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Cox-Counter-Point:
Biomechanics or Biomythchanics In Cox Distraction
Adjusting? An analysis of the Literature. Part I of III
By
Deed E.
Harrison, DC
I would like to begin this counter-point article with a
complement to Dr. Cox. Dr. Cox should be commended for spearheading
clinical trials with his method and congratulated for such a detailed
literature review supporting his analysis and treatment protocols.1
However, I have found several errors in Dr. Cox’s interpretation of
the literature, with selective referencing to support his position.
Several of the references cited by Dr. Cox are outdated (i.e., they have
been shown to be inaccurate or fraught with methodological flaws) or are
merely opinion sources. In addition, in his article1, there
are several areas where, instead of referencing the available
literature, Dr. Cox promotes his opinions as mechanical fact. Because
Dr. Cox’s article1 was rather lengthy with multiple,
redundant topics, I have
elected to respond paragraph by paragraph and, in some cases, in the
order that his ideas are presented.
In his opening paragraph, Dr. Cox believes we (DD Harrison, DE
Harrison and CBP® practitioners) do not believe canal stenosis is an
important issue and that hyper-extension has no effect under these
conditions. Clearly, Dr. Cox has misinterpreted our position. For
example, in a recent publication in JMPT, regarding canal stenosis we
stated, “We do not deny the clinical significance of this issue, nor
do we intend to minimize it. However, we believe that an equally
important issue, and more prevalent, has typically been under
appreciated by many clinicians and researchers. This issue being neural
tissue stress and strain in the absence of stenotic conditions. Since
stenotic canals are present in only a minority of individuals, we feel
that the latter condition may encompass a larger volume of patients and
neurologic conditions. This is because altered alignment of upright
posture, viewed as rotations and translations in three dimensions, and
poor ergonomics are relatively common place among today’s patient
populations.” 2
Dr. Cox would have us believe that the vast majority of our
patients have nerve root compression and spinal cord compression due to
canal stenosis, when in fact these patients represent less than 5.0% of
patients coming to healthcare providers with low back pain.3,4
“Pure osteoligamentous lateral stenosis is a fairly uncommon
condition.”5 Thus, 95.0% of the patients we chiropractors
take care of have neither IVF encroachment nor canal stenosis as a cause
of their complaints.
Still in the opening paragraph, Dr. Cox would have us believe
that pathological changes (degenerative changes in various spinal
tissues) occur all by themselves (without abnormal loads first) and that
“these changes cause us two legged bipeds to seek postural relief and
loss of lordosis is often that relief.”1 This statement is
an example of Dr. Cox’s personal opinion being promoted as fact. In
reality, anyone with a basic understanding of Hueter-Volkmann’s law,
Wolff’s law, and Davis’s law would know that Dr. Cox’s statement
is false. For examples, Hueter-Volkmann’s law governs the modeling of
bone. This law applies to immature, developing bone. Several studies
have proven that during development, compression loads inhibit growth
while tensile loads accelerate growth.6,7 In order to create
asymmetrical bone in the sagittal or transverse planes (wedged shaped)
an asymmetrical alteration in the structure of the spine must be present
first.8,9 Hueter-Volmann’s law also applies to the
intervertebral disc.10
Wolff’s law and Davis law apply to the remodeling
(degenerative and non-degenerative changes) of developed bone and
tissue. In the cervical spine, using an engineering analysis of slope
and bending moment, Matsunaga et al.11 proved degeneration
and consequent subluxation will developed in abnormal kyphotic
configurations termed “buckling” alignment. Using an engineering
analysis of strain, Matsunaga et al.12 found ossification of
the posterior longitudinal ligament (PLL) to progress in the areas
showing uneven and abnormal strain at the adjacent intervertebral disc
and PLL. Specifically, strain in the tensile direction was found to
correlate with ossification of the PLL.
