Abstract: Tethered spinal cord, or tethered cord syndrome, describes a disorder manifested by progressive motor and sensory deficit in the legs and by incontinence. Tethered cord syndrome occurs when the elongated spinal cord is anchored by a thick filum terminale or other pathological structures. The underlying mechanism is impairment of oxidative metabolism in the lumbosacral cord. The authors studied the extensibility of various parts of lumbar, sacral, and coccygeal segments in experimental animals and correlated this with the oxidative metabolism in these segments. The filum terminale possesses far greater extensibility than any spinal cord segments and functions as a buffer in preventing the cord from overstretching. The lumbar, sacral, and coccygeal segments elongate under traction only below the attachment of the lowest pair of dentate ligaments. The lower the cord segment, the greater the percentage of elongation in spite of limited elasticity of the cord tissue; this greater percentage of elongation of the spinal cord correlates with increasing impairment of the oxidative metabolism and more severe neurological deficit. These findings explain such symptoms and signs as motor and sensory deficits in the legs associated with the human tethered cord syndrome, and correspond with the high clinical incidence of incontinence. The lower spinal cord segments elongated promptly within 3 seconds after the start of traction. This implies that repeated acute hyperextension and hyperflexion, as occurs in humans, may accentuate oxidative metabolic changes that have already been caused by chronic cord tethering. The authors conclude that the elongation of the spinal cord under traction parallels the degree of metabolic dysfunction. 
Question: Does the abstract contain any numerical data?
Yes