Low Back Pain Studies?

[Guest guest]

The following web page on the issue of lower back pain (LBP) was being

discussed on another list. It is about some of the current research and

therapy for Low Back Pain (LBP). I have a tendency, having done much

personal research, to see the current trends as misguided or at least

incorrect in direction. It seems that current research is " full bent "

on finding some " magic muscle " that, when conditioned with complicated

and specific exercise/therapy, will eradicate LBP.

Don't we ever learn? The body works with the " sum of its parts " , not

the as an isolated unit here and there.

Mel has posted the following information and web address that has the

article that, according to the author, has finally " proved " what causes LBP

and how to cure it.

NOT SO!!!

The darling muscle this time is the Multifidus Muscle (MM) which to be

sure is very valuable in " helping " keep the spine stable, but a " bit

player " in the overall Torso Stabilization Mechanism (TSM). Since this

might be a muscle (group) that many are not familiar with here is a site

that offers a anatomy chart showing where it is located:

<http://www.meddean.luc.edu/lumen/MedEd/GrossAnatomy/dissector/mml/mult.htm>

Below is information that Mel has posted regarding portions of that article.

I have posted my comments that I sent to the list in question at the end.

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<http://www.ptlitup.com/frameset_800.html>

<<In 1994/1996, Hides et al (1,2) had already found that the diameter of the

multifidus muscle (MM) is diminished with more than 30% in acute LBP

patients, and does not automatically recover after an episode of acute LBP,

not even when the ADL pain has long subsided. What is important is that they

found that the MM atrophied only at the exact site of the pain, so on the

ipsilateral side and on the segmental level. Why this is important, is that

quite recently, Yoshihara et al (3) and Zhao et al (4) found as good as

perfect correlations between disc damage and side- and level-corresponding MM

atrophy. These results taken together actually prove that acute LBP is in

fact acute disc pathology, in most cases!

The question " what comes first? " has to my knowledge not been proven

conclusively, but it is very unlikely that such a local MM atrophy would

occur without preceding local pathology. There is in my opinion therefore

reason enough to accept that acute LBP starts with acute disc pathology.

The resulting pain then causes the local MM to atrophy, by means of

inhibition, and that atrophy, in turn, could very well sustain the disc

pathology,

since segmental stability is then diminished.

For McKenzie adepts, the fact that most cases of acute LBP are actually

caused by acute disc pathology will not come as a surprise. It has

however never been clearly proven, and most medical guidelines, also the latest

ones, all state that a substrate for sub/acute LBP has not been found. But

that has now clearly changed........

On a research level, this will in my view demonstrate to effectively

prevent recurrences, also in other patient populations than the one studied -

and personally coached - by Hides et al. Such a study should nevertheless

also include screening for dominant psychosocial factors at baseline, to see

whether eventual non-successful cases can be contributed to those factors......

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Below is a portion of the original post I commented on:

----- Original Message -----

It was written:

<<What has been a puzzle for decades, evidence-wise speaking, has now

largely been solved/proven: the substrate of what is/was known as

non-specific LBP. I couldn't believe it myself, but it is true.>>

Casler writes:

** I have read this " proof/solution " and find it less than either proof or

a solution. While I concur that most chronic or recurring LBP can be

traced to disc pathology, that is where our paths diverge.

In general, structural disc damage is caused by force beyond tissue and

support mechanism strength, plain and simple. To even ask questions like

" what comes first " demonstrates that some are trying (in vain I might

add) to force an answer that cannot be answered.

The discovery that the Multifidus Muscle (MM) may atrophy from

" inhibition " during a bout of LBP is not significant to any degree.

Keep in mind that the MM is but a rather insignificant (and rather weak)

portion of two systems (local and global) that when sufficiently

conditioned work together to supply the " Torso Stabilization Mechanism "

(TSM).

The TSM is the sum of all systems and structures that work sequentially

and concurrently to provide a static or dynamic support to the force

creating and absorbing structures of the torso.

LBP is caused when the conditioning and support level of these

structures and tissues is forced beyond their capacity. Due to the fact

that a disc can be forced into protrusion or herniation from the simple

act of tying ones shoes, yet can support in a well conditioned

individual hundreds if not a thousand pounds, we have a broad range of loads and

forces that are in play. There is enormous significance in why this is.

How can simply bending and twisting (with no external loading other than

bodyweight) have the potential to cause damage that does not happen even

with hundreds of pounds of external load?

It all simmers down to the proper activation of the TSM.

To single out the MM or the other " darling " , the TvA is the height of

speculation. To then tout this speculation as " proof " and " solution " ,

to me, demonstrates that there are many well respected in the field who

haven't the slightest idea how to deal with LBP at all. The current

trend is well too specific, speculative, forced opinion, and theory

If we are talking about " insurance " to reduce the probability of LBP,

then those who advocate anything but a comprehensive " global/local "

conditioning of the TSM are doomed to failure or at best partial

success. And this will only provide " higher coverages " of LBP

conditioning insurance. It will not and cannot provide total insurance

to all forces. It will however provide substantial and overwhelming

protection against reoccurrence from normal everyday activity.

What? The general conditioning system has been tried before and didn't

work? Show me! Sit-ups, hyperextensions, and crunches are NOT the

answer. That just shows that again, " many " know too little.

So like our " immune system " is a system of many mechanisms working

together to fight against infection, the TSM is the immune system for

LBP. If it is working well we will reduce LBP and the reoccurrence of

such. If it is compromised, we are at risk.

The MM is but a small cog in that wheel, and focusing on it, only

reduces the effectiveness that can be realized with a more comprehensive

program.

And a word about exercise and conditioning. I have yet to see a program

of exercise from " any " back expert that even remotely resembles what is

needed to help a patient bend, lift, walk, run, and in other words lead

an active life and be pain free. I am so tired of these stiff incorrect

lifting postures and stretching exercises.

The exercises recommended by and Jull are all but useless.

The Danneels exercises are a joke. To be sure, they can be useful to a

small degree, but they are nothing but slight muscle toners. In fact,

they are so removed from the actual acts of daily activity such as

lifting the baby or lifting the garage door that they serve little

purpose.

You can damage a disc by getting out of a sports car incorrectly

(believe me I have done so), so why do exercises that do nothing to help

" real, everyday loads " ??

When was the last time you helped a patient learn a Valsalva maneuver?

Just how important is diaphragmatic hypertrophy? How do you strengthen

the major abdominal muscles for torso support? How much IAP can the TvA

really produce? What can produce more?

Let me assure you that the Multifidus Muscle is a small element of the

system.

Sorry to gore so many oxen, but this path is leading nowhere fast. I

would suggest that every back researcher who does not have disc

pathology personally and has not cured such has absolutely no idea what

will work. I have been blessed./cursed, with a lifelong " classic " BAD

BACK. It lasted for over 35 years until I took the problem into my own

hands and let me assure you I know every system and how it contributes.

So don't Mutifidus Muscle ME!!!

Regards,

A. Casler

Century City, CA

TRI-VECTOR 3-D Force Systems

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