spinal stenosis
Adolescent idiopathic scoliosis is a multi-factorial condition involving both genetic and environmental risk factors. Neither seems to be enough to cause the condition on their own, but it can be positively devastating when they do combine to form progressive scoliosis. Two separate questions keep popping up in regards to scoliosis; 1. Why does it occur in some child and not in others? 2. Why do some spinal curves progress and others do not?
Genetic factors + Environmental factors = Progressive Scoliosis
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.)
These include multiple theories, which I'll elaborate more on individually later in this article.
- Rotational preconstraint theory
- Uncoupled spinal neuro-osseous growth (The String and Spring Theory)
- Brain, nervous system, and skull concepts
- Neuro-Osseous timing of maturation theory (NOTOM)
- Transverse plane pelvic rotation, skeletal asymmetric, 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, etc) with eccentric loading (having axis away from the center) and vertebral 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 adolescent AIS only
- Origin in contracture at the hips
- Osteopenia - a risk factor for curve progression?
- Melatonin deficiency
- Platelet calmodulin dysfunction
- Biomechanical spinal growth modulation
1. 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 vertical loading lead the formation of scoliosis. The lingering question is... what causes the interference of the postural reflexes?
2. Uncoupled spinal neuro-osseous growth (The String and Spring 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 Breig's 1978 work shows changes in relative lengths of spinal canal and cord CAN lead to pathologic axial tension. JD Reid's research confirms this when his research 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 curve). Essentially, an acquired spinal cord tethering is the result from a loss of the normal side view cervical curvature.
Roth built 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 mal-adaption 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 mal-adapation of the spine to the subclinical tether of a relatively short spinal cord.
3. 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 evoked potentials (SSEPs) via a higher CNS disturbance producing visuo-spatial perceptional impairment, motor adaptation, and learning deficits which lead to faulty recalibration of the proprioceptive (bodily awareness in space) from axial musculature.
2. leading to impaired balance control, with...
3. Low lying cerebellar tonsils due to acquired spinal cord tethering, together with...
4. Other intracerabral structural abnormalities (Ex: abnormal skull base and vault) that could contribute to...
5. Inappropriate postural adjustment during...
6. The adolescent growth spurt that leads to...
7. Progressive AIS.
4. 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 adolescent growth spurt occurs post postural maturity.
Essentially, they are viewing the problem as a dis-coordination 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.
5. 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 demonstrates correlation between thoracic curvatures 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 dis-coordination 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.
6. Relative Anterior Spinal Overgrowth (RASO)
Relative Anterior Spinal Overgrowth (RASO) essentially states that in many AIS cases the anterior elements (vertebral body) are longer than the posterior elements (the posterior joint complex) resulting in a structural hypo (decreased) thoracic kyphosis (the normal reversed side view curve seen in the mid back area).
It is not clear if this phenomenon is the result of an intrinsic abnormality of skeletal growth in patients with AIS which may genetic or an adaptation to biomechanical bone stress....which is the more accepted premise thus far... via the Hueter-Volkmann principle(bone under stress grows slower then bone not under stress) which would mean AIS has primarily a mechanical basis (aka: Dorsal shear forces theory).
The dorsal shear forces theory states the initial event is a lordotic segment in the thoracic spine with the spinal rotation and cobb angle being created by secondary torque forces from the posterior musculo-ligamentous structures.
Castelein has outlined 6 link/overlapping processes of the dorsal shear forces leading to AIS.
1. Upright human posture
2. Backward inclination of the vertebra in the sagittal plane (lordotic segment in the thoracic spine) creates...
3. Dorsal shear forces that render the facet joints inoperative and introduce...
4. Axial rotational stability enhancing slight asymmetries in the transverse plane with already exist.
5. Asymmetric loading of the posterior part of the vert. lead to asymmetric growth in 3-D of the pedicles, vert bodies, arches in accordance with the Hueter-Volkmann effect.
6. Progressive AIS
7. Thoracospinal concept - girls with right thoracic adolescent AIS only
Dr Sevastik developed a "thoracospinal concept" based on experimental, clinical, and anatomical data and it only applies to females with right thoracic curves.
His 6 steps has a linear causality mechanism...
1. Dysfunction of the autonomic nervous system (which is responsible for involuntary neurological postural control)
2. Increase vasularity of the left anterior hemithorax
3. Overgrowth of the left peri-apical ribs which...
4. disturbs the equilibrium of the forces that determine normal alignment of the thoracic spine, in a putative growth conflict, that...
5. triggers the thoracospinal deformity simultaneously in the three planes.
6. Biomechanical spinal growth modulation.
Basically, he is staying that asymmetrical blood flow between the left (increased) and right (decreased) to the anterior chest wall which causes and elongation of the left ribs.
8. Origin in contracture at the hips
Dr. Karski developed this concept of AIS orgin/progression based on 3 step linear process.
1. Hip abduction (external rotation)...which equates to a limitation of internal hip rotation...mostly of the right hip.
2. Disturbance of growth of the pelvi-sacral lumbar region with development of a left lumbar curvature.
3. Development of a compensatory right thoracic curvature.
Based off this theory he developed 3 groups with varying degrees of hip contractor to explain the "S" and "C" curve patterns.
