Tethered cord in children with spina bifida

Any process that attaches and fixes the spinal cord, inhibiting movement of the cord in the spinal canal, has the potential to cause tethered cord syndrome. Motion of the head and trunk changes the length of the spinal canal and the cord must move cranially to accommodate increases in length. If the cord is unable to move, it must lengthen to accommodate increased distance. The epipial layer of the spinal cord contains abundant collagen and extension narrows the cord and causes this layer to squeeze the interior of the cord, elevating intramedullary pressure. This is much like the children's toy, the finger trap. The harder you pull the tighter the squeeze. When intramedullary pressure exceeds perfusion pressure, the cord becomes ischemic and metabolism ceases. Repetitive or prolonged stretching of the spinal cord leads to infarction and a deficit. As would be expected, the deterioration is usually subtle, progressive, may be reversible and only rarely catastrophic. Hoffman, Hendrick, and Humphreys described this problem in children in 1976 [1]. Yamada demonstrated the physiology in the laboratory in 1981 [2].