The Fall of The Postural-Structural-Biomechanical Model in Manual and Physical Therapy

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Is a postural-structural-biomechanical model, within manual therapies, viable 131

manual treatment, towards cognitive and re-educational to question, what we need to know, and how we need to
strategies - which is a less extreme position to that taken by practice.
Lederman.
In order to unpick these arguments, JBMT has invited
five leading experts from the world of manual medicine to References
respond to Dr Lederman’s thesis. These clinicians (from the
world of osteopathy, chiropractic and physiotherapy) as Chaitow, L., 2010. Fascia Directed Therapies for the Treatment of
well as researchers into biomechanical dysfunction and Low Back Pain: Review and New Directions. Presentation: 7th
therapeutic methods, offer their perspectives,in alpha- Interdisciplinary World Congress on Low Back and Pelvic Pain.
betical order, following Dr Lederman’s paper. Los Angeles. November 11 2010.
Irvin, R.E., 2007. Why and how to optimize posture, chapter 16. In:
It is important to observe that by no means all of these
Vleeming, et al. (Eds.), Movement, Stability and Lumbopelvic
expert responses are wholly critical of Dr. Lederman’s
Pain, second ed. Elsevier, Edinburgh.
arguments, and ultimately it is for you, the reader, to Lederman, E., March 2010. The fall of the postural-structural-biome-
decide which aspects of the debate are most persuasive, chanical model in manual and physical therapies: exemplified by
and where the relative clinical truth lies. lower back pain. CPDO Online J. http://cpdo.net/jour/jour1.html.
It is hoped that this examination of controversial ideas O’Sullivan, P., 2010. Diagnosis and Classification of Chronic Low
will lead to a better understanding of what we hold to be Back Disorders. Proceedings Book 7th Interdisciplinary World
true, based on current evidence, as well as what we need Congress on Low Back and Pelvic Pain, pp. 160e177.

The fall of the postural-structural-biomechanical


model in manual and physical therapies:
Exemplified by lower back pain
Eyal Lederman, PhD DO

CPDO Ltd, 15 Harberton Road, London N19 3JS, UK

Summary Manual and physical therapists often use a postural-structural-biomechanical


(PSB) model to ascertain the causes of various musculoskeletal conditions. It is believed that
postural deviations, body asymmetries and pathomechanics are the predisposing/maintaining
factors for many musculoskeletal conditions. The PSB model also plays an important role in
clinical assessment and management, including the choice of manual techniques and the exer-
cise prescribed. However, the most important question is consistently being ignored e can
a person’s physical shape/posture/structure/biomechanics be the cause of their lower back
pain?
.

Is development of LBP associated with PSB Prospective studies are particularly useful to examine
factors? the causal relationship between PSB factors and LBP. In
these studies groups of asymptomatic individuals are
assessed for PSB factors initially and tracked over several
In the last two decades the PSB model has been eroded by
years noting the episodes of LBP. Other less ideal studies
clinical studies examining the relationship between PSB
compare subjects with LBP to an asymptomatic group.
factors and lower back pain. The balance of evidence
However these studies can only be used to inform us about
suggests that there is no association between LBP and PSB
the changes that are due to the condition but they cannot
factors (see summary, Figure 1).
indicate its cause, i.e. the consequence of LBP is not
necessarily its cause. This distinction is important clinically.
Often the PSB assessment is made when the patient is
already in pain, once the individual/body has reorganized
E-mail address: [email protected]. to cope with the condition.
132 E. Lederman

Figure 1 PSB actors not associated with LBP.

