Multiple sclerosis (MS) is the most common inflammatory demyelinating disease of the central nervous system (CNS) in young adults. The proinflammatory cytokines such as interferon-gamma (IFN- ), tumor necrosis factor-alpha (TNF- ), and nitric oxide (NO) which are known to be produced by inflammatory cells play a key role in the pathogenesis of MS. Some metabolic changes may have an effect on axonal transmission, and white blood cells NO and other inflammatory mediators such as cytokines may be affected from cooling process. In this study, we evaluated the effects of body cooling procedure on proinflammatory cytokines such as TNF- , IFN- , and NO levels. Twenty patients with MS were evaluated. Thirteen of the patients were women, 7 were men (mean age: ？yrs.). Body temperature was reduced by an average of 1°C approximately in 1 hour with using the “Medivance Arctic Sun Temperature Management System” device. In our study, the decrease in TNF- , IFN- levels after the cooling procedure has no statistical significance, whereas the decrease in the mean level of NO level after the cooling procedure is ？ mol/L which has statistical significance ( ). These results suggested that the decrease in NO level improves conduction block in demyelinated axonal segments after cooling procedure in multiple sclerosis. 1. Introduction Multiple sclerosis (MS) is the most common inflammatory demyelinating disease of the central nervous system (CNS) in young adults. Current knowledge indicates that tissue damage in MS is due to a T-cell-mediated autoimmune process. Once MS has been triggered, a pathogenic autoimmune T-helper ？17 subtype of T cells response directed against myelin/CNS components perpetuates the disease [1, 2]. The proinflammatory cytokines such as interferon-gamma (IFN-γ), tumor necrosis factor-alpha (TNF-α), and nitric oxide (NO) which are known to be produced by inflammatory cells play a key role in the pathogenesis of MS [3–6]. Many individuals diagnosed with MS are sensitive to increased body temperature. The earliest medical reports of thermal sensitivity in MS are derived from Ollivier d’Angers in 1827 [7]. However, Wilhelm Uhthoff’s description of this phenomen on occurring after a hot bath or with exercise in MS patients with a history of optic neuritis has most commonly been cited as the landmark observation of the pathophysiological principle of temperature-induced conduction block in demyelinated axonal segments [8]. It is estimated that 60–80% of the MS population experiences transient and temporary worsening of clinical signs and neurological
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