1. The orgins of AIS is most likely linked to a genetic defect of the central control or processing by the central nervous system (Pons and hind brain) that affects the growing spine.

2. It appears that factors that pre-dispose/initiate AIS are separate from the factors that drive curve progression.

3. The consensus is that RASO results largely from biomechanical spinal growth modulation.

4. The NOTOM concept was formulated to explain why adolscent girls are more susceptible than boys to curve progression. Based on the timing of adolescent growth spurts (earlier in females) in relation to the timing of postural maturity (similar in boys and girls).

Transverse plane pelvic rotation, skeletal asymmetrics, and the "developmental theory: timing of maturation from the top-down to bottom-up organization of postural control.

This theory demostrates coorelation between thoracic cuvatures and pelvic rotation in the same transverse plane. They speculate that the feet, pelvis, and "bottom-up" organization of postural control emerges prior to postural control and the "top-down" postural control re-organizes around age 7. It is possible that a discoordination of timing between the top-down (visual and vestibular) from the "bottom-up" (feet) organization of postural control could serve as the initiation and progression of AIS.

 

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Neuro-Osseous timing of maturation theory (NOTOM)

This theory was introduced in 2002 by Burwell and Dangerfield and it suggests that the maturation of postural mechanisms in the CNS may be complete about the same time in boy and girls and the higher prevalence of progressive AIS in girls may be the result of entering there adolescent growth spurt in postural immaturity vs boys whose later adolscent growth spurt occurs post postural maturity.

Essentially, they are viewing the problem as a discoordination between the Osseous (bone) escalator (increasing skeletal size, changing skeletal shape, and relative mass of the different body segments) and the neural escalators (postural maturation with the CNS body schema being recalibrated as it continually adjusts to skeletal enlargement, shape, and relative mass changes to enable it to coordinate motor actions.

Uncoupled spinal neuro-osseous growth (The String Theory)

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 AIS 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 AIS 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 AIS patients with severe curvatures vs normal subjects) in 2007. They found the vertebral column in the AIS population was significantly longer, yet the there was no detectable change in spinal cord length. The speculated that the initiation and progression of AIS result from vert. column overgrowth through a maladapation of the spine to the subclinical tether of a relatively short spinal cord.