Spinal curves, asymmetry and motion failed to show an association with the future development of
LBP (Hellsing, 1988b; Burton and Tillotson, 1989; Hamberg-van
There was the lack of association between postural spinal Reenen HH 2007, syst review; Mitchell et al., 2008).
asymmetry, thoracic kyphosis and lumbar lordosis in teenagers
and developing LBP in adulthood (Papaioannou et al., 1982; Segmental pathomechanics
Dieck, 1985; Poussa, 2005). Even obvious increases in lordosis
and sagittal pelvic tilt during pregnancy lack an association One important area to examine is whether the profound
with back pain (Franklin and Conner-Kerr, 1998). Stronger biomechanical changes brought about by segmental
predictors of the development of back pain during pregnancy biomechanics can give rise to lower back symptoms.
were body mass index, history of hypermobility and amenor- A systematic review from 1997 suggests an association
rhea, low socioeconomic class, previous LBP, posterior fundal between disc degeneration and non-specific low back pain
location of placenta and fetal weight to LBP with radiation to (van Tulder et al., 1997). However, it might not be the
leg (Orvieto et al., 1990; Mogren and Pohjanen, 2005). cause of it -there is strong evidence that X-ray and MRI
In adults, the extent of lumbar lordosis as well as the pres- findings have no predictive value for future LBP or disability
ence of scoliosis failed to show an association with back pain (Waddell and Burton, 2001, review). Several studies since
(Dieck, 1985; Haefeli et al., 2006; Norton, 2004; Christensen have failed to show a clear relationship between spinal/
and Hartvigsen, 2008, syst. rev.) Also differences in regional disc degeneration and LBP (Savage et al., 1997; Borenstein
lumbar spine angles or range of motion between the segments et al., 2001; Jarvik et al., 2005; Carragee et al., 2005;
Is a postural-structural-biomechanical model, within manual therapies, viable 133