It is important to note, the only way to increase the tensile
strain in the PLL is to have concomitant hypolordosis or kyphosis
(flexion).13 Using flexion loading in rabbits, Yu14
found “the greater the level of the strain and the longer time the
strain was loaded, the more evident the morphological abnormalities of
the cervical vertebrae.” Several other studies indicate that loss of
cervical lordosis or kyphosis is a cause or is associated with a high
incidence of degenerative changes in the disc and vertebral bodies.15-17
In the lumbar spine, several investigators have shown that degeneration
in the vertebral bodies, discs and ligaments (including the ligamentum
flavum) occurs due to loss or reversal of the lumbar curvature.18-23
In the anterior-posterior view alteration from true vertical alignment
has been shown to cause disc degeneration, vertebral body degeneration,
and facet arthrosis.18,24,25,26
According
to the above brief review, it is apparent that abnormal posture comes
first and causes abnormal loading of spinal tissues leading to
degenerative changes. This is an example of a one-way implication in
logic, i.e., if abnormal structure exists then degeneration will occur
not vice versa. Dr. Cox’s position concerning loss of lordosis or
kyphosis being a relief position for pain patients is incorrect for any
condition other than extreme
canal stenosis. In the lumbar spine, multiple studies using age,
weight, sex, and/or height matched controls have found that acute and
chronic back pain patients have statistically significant increases or
decreases or reversals in their lumbar curvatures compared to normal
volunteers.28,32-34 Recent non-surgery and surgery studies
have found that patients with increased post surgical pain have
decreased lumbar lordosis compared to those with no pain.27,29,30,31
Most importantly, it is now known that decreased lumbar lordosis
is a risk factor for the first time occurrence of serious low back pain
requiring medical attention.35 In the cervical spine headache
sufferers, neck pain and shoulder pain patients, and post-surgical
patients with pain all have been found to have statistically significant
decreases or reversals of the cervical lordosis compared to normal,
pain-free subjects.36-45 If Dr. Cox were correct, then all
the patients in the above studies should be pain free because they are
relieving their symptoms by flexing (loss of lordosis) their necks and
backs. HOW ABSURD!! These people hurt and suffer due to abnormal
structure of their spine.
Paragraph #2
In paragraph #2, Dr. Cox attempts to “clarify some
misconceptions concerning his work”. Dr. Cox states “I treat all
conditions of the low back with axial distraction adjustments” and
“These patients are treated with axial distraction adjustments, always
starting with axial flexion distraction.” To this, I can only shake my
head in dismay and disbelief. To claim that every clinical condition
(mechanical in origin) affecting the Lumbar spine should be treated the
same is utterly absurd. I ask you Dr. Cox, should a lumbar kyphosis be
treated with flexion? Should an anatomical short leg be treated with
flexion? Should a spondylolisthesis or anterolisthesis be treated with
flexion so as to make it translate further anterior? Should a segmental
flexion instability be treated with more flexion? Should a lateral
flexion of the thorax relative to the pelvis be treated with flexion?
Should a lateral translation (trunk list) be treated with flexion?
Should a posterior vertebral spur be treated with flexion so as to cause
transverse loading of the neural tissue? Should non-surgical
syringomyelia be treated with flexion so as to make the syrinx (fluid
filled cavity) larger? Should multiple sclerosis be treated with flexion
so we can cause Le Hermitte’s sign? I ask you Dr. Cox how is your
statement different than some mis-informed medical doctor prescribing
heat, bed rest, muscle relaxants, and or anti-inflamatory agents for
every patient with low back pain. One cause one Cure?
In paragraph #2 and 6 Dr. Cox brings forth the concept of
restoring physiologic ranges of motion to the functional spinal unit (FSU).
He states, “they are then adjusted by placing their facets through the
five physiological ranges of motion while under distraction. Those
motions are flexion, extension, lateral flexion, circumduction, and
rotation.” This statement demonstrates Dr. Cox’s lack of knowledge
and understanding of human biomechanics. To claim there are only 5 physiological motions and that
circumduction is one of them is nonsense.
