Biological and Biomechanical Basis of Low Back Injury
THERE IS A BIOLOGICAL AND BIOMECHANICAL BASIS OF LOW BACK INJURY.
Australia once again leads the world down an intellectual black hole with “Pain Science” education taught in place of the biomechanics of human movement and low back injury.
There has been a recent shift in Australian University education, for Health Professionals, away from almost 400 years of biomechanical science and nearly 100 years of published anatomical evidence for the assessment and treatment of Low Back Pain towards a “Pain Science” model based upon what appears to be the clinical inabilities and educational inadequacies of the academics involved. This article is written for the grand tide of Health Professionals who contact me daily for help due to the paucity of their spinal education upon graduation.
This is not a new development is Australian Universities. We apparently follow so called “evidence based” research, produced by Australian Academics often to the exclusion of the reality of basic sciences. Ever hear of the Transversus Abdominis and Multifidus co-contraction solution to Low Back Pain? It was wrong when it was published in a low impact journal called “Manual Therapy” in 1995 (1). The researchers actually misquoted their own references and no one ever picked it up until I wrote upon it (2) years after the articles publication. That theory led us down a 20-year dead end that Pilates practitioners initially used to validate their reformer beds. Now even many of them don’t support the model, but that horse has well and truly bolted (even Insurance companies in Australia now don’t rebate Pilates anymore). The VMO fiasco of knee pain rehabilitation was also an Australian invention, I’ll leave that for another article. Now it’s the turn of “Pain Science” to misdirect a new generation of health professionals.
This article is to briefly clarify, and introduce, the basic science on Low Back Injury for Health Professionals. You will hear names never mentioned during your under-graduate and post-graduate years in Australia. They just happen to be the most important figures in Science and Low Back Rehabilitation methods world-wide, also they are not Australians.
Essentially, we should have 2 Gold Standards to consider - Biomechanics (Physics as applied to the Human Body) and Anatomy. If “evidence-based research “conflicts with these two standards then perhaps a more critical eye needs to be applied to that “research”. Our Tertiary Health Science educators appear to be allowed to avoid the reality demands that apply to other Tertiary Departments such as Mathematics, Medicine and Engineering Departments.
LET US DEAL IN REALITY
Biomechanics really finds its foundation stone upon the publication of De Motu Animalium by Borelli in 1680. Here began the application of Physics to biological tissue and its movement. This was six years prior to 1686 when Sir Isaac Newton published his classic 3 laws of motion in the "Principia Mathematica Philosophiae Naturalis.". Can you comprehend that over the centuries biomechanics has continued to progress and world-wide textbooks are now published and updated yearly but the evidence and solid science of spinal biomechanics are not taught to Australian Physiotherapists in their undergraduate years? How is it possible that McGill’s “Low Back Disorders” and Adams “The Biomechanics of Back Pain” are not required texts? There is over 2000 references within these 2 texts alone supporting the biomechanical assessment and treatment of low back pain. These texts are written by authors who are not Australian. I constantly hear from Physios saying they graduate knowing nothing about spinal biomechanics, but they have been taught about “Pain Science” which has been championed by Australian academics. Graduates have told me they cannot assess a low back injury or even hypothesize upon the injured structure (because they have been told they cannot ever do so), yet there are thousands of research papers and texts that hold these answers.
It is a fact that all biological tissue has a fatigue capacity. Apply too much stress to a tissue and it will break down. A rapid inversion injury to an ankle ligament is an example, as is the slow loading over a longer time period when a ligament is constantly loaded such as creep fatigue upon the posterior ligamentous structures of the spine in poor flexed posture (10). The elastic recoil mechanism of spinal flexion is another fact of movement science and is well discussed in the work of Professor Gracovetsky (3) (I get blank looks from physios when I explain this, they have never heard of it). Further studies and observations of myoelectric silence into flexion, as published by McGill (4), clearly demonstrate the mechanism. Yet how many undergraduates/graduates are made aware of this when it comes to understanding the mechanism of low back injury. Were they ever told that as a person moves into spinal flexion their spinal erectors do enter myoelectric silence and the passive tissues including ligaments become loaded? Ligaments have a load capacity and hence a fatigue capacity and it is a mechanism of injury. Undergrads actually are told that there is no evidence for a best lifting posture. Its like telling architects that there are no principles for building structures. The evidence for lifting involves individual anthropometric evaluation of joint, limb and lever variables. It’s just physics applied to a human body. Everybody is different so there is no universal single rule on lifting posture, you have to know how to evaluate the individual components and Physios are graduating without being taught what these tests are!
