The tethered cord syndrome is a clinical entity manifested by progressive motor and sensory changes in the legs, incontinence, back of leg pain, and scoliosis. In order to elucidate the pathophysiology involved in the tethered cord, the reduction/oxidation ratio (redox) was used in vivo of cytochrome alpha,alpha 3 to signal oxidative metabolic functioning in human examples of tethered cord and in animal models. Studies in experimental models indicate marked metabolic and electrophysiological susceptibility to hypoxic stress to lumbosacral cord under traction with greater weights (3, 4 or 5 gm). Similar effects were demonstrated in redox behavior of human tethered cord during surgical procedures. The authors conclude that symptoms and signs of tethered cord are concomitant with lumbosacral neuronal dysfunction which could be due to impairment of mitochondrial oxidative metabolism under constant or intermittent cord stretching. It is assumed that prolonged or accentuated neuronal dysfunction may lead to structural damage to the neuronal perikarya and later of the axons. Untethering procedures in human tethered cord improve oxidative metabolism, and probably facilitate the repair mechanism of injured neurons.