This is an example of Biomythcanics
in Cox distraction adjusting. According to the best available
biomechanics literature, the typical vertebrae has six degrees of
freedom, i.e., translation along and rotation about each of three
orthogonal axes (see Figure 1). Since rotation and translation along or
about an individual axis can be in a positive or negative direction, the
typical vertebrae can only be displaced in 12 single directions (see
Figure 2)13,46,47. These
movements are: 1) left axial rotation, 2) right axial rotation, 3) left
lateral bending, 4) right lateral bending, 5) flexion, 6) extension, 7)
left lateral translation, 8) right lateral translation, 9) anterior
translation, 10) posterior translation, 11) vertical translation, and
12) inferior translation. Note, that circumduction is not a
physiological range of motion nor a degree of freedom, it is a
combination of axial rotation, lateral bending, and flexion or
extension. Dr. Cox’s 5 physiological ranges of motion are only 3 out
of 6 degrees of freedom or ½ of the possible physiological ranges of
motion.
Figure 1. The typical
vertebra has 6 degrees of freedom. These are 3 translation axes and 3
rotation axes.
Figure 2. The 12 simple movements of
a vertebra are depicted in the 6 degrees of freedom.
Biomechanics of the Intervertebral disc
Dr. Cox makes several erroneous statements concerning the
mechanics and/or treatment of the intervertebral disc:
1.
Lumbar manipulation injures or ruptures the intervertebral disc
2.
Flexion increases metabolite transport into the disc, while
extension decreases it.
3.
Flexion decreases posterior disc stress.
4.
Extension causes the nucleus to move posterior, while during
flexion it does not move.
5.
Extension increases the posterior disc stress.
6.
Intra-discal pressure is higher on extension and lower during
flexion.
7.
Extension is detrimental to the disc and decreases disc height.
8.
A herniated nucleus pulposus will be sucked back into place
during flexion/distraction.
Concerning item #1 above, first, Dr. Cox appeals to our emotions
by presenting a supposed case study of his where a side posture
adjustment “ruptured” a lumbar disc in a patient of his. He
continues this emotional appeal by stating that some patients cannot
even get into position for side posture adjusting and that the million
dollar role is the #1 cause of iatrogenic disc injuries in malpractice
cases. Lastly, Dr. Cox using the old “appeal to authority” by
letting us know how Dr. Dvorak feels about manipulation and disc
injuries. Dr. Dvorak’s personal opionion concerning spinal
manipulation and disc injuries should not be used to counteract the
biomechanical data on the topic.
To begin, Dr. Cox’s case study of one means absolutely nothing.
According to Hamilton, “no conclusion can be drawn from a single
case.”48 Secondly, I’ve been in private practice now for
26 months and delivered an average of 275 adjustments per week for a
total of 113 wks x 275 adjustments = 31,075 adjustments. Never have I
had a patient whom could not get into the side posture position given a
little time and effort. Perhaps the day will come but I doubt it.
Secondly, the fact that the “million dollar roll” is linked to
malpractice cases in no way indicates this adjustment herniates or
ruptures discs. The only way to prove or disprove this issue is with
biomechanical testing on injured and non-injured discs.
In
biomechanical testing of intervertebral disc (IVD), it is well
documented that the IVD resists torsion or axial rotation.49
However, this does not mean that torsion injures the IVD. For example,
the IVD also resists compression and it is well documented that an
abruptly applied compressive force to the spine in a neutral position
will damage the vertebral body before the IVD.13 Hukins50
has suggested that an annular fiber strain of 3.0-4.0% is necessary
before torsion can damage the disc and that a 5.0 degree axial rotation
angle is necessary to achieve this annular fiber strain. Importantly,
Adams and Hutton51 have shown that the disc will recover
completely from rotations of up to 9.0 degrees with the facets removed.
In intact lumbar spines in vitro and in vivo, the articular processes
only allow a maximum of 3.0 degrees and in most cases only 1.0-2.0
degrees of axial rotation per side can occur.52-59 It
appears, therefore, that torsion is incapable of inducing the rotation
required to cause annular damage or failure.
