sjmcphee
10-27-2004, 11:02 PM
I'd like to bring the following to the attention of all people involved with, or affected by idiopathic scoliosis.
Its been over a year since I started this thread - "The Future Of Scoliosis Research".
During that time I have been able to learn a lot more, and I can now express my ideas much clearer.
I have knowledge which is important to the future of scoliosis research and I would like to share it.
Id firstly like to summarise some things about scoliosis.
It is known to researchers that individual scoliotic curve patterns have their own particular characteristics, predicted course and outcomes.
Despite this, the exact biomechanical (muscular) systems relating to or responsible for scoliosis are not understood.
In the search for the etiology of idiopathic scoliosis, research is focused on finding a genetic link responsible for spinal deformity.
With the existance of 2nd and 3rd generation scoliosis families, it's hard to deny that a genetic factor may be involved, but despite thousands of patients and their families tested, no conclusive abnormality within the genetic structure of DNA or a mode of inheritace has been identified.
My opinion is that too much emphasis is placed on genetic scoliosis research, and that ultimately the answer as to whether a genetic factor is responsible for idiopathic scoliosis is of little importance in the actual treatment of scoliosis patients. There are only 2 possible answers. Either there is a genetic factor, or there isn't.
If there is a genetic factor, then what have we really learned ? People cannot be stopped from having children, so how exactly does this bring us closer to finding a better treatment for scoliosis ? If there is no genetical factor, then all the time and money spent in this area will have been a waste when it could have been put to better use elsewhere. Either scenario brings us to a point where the only stumbling block left to overcome is through complete understanding the biomechanical systems responsible for individual curve patterns.
There are many problems relating to accurately testing the musculative properties of scoliosis subjects.
Electromyography data is approximate, and the number of muscles that can be recorded is limited.
It also seems to me that the studies themselves are not curve pattern specific which in turn would make the studies almost worthless.
The moral to this story, and the reason I am updating this thread is because I am a scoliosis patient with exact knowledge of the biomechanical systems relating to scoliotic curve patterns. Going in to the exact details is rather complicated, but I wish to make some things clear.
A scoliotic curve pattern is created through a malfunction or misalignment within the spinal column that corrupts a natural curve of the spine.
The reason no evidence can be found of this "injury or misalignment" is because all evidence is accounted for by understanding the relative load geometry of the curve pattern. The injury itself, I refer to as "asymmetrical load geometry". This relates to the creation of a scoliotic curve pattern.
Once "asymmetrical load geometry" has occurred to create a scoliotic curve pattern, the stretched and unstretched connective tissue (from the asymetrical load geometry) have a systematic effect on the junctions of the spines remaining curves. I call this secondary system "relative scoliotic load geometry" which relates to the progression of a curve pattern. Relative scoliotic load geometry is a vicious circle of decompensation where changes in the spine occur in relation to changes that have already occurred.
The location of "asymmetrical load geometry" determines the curve pattern. Either 'C' or 'S' curve depending on whether the misalignment originated within the kyphosis or lordosis curvature.
The reason scoliosis is more likely to progress in females is because of a difference in pelvic angle.
The speed of progression relates to skeletal maturity at the time the curve pattern was created, in relation to the growth spurt during puberty.
There is an increase of interverterbral pressure during puberty attributible directly to rapid growth.
This increased interverterbral pressure has a subsequent effect on relative scoliotic load geometry.
The actual geometry is a corruption of the loading forces of compression, forward shear, and axial rotation, (working for the convex of the original misalignment ) against an opposing geometric system of compression, forward shear and axial rotation (working for the concave of the original misalignment). The loading equilibrium is satistied at all junctions above below in both the saggital and coronal planes.
This system of relative scoliotic load geometry is probably also responsible for congenital deformities.
Supporting the musculative structure of the spine is the rationale behind bracing and other treatments.
In summary, there is a method to calculate the position of every single piece of connective tissue at any given time in any curve pattern.
This information should be used to establish better practice in the diagnosis and treatment of spinal deformities.
Despite my efforts, I have had little or no interest from professional or patient scoliosis organisations.
I am willing to cover the costs of this research personally, I seek no fame or reward for my efforts, only the right as a patient to help myself.
In regards to scoliosis research the situation as a whole is very much a case of the blind leading the blind.
I can safely say that there will be no major improvements in the diagnosis or treatment of spinal deformities until this research has been addressed.
