CHRONIC CENTRAL PAIN AFTER SPINAL-CORD INJURY

Spinal cord injury (SCI) frequently results in dysesthesias that have remained refractory to clinical treatments despite a variety of interv entions. The failure of therapeutic strategies to treat dysesthesias a fter SCI is due to the lack of attention given to mechanisms that elic it chronic pain following SCI. An overview of the literature with resp ect to the development of chronic pain in the SCI patient population w ill be given. In addition, a mammalian model of chronic central pain f ollowing spinal cord trauma will be presented. The model is characteri zed by the development of mechanical and thermal allodynia, as demonst rated by measuring the thresholds of accepted nociceptive tests, the p aw withdrawal responses accompanied by changes in behavior consistent with the experience of noxious stimulis. In addition, vocalization res ponses that are accompanied by postural and behavioral changes consist ent with the receipt of a noxious stimulus and involving supraspinal p athways are measured. Locomotor function was also tested and scored us ing the Basso, Beattie, and Bresnahan (BBB) open field test scale. Our data indicate that somatosensory thresholds for both mechanical and t hermal stimuli that elicit paw withdrawal (flexor reflex) or vocalizat ions, accompanied by complex changes in behavior, are significantly di fferent following SCI. These changes represent the development of mech anical and thermal allodynia. To determine the underlying mechanism fo r the altered sensory responses, we used electrophysiological techniqu es to determine if nociceptive dorsal horn neurons demonstrated increa sed excitability to peripheral stimulation as evidenced by increased r esponses to natural somatosensory stimuli. The data presented support the development of central sensitization of dorsal horn neurons after spinal cord hemisection. This provides a mechanism for the development of mechanical and thermal allodynia after SCI. Hypotheses that accoun t for the development of the central pain state after SCI, as well as therapeutic interventions to ameliorate the pain state, are discussed.