“Spec Letters”
Over
many years, I have I have written letters "on spec" to researchers,
surgeons and others who might take-up these ideas. I have tried many different ways to get the
basic ideas across in a short letter. I am
adding a selection of these here. They
will all be on this one page with the most recent the top.
Professor Nikolai Bogduk Dept of Clinical Research University of
Newcastle New South Wales Australia. Posted July 2005 Reposted 8th
Nov 2005 Reposted April 2006
John
Gorman
First sent July 2005 as email
UK
Registered Chiropractor
Dear Nikolai Bogduk.
I am an engineer and an independent
researcher into low back pain -- and now a chiropractor too. I have on my desk the first, third and fourth
editions of your book, The Clinical Anatomy of the Lumbar Spine and
Sacrum. I used your first edition and
your previous papers as the basis of my submission to Spine in 1987. (Not published). In my own 1992 book I referred to yours as
"the definitive book containing all the correct muscle and ligament
connections in the lumbar spine".
It is therefore very pleasing to me to
see, in your third and fourth editions, the way in which your ideas "home
in on" access by the nucleus to the nerves in the posterior annulus as
being in some way the centre of the low back problem. This has been the centre of my hypothesis
since 1987.
You cover this in considerable detail in
your "low back pain" chapters all of which I am very happy with. Accepting that mechanism, many new questions
are raised. The two most important to me
are:
-- why should these nerves cause such
initially paralysing and ultimately persistent pain?
-- what can we do to correct the situation
or avoid it in the first place?
Taking the second question first: my
hypothesis is that the L4 /5 and L5 S disks should remain wedge shaped at all
times even in full flexion. It would
seem likely that this will tend to keep the nucleus away from the nerves in the
posterior annulus. (I hope you agree
that these two joints are, in some way, the centre of the low back pain
problem.) To support my suggestion on
this wedging, may I quote an e-mail I sent recently to another researcher.
(
ps his paper is at http://www.mubabol.ac.ir/Babol/19-L.htm#3
Yours is the only paper that I have seen which
specifically looks at the wedge angle of all the lumbar discs. If we look just
at the lowest two discs your wedge angles are 14° for L4 5 and 21° for L5 S. I
believe that your figures are correct because they are more or less the same as
my measurements. I was able to examine the x-rays of the group of English
people selected by Piercy etc as being free of back
problems for their paper in Spine 1984. Professor van Niekerk
(of Jonk and van Niekerk
1961) was also able to obtain for me some x-rays of the lumbar spine of tribal
living Africans, which had very similar angles of wedging (slightly greater).
If we now look at the flexion mobility of these joints
in the above paper from Spine in 1984 we have 13° for L4 5 and 9° for L5 S.
These figures are again confirmed by various papers including Adams and Hutton
in Spine 1981. In other words in full flexion these joints will not flex beyond
parallel sided and will always maintain a wedge shape with the wide end
anterior (for people who are chosen as free of back pain in England, Iran or
South Africa!)
(I
wonder if it is significant that an x-ray survey of 100 healthy individuals
would probably not be permitted now in England or Australia!).
In
your book, you do remark on the wedge shape of the L5 S disk in the lordosis
chapter but you very specifically include the L4 5 disk as similar to the other
lumbar discs. Your picture on page 2
shows the L4 5 parallel sided and the L3 4 is wedge shaped. This is also true of the outline that has
graced the front cover of each of your editions.
This
tendency to show the L4-5 disk as parallel sided is fairly universal. It applies to wall charts, chiropractic books
and many other publications. I have
always suspected that this is because x-rays of back sufferers are so much more
readily available than lateral x-rays of people with no back problem.
I
believe that both the L4 5 and the L5 S. discs have to be looked upon as
different from other lumbar discs and always wedge shaped in the
"normal" spine. (Normal used
here in the sense of ‘totally as designed’ even though it may only apply to a
minority of those of us living a western lifestyle.) In these discs the wedge
shape is always maintained even in full flexion. (I admit that the situation
for L4 5 is less clear than for L5 S, but surely this fits well with the
general belief that L4 5 is so often the trigger for a back problem.)
Do I have any evidence that the pain behaves in the
way that I suggest? i.e. that the pain
switches on when flexion occurs beyond parallel sided and can be switched off
by extension.
By far the most important bit of evidence for me is
provided by the Mackenzie system of therapy.
