What Do Scientists Tell Us about Back Pain?

Notes from the Fourth World Congress on Low Back and Pelvic Pain

by Robert Schleip

 

First published in ‘Structural Integration: The Journal of the Rolf Institute’, September 2002, Vol. 30, No.3

 

Every three years, the world's leading academic researchers on low back and pelvic pain meet to exchange their latest insights and discoveries.  They present new studies, new theoretical concepts and engage in debates with each other.  Like several other Rolfers, I attended the most recent of these interdisciplinary congresses, held in Montreal last November.  Having profited immensely from attending the previous congress in Vienna in 1998 and from studying the papers of the first two of these congresses (1992 and 1995), I was particularly intrigued by the new subtitle of this congress:  "Moving from Structure to Function".  Here are my digested notes from this inspiring and informative congress.

 

A Context

Two thirds of all people in the industrial world suffer from debilitating back pain at least once in their lives.  Low back pain produces the largest health-related expense in our national economies.  Most bodywork practitioners have either their private philosophy - or share their particular school's believe system - about what factors are causing this pathology, and about how to best treat or prevent it.  Orthopedic physicians tend to see the problem in the lumbar discs; visceral osteopaths tend to treat the viscera; manual therapists focus on adjusting the sacroiliac joint or individual vertebrae; physiotherapists tend to look for weak muscles, which need strengthening; their colleagues see the problem in tight muscles which need relaxation; yet others focus on psychological components, and so forth.  As contradictory as their assumptions often are, all of these approaches seem to have plenty of impressive case histories to back up their conclusions.  As a patient "whom you see is what you get."  At worst, it looks like an esoteric carnival.

 

To orient in this situation - either as a suffering patient or as a serious practitioner - is not easy.  Provided one studies any one of these systems in any depth, or meets a charismatic and convincing representative, most of these explanation concepts have some logical and/or appealing plausibility.  Which means that, unfortunately, plausibility cannot serve as a sufficient orientation.  Anecdotal reports (also called "clinical experience"), personal experience ("this seemed to help last time") or word-of-mouth recommendations are also not reliable, since without a proper statistical study design, it is almost impossible to judge whether the "healing success" is incidental with - or is clearly above - the spontaneous recovery rate (e.g., 75% of all back pain, if not treated, disappears within four weeks[1]).

 

It would be nice if we Rolfers could conduct our own scientific research to test some of our most popular in-house hypotheses.  Yet for such studies to be at all meaningful and to go beyond an amateurish "self-fulfilling prophesy study design", huge amounts of resources are needed that we haven't mastered so far.  Cottingham's studies around the Rolfing pelvic lift have been a good beginning, but their relationship to low back pain remains tenuous[2].  Nevertheless, scientists outside our school - yet worldwide - have been busy to conduct all kinds of research in order to try to understand back pain.  Some of their research findings have been quite inspiring and seem to have relevance for our work.

 

While it again became obvious to me at this congress - as at the last - that academic scientists tend to have their own biases and shortcomings, and that often-accepted "facts" and concepts of today will be shown to be outdated in the future, I do admire the rigor and care with which they tend to question most of their hypotheses.  It therefore has been a pleasure for me to connect with the series of "Interdisciplinary World Congresses on Low Back and Pelvic Pain" and to update my input from that side every three years.  I am still thankful to my colleague and Rolfing instructor Jim Asher (who I believe has attended all of these congresses so far) for having recommended these high-profile conferences to me.

 

A Brief History of the Congress

Most of the top names in scientific back pain research have contributed to this congress series:  Greenman, Don Tigny, Paris, Mooney and Dorman from the United States, Gracovetsky and Lee from Canada, Vleeming and Snijders from the Netherlands, Oostgaard and Sturesson from Sweden, McKenzie from New Zealand, Adams from England, Tilscher from Austria, Richardson/Jull/Hodges from Australia, and many others.   The first congress (San Diego, 1992) mostly explored structural features of the sacroiliac (SI) joint.  Yet it soon became scientifically clear that back pain is more complex than that, and that other features need to be included for understanding the widespread existence of this common pathology.  The second congress, which was also hosted in San Diego, then explored a vast array of possible interrelationships between the lumbar spine and the pelvis.  The third congress, in Vienna, finally focused on the efficacy of treatment modalities, with a special emphasis on muscular recruitment techniques.  It was at this previous congress in Vienna that the concept of spinal segmental stabilization was presented by several Australian researchers and subsequently gained worldwide attention.[3] 

 

The invitation to this most recent congress promised to cover a more detailed anatomy of the lumbar spine, a further exploration of the segmental stability concept, and a deeper view into psychosocial factors.  At their opening address, Andrew Vleeming and professor Nicholas Walsh related the meeting to "The Bone- and Joint Decade" (2000 - 2010, HYPERLINK "http://www.boneandjointdecade.org" www.boneandjointdecade.org), and pointed out that the number of people older than 65 is expected to double between 1990 and 2020, meaning that degenerative joint pathologies will demand increasing attention.