Kanayama et al., 2009; Kalichman et al., 2010). In a pop- a mean of 5.2 mm. The evidence suggests that for most
ulation-based study of 34,902 Danish twins 20e71 years of people anatomic leg length inequality is not clinically
age there were no meaningful differences in the frequency significant (Papaioannou et al., 1982; Grundy and
in LBP between younger and older individuals (Leboeuf-Yde Roberts, 1984; Dieck, 1985; Fann, 2002; Knutson, 2005,
et al., 2009), although greater degenerative changes are review), until the magnitude reaches approximately 20 mm
expected in older individuals. (Gurney, 2002 review; Knutson, 2005, review). Although
In studies that show some relationship between disc some earlier studies comparing people experiencing back
degeneration and LBP it has been suggested that the genes pain with asymptomatic controls suggest a correlation
that play a part in the heritability of back pain also play (Giles and Taylor, 1981; Friberg, 1983 and 1992), more
a part in disc degeneration, i.e. pain may not be due to the relevant are prospective studies in which no correlation
mechanical changes in the spine but to shared biological was found between leg length inequality and LBP (Hellsing,
factors (Battie et al., 2007). These hereditary factors are 1988a; Soukka et al., 1991; Nadler, 1998).
not associated with the shape of the back but linked to Patients who have acquired their leg length differences
variations in the collagen and immune-repair system/ later in life as consequence of disease or surgery may also
processes between individuals (Paassilta et al., 2001; help to shed light on the relationship between patho-
Valdes et al., 2005; Battié et al., 2009; Videman, 2009). It mechanics and LBP. Individuals who developed a shorter leg
was demonstrated in twins that as much as 47%e66% of due to Perthe’s disease had a poor correlation between leg
spinal degeneration is due to hereditary and shared envi- length inequality, lumbar scoliosis and low-back disorders,
ronmental factors, whereas only 2%e10% of the degenera- assessed several decades after the onset of the condition
tion can be explained by physical stresses imposed by (Yrjönen et al., 1992). In studies of patients who had
strenuous occupations or sporting activities (Battié, 1995; marked changes in leg length due to hip fractures or
Battié et al., 2009; Videman et al., 2006 and 2007). replacement, such changes were not associated with back
No association has been found between congenital pain assessed several years after surgery (Gibson et al.,
abnormalities in the lumbar spine and pain in that area 1983; Edeen et al., 1995; Parvizi et al., 2003).
(spina bifida, transitional lumbar vertebra, spondylolysis One of the arguments in favor of an association between
and spondylolisthesis: van Tulder et al., 1997, syst. review, leg length differences and LBP is the supposed success of
Luoma et al., 2004; Brooks et al., 2009). Although spina heel lifts in reducing back pain (Giles and Taylor, 1981;
bifida and transitional vertebra may not be the cause of Gofton, 1985; Helliwell, 1985; Friberg, 1983 and 1992;
LBP, they may determine the pain levels (Taskaynatan et Brady et al., 2003 review). However, all these studies
al., 2005, weaker study). failed to include controls or sham heel lift (such as ineffi-
Another popular and enduring biomechanical concept is cient soft foam lift).
the spinal “neutral zone”. It claims to be related to stability Prospective studies of inflexibility of the lower extrem-
and LBP (Panjabi, 1992a and b; Panjabi, 2003; Suni et al., ities and hamstrings and psoas tightness also fail to predict
2006). This mechanical concept is derived from mathemat- future episodes of LBP (Hellsing, 1988c; Nadler, 1998).
ical models and cadaver experiments on which an extensive As for foot biomechanics there is strong evidence that
amount of spinal joint damage had to be inflicted before the orthotic corrections have no effect on preventing back pain
findings could fit the model (Gracovetsky, 2005). Since its (Sahar et al., 2007, syst. review).
inception three decades ago, no study exists to show Surprisingly even whole body changes such as over-
a correlation between mechanical changes in the neutral weight/obesity have a low association with LBP (Leboeuf-
zone changes and LBP (Leone et al., 2007, review). Yde, 2000 syst. review). Contrary to common beliefs,
The disparity between pathomechanics and symptom- a recent study has shown that cumulative or repetitive
atology can be observed in other segmental conditions. For loading due to higher body mass (nearly 30 pounds on
example, in an MRI study of patients with nerve root pain it average) was not harmful to the discs. The study found
was found that the degree of disc displacement, nerve root a slight delay in disc desiccation (L1-L4) in the heavier men
enhancement or nerve compression did not correlate with when compared with their lighter twin brothers (Videman
the magnitude of the patients’ subjective pain or level of et al., 2009).
functional disability (Karppinen et al., 2001; see also
Beattie et al., 2000). However there is a strong association Neuromuscular factors
between severe nerve compression, disc extrusion and
distal leg pain (Beattie et al., 2000). Although not fully within the scope of this article, motor
control of the trunk is relevant in relation to muscle func-
Non-spinal structures tion and posture. Certain neuromuscular components also
failed to show a clear association with LBP.
Studies have also failed to identify an association between Although earlier studies demonstrated an association
other structures beyond the spine and back pain. For between muscle endurance and LBP (Biering-Sørensen,
example, there is no correlation between pelvic obliquity/ 1984; Alaranta et al., 1995), a recent systematic review
asymmetry and the lateral sacral base angle and lower back found strong evidence that low trunk muscle endurance is
pain (Dieck, 1985; Levangie, 1999a and b; Fann, 2002; not associated with LBP (Hamberg-van Reenen, 2007 syst.
Knutson, 2002). rev). This review found inconclusive evidence for an asso-
Leg length differences as a cause for back pain has been ciation between low trunk muscle strength and LBP. Also
debated for the last three decades. It is estimated that there is no association between erector spinae pairs
about 90% of the population has a leg length inequality with imbalances during extension and LBP (Reeves et al., 2006;
134 E. Lederman

