The majority of individuals who sustain spinal cord injuries do not suffer a complete transection of their spinal cords, even if they have functionally complete paralysis. Rather, while the initial "primary" mechanical impact interrupts axons at the site of injury and disrupts the local neuronal and glial cytoarchitecture, a proportion of the spinal cord (usually the outer rim) escapes intact. This spared tissue, however, is then subject to a complex cascade of acute pathophysiologic processes that cause further "secondary" damage. These interrelated processes include ionic homeostasis abnormalities, excitotoxicity, programmed cell death, tissue ischemia, and inflammation (Kwon et al., 2004b). Neuroprotective therapies aim to counteract these processes, thereby averting further secondary damage and maximizing the extent of spared cord tissue. Animal studies have demonstrated that significant neurologic function can be mediated by small amounts of spared cord tissue, and in this regard, even small neuroprotective effects might reap substantial functional benefits to patients.