 

From Structure to Function

Although many of the leading researchers had hoped to find the key for understanding low back pain (LBP) in a detailed structural analysis of related anatomical features, the new research in the last few years has made it increasingly clear that disc degeneration and other structural aberrations account only for a small portion of LBP.  For example, MRI studies have shown that people with LBP have just as many disc degenerations, annular tears and disc protrusions as healthy people of the same age with no back pain[4].  The subtitle of this particular congress, "From Structure to Function", symbolized a stronger interest in neuromuscular movement orchestration and its relationship to back pain.  Jean Paul Wingerden spoke at this congress of a shift in contemporary research "from form to function".  At the congress of 1998, Panjabi's illustration of three elements of joint stability (Fig 1) was probably the most often repeated illustration.  It signaled the inclusion of neural and muscular factors (together with the osteoligamentous aspect that most researchers had been focusing on before).

Fig. 1 The three interrelating subsystems of spinal stability based on Panjabi. This classical illustration served as the most common graphic at the 1995 congress in Vienna. (Reprinted with kind permission of Lippincott Williams & Wilkins, from Panjabi M M 1992 The stabilization of the spine. Part 1. Function, dysfunction, adaptation, and enhancement. Journal of Spinal Disorders 5(4): 383-389)

  

Two of the main organizers of the Montreal congress, Diane Lee and Andrew Vleeming, presented Fig. 2 as their latest model for understanding both healthy and pathological joint function.  It reflects the model of joint stability for the SI joint as developed by Vleeming and Snijders (both from Rotterdam), which had been presented at previous congresses, and which had combined passive joint stability by form closure (via wedge-like orientation of the joint in relation to gravity) with active muscular control from "local stabilizer" muscles.  Yet it also adds the factor of emotions and awareness.

 

Fig 2: "An Integrated Model of Joint Function" as presented by Lee and Vleeming at this congress. Reprinted with kind permission of Diane Lee

 

Pain from Discs or Facets?

Nevertheless, the first day of this three-day conference was still devoted to the traditional preoccupations of back pain researchers:  the anatomy and biomechanics of the lumbopelvic area.  Several presentations explored the question of which tissues are potential pain generators around the lumbar spine.  Based on injecting pain-blocking substances into specific tissues (which then sometimes distribute it to other tissues and distort this "gold standard test"), the following percentages for common pain generators where presented:

• discs 40%
• facets: between 15% (in younger patients) and 42% (in older patients)
• SI joint 16-30%
• plus possible minor amounts for nerve roots, dura, and muscles.

 

This seemed to correspond to the report of Michael Adams, who believes that 40-55% of chronic LBP originates from discs (mostly from the posterior annulus), from the posterior longitudinal ligament, followed by the SI joint and facet joints.  Adams also stated that 50% of discogenic LBP shows centralization/peripheralization of pain in relation to lumbar spine extension/flexion, whereas this happens in 0% of symptomatic facets (this partially supports the McKenzie concept of LBP diagnosis and treatment).  Pain-provocation and pain-blocking studies on sedated patients "have shown that the posterior annulus is the most frequent source of lower back pain, followed by the sacroiliac and apophyseal joints.  Muscles and ligaments tend to cause very localized back pain, and nerve roots cause leg pain."

 

According to Adams, Bogduk - who is usually quoted as an authority on lumbar spine research - was wrong in saying that the outer posterior annulus fibrosus is innervated by branches of the sinuvertebral nerve.  Recent studies have shown that in healthy subjects it is only the outer few millimeters which are innervated, and that further ingrowth seems to be inhibited by hydrostatic pressure in healthy people.  However, with degeneration and loss of hydrostatic pressure one also often sees the incursion of blood vessels and nerves into the center. 

 

Regarding discogenic pain, there is now also the new concept of internal disc disruption.  Plus of course the concept of pain sensitization (due, e.g., to extrusion of nucleus pulposus material, which is highly acidic) happening both locally and in the brain and spinal cord.

 

Adams also reported  that "studies on identical and non-identical twins have shown that approximately 70% of intervertebral disc degeneration and 50% of back pain can be attributed (in a statistical sense) to genetic inheritance.  The race is now on to find the genes responsible."  Several genes have already been implicated, especially some which code for vitamin D metabolism, collagen type IX, aggrecan, proteoglycans (which are responsible for holding water in cartilage, and which degrade with age), and with biomechanics.  Probably Adams was referring to what was later quoted as the "McGregor twin study of 1999", which had found a dominant role of familial factors (genetics and childhood environment) for LBP.  For example, very similar x-rays were found between monocygotic twins.