Hamberg-van Reenen, 2007 syst. rev; Van Nieuwenhuyse et works in perfect harmony within itself and other body
al., 2009). Furthermore, no study to date has shown that systems. However, the research suggests that biological
back pain is due to timing differences in specific muscle systems contain reserve capacity to accommodate for loss
such as transversus abdominis (see discussion Lederman, and imperfections without failure or symptoms. Further-
2010b). These control changes have been observed only in more, within a biological dimension, structures such as the
individuals who already have back pain. They probably spine are capable of self-repair and are able to adapt and
represent the outcome rather than the cause of back pain change according to needs and demands. Hence, the spine
(see discussion Lederman, 2010a). can undergo profound physical changes that are well
Two studies using the same methodology appear to tolerated without the development of a symptomatic
demonstrate that in athletes a delayed reflex muscle condition.
response at the trunk could increase the risk of lower back Perhaps there is a critical level where PSB factors will
as well as knee injury (Cholewicki et al., 2005; Zazulak et exceed the reserve of the system. Clinically, this still
al., 2007). Unfortunately, the obvious was not examined remains unquantified (and probably unquantifiable). If we
in these studies e the reflex response to a sudden pertur- were to overlook this obstacle, the next hurdle to overcome
bation of the trunk should have been examined in other is the reliability of assessing PSB factors. It is now well
body areas (e.g. a control recording from the leg). This established that many of the examinations that assess PSB
would have helped establish whether the injuries are due to factors are either low on validity or reliability (McCaw and
delayed muscle onset-timing, specific to the trunk or, the Bates, 1991; Mannello, 1992; Panzer, 1992; Levangie,
alternative more plausible explanation that athletes with 1999a; Hestbaek and Leboeuf-Yde, 2000; Seffinger et al.,
sluggish muscle reaction times/reflexes may be more 2004; Dunk et al., 2004; van Trijffel et al., 2005;
susceptible to injury. Hollerwöger, 2006; May et al., 2006; Paulet and Fryer,
2009). A third clinical hurdle to overcome is whether
Postural behavior factors manual techniques or specific exercise are effective in
modifying inherent PSB factors. Can foot mechanics, leg
length differences, pelvic tilts, vertebral positions and
An area that is often assessed in manual and physical
spinal curves be permanently changed, solely, by these
therapy is how “correctly” a person is using their body e
clinical tools?
their “postural behavior”. It is believed that prolonged
There are no known studies that examine the influence
postural stresses at work or sporting activities could be
of manual techniques on PSB factors in the medium- or
the cause of LBP. The results of recent systematic reviews
long-term, in particular at the cessation of the treatment.
challenge these widely held beliefs. These studies
However we know from the allied sciences that a herculean
demonstrate lack of association between work-related
effort would be required to modify many of the inherent
posture and LBP. They include postures such as prolonged
PSB factors (Maruyama et al., 2008; Maruyama, 2008;
standing, bending, twisting, awkward postures (kneeling
Lonstein, 1999; Marks and Qaimkhani, 2009; Willy et al.,
or squatting) sitting posture at work and prolonged sitting
2001; Harvey et al., 2002; Williams et al., 1986; Goldspink
at work and leisure time (Hartvigsen et al., 2000 syst.
et al., 1992; Arnoczky et al., 2002; Bosch et al., 2002;
review; Chen et al., 2009 syst. review; Bakker et al., 2009
Magnusson et al., 1995; Magnusson, 1998; Light et al.,
syst. review; Roffey et al., 2010 syst. review; Wai et al.,
1984; Roberts and Wilson, 1999. see full discussion of this
2010, syst. review). Also physical leisure time activities
topic and references in, Lederman, 2010a). As such, the
such as sport or exercises, sitting, and prolonged
therapeutic investment in correcting PSB factors is irra-
standing/walking were found not to be associated with
tional, in particular, as it is unlikely to influence the course
LBP (Bakker et al., 2009 syst. review). Heavy manual
of the patient’s LB condition.
lifting is strongly associated with LBP, however the effect
size is considered to be modest (Waddell and Burton, 2001
review). Implications for practice
Prediction of back pain by PSB assessment The lack of association between PSB factors and back pain
has far-reaching implications for the way we conceptualize
In a recent prospective study on young workers (n Z 692) musculoskeletal conditions, the clinical examination and
examined by physical therapists, PSB factors failed to show the goals/objectives of the techniques and the exercise
a correlation with future development of LBP (Van prescribed.
Nieuwenhuyse et al., 2009). A number of factors were From the evidence so far many of the clinical examina-
evaluated including iliac crest height inequality, scoliosis, tions assessing PSB factors have no obvious value in
lumbar flexion, extension and lateral flexion, length of explaining why the patient has developed their back
hamstring muscles and strength testing in the motor condition. It implies that the PSB model and the related
distribution of L4/L5/S1. clinical examinations are mostly redundant.
The lack of association between PSB factors and LBP has
Biological not mechanical also important implications for what we aim to achieve and
There seems to be a disparity between pathomechanics and for our choice of techniques and exercise used to manage
the experience of a low back condition. In this biome- the condition. We can no longer justify the use of manual
chanical model the musculoskeletal system is seen as techniques to readjust, correct or balance-out the mis-
a precision engine where every system, organ and cell aligned structure. There is an urgent need to redefine what
Is a postural-structural-biomechanical model, within manual therapies, viable 135

