfortunately, the study of chronic pain after SCI has been neglected in the past due in part to the lack of good animal models but also largely due to the clinically held dogma that CCNP is not a real phenomenon based on described pathophysiological mechanisms. The purpose of this article is to offer standardized terminology of pain, insight into animal modeling issues of CCNP, descriptions of current clinical therapies, and discussion of the pathophysiological mechanisms that provide the substrate for CCNP that will lead to innovative new therapies. This information will give health care professionals insight for the care of SCI individuals and will be generalizable to many other CCNP syndromes.

central sensitization, excitatory amino acids, glutamate, glutamate receptors
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