 

A New Nomenclature

Up until recently, no generally accepted nomenclature existed for the classification of lumbar disc pathology.  Based on the wise statement of the ancient philosopher Socrates, "The beginning of wisdom is the definition of terms", several international associations recently worked together to develop an extensive reference document for terminology and classification.  This document was then published in the journal Spine, is additionally available for public orientation at the internet[5], and was presented at this congress by Pierre Milette.  According to these new guidelines, each lumbar disc can be classified in terms of one of the following six diagnostic categories:

·      normal;

·      congenital/developmental variation;

·      degenerative/traumatic;

·      infectious/inflammatory;

·      neoplastic; and

·      morphologic variant of uncertain significance.

 

Among the degenerative/traumatic lesions, the following three subcategories exist:

• annular tear (without herniation);
• (disc) herniation; and
• (disc) degeneration.

 

The term "herniation" can then be further classified as:

• protrusion;
• extrusion;
• intravertebral.

 

Note that the common yet less precise term "disc bulging" no longer exists in this classification, and should therefore be avoided.  Clear guidelines are given to differentiate between these subcategories based on MRI, CT, and x-ray findings.  For the imaging specialist there are then three confidence levels: 

• "possible", with less than 50% certainty;
• "probably" for above 50%; and
• "definite" with 100%.

 

The above-mentioned MRI study[6] in the NEJM showed that people without LBP usually have the same amount of disc degeneration, intravertebral herniations, annular tears and protrusions (yet usually not extrusions) as patients with LBP.  Therefore, the following differentiation from Milette between extrusion and protrusion becomes useful for clinicians:  "Extrusion is present when, in at least one plane, any one distance between the edges of the disc material beyond the disc space is greater than the distance between the edges of the base in the same plane, or when no continuity exists between the disc material beyond the disc space and that within the disc."  In other words, most of what is called a slipped or herniated disc is a simple protrusion (i.e., extrusions are extremely rare), and there is therefore no clear causal relationship between this disc pathology and LBP.  Yes, the pain might be generated by tissues in or around the joint.  But since asymptomatic people of the same age tend to have almost the same frequency of protrusions, other factors are necessary to explain why such changes trigger pain in these LBP patients and not in their pain-free contemporaries.  Ollie Miettinen expressed this humbling insight (humbling for the structurally-oriented clinicians) later in the brief sentence:  "the vast bulk of LBP should be considered idiopathic"

 

Asymmetrical Overload Syndrome

Jim Porterfield and Carl de Rosa gave an interesting presentation on what they called AOS, or "asymmetrical overload syndrome".  According to them, the facet joints carry 15-20% of load, the discs 80-85%.  As the discs are breaking down, the facet joints take more load.  Asymmetric weight bearing potentially results in altered tissue loading patterns on the right and left side of the body.  A left frontal plane asymmetry is present when in standing all bony prominences of the pelvis are lower on the left than on the right side. This tends to produce the following AOS symptoms:

• increased compression on the lumbar discs on the high (right) side;
• SI pain on the long leg side;
• piriformis syndrome ("as a term to depict tensile overuse syndromes of the deep rotators and abductors of the hip") on the high side;
• knee problems on high side ("varus from above, valgus from below") which often results in medial patellar facet compression;
• lateral epicondylitis on low side; and
• early onset degeneration of hip on long side.

 

As plausible and convincing as their biomechanical and graphically demonstrated explanations were, the small sample of patients (only six) on which Porterfield and DeRosa had based their data appeared to weaken their model to some degree for me.

 

Gracovetsky's Spinal Engine

Serge Gracovetsky developed a theory in 1985 to explain how the human spine evolved from our fish ancestors and how this is related to human gait.  Some of our old-timers will remember his impressive presentation of that concept at an Annual Meeting of members of the Rolf Institute in the late Eighties.  Up until recently his model did not describe the specific interactions of the spine with the legs and the upper extremities.  Gracovetsky had the pleasure to achieve this at this congress in his home town of Montreal. 

 

When walking with a corset, energy consumption goes up, which shows that it interferes with an important element of the economic orchestration, i.e. with trunk rotation.  According to him, there are currently two opposing concepts about the role of trunk rotation in walking (Fig 3).  In one concept, trunk participation is seen as passive, while in the other as an active movement.  Current data still support both interpretations of gait.  The passive concept is supported by the fact that velocity in runners can be improved by proper trunk stability.  Whereas the active trunk model is supported by Gracovetsky's finding (which he already demonstrated at our Rolfing meeting long ago) that the absence of lower extremities does not significantly affect the motion of pelvis, spine and trunk.

