Nociceptive (Pain) Input After Spinal Cord Injury (SCI) Enhances Secondary Injury: Identifying Treatments that can be Translated to Clinical Practice
Technical Report,30 Sep 2018,29 Sep 2019
Texas A and M University College Station United States
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Using an animal model, we have shown that nociceptive pain input after spinal cord injury SCI amplifies secondary injury and undermines long-term recovery. These observations are important because SCI is often accompanied by additional tissue damage polytrauma that provides a source of nociceptive input. The consequences of pain nociceptive input on recovery after a lower thoracic contusion injury have been studied using an animal rat model. Prior work has shown that engaging nociceptive fibers 24 hr after injury increases tissue loss, undermines long-term recovery, and fosters the development of pain and spasticity. Recent studies have related these effects to pain induced hemorrhage at the site of injury and shown that this can be blocked by means of a local lidocaine or general pentobarbital anesthesia. Experiments will determine when nociceptive input affects tissue loss, the time period over which hemorrhage occurs, whether these effects are observed in both male and female animals, and whether chemically engaging pain C fibers with the irritant capsaicin has the same effect. Having demonstrated that capsaicin induces hemorrhage and impairs long-term recovery, we are assessing whether this effect can be prevented by means of a pharmacological transection or general anesthesia. To further evaluate the clinical relevance of these findings, we will test whether they are effective when initiated soon after injury or the initiation of painful stimulation.
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