Actual Aspects of Treatment Strategies in Spinal Cord Injury

Abstract

Treatment in the Acute Phase: Processes of secondary injury significantly enlarge tissue damage after spinal cord injury (SCI). Ischemic and inflammatory processes play a major role. Animal models have shown that in the acute stage, there are numerous possibilities of preventing secondary tissue damage after SCI including barbiturate coma, hypothermia, tissue oxygenation, administration of antioxidants and neuropeptides, as well as maintenance of the ionic homeostasis and balance between anti- and pro-inflammatory strategies. Only methylprednisolone (MP) has given consistent enough results in clinical trials to justify its wide use today, although the effects are small and the mechanism of action (radical scavenger, anti-inflammatory, anti-edema) is not understood. The role of inflammation is also far from being clear; damaging as well as positive, tissue-protecting effects are described and probably occur simultaneously.

Threatment in the Chronic Phase: In the chronic stage, strategies to promote axonal regeneration and compensatory sprouting of fibers include support of neuronal survival, promotion of axonal growth by the use of antibodies to block white matter inhibitors or influencing the surrounding through application of neurotrophins or substances that minimize scar formation or bridge the damaged tissue through transplantation. Although several of these procedures have yielded exciting results in animal models, none of them has reached the level of clinical trials yet.