Although I am qualified as a chiropractor, I am trained in Mackenzie by
the Mackenzie Institute UK and I use it in most back pain cases. In the trial published in the BMJ in 1990,
neither manipulative physiotherapy nor chiropractic was particularly effective
in the early stages of an acute LBP attack.
This is exactly when Mackenzie is most effective. It can completely stop the attack in its
tracks. If the person is careful with sitting and uses my pelvic supports when
driving they can be back to square one quite quickly. My interpretation is that the Mackenzie
extension exercise squeezes the nucleus back to the anterior of the disk where
it should be all the time in L 4 5 or 5 S.
I know that Mackenzie has a slightly dubious reputation
inside orthopaedic circles. I assume
this is because they see those cases where the nucleus squeezes in the wrong
direction! In daily therapy, with normal
back pain and no evidence of prolapse to start with, it is very effective.
I have always looked upon the "peripheralisation" part of Mackenzie as rather a red
herring so I was happy to read in your low back pain chapter that more pain
stimulation in a disk can send the pain further down the leg.
Although the Mackenzie extension exercise works well I
find it even more effective to apply the extension force directly to the
pelvis, rather than using the legs as lever.
With the patient supine I put a cushion under the knees to take the
tension out of the psoas and then I lift the iliac crest on each side with both
my hands. I pull upwards and towards the
patient's feet to apply an extension plus tension to the lumbo sacral junction
area. For a light person where I can
apply sufficient force this is much more effective than standard
Mackenzie. Sometimes I, and the patient,
can feel the nucleus oozing back to where it should be!
In the standard Mackenzie extension exercise, the
psoas muscle will be working against the extension of L5 S and L4 5. This must be one of the important functions
of the psoas muscle although I have not seen it mentioned in published
papers. The line of action of the psoas
lies anterior to the discs of L4 5 and L5S and will therefore apply a flexion
force to these joints. This would occur
at the completion of the running stride as the extension of the hip joint
applies a direct tension to the psoas.
The L4 5 and L5 S joints need this protection because they have such an
extended shape in the normal standing position and would otherwise be damaged
by running or other activities, which tend to take the hip joint into
hyperextension.
I am pleased to see that you have extended the scope
of your book to the pelvis and particularly the sacroiliac joints. I always say that osteopaths and
chiropractors make most of their money by loosening off the sacroiliac
joints. If a patient has had a low back
problem for several months or years and the location of the pain seems to be
the sacroiliac, buttock or thigh, I can be very confident that a few normal
chiropractic treatments will solve the problem.
This is where chiropractic did so well in that 1990 trial.
What exactly locks up in the sacroiliac joint is not
so clear to me. I have modified my
plastic demonstration pelvis with nylon cord rather than pins to hold the pubic
symphysis together and to simulate the interosseous sacroiliac ligament and the
sacro-spinous ligament. If I twist one
side of this in relation to the other then one ASIS (anterior superior iliac
spine) will be about one inch higher than the other with the iliac crests
level. Twisting the opposite way gives
the opposite situation. This is with the
simulating nylon cord pretty tight.
This is exactly the same situation that I find with
the human pelvis when the person has no problem. When there is a problem, the pelvis always
seems to be stuck in the twisted position.
Usually there is sensitivity over the sacroiliac joint so I had assumed
that the locking was associated with some muscles that crossed the joint. Unfortunately your book does not mention any
muscles crossing the sacroiliac joint so this is an ongoing question for me.
I had hoped that you would show that the laminar
fibers of the multifidus below S1 had evolved to cross and strengthen the
joint. (Where have they gone? Don't they
exist? Page 102 Fig 9.4A). This would
have been nice because the locking of the sacroiliac joint would then have been
of exactly the same nature as the locking of any other spinal joint as recognised by the chiropractor and osteopath. It is these fibers, and correspondingly the
rotatores in the thoracic spine, which I believe are responsible for the
sublesation (I don’t use the term
‘chiropractic subluxation’ because it is a wrong use of a medical term.
See ).
I was also interested to find recently
that the Australian writers on core stability concentrate on these parts of the
multifidus in their book ‘Therapeutic Exercise for Spinal Segmental
Stabilization in Low Back Pain’.
I still have one contribution to the first
half of the question ‘what can we do to correct the situation or avoid it in
the first place?’
If in a particular case a person's severe or
persistent low back pain seems to be caused by flexion of one of the lowest to
two joints beyond this parallel sided limit then the lack of a supraspinous
ligament at this level would seem to be important. The posterior ligamentous system is
presumably adequate but works in a significantly different way. The insertion of a prosthetic supraspinous
ligament between the spinous process of L4 and some point on the sacrum might
be very effective in switching off the pain and "curing" an
"unstable" joint before serious disk damage had occurred.