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Invited response
Gary Fryer, PhD, BSc(Osteopathy), ND a,b,c

a
School of Biomedical and Health Sciences, Victoria University, Melbourne, Australia
b
Institute of Sport, Exercise and Active Living, Victoria University, Melbourne, Australia
c
A.T. Still Research Institute, Kirksville, MO, USA

The philosophical foundations of many manual therapy states that the most important question is consistently
disciplines, including osteopathy, have been deeply being ignored: ‘can a person’s physical shape/posture/
rooted in the postural structural model (PSM) paradigm, structure/biomechanics be the cause of their lower
which emphasizes the role of altered posture, anatomical back pain?’ The cause of back pain is multi-factorial and
structure, and biomechanics as a cause of pain and may involve genetic, biopsychosocial, and environmental
disturbed function. This paradigm has been reinforced by factors. The key questions, therefore, are not whether
catch cries such as ‘structure governs function’ and by physical shape or posture can cause lower back pain, but
enduring concepts of misaligned or malpositioned joints. whether these factors influence or contribute to back
Lederman has highlighted the lack of scientific support for pain and, if so, whether practitioners can identify and
abnormal posture as a cause of low back pain and provided treat these factors to influence the health of patients.
a well-reasoned argument that research has eroded many The studies reviewed by Lederman typically examine
aspects and practices associated with PSM. While I the influence of a single PSM factor (e.g., pelvic asymme-
applaud Lederman’s critical approach to this model and try), without accounting for other PSM factors or
agree that postural and biomechanical factors have been other multidimensional aspects of pain. Comparison of
overemphasized in the past, I believe it would be posture between individuals may not be meaningful
a mistake to conclude that posture and biomechanical because posture is highly variable and idiosyncratic, but
factors have no relevance in the assessment of patients exaggeration of an individual’s postural pattern may be
with pain. more clinically relevant, as may treatment aimed at
The causes of spinal pain are unclear, but pain is multi- minimizing deviations. For example, examination of head
factorial, and an overemphasis of any one aspect, such as carriage in a group of office workers may not reveal those
mechanical factors, is inappropriate. Lederman correctly individuals with pain, but exaggeration of head forward
draws attention to the literature that shows most diag- posture in a worker with recurrent pain will likely aggra-
nostic findings associated with PSM cannot be used to vate the pain, whereas attention to better posture
differentiate individuals with pain from those without pain alleviates it.
or to predict whether individuals are more likely to have Although direct evidence for the association of posture
pain. This literature does not, however, demonstrate that with low back pain is lacking, there is a strong theoretical
postural factors have no influence on pain. Lederman rationale of why posture may influence pain. Mechanical
loading on ligaments, either sustained or cyclic, causes
viscoelastic change, hysteresis, strain, inflammation, and
abnormal motor activity (Solomonow, 2006). Thus,
E-mail address: [email protected].