  

Fig. 3 Trunk rotation as an essential element in walking. Reprinted with kind permission of Serge Gracovetsky

 

The adaptations of the trunk in locomotion mainly serve three goals:  rotation of the pelvis, counterrotation of the shoulders, and stabilization of the head.  With the use of a high-resolution opto-electronic tracking system, Gracovetsky studied the fine details of those adaptations.  He proposed that directly after heel strike the opposite latissimus pulls on the spine to counterrotate.  Gluteus maximus and hamstrings then extend and derotate the spine directly or indirectly, which involves the lumbodorsal fascia transmitting those forces in an oscillating manner.  The torque is transmitted by the intervertebral joints via a dual (facet and annulus) but complementary mechanism.  When pelvic rotation is at its maximum, the interlocking facets transmit virtually all the available torque; whereas during double-stance phase, the facets are substantially aligned and do not transmit any torque.  In contrast, the torque transmitted by the annulus fibrosus is maximum when the velocity is maximum (double-stance).

 

Occupational Factors

The McGregor twin study mentioned above also looked at the influence of job-related factors on LBP.  The result might be surprising to many:  apparently job factors such as lifting or driving explain only 2-7% of LBP.  Tapio Videman summarized the present practical conclusion of this and other back pain studies of the last few years as follows:

 

1) LBP is very poorly correlated with structural findings in imaging;

2) X-rays and MRIs are not indicated;

3) Do not recommend lumbar belts and supports;

4) Traditional biomedical education based on an injury model does not reduce LBP and work loss;

5) High job satisfaction and good industrial relations have a strong influence.

 

Videman's recommendation:  intervene in the domain of psychosocial factors.

 

Psychosocial Factors

Andrew Vleeming has been a strong supporter (and developer) of the concept of form and force closure of the sacroiliac (and lumbar spine) joints.  At this congress he surprised me by suggesting that in order to understand inappropriate force closure, a shift from quantity ("how much") to quality ("how a joint moves") is necessary.  Often it is not helpful to try to find out which muscles are statically weak or tight, rather to understand the dynamic orchestration of their actions.  This orchestration is regulated via the central nervous system, and seems to be strongly influenced by emotions.  Reminding us that the word e-motion signals that emotions express themselves best in the motor system, Vleeming suggested - similarly to Videman before him - a stronger "inclusion of psychosocial factors, yet," as Vleeming says, "from a medical perspective."

 

A study by Whitehall[7] has shown that the most significant predictor for general health is not genetics, not eating, religion, sports or whatever; it is social rank and socioeconomic status (I did not like that finding, as it might mean that connecting my clients with a good career coach, personal image trainer or investment advisor might help their back health over the long term more than any of my direct treatments).  Sapolsky's now famous study of baboons was quoted, which demonstrated that a lack of social control leads to very high stress level in terms of cortisol and adrenaline.  Vleeming mentioned strong correlations between specific neuropeptides and altered postures. This sounded very interesting to me; but he mentioned only one example:  that adrenergic states tend to go along with a higher basal motor tone.

 

Nevertheless, a later presentation of Gert Holstege on "The Emotional Motor System" continued to satisfy my hunger for more detailed information about these neuroendocrino-postural relations.  Holstege showed that a neural center in the midbrain, called PAG (for Periaqueductal Grey) plays a key role in regulating the influence of emotions on the motor system.  This area is strongly connected with the limbic system, and stimulates changes in nociception, blood pressure, vocalization, locomotion (jumping and stepping), micturition, and lordosis.[8]

 

The influence on lordosis, or what Holstege also called "arching of the back", is of course of special interest for us Rolfers.  Apparently stimulation of the lateral and dorsal PAG facilitates a so-called "lordosis reflex".  In mammals, lordosis often is a female receptive behavior which is driven by the PAG.  To quote from Holstege's picturesque description of that reflex in the congress book:  "In the cat the full receptive posture consists of crouching (forelegs collapsed), lowering of the head, perineal elevation, tail deviation, and treading, often in combination with calling and vulval excretion.  The PAG is essential in the control of lordosis.  Stimulation of the lateral and dorsal PAG facilitates lordosis, whereas lesions suppress it."  Based on their neural connections with the PAG, the following muscles appear to be particularly involved in the lordosis reflex:  iliopsoas, medial longissimus, hamstrings, adductors and pelvic floor muscles.  In laboratory rats, for example, mechanical stimulation of the cervix activates their iliopsoas.

 

Interestingly, this influence of the PAG on lordosis is dependent on the presence and relative amount of the hormone estrogen.  The PAG also receives direct and indirect projections from the sacral spinal cord and it is known to "respond to lordosis-relevant somatosensory stimulation", which means that "In freely moving animals, lordosis is initiated easily by applying tactile stimuli to the skin of the flanks, posterior rump, tail base and perineum".  While fortunately no human studies were quoted about these peculiar relationships, I wondered to what degree these studies apply not only to mating female cats and other mammals, but also to biped humans of different gender and age.  It seems possible to me that at least for some of my young female patients these PAG driven neural mechanisms might be contributing to their degree of lordosis.  And, heaven forbid, could this be true for 48-year old therapists like me as well?

 

Coming back to Vleeming's talk on the role of emotions on altered motor control.  According to him, emotions override somatic motor control.  He mentioned the so-called "bud grip" as an example of too much force over the pelvic region.  His suggestion for therapeutic retraining approaches:  "Create deep riverbeds of facilitated motor action", which are linked with a more positive emotional pattern.

