Displaying items by tag: causes of scoliosis

The developmental theory cause of scoliosis

Transverse plane pelvic rotation, skeletal asymmetrics, and "developmental theory"

 

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.

 

Please click here to receive a FREE SCOLIOSIS TREATMENT INFORMATION KIT ASAP.

 

The NOTOM cause of scoliosis theory

Please click here to receive a FREE SCOLIOSIS TREATMENT INFORMATION KIT ASAP.

 

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.

7 step cause of Scoliosis?

Please click here to receive a FREE SCOLIOSIS TREATMENT INFORMATION KIT ASAP.

 

Brain, nervous system, and skull concepts

Dr. Chu (the same researcher who re-investigated the uncoupled neuro-osseous growth concept) developed a concept of AIS progression with 6 linked and overlapping processes a follow......

1. Longer latency somato-sensory envoked potentials (SSEPs) via a higher CNS distrubance producing visuo-spatial perceptional impairment, motor adpatation, and learning deficits which lead to faulty recalibration of the proprioceptive (bodily awarenss in space) from axial musculature.

2. leading to impaired balance control, with.......

3. Low lying cerebellar tonsils due to aquired spinal cord tethering, together wilth.....

4. Other intracerabral structural abnormalities (Ex: abnormal skull base and vault) that could contribute to.....

5. Inappropriate postural adjustment during......

6. The adolscent growth spurt that leads to.....

7. Progressive AIS.

What causes scoliosis

Uncoupled spinal neuro-osseous growth (The String Theory)

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.

Cause of scoliosis theory

Rotational preconstraint theory

This theory is pretty straight forward and not too complex......on the surface. It basically states that paravertebral muscle imbalance with interference of the postural reflexes and body weighted related verticle loading lead the formation of scoliosis. The lingering question is....... what causes the interference of the postural reflexes?

This study on frogs may hold some clues.....


Vestibular asymmetry as the cause of idiopathic scoliosis: a possible answer from (Frog) Xenopus.

Lambert FM, Malinvaud D, Glaunès J, Bergot C, Straka H, Vidal PP.
J Neurosci. 2009 Oct 7;29(40):12477-83.
Centre National de la Recherche Scientifique , Unité Mixte de Recherche 7060-Université Paris Descartes, 75006 Paris, France.

Human idiopathic scoliosis is characterized by severe deformations of the spine and skeleton. The occurrence of vestibular-related deficits in these patients is well established but it is unclear whether a vestibular pathology is the common cause for the scoliotic syndrome and the gaze/posture deficits or if the latter behavioral deficits are a consequence of the scoliotic deformations. A possible vestibular origin was tested in the frog Xenopus laevis by unilateral removal of the labyrinthine endorgans at larval stages. After metamorphosis into young adult frogs, X-ray images and three-dimensional reconstructed micro-computer tomographic scans of the skeleton showed deformations similar to those of scoliotic patients. The skeletal distortions consisted of a curvature of the spine in the frontal and sagittal plane, a transverse rotation along the body axis and substantial deformations of all vertebrae. In terrestrial vertebrates, the initial postural syndrome after unilateral labyrinthectomy recovers over time and requires body weight-supporting limb proprioceptive information. In an aquatic environment, however, this information is absent. Hence, the lesion-induced asymmetric activity in descending spinal pathways and the resulting asymmetric muscular tonus persists. As a consequence the mostly cartilaginous skeleton of the frog tadpoles progressively deforms. Lack of limb proprioceptive signals in an aquatic environment is thus the element, which links the Xenopus model with human scoliosis because a comparable situation occurs during gestation in utero. A permanently imbalanced activity in descending locomotor/posture control pathways might be the common origin for the observed structural and behavioral deficits in humans as in the different animal models of scoliosis.

Translation:

"Vestibular dysfunction PLUS lack of proprioceptive feedback has now been proven to create scoliosis.

Also proven: the root cause of scoliosis can be reversed by restoring correct proprioceptive feedback from body to brain."

What are the causes of scoliosis?

Please click here to receive a FREE SCOLIOSIS TREATMENT INFORMATION KIT ASAP.

 

Ok, so there seems to be 2 types of pathogenic factors in AIS.

1. Initiating/inducing factors.....which is thought to involve a genetic pre-disposition....undetected neurological development/dysfunction which affects control of posture and coordinated movements in relation to the central nervous system body schema.... ('Body scheme' or 'body set' is the neural representation in our brainstem of our body. It is a sort of reference frame for our brain.
fMRI studies can show us the we can increase activity there by doing certain activities.)


- Rotational preconstraint theory
- Uncoupled spinal neuro-osseous growth (The String Theory)
- Brain, nervous system, and skull concepts
- Neuro-Osseous timing of maturation theory (NOTOM)
- Transverse plane pelvic rotation, skeletal asymmetrics, and the "developmental theory: timing of maturation from the top-down to bottom-up organization of postural control.

2. Curve progression factors (which is generally thought to involve a mechanical process (torsion, vicious cycle, dorsal shear forces, ect) with eccentric loading (having axis away from the center) and vertbral growth modulation....AKA:Hueter-Volkmann principle. These are generally accepted to have both neural and osseous components.

These include theories on curve progression that appear after the initial onset of AIS.

- Relative Anterior Spinal Overgrowth (RASO) (although this could possibly be controlled via genetic factors in some AIS cases)
- Thoracospinal concept - girls with right thoracic adolscent AIS only
- Origin in contracture at the hips
- Osteopenia - a risk factor for curve progression?
- Melatonin deficiency
- Platelet calmodulin dysfunction
- Biomechanical spinal growth modulation