As stated earlier, secondary damage to the spinal cord after the initial mechanical impact is mediated by a number of pathophysiologic processes, including ionic homeostasis abnormalities, excitotoxicity, programmed cell death, tissue ischemia, and inflammation. The preceding discussion has focused on tissue ischemia and how this might be affected by CSF drainage. Inflammation appears to also play an important role in the pathophysiology of acute spinal cord injury, and has thus been the focus of increasing attention in recent years. The inflammatory response to spinal cord injury is mediated by cytokines that influence vascular permeability and regulate migration of inflammatory cells such as neutrophils and macrophages into the spinal cord (Kwon et al., 2004b). The list of cytokines thought to be relevant to the inflammatory response after spinal cord injury is long, and includes IL-1 , IL-1 , TNF , IL-6, IL-10, VEGF, and a variety of leukotrienes. (Mueller et al., 2003;Widenfalk et al., 2003; Mitsuhashi et al., 1994; Xu et al., 1990; Bartholdi and Schwab, 1997; Carmel et al., 2001; Hayashi et al., 2000; Pan et al., 2002; Wang et al., 1997) Recently, a study of the injured spinal cords of 11 patients who died shortly after their trauma demonstrated the presence of IL-1 , IL-6, and TNF positive cells within the spinal cord within 24 hours of injury. (Yang et al., 2004)