 

How Stiff Is the Sacroiliac Joint?

Bengt Sturesson from Sweden had shocked many practitioners at the previous congress in Vienna with his precise measurements of SI motion.  Using radiostereometric x-ray imaging, he had shown that SI joint mobility in healthy people is much less than had been assumed before (i.e., it is only 0.5 -1.6 mm translation or 2-4 degrees rotation in a standing or sitting position), and that manual tests in which the practitioner assumes to palpate SI motion in these positions, are therefore very questionable[9].  At the congress in Montreal, Sturesson presented an additional study[10] with the same expensive technology, which seriously questions the standing hip flexion test (also called the Gillet, Stork, or Rucklauf Test) for SI joint diagnosis - which, by the way, has recently become popular among Rolfers.  His conclusion:  "The small movements registered support the theory of form and force closure in the sacroiliac joints.  The self-locking mechanism that goes into effect when the pelvis is loaded in a one-leg standing position probably obstructs the movements in the sacroiliac joints. Therefore, the standing hip flexion test cannot be recommended as a diagnostic tool for evaluating joint motion in the sacroiliac joints."

 

One of the highlights for me at this congress was the presentation of a new and simple diagnostic technique for analyzing joint stability:  Color Echo Doppler imaging. For the SI joint it provides a real breakthrough, especially since not everybody is willing to shoot tantalum balls into the sacrum and innominate bones in order to use Sturesson's radiostereometric imaging devices; and other measurement techniques for SI motion have not shown to be precise enough.  Yet the idea for Doppler imaging is quite simple:  vibration is applied to the ilium and detected again at the sacrum.  If they vibrate pretty much together, the SI joint is stiffer.  And if there is a lag in the vibratory response of the ilium, there is more laxity in the joint.  Using this new diagnostic idea together with EMG measurements, van Wingerden, Buyruk and  Snijders studied the effect of several muscles on SI joint stiffness and published the following result:  "It was demonstrated that SIJ stiffness increased when selected muscles where activated.  The erectors spinae, biceps femoris and gluteus maximus showed the greatest effect on joint stiffness.  The latissimus dorsi only had a small effect on SIJ stiffness."

 

Unfortunately, they did not include any abdominal muscles in that study (which used surface electrodes only).  However, they suggested that their findings could explain how usually intra- and inter-tester reliability of manual tests to examine SI stiffness is quite low.  Their suggestion is that the "poor reproducibility of manual tests could be related to variance in muscle tension and hence joint stiffness between tests."  The study shows “that besides structural quality and integrity of the joint, joint stiffness is also influenced by muscles.  It can be assumed that joint stiffness is already influenced by basic muscle tone, when no muscle activity is detected by EMG.  Emotional states are known to influence muscle tone and patterning.  Therefore, the effect of emotional states on specific muscle patterns needs to be taken into account when analyzing SIJ stiffness.  Presumably this assumption can be applied to joints in common."  They also quoted - and the high number was new to me - that 30% of the biceps femoris fibers go directly into the sacrotuberous ligament without any attachment to the ischial tuberosities.

 

In a brilliant talk on the concept of SI lesions, Carolyn Richardson reviewed the history of changing opinions around this theme.  The famous Mr. Cyriax, for example, wrote about SI lesions:  "years ago I believed them to be common, then to be rare.  Now I regard them as a misdiagnosis".  Greenman, on the other hand, teaches that 60% of postsurgical lumbopelvic pain is due to SI lesions.  Recent studies of gait changes after SI manipulations have shown that 60% of the treated patients showed increased motion of the SI joint, and 25% decreased motion.  Richardson's convincing conclusion:  "Bone position is irrelevant. Function is more important".  By "function" she means things like reflex activity and EMG.  For example, she reports that H-reflex activity is restored to normal after manipulation.

 

An overview of standard pain provocation tests around the SI joint showed that none of the common tests has sufficient reliability.  But if several of these tests are done, and three or more of them provoke pain, this might indeed be a pretty decent indication for SI dysfunction.  It was repeated a few times that the SI joint is richly innervated, receiving branches from L3-S4.  The statement was made that "most understanding of the SI joint comes from anthropology", which in the light of the biomechanical changes from quadruped to biped anatomy makes a lot of sense to me.

 

Pelvic Pain in Pregnancy

It seems that most research and treatment around pregnancy-related pelvic pain happens in Scandinavia.  According to Hans-Christian Ostgaard, from Sweden, posterior pelvic pain in pregnancy (PPPP) usually starts in the 18th week and disappears after three months. If not, it has a bad prognosis.  Usually one or several pelvic pain provocation tests are positive, such as active straight leg raise (ASLR), posterior pelvic pain provocation, and palpation tenderness of the iliopsoas muscle or of the sacrotuberous or the long dorsal SI ligaments.  Hanne Albert from Denmark added that 14-20% of pregnant women get pelvic pain, and that two in three are pain-free one month after delivery.  According to her study, acupuncture has been shown to be helpful, even more than physiotherapy.  Water gymnastic therapy proved to be helpful as well; same for massage.  She also presented clear figures that demonstrated that prophylactic ergonomic advice and exercises are helpful, but only if they are individually designed.

