Current Agents and Related Therapeutic Targets for Inflammation Following Acute Traumatic Spinal Cord Injury

Abstract Background Infliction of a traumatic spinal cord injury propagates damage that is seen in two stages. The first phase of trauma occurs from the initial mechanical insult, while the second phase involves the degradation of nervous tissue but is likely not affected by the initial insult. Thus therapeutic targets with a high specificity for these secondary injury processes are of increasing interest. The pathophysiologic cascades of inflammation after spinal cord injuries and potential therapeutic targets are reviewed. Methods Databases (e.g. PubMed and EMBASE) were queried with appropriate medical subject headings for studies involving TNF-alpha, NF-kB, iNOS, IL-1 beta or FAS ligand targets. Relevant studies found were graded into three levels (namely A, B or C) according to the their quality of evidence. Results The basis of neurological damage for the five chosen targets of inflammation after spinal cord injury was summarized. In all, seventeen studies were rated, each of which reported histological, biochemical, physiological, and behavioral outcomes based on the treatment that focused on the aforementioned targets. Conclusion TNF-alpha, iNOS, NF-KB, IL-1beta and FAS ligands are active within minutes after spinal cord injury. Adverse effects from activity of these receptors include inflammation and other important neurological damage. Each of these targets can be modulated by specific agents with various degrees of efficacy according to evidence found in the literature.