logically complete injuries show some amount of tissue and axonal sparing across the site of the lesion (Bunge et al., 1997).

A spinal cord injury immediately injures or kills cells, but it also causes delayed damage and death to cells that survive the original trauma. The biological response to a spinal cord injury is divided into three phases that follow a distinct but somewhat overlapping temporal sequence: acute (seconds to minutes after the injury), secondary (minutes to weeks after the injury), and chronic (months to years after the injury). A general overview of the three phases is presented in Table 2-4. Diverse groups of cells and molecules from the nervous, immune, and vascular systems are involved in each phase. Most participating cells reside in the spinal cord, but others are summoned to the site of injury from the circulatory system (Table 2-5). To carry out many of their functions, the cells depend on changes in gene expression. As would be expected, injury triggers certain cells to up-regulate (increase expression) or down-regulate (decrease expression) genes responsible for a host of proteins involved in inflammation, neurotransmission, regrowth and repair, and other local responses to injury (Bareyre and Schwab, 2003). The final pattern of sensory and motor losses from the