Yamada S, Zinke D E, Sanders D
J Neurosurg. 1981 Apr;54(4):494-503. doi: 10.3171/jns.1981.54.4.0494.
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.
脊髓拴系综合征是一种临床病症，表现为腿部进行性运动和感觉改变、大小便失禁、腿痛以及脊柱侧弯。为了阐明脊髓拴系所涉及的病理生理学，在人体脊髓拴系病例和动物模型中，使用细胞色素α,α3的还原/氧化比（氧化还原）来指示氧化代谢功能。实验模型研究表明，在更大重量（3、4或5克）牵引下，腰骶部脊髓对缺氧应激具有明显的代谢和电生理易感性。在手术过程中，人体脊髓拴系的氧化还原行为也表现出类似效应。作者得出结论，脊髓拴系的症状和体征与腰骶部神经元功能障碍同时存在，这可能是由于在脊髓持续或间歇性拉伸下线粒体氧化代谢受损所致。据推测，长期或加重的神经元功能障碍可能导致神经元胞体以及随后轴突结构受损。人体脊髓拴系的松解手术可改善氧化代谢，并可能促进受损神经元的修复机制。