 

In another paper presented there, Bengt Sturesson from Sweden had studied SI mobility in pregnant women who suffer from posterior pelvic pain, which is also often accompanied by "catching" of the leg when walking.  He found that "The most probable explanation for the catching is that local nociception disturbs muscular function in women with posterior pelvic pain because changes in the sacroiliac joint's range of motion, which is very small, cannot cause this symptom."

 

A New Anatomical Definition of "Core"

The concept of segmental stabilization was originally developed by a group of researchers around the University of Queensland in Australia, and was already powerfully presented at the previous congress[11].  For me it has become a major inspiration and clarification for Rolf Movement as well as for structural work.  The concept has gained worldwide attention very rapidly, and has already been taken over by thousands of Pilates instructors and professionals in other fields.  According to it, there are several muscles that are activated in healthy people to stabilize the vertebrae of the lumbar spine as well as the SI joint.  But in LBP patients, as well as in people who are prone to develop LBP, these muscles have become weak or their orchestration is out of phase (i.e., they fire too late or not strongly enough when needed).  These muscles are called "inner unit" and include the transversus abdominis (TrA), multifidus, pelvic floor, diaphragm and possibly the lower part of the obliquus abdominis internus.  Together they form a "deep musculo-fascial corset" (Richardson) to support segmental stability from the inside and to allow outer and more global muscles to work less.  Anyone familiar with Ida Rolf's body ideal in which the "intrinsics" - or what she sometimes called "core" - provide an inside support and allow the "girdles" to relax more, should be excited about this scientific reconfirmation.  At least I am! - even more so as Diane Lee suggested at this conference a name change from "inner unit" to (hold your breath)..."core".

 

Transversus Abdominis

Particularly the function of the TrA has been thoroughly researched based on that concept.  In healthy people this muscle is subconsciously pre-activated to initiate and to accompany movements like a standing leg raise, lifting an object, or even a standing arm raise in any direction.  An anatomical and biomechanical analysis has also shown this muscle (as well as the deeper fibers of the multifidus) to be able to guard individual vertebrae from dislocation in active and loaded trunk movements.

 

Teaching LBP patients to recruit their TrA has been shown to shorten recovery time significantly; and - most impressive of all - the recurrence of pain of these patients within one year as well as within three years is only half of that of other tested rehabilitation methods.

 

Carolyn Richardson (a main representative of the Australian research group) presented a further study, demonstrating that isolated activation of the TrA (with hollowing exercises, or pulling in of the lower belly wall) reduces SI joint laxity more than a bracing action using all the lateral abdominal muscles.  This supports her model of the biomechanical effectiveness of TrA activation to treat LBP.  She reported that her measurements have shown the TrA often to be weak or inactive on one side of the body only.  Also she found that in LBP patients the outer system is normally not only overactive; it is even less fatiguable, according to a new study in Spine by Ng (yes, that is a complete surname).

 

Measuring Psoas and Pelvic Floor

Also new at this congress was a study by Sean Gibbons that demonstrated that the deep fibers (or posterior fascicles) of the psoas major can be seen as local stabilizers of the lumbar vertebrae (as well as the SI joint), and should therefore be included as part of the core.  Peter O'Sullivan shared the observation that an ASLR is often less painful if the pelvis is compressed by the therapist.  He therefore suggested that instability patients should hold their breath in low-level exercises (like ASLR), which means to apply the same stabilizing strategy as normal persons in high-level loads.  To monitor pelvic floor activity during exercise, he applied a brilliant and simple idea (which was first suggested by Julie Hides from the Australian research group):  the use of a portable ultrasound unit to see whether the bladder drops during trunk loading or not.  Patients with SI pain during ASLR were taught a core-activation training consisting of "lifting" their pelvic floor with controlled respiration and in co-contraction with the deep abdominal muscles and lumbar multifidus.  This training resulted in marked reduction in pain and disability.

 

The Multifidus as an Avocado

Previous studies of the Australian group had already demonstrated that in LBP the multifidus usually diminishes in size on the ipsilateral side.  Regular back strengthening exercises do not result in getting the multifidus to regain its original size, yet specific lumbar stability exercises (as developed by the Australian school) evidently do so.

