• W D Dietrich, K Chatzipanteli, E Vitarbo, K Wada, and K Kinoshita.
• Department of Neurological Surgery, Neurotrauma Research Center, Miami Project to Cure Paralysis, University of Miami School of Medicine, Miami, FL 33101, USA. ddietrich@miami.edu
• Acta Neurochir. Suppl. 2004 Jan 1; 89: 69-74.

AbstractTraumatic injury to the brain and spinal cord results in an early inflammatory response that is initiated by the release of proinflammatory cytokines followed by the infiltration and accumulation of polymorphonuclear leukocytes (PMNLs). The role of the inflammatory cascade on traumatic outcome remains controversial. Pleiotropic cytokines appear to function both protectively and destructively. The induction of cytokines can lead to the expression of the inducible form of nitric oxide synthase (iNOS), which in turn provokes the release of excessive amounts of nitric oxide (NO) that may participate in the pathogenesis of tissue injury. Hypothermia has been reported by various groups to be neuroprotective in brain and spinal cord trauma. We studied the effect of therapeutic hypothermia on cerebral IL-1beta concentrations, PMNL accumulation and iNOS activity after traumatic brain injury (TBI) and spinal cord injury (SCI). Based on current data therapeutic hypothermia may protect in models of traumatic injury by modulating deleterious inflammatory processes.

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