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The effects of scoliosis on the spinal cord has always been relatively "poorly understood" not only in terms of bio-mechanical stress placed on the cord, but in regards to the symptoms of scoliosis and scoliosis pain it may cause.

 

It is important to note that idiopathic scoliosis is a 3 dimensional spinal distortion and the bio-mechanical stress placed on the spinal cord much be taken into account in the vertical, horizontal, and side view dimensions as a summation of the total amount of bio-mechanical stress placed on the spinal cord, because of a scoliotic curvature.

 

Here are all 3 parts of a study examining the effects of bio-mechanical stress on the spinal cord.

 

 Biomechanics_of_CNS_I.pdf

 Biomechanics_of_CNS_II.pdf

Biomechanics_of_CNS_III.pdf

 

While the scoliosis pain syndromes bio-mechanical stress on the spinal cord are varied and unpredictable, but perhaps the most important aspect on bio-mechanical stress on the cord caused by a scoliotic curvature may be increased risk of rapid progressive scoliosis.

 

Biomechanically speaking, the continuous axial tissue tract of the pons, medulla oblongata (the CNS postural control centers) and spinal cord are all functionally linked together and anchored vertically from the skull to the caude equina at the base of the spine. It is also anchored laterally through out the spine by dentiulate ligaments, nerve roots and nerve sleeves. Take home message: The spine is tied down in the spine pretty tightly.

 

Alf Breigs 1978 work shows changes in relative lengths of spinal canal and cord CAN lead to pathlogic axial tension. JD Reid's research confirms this when his reseach found physiological lengthening of the cord chiefly between C2-T1 up to a maximum of 17.6% in flexion (AKA: reversal of the normal cervical lordosis). Essentially, an aquired spinal cord tethering is the result from a loss of the normal cervical lordosis.

 

Roth build off this information in 1981 when he speculated that adolescent idiopathic scoliosis is a disproportion of vertebro-neuro growth due to either a short spinal cord or a too rapid growth spurt of the spine. In this spring/string model, he found that shortening of a string running though a spring model (think of a slinky with a string running though it) hindered elongation of the spring resulting in a scoliotic deformity.

 

Porter supported the uncoupled neuro-osseous growth concept of adolescent idiopathic scoliosis being a physical manifestation of the maladaption of the growing immature spine to the tether created by the short spinal cord. This evidence for this was the finding that the conus medullaris (the end of the spinal cord) position is NOT significantly different from that of a normal spine.

 

Dr. Chu re-examined the Roth-Porter theory via an MRI study (comparing adolscent idiopathic scoliosis patients with severe curvatures vs normal subjects) in 2007. They found the vertebral column in the adolescent idiopathic scoliosis population was significantly longer, yet the there was no detectable change in spinal cord length. The speculated that the initiation and progression of adolescent idiopathic scoliosis result from vert. column overgrowth through a maladapation of the spine to the subclinical tether of a relatively short spinal cord.