Understanding the tissues involved in the origin of low back pain has also been well investigated. Let’s consider the modern age of structural injury understanding beginning in 1934 when Mixter and Barr(5) presented a correlation of disc prolapse and the clinical syndromes associated with the resulting nerve and cord compression. It has been over 80 years now and thousands of published papers demonstrating the relationship between structure and pain production. Let’s consider an important paper by Kuslich et al (6). Kuslich investigated the tissue origin of low back pain by stimulating tissues under local anaesthesia in 193 consecutive patients. Sciatica could only be provoked by nerve root stimulation; low back pain could most commonly be provoked by the outer layer of the posterior annulus and posterior longitudinal ligament. Buttock pain by simultaneous stimulation of the nerve root and posterior annulus. Facet joint capsule rarely produced low back pain. Facet synovium and cartilage never produced low back pain. This is consistent with Hirsch (7) and Mixter and Barr published prior. Outcome studies prove the relationship between disc herniation and pain when compared between surgical and non-surgical outcomes (8). There is no dispute amongst educated professionals about the disc as a source of low back pain, yet in Australia Physios actually argue about it! We can clearly see that the source of low back pain has been examined, and established, on a tissue basis for almost 100 years, yet our students are not informed of this fact.
Robin McKenzie in the 1950’s showed a clear relationship between directional assessment (both subjective and objective) and low back diagnosis and treatment. This correlates with the thousands of papers on the biomechanical evidence of lumbar disc behaviour. Directional assessment and its hypothetical basis are also not taught to Australian Undergraduates. Structure and function, it’s simple anatomical application to movement and then it’s not hard to understand why the directional assessment produced by McKenzie is predictive of the injured structure.
I’ll summarize for clarity. The mechanism of the vast majority of low back injury is into lumbar flexion. This occurs due to exposure of the passive tissues (outer annulus and posterior ligamentous structures) when myoelectric silence of the musculature loads the passive tissues. Biological tissue has a fatigue capacity, when the load on the passive structures exceeds the capacity then injury occurs and pain is consequent. The injurious load may occur due to movement pattern disorders such as segmental buckle, which are also easy to assess but not taught in Australia, or an increased neutral zone as demonstrated by Panjabi (9). Neutral zone laxity is also easy to test in both axial skeleton and peripheral joints. It is not hard to examine both subjectively and objectively the directions, loading patterns and tests that both produce and reduce a patient’s pain.
Over the last 20 years I have pursued spinal injury and its evidence in an unrelenting quest. The basic biological and biomechanical science is not debatable, except by those who don’t know the science. As a result I created a very straight forward approach to lumbar spine injury and rehabilitation based upon these solid sciences. At its core lies the understanding that most lumbar spine injury is to passive structures, due to a weakness in an active muscle group and an inefficient neurological static or movement pattern. The resolution of the problem lies in assessing the problematic pattern, the active muscle control of the pattern, and the integrity of the passive structure that was exposed. This could never have been achieved if I had not learned both indirectly and directly from some of the giants of Rehabilitation Science such as Professor Stuart McGill (Canada) and Robin McKenzie (New Zealand), Educators such as Pavel Tsatsouline (Russia) and Grey Cook (USA). These people stand on the shoulders of past giants and if we care to use their broad shoulders then we too will see further again.
I see that there will now be a necessary split within the health professions, especially Physiotherapy. Those of us who will pursue a biomechanical and biological science-based protocol that honours nearly 400 years of evidence and involves anatomical assessment and strengthening for rehabilitation, opposed by those who will find any excuse not to learn, based in the concept that no knowledge is certain, and that their “evidence-based research” has no answers.
So, to the Australian Academics and Professionals who proudly say they don’t know the source of a patient’s low back pain, or he mechanism of injury, and wear it as some sort of badge of honour, I say “that’s O.K, because there are professionals in Australia, and around the world who do”.
Dr. Andrew Lock’s various educational courses on Lumber Spine, Shoulder and Hip run throughout the year. He can be found on Instagram @andrew_lock_strength and Facebook “Functional Strength Rehabilitation”.
- Richardson CA, Jull GA. Muscle control-pain control. What exercises would you prescribe? Man Ther. 1995 Nov;1(1):2-10.
- Gracovetsky Serge. The Spinal Engine. Springer-Verlag; 1st edition (March 1, 1989)
- McGill SM, Kippers V. Spine (Phila Pa 1976). 1994 Oct 1;19(19):2190-6. Transfer of loads between lumbar tissues during the flexion-relaxation phenomenon.
- Mixter, W. and Barr, J. (1934) Rupture of the Intervertebral Disc with Involvement of the Spinal Canal. The New England Journal of Medicine, 211, 210-215.
- Kuslich SD1, Ulstrom CL, Michael CJ. Orthop Clin North Am. 1991 Apr;22(2):181-7. The tissue origin of low back pain and sciatica: a report of pain response to tissue stimulation during operations on the lumbar spine using local anesthesia.
- Carl Hirsch (1949) An Attempt to Diagnose the Level of a Disc Lesion Clinically by Disc Puncture, Acta Orthopaedica Scandinavica, 18:1-4, 132-140
- Weber H. Lumbar disc herniation. A controlled, prospective study with ten years of observation. Spine (Phila Pa 1976). 1983;8:131–140.
- Panjabi MM. J Spinal Disord. 1992 Dec;5(4):390-6; discussion 397. The stabilizing system of the spine. Part II. Neutral zone and instability hypothesis.
- Henryk Tkaczuk (1968) Tensile Properties of Human Lumbar Longitudinal Ligaments, Acta Orthopaedica Scandinavica, 39:sup115, 1-69
JOIN THE COMMUNITY
Stay up-to-date with our latest research, education, workshops and other resources.
No spam. Only education.