I have done a preliminary but fairly detailed document
on this suggestion at
Now to second part of that question: "or avoid it
in the first place". The
association of sitting, particularly civilised
sitting, goes back a long way in the literature and human experience. However this new geometrical limit on the
flexion of L4 5 and L5 S makes the association with civilised
sitting so much more specific.
The most important point here is that backrests, and
particularly lumbar support, do not limit the flexion of the lumbo sacral
junction, they increase it. This was
clearly shown in the tabulations in the paper in Spine in 1979 " The
Influence of Backrest Inclination and Lumbar Support on Lumbar Lordosis" (Spine 4: 52-58, 1979 by Anderson,
Nachemson et al.).
That
paper clearly showed that lumbar support flexed the L5 S joint in comparison
with slumped sitting and that increased lumbar support flexed it more. This corresponds to mechanical common sense
but I have not found any reference to this obvious point in any literature (and
the authors didn’t notice it either!)
Putting these two points together makes it is
unsurprising that driving is the one activity that shows up in any
epidemiological survey of back pain incidence.
My personal starting point from Easter 1981 is that car seats should be
designed to support the pelvis and not the lumbar spine.
I do of course have a patent on pelvic support in
seating and you might assume, as I did, that I would become rich beyond the
dreams of avarice when this argument was accepted. Sadly the patent, applied for in 1982 or
three, expires next year so that dream has long since faded and with it any
unreasonable bias on my part! May I sum
up the car seat situation by quoting from another letter of mine?
“The
only clear statistical association is with driving cars. This was first shown by Kelsey and Hardy in
1970 and has been confirmed by many studies since. Would we expect this mechanically? The answer is definitely yes. Car seats tip the thighs and therefore the
pelvis further back than almost any other seat.
Car seats incorporate far more direct support for the lumbar spine than
any other seats. We sit still in a car seat for far longer than we ever sit
anywhere else. This mechanical situation could not be better designed to cause
the problem outlined above.
If we combine Kelsey and Hardy's work with
the surveys by Mark Porter, Professor of Ergonomics at Loughborough University
UK it appears that a high mileage car driver is about twelve times as likely to
have a serious low back problem as anyone who never uses a car at all.
This suggests a far higher correlation
between driving cars and low back pain than between smoking and lung
cancer. Comparison of these two surveys
also suggests that the situation is far worse for the high mileage driver in
the late nineties than it was in the late sixties. Is this compatible with the mechanical
argument proposed?
Yes.
It is more than compatible. It's
predictable. In the eighties and
nineties the angle of the sitting surface of car seats was tilted further
backwards in order to counter the problem of slipping under the seat belt in an
accident. At the same time lumbar
support was introduced generally into car seats. The combination of these two is bound to
increase the flexion force in the spine at the lowest spinal joints. We should expect the statistical situation to
be worse and judging by these published statistics it is”
Believe it or not, this was meant to be a short
e-mail. I am sure that you also find
that writing a document of this type raises new questions that need to be addressed
but that is an infinite road so I had better get back to my first important
question:
-- why should these nerves cause such initially paralysing and ultimately persistent pain?
There is something illogical about asking why in a
case like this. After all, we can never
prove that evolution has worked in a particular way at some time in the distant
past. Maybe it is because I am an
engineer and also because back pain has played such an important part in my life
that I need an answer to this question even if I can’t prove it.
My explanation is as follows:
In your book your cover in detail the deterioration of
the disk, which can eventually lead to prolapse. You quote the experiments, which show that
compression of a disk does not result in prolapse almost regardless of the
circumstances. There is one case,
however, that you do not seem to cover.
This is the case of compression combined with flexion
beyond the normal flexion limit of that disk.
This is the situation studied by Adams and Hutton to win
the Volvo Prize in 1981. (Your reference
317 page 200) I accept that this is not the normal mode of failure or prolapse
but the question is: why not?
Adams and Hutton showed that hyper-flexion of a
healthy disk combined with compression would, in most cases, result in sudden
prolapse of the nucleus into the neural canal or intervertebral foramen. This seems to correspond to mechanical common
sense. If the flexion is sufficient then
the posterior annulus will be in vertical tension despite the compression of
the whole disk. It does not seem
surprising that it is unable to contain the large hydrostatic pressure in the
nucleus while simultaneously being torn vertically.
