| dc.description.abstract | When a person suffers a spinal cord injury, peripheral damage often accompanies it, such as damage to the legs, for instance. The pain (nociceptive) signals from this peripheral injury are being sent to the damaged spinal cord, but the patient might not “feel” any pain because the ascending pathways are damaged by the spinal injury. Even though the affective component of pain is not present, the stimulation from peripheral injury could be damaging to locomotor recovery. This has been studied using a spinal contusion surgery on rats to simulate spinal cord injury, and uncontrollable shock to act as pain signals from peripheral injury. Although it is known that the brain is necessary for this destructive effect to occur, it is not known whether the brain initiates the effect, or if the signal must travel through the injury to induce the effect, making the spinal cord the primary initiator. This was examined by comparing the recovery of groups given shock above, versus below, the spinal cord injury. To minimize pain in shocked animals, all subjects received an analgesic dose of morphine. Prior work has shown that this treatment blocks behavioral signs of pain, but does not block the adverse consequences of stimulation on recovery. I found stimulation below, but not above, the site of a spinal contusion injury in rats impaired recovery. This supports that nociceptive signals only impair recovery if they engage spinal neurons below (caudal to) the site of injury. | en |