 

My favorite presenter, both in intellectual content as well as the elegance of delivery, was Diane Lee from Canada.  In describing how she teaches her students diagnostic palpation of the multifidus she used some helpful imagery:  If this muscle is healthy, it feels "like ripe avocado for salad.  If it feels like avocado for guacamole, it is too mushy".  She also recounted that Echo Doppler studies have shown a wide variation in SI mobility among people.  It seems that if a SI joint has only little form closure (e.g., because of the individual design of the joint), more force closure is needed for stabilization.  The amount of SI motion does not correlate with LBP or pelvic pain, yet there is a higher incidence of asymmetrical SI motion in symptomatic patients.  She therefore uses both the standing leg raise (or Gillet) test and the common forward-bending test to look for asymmetries.  However, "a positive Gillet test doesn't mean anything, besides that this patient cannot maintain pelvic stability"; or, it signifies what she also called "failed load transfer in one-legged standing".  Same for the forward bending test:  if the sacrum does not move symmetrically in forward flexion (or backward bending) of the trunk, it could be the SI joint, the hamstrings, pelvic ligaments or many other things.  It only means that the force closure is asymmetrical and most likely that the orchestration of that action is not optimal.  Pointing to the second and third component of her and Vleeming's illustration of "An Integrated Model of Joint Function" (see Fig. 2), she explained her proposed shift from a static towards a dynamic analysis and training concept:  "Force closure is like learning to conduct an orchestra."

 

PPPP has been shown to correlate with weakness in hip adductors and abductors, and such abductor weakness has also been shown to result in a "waddling gait".  Lee therefore looks for a minimum sideways deviation of the center of gravity in walking.  She also uses the ASLR to look for (and sometimes teach) proper orchestration of hip flexion.  In LBP she often sees what she calls "the tail wagging the dog":  an anterior pelvic tilt initiating the leg raise.  With proper orchestration of what she calls the core, patients can learn to stabilize their lumbar spine in a more neutral position during this as well as other movements.  Based on Eric Franklin's ideokinesis books, and also on some good inventions of her own, she uses imagery to guide the training of such proper core activation.

 

Painful Australian Experiments

Paul Hodges from the Australian group presented some drastic experiments to study the chicken-or-egg question of what comes first in the relationship between pain, fear, and altered motor control.  "EMG activity of the trunk muscles associated with arm movement was recorded during low back pain induced by injection of hypertonic saline into the longissimus muscle.  While changes were observed in the timing and amplitude of muscle in all trunk muscles, changes in the TrA were most consistent and were similar to those changes in clinical LBP".  In a second test, inducing not pain but fear, he got the same delay in TrA activity - not, however, by inducing attention or stress.  This shows that both LBP and an emotional state of fear cause "motor control deficits of the trunk muscles, in particular TrA, and supports motor control training in LBP rehabilitation".  According to Hodges, the fear response is mediated mostly by three elements: "catastrophizing, somatic hypervigilance, and the threat value of pain."

 

New Training Directions

Vert Mooney from San Diego had studied and worked with a group of scoliotic patients.  He found that all of them had asymmetric strength in trunk rotation.  His training with a newly developed MedX trunk rotation machine led to improvements in the degree of scoliosis, which he documented with "PosturePro" software for measurements.  Regarding similar spine extension exercise machines, Simo Taimela added that when training in such machines the multifidus is most involved in low(!) loads.

 

Stuart McGill, a kinesiology professor from Canada who apparently loves weight training, shared a video of a weight lifter, who - as it happened -  injured his back at the time of videotaping during repeated weight lifting in the laboratory studio.  Measurements showed that the spine buckled at L2/3 with an instability catch or "clunk" as this region had not been securely stabilized by the TrA and other core muscles.  McGill also pointed out that, in spine flexion, the longissimus doesn't have an efficient angle to work.  Whereas in folding forward with a neutral spine, the longissimus fibers act in good oblique directions and can better function as shear stabilizers.  He suggested that good exercises are therefore not about strength, but about symmetric endurance to ensure symmetric stiffness and a "grooving of stiffening motor patterns".  As an admirer of Vladimir Janda's writings, I was impressed by McGill telling us that at least one of Janda's assumption has been proven to be wrong.  When leaning backwards while seated on the floor, as in Fig. 4, Janda had suggested that hamstring activation (in the form of a pulling action of the feet on the floor) would inhibit iliopsoas activity.  Yet recent measurements have shown just the opposite.

Fig. 4. A hamstring-mediated pulling movement of the feet along the floor in this seated trunk stability exercise does not inhibit iliopsoas activity (as Janda had suggested). It actually tends to increase iliopsoas involvement.

 

Hollowing or bracing? Such have been - and still are - the questions about the best training methods for the core in order to treat or avoid LBP.  McGill sees value in both approaches.  Hollowing of the lower belly (as advocated by the Australian group) seems to be best for a controlled motor retraining, and yet it also reduces the base and takes the internal and external abdominal obliques out, which are critically important for stability.  Therefore, bracing exercises seem to be better for stability (and might have prevented the injury to the poor weight lifter in that video).  Regarding the now-popular training on labile surfaces, McGill pointed out that this involves more (though sometimes too much) muscle activation.