The shape and muscle connections of the human lumbo
sacral region can produce exactly these conditions. Many of the most important muscles have their
origin on the prominence of the sacrum or the posterior iliac spines. However one evaluates the "hinge point"
of the lower lumbar spine on flexion, it will be above (more rostral than) these
muscle connection points. To the eye of an engineer, this whole structure is an
"over-centre mechanism".
Beyond a certain angle of flexion, on lifting, the line of action of the
muscles will get so close to the hinge that the structure will collapse. The flexion of the lowest discs will increase
rapidly while compression remains high.
The result will be prolapse by hyperflexion as shown by Adams and
Hutton.
Your reference 69 on page 114 does not pick up this point
because it covers only the normal range of motion. Figure 4 B in that paper shows L4 5 and L5 S
parallel sided in full flexion. This corresponds exactly to the criterion
suggested earlier in this e-mail. It
seems good evolutionary design that total muscle moments remain approximately
constant within the normal range of motion.
However there is nothing that can be done mechanically beyond this range
to avoid the "over-centre effect".
The only solution is to stop the person using the spine in that range by
a warning pain that is initially paralysing and very
persistent.
I suggest that it is the coincidence, that muscle
offsets become inadequate in flexion as L4 5 and L5 S flex through the parallel
sided shape, that has allowed such an effective warning pain to evolve so
easily by such a simple mechanism. (The
shape of the sacrum is of course defined more by the need to maintain an
adequate birth canal than any other consideration.)
I used your papers on spinal musculature to do my own
detailed analysis of the effect of flexion in 1987. This paper (The
Obstetric Reason for Lordosis and the Implications for Lifting and Low Back
Pain-unpublished) is
available at This
included flexion of L4 5 and L5 S to a wedge shape of 10 degrees, wide end
posterior, and confirmed the “instant evaluation” above.
It would have been nice if the warning pain had
evolved to apply only when flexion was excessive and to switch off completely
when the safe shape had been restored. As we all know this is not the case. The
characteristics of the pain are what one would expect of the mechanism that you
describe. The nucleus ‘leaks’ to the nerves in the annulus and there is obvious
difficulty in correcting the situation quickly. I have listed various characteristics
at
such as the following:
6) The pain is most severe when it first occurs and
can take a long time
to die away.
10) In some cases (possibly in a lot of cases) the shape can have been
wrong from
childhood. In that case the phase of severe warning pain will
not have occurred and the person will simply have a
‘weak’ back with a
tendency to bouts of ache due to sitting, bending or
lying in bed.
11) Usually this gets worse with age.
I enjoyed your new chapter on instability because, I
think, your views are exactly the same as mine.
The description ‘unstable’ is often used to describe
the whole situation of an acute back.
The spine seems to have lost the stability that we normally rely on and
the sufferer has to hang onto things for stability. Somehow this use of "unstable"
seems to have been taken by biomechanists to refer to
the spine with its passive components for stability. But the spinal column with only the passive
components doesn't have any stability.
As a column, it isn't even straight for heaven's sake!
The stability of the spine relies completely on the
muscles. Pushing on a person's spine
doesn't distort it at all whether they have a back problem or not and
regardless of whether they are standing or lying down relaxed. It is the muscles that give this stability or
rigidity. The spine only bends as a part
of the movement of the body under muscular control. (I have always suspected that this is why
Anderson, Nachemson et al. didn't notice the effect of lumbar support in their
1979 paper in Spine. The instantaneous
effect of lumbar support is very small. Civilised
sitting however is not an instantaneous effect.
It applies for hours and hours and years and years.)
Many radiographic surveys have shown that one totally
degenerated disk is often asymptomatic so long as the spinal muscle system is
working normally. The instability
referred to by any clinician is a muscular effect and is always associated with
pain. I would refer to it as a part of the "shape warning pain".
I am comparing your criticisms and quite strong words
in this chapter on instability with your comments on internal disk disruption
in your back pain chapter. I think you
see far more value in fully understanding the latter. So do I.
In my 24 years of studying low back pain I have spent much time
developing chairs and car seats. I
thought that this would lead on to a wide acceptance of these basic points
about the spine. In fact it hasn't done
anything of the kind. I have therefore
decided to approach researchers like yourself in the hope of working towards a
more general understanding of low back pain and some real solutions. I hope that you will see some value in the
suggestions that I have made in this e-mail and that you might have some ideas
on how we could take cooperation further.
I hope that I will hear from you.
Yours sincerely,
John Gorman.