ABSTRACT
Despite recent advances, spinal cord injury (SCI) remains a leading cause of chronic disability with significant socioeconomic consequences. Accordingly, a large effort has been devoted to understanding and preventing the longterm effects of both the immediate primary and delayed secondary damage after SCI. Traumatic SCI is characterized by well-defined spatial and temporal patterns of tissue injury that evolve over time (1). The acute stage is characterized by hemorrhage and edema in and around the lesion epicenter (2). This is followed by a delayed stage with secondary injury due to oxidative stress, excitotoxicity, and inflammation, resulting in both neuronal and glial cell death (2). Pharmacological and=or cell-based approaches that mollify the immune response, reduce glial scarring, enhance axon regeneration, promote neuroprotection and restore irreparably damaged cells have thus far been among the most widely employed strategies for SCI therapy. Although these therapeutic approaches may significantly improve functional outcome in experimental animals, successful translation to the human condition remains to be proven.
