cal research efforts from many related fields of neuroscience, bioengineering, and rehabilitative research.

ACUTE INJURY

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

Strategy

Examples of Therapeutic Classes or Agents

Reduce ischemia

  • Antivasospasm agents

  • Protein kinase inhibitors

  • Steroids

  • 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)

  • Increase intercellular cyclic AMP levels



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