 

Value of Proprioception

Andrea Radebold from Yale shared a study showing that LBP patients have more postural sway when sitting on a wobble board, have a diminished lumbar spine position sense, and maybe therefore have a longer reaction time by trunk muscles to an increase in load.  Among many other things, her patients had to sit blindfolded on a horizontally sliding platform (see Fig. 5).  Compared with normal subjects, LBP patients could detect only large sliding movements of their pelvis, not the small ones.

Fig. 5: Low back pain patients have a diminished lumbar spine position sense.  When their pelves are moved relative to their thoraces, these patients notice only much larger movements than healthy subjects.

 

This confirmed a finding already presented at the previous congress by Christine Hamilton, namely that LBP patients usually cannot fold forward in sitting more than 15 degrees with a neutral spine.  Several presenters spoke at the Montreal congress of the "decreased sensory acuity" or proprioception in LBP patients.  Diane Lee added that "sustained emotional states diminish body awareness."  It was therefore suggested that proprioception training should be an essential part of rehabilitation.

 

Fig. 6 was used to show one of the new physical therapy concepts:  combining proprioception and coordination training with classical endurance and strength exercises.  Other presenters added flexibility to that list, but did not have studies to back that up.  Nevertheless, there was apparent agreement that stability training without strength training is not sufficient in cases of chronic LBP.

Fig. 6: One of the current physical therapy concepts.  Stability training forms a basis, but, at least for chronic LBP patients, additional strength and endurance training is needed to avoid reinjury in the future.

 

Lieven Danneels from Belgium compared three rehabilitation programs for the lumbar multifidus.  Results were measured as the cross sectional area (CSA) of the multifidus.  Group 1 did a stability training only; Group 2 did a stability training plus dynamic resistance training; and Group 3 did a stability training plus dynamic-static resistance training.  Interestingly, only Group 3 showed significant increase in CSA.  This result emphasizes the static holding component (between the concentric and eccentric phase) for rebuilding the muscle.  However, all three groups had the same significant reduction in pain and functional disability during the training period.  But a one-year follow-up study showed that disability had increased in Group 1, not in Groups 2 and 3.  For long-term disability her advice therefore is "a combination of stabilization exercises and intensive lumbar resistance training, independently of the dynamic or dynamic-static modality."

 

Posture; Pain and Rolfing

It was stated that the relationship between posture and LBP is still unclear.  Yet a study was presented by O'Sullivan which showed that internal abdominal oblique, multifidus and thoracic erectors spinae show a significant decrease in activity in "postures of defeat" such as sway standing and slump sitting.  He hypothesized - he has as yet no proof - "that individuals who habitually adopt passive postures for long periods, may de-activate and potentially de-condition the stabilizing muscles of the lumbo-pelvic region."  In other words, and which resonates very well with our Rolfing assumptions:  if a client gets to improve their everyday average posture - e.g., through our manipulation and movement education - this may lead to a lesser likelihood of LBP.  If this hypothesis can be scientifically validated (who knows, maybe someone will present such a study as soon as the next LBP congress!), it should be a big moment for the history of our work and its relationship with the established scientific world.

 

Bits and Pieces

Here are some other pieces and information from my notebook of the congress:

·           A group around Spanish researcher Kovacs announced the establishment of a website that routinely evaluates scientific studies in LBP research and comments on their strength and weaknesses: 

·           The journal Spine was quoted the most often, and appeared to be the place where most of the substantial studies around LBP are being published.  Checking their website and screening for abstracts which are NOT related to surgical procedures has become a good source of input for me since the last LBP congress.

·           Vert Mooney mentioned that in trunk rotation (against resistance) there is a coactivation of latissimus and gluteus maximus.  Yet the gluteus maximus is used only for SI joint stability.

·           Carl de Rosa from Arizona showed impressive slides on new myofascial details. He mentioned, e.g., that the internal abdominal oblique is usually thicker than the external oblique or the transversus abdominis.  This might be related to the fact that the internal oblique is involved in bringing the pelvis forward (such as in what I call a "banana posture").

·           According to Carolyn Richardson the pelvic floor won't work in lumbar flexion.

·           Paul Hodges showed that intra-abdominal pressure is by itself not a powerful spine extensor, yet it can add to stabilization.

·           Some of the punch lines from the congress regarding best treatment approaches:  "Don't take back pain lying down"; "Treatments should toughen the mind as well as the body."; or, even better, "Be aware, don't seek care."

·           Serge Gracovetsky was selling a nice computer CD with power point presentations (including two motion videos) of his presentation plus that of Jim Porterfield (on the Asymmetric Overload Syndrome), and of Carl de Rosa (with anatomy slides) for $50. His e-mail is:  gracovetsky@videotron.ca

·           Even better, many abstracts or papers from this congress are currently posted on Don Tigny's website

 

Robert Schleip’s report of the previous congress in Vienna 1998

 

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