Yours Truly,
Scott J McPhee
Its been over a year since I started this thread - "The Future Of Scoliosis Research".
During that time I have been able to learn a lot more, and I can now express my ideas much clearer.
I have knowledge which is important to the future of scoliosis research and I would like to share it.
Id firstly like to summarise some things about scoliosis.
It is known to researchers that individual scoliotic curve patterns have their own particular characteristics, predicted course and outcomes.
Despite this, the exact biomechanical (muscular) systems relating to or responsible for scoliosis are not understood.
In the search for the etiology of idiopathic scoliosis, research is focused on finding a genetic link responsible for spinal deformity.
With the existance of 2nd and 3rd generation scoliosis families, it's hard to deny that a genetic factor may be involved, but despite thousands of patients and their families tested, no conclusive abnormality within the genetic structure of DNA or a mode of inheritace has been identified.
My opinion is that too much emphasis is placed on genetic scoliosis research, and that ultimately the answer as to whether a genetic factor is responsible for idiopathic scoliosis is of little importance in the actual treatment of scoliosis patients. There are only 2 possible answers. Either there is a genetic factor, or there isn't.
If there is a genetic factor, then what have we really learned ? People cannot be stopped from having children, so how exactly does this bring us closer to finding a better treatment for scoliosis ? If there is no genetical factor, then all the time and money spent in this area will have been a waste when it could have been put to better use elsewhere. Either scenario brings us to a point where the only stumbling block left to overcome is through complete understanding the biomechanical systems responsible for individual curve patterns.
There are many problems relating to accurately testing the musculative properties of scoliosis subjects.
Electromyography data is approximate, and the number of muscles that can be recorded is limited.
It also seems to me that the studies themselves are not curve pattern specific which in turn would make the studies almost worthless.
The moral to this story, and the reason I am updating this thread is because I am a scoliosis patient with exact knowledge of the biomechanical systems relating to scoliotic curve patterns. Going in to the exact details is rather complicated, but I wish to make some things clear.
A scoliotic curve pattern is created through a malfunction or misalignment within the spinal column that corrupts a natural curve of the spine.
The reason no evidence can be found of this "injury or misalignment" is because all evidence is accounted for by understanding the relative load geometry of the curve pattern. The injury itself, I refer to as "asymmetrical load geometry". This relates to the creation of a scoliotic curve pattern.
Once "asymmetrical load geometry" has occurred to create a scoliotic curve pattern, the stretched and unstretched connective tissue (from the asymetrical load geometry) have a systematic effect on the junctions of the spines remaining curves. I call this secondary system "relative scoliotic load geometry" which relates to the progression of a curve pattern. Relative scoliotic load geometry is a vicious circle of decompensation where changes in the spine occur in relation to changes that have already occurred.
The location of "asymmetrical load geometry" determines the curve pattern. Either 'C' or 'S' curve depending on whether the misalignment originated within the kyphosis or lordosis curvature.
The reason scoliosis is more likely to progress in females is because of a difference in pelvic angle.
The speed of progression relates to skeletal maturity at the time the curve pattern was created, in relation to the growth spurt during puberty.
There is an increase of interverterbral pressure during puberty attributible directly to rapid growth.
This increased interverterbral pressure has a subsequent effect on relative scoliotic load geometry.
The actual geometry is a corruption of the loading forces of compression, forward shear, and axial rotation, (working for the convex of the original misalignment ) against an opposing geometric system of compression, forward shear and axial rotation (working for the concave of the original misalignment). The loading equilibrium is satistied at all junctions above below in both the saggital and coronal planes.
This system of relative scoliotic load geometry is probably also responsible for congenital deformities.
Supporting the musculative structure of the spine is the rationale behind bracing and other treatments.
In summary, there is a method to calculate the position of every single piece of connective tissue at any given time in any curve pattern.
This information should be used to establish better practice in the diagnosis and treatment of spinal deformities.
Despite my efforts, I have had little or no interest from professional or patient scoliosis organisations.
I am willing to cover the costs of this research personally, I seek no fame or reward for my efforts, only the right as a patient to help myself.
In regards to scoliosis research the situation as a whole is very much a case of the blind leading the blind.
I can safely say that there will be no major improvements in the diagnosis or treatment of spinal deformities until this research has been addressed.
Yours Truly,
Scott J McPhee