CPDO Online Journal (2010), March, p1-14. www.cpdo.net

The fall of the postural–structural–biomechanical model inmanual and physical therapies: Exemplified by lower backpain
Eyal Lederman*
CPDO Ltd., 15 Harberton Road, London N19 3JS, UK
KEYWORDS
Biomechanics, lower back pain,
pathomechanics, posture, spine,
structural asymmetries.

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 andpathomechanics are the predisposing/maintaining factors for many musculoskeletal conditions. The PSB model also plays an important role in clinicalassessment and management, including the choice of manual techniques andthe exercise prescribed. However, this model has been eroded by research in
the last two decades introducing profound challenges to the practice of manualand physical therapy. This article will examine how the sciences are challenging the PSB model, using lower back pain (LBP) as an example.

Introduction
There is a basic belief among manual and physicaltherapists that structural imbalances and asymmetry
in the body can result in painful musculoskeletal conditions. In this model, the imbalances and asymmetries increase the abnormal mechanical/physicalstresses imposed on the musculoskeletal system. This
may lead to recurrent injury or the development ofchronic conditions through a gradual process of wear
-and-tear. This conceptual model manifests clinicallyin the form of postural, structural and biomechanical(PSB) assessments, manual treatments and exercisethat aim to correct these structural factors. The PSB
model is frequently used in clinic to manage patients
suffering from low back pain (LBP).
The PSB evaluation/assessment often includes astatic postural examination, observing the shape ofthe back, whether there are any increases in spinal
curves such as scoliosis, kyphosis or lordosis. The
assessment may also include measuring pelvic angles
in the coronal plane, pelvic nutation/counternutation
angles, the relative position of the sacrum to the ilia
and leg length differences. It is believed that such
misalignments impose excessive stress on the spine
leading to degeneration/damage or dysfunction and*Correspondence author e-mail: cpd@cpdo.net

eventually to painful back conditions. These static
observations are often followed by a dynamic assessment during standing in which the spine is examinedin all planes of motion. Observed regional and segmental movement losses/stiffness is often used todetermine the severity of the spinal condition and isalso used to explain the cause of the condition. The
PSB examination may sometimes include an assessment of the feet. The rationale here is that any problems in the physical foundations upon which the
body rests will have repercussions on structures further up the mechanical chain, such as the knees or the
lower back.
A palpatory examination is often incorporated
into the PSB assessment during standing or lying on
the treatment table. Information is gathered aboutabnormal tissue textures, unusual muscle stiffness orabnormal relationships between body masses, muscle
bulks or position of vertebral landmarks. Althoughthese findings are often used to estimate the locationof damage or tissue-causing symptoms they are also
used to indentify predisposing local segmental PSB
factors.
The structural model also includes beliefs about
imbalances and misalignments in specific body subsystems or tissues as the causes of spinal and otherpain conditions. These include adverse neural ten-

Fall of PSB model in manual and physical therapies
sion, specific muscles such as multifidus or shortened
hamstrings, muscle chains, kinematic chains and thefascia system.
Every few years this model shifts in focus to otherbody systems. In the last decade, this biomechanicalmodel has