9. Osteopenia- a risk factor for curve progression?
Low bone calcium has been found and noted in approximately 50% of AIS females in which their curve progressed 6 degrees or more and especially in the femoral neck of the hip on the side of the curve convexity (the outside of the curve) due to more weight bearing loading on the side of curve concavity (the inside of the curve). The researchers feel some of these findings could be explained via low calcium in-take, but felt that a lack of weight bearing activity and programmed exercise due to spinal brace treatment may be a primary contributor to the osteopenia in AIS.
10. Melatonin Deficiency
Virtually all of the work done in area of Melatonin deficiency and AIS has concluded that it may be factor in curve progression, but probably not related to initial onset of the condition. Machinda and colleagues postulated that in the development of progressive AIS, melatonin acts through the nervous system.
1. An inherent disorder of neurotranmitters from neuro-hormonal origin affect in melatonin,
2. associated with the bipedal condition, and......
3. a horizontal localized neuromuscular imbalance with torsion produces.....
4. a scoliotic deformity of the fibro-elastic and body structures of the spine.
Dr. Alan Moreau reported a melatonin-signaling transduction to be impaired in osteoblasts (bone builders) caused by the inactivation of Gi proteins. Which could serve as a biological marker with potential for curve progression prognosis via a blood test using lymphocytes.
11. Platelet Calmodulin Dysfunction
This curve progression theory also incorporates melatonin and the RASO concepts. Calmodulin is a protein that helps regulate skeletal muscle contraction via regulation of calcium within the muscle. Melatonin functions may include modulating calcium-activated calmodulin.
It is suggested that altered para-spinal muscle activity explained the relationship between calmodulin level changes and cobb angle in AIS.
Lowe offered an alternative calmodulin concept in 5 linear steps which ends in with development of RASO (relative anterior spinal over growth in the thoracic spine).
1. A small scoliotic curve.
2. Increased axial loads (growth spurt) create micro-damage to the vert. body growth plates...
3. causing vertebrae vascular damage...
4. combined with genetic pre-disposition calmodulin changes occurs with dilated blood vessels of deforming vert. bodies
5. which releases growth factors, which in a mechanically compromised vertebral endplate promotes RASO
12. Mechanical spinal growth modulation (AKA: The vicious cycle)
This theory is the most supported and generally accepted theory. Purposed by Dr. Ian Stokes (one of my personal favorites) as early as 1996, the biomechanical spinal growth modulation suggests spinal imbalance through gravity and continuous muscle action leads to asymmetric loading of the vert. growth plates and hence asymmetric growth via the Heuter-Volkmann principle.
Perdriolle reports that the onset of AIS occurs as a result of a mechanical process termed "geometic torsion of the vertebral bodies" but worsening was caused by deformation of the vert. bodies.
Stokes developed a 2-D mathematical simulation of the lumbar vertebra (not the discs) and tested whether the calculated loading asymmetry created by muscles in a spine with scoliosis could explain the observed rate of scoliosis. The results were consistent with the clinical observations.
Stokes' "Vicious Cycle"
1. Pre-existing scoliosis curve of unknown etiology (probably genetic underdevelopment of the neurological postural control centers in the CNS from the current knowledge provided by Axial bio-tech (developers of Scoliscore).
2. Putative neuromuscular dysfunction with the most physiological strategy causing loads more the concavity at the apex of the curve.
3. Neuro-muscular determined left-right asymmetric loading of vertebral bodies sustained over a substantial portion of the day.
4. Vertebral body growth plates (sensitive to altered asymmetric compression) with mechanically modulated alteration of growth leads to AIS curve progression
*** Different individuals adopt different neuromuscular strategies which explains curve patterns and varied progression rates.
What does it all mean? Well, there are a few conclusions that can be out of this massive amount of data and theory.
1. The origins 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 adolescent 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).
So how will all of this new information change the future of scoliosis treatment? No one really knows for sure, but it obviously will and has even spun an new concept in scoliosis treatment called Bernstein's Problem.
The Bernstein's problem: The brain is responsible for coordinating an amazing number of mechanical linkages, so Bernstein theorized the nervous system organized movement in a hierarchical manner which places the "body schema" at the top.
During the development of the body Schema the overwhelming evidence suggests it is tied to growth of the muscular-skeletal system and brain.
The key theoretical issue centers around how the brain adapts circuitry controlling muscles/joints and matches them to the developmental biomechanical changes during growth spurts.
The body schema is developed long-term from both somatotrophic body maps and immediate sensory input. (AKA: it is partly genetic and partly acquired through adaptation to the environment)
The first part of the body to develop postural organization is the head via visual and vestibular sensors (Top-Down mode by postural organization by age 7)
The NOTOM escalators may influence the CNS body schema during growth via proprioceptive inputs and brain plasticity. Particularly the decoupling that occurs between the head and torso past the age of 7 years old.
The evidence is continuing to support the notion that early stage scoliosis intervention using a neuro-muscular system of involuntary postural control may be the only way to alter the natural course of adolescent idiopathic scoliosis.
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