When all the information is pooled, it is apparent that torsional
loading during a side posture adjustment is an inadequate cause of
damage to the annulus and most certainly does not cause or lead to
nuclear herniation.5,47,51,52,58,60-65
Item #2. Dr. Cox states “flexion increases metabolite transport
into the disc” and that extension decreases it. He uses this statement
to support the use of flexion distraction on disc injured patients.
There are two serious problems with his claim. Firstly, I note that the
biomechanical article cited by Dr. Cox in his support is from Adams and
Hutton66. Adams and Hutton66 did find that flexion
accentuated fluid loss from the nucleus and flow through the posterior
annulus. However, Adams and Hutton utilized flexion combined with
COMPRESSION loading. I now note that Dr. Cox utilizes flexion combined
with DISTRACTION loading. Adams and Hutton’s66 finding cannot
be extrapolated to the totally different loading environment in Dr.
Cox’s flexion/distraction treatment, the two are not the same.
Secondly, the study by Adams and Hutton66 which
claimed that the posterior annulus does not receive nutrition without
flexion and compression is methodologically flawed. In 1997, Bass et al.67
reported that freezing of cadaveric discs (as in Adams and Hutton’s
methods) will permanantly damage the disc and cause more fluid to go
through the endplates and less to the posterior annulus due to expansion
cracks in the vertebral endplate. In summary of item #2, there is an
inadequate amount of evidence presented by Dr. Cox and most certainly
this evidence cannot be used to claim that flexion/distraction improves
disc nutrition.
Item #3. Dr. Cox claims flexion “...reduces posterior disc
stress.” Again, Dr. Cox cites Adams and Hutton for this statement.
Aside from the problem mentioned above, this study is again inadequate
for Dr. Cox’s claim. The study by Adams and Hutton utilized Functional
Spinal Units (FSU) for their analysis. In 1999, it is now well known
that FSU’s do not adequately represent the complexity of spinal
behavior.68 Additionally, the direction of force application
(i.e., centric, eccentric, or tangential to the curve) can change the
results.69
Concerning posterior disc stress in whole lumbar spines
(L1-S1) during flexion and extension, Hedman and Fernie68
found “no significant difference between the two postures in posterior
disc force.” Their statement is in regards to posterior compressive
stress. Hedman and Fernie go on to state, “The posterior ligament
force in the flexed posture, however, remained roughly three times the
anterior ligament force in the extended posture over the period of the
experiment. Disc shear force increased 9% in the flexed posture and
decreased 75% in the extended posture”, and “...compressive forces
on the disc, whether from compressive loads transmitted through the
endplates or from tensile forces on the adjacent ligaments, are lessened
in extended postures” 68. In 15 cadaveric whole lumbar
spines (L1-S1), Steffen et al. 70 demonstrated that posterior
disc pressure is larger in flexion combined with axial rotation than in
extension with axial rotation. They state “this supports the
hypothesis that a focal increase in IVD pressure leads to traumatic IVD
injury during flexion/rotation.” Gordon et al. 71 found
that the only reproducible method to create posterior annulur
protrusions and/or nuclear extrusion is to combine flexion with
compression, lateral bending or axial rotation. Concerning flexion and
disc failure, Adams et al. 72 state “disc failure in
bending occurs through overstretching of the outer annulus in the
vertical direction. In life, the posterior elements may not adequately
protect the posterior annulus from fatique damage.” McNally et al.
73 state “It is concluded that some discs are predisposed to
prolapse because of damaging, localized concentrations of stress in the
posterior annulus in combined anterolateral bending and compression.”
Natarajan et al. 74 state “The analyses also showed that
annular injuries are unlikely to be produced by pure compressive loads.
The model predicted that it would require a larger extension moment as
compared to flexion moment to initiate and propagate failure in a motion
segment, which leads to the conclusion that the motion segment is
stiffer in extension.” Several other researchers have also found that
the only way to cause posterior annular protrusion and/or disc
herniations is with flexion, not extension. 46,47,60,6375,76
In light of this information, how is it possible that Dr. Cox believes
flexion decreases posterior disc stress?
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