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Spinal Cord Injury: Progress, Promise, and Priorities
cal research efforts from many related fields of neuroscience, bioengineering, and rehabilitative research.
Reduction of Edema and Free-Radical Attack
A complex series of biochemical reactions that cause ischemia and edema, followed by necrosis and inflammation, occur as a result of a spinal cord injury. Each reaction could provide a target for early intervention and treatment. The key is to pick out, from among the myriad of reactions, the dominant and most specific players and then target them for treatment.
Many different therapeutic approaches have been tested in vitro or with animal models of spinal cord injury (Table 5-1). Some are aimed at
TABLE 5-1 Examples of Strategies to Reduce the Effects of Acute Spinal Cord Injuries Tested with Animal Models
Examples of Therapeutic Classes or Agents
Protein kinase inhibitors
Prevent disruption to the blood-spinal cord barrier
Mild to moderate regional hypothermia
Reduce calcium influx
Blockers of ion channels or exchangers
Reduce edema and formation of free radicals
Antioxidant enzymes, including free-radical scavengers (e.g., superoxide dismutase, glutathione peroxidase, catalase, and melatonin)
Inhibitors of nitric oxide synthase
Control inflammation or enhance protective immunity
Steroids and other anti-inflammatories (e.g., COX-2 inhibitors and anti-inflammatory cytokines)
Activated macrophages and monocytes
Inhibitors of immune cell infiltration of the CNS
Antibodies against integrin on the vascular surface to prevent egress of neutrophils
Reduce tissue loss
Cell transplantation (e.g., Schwann cells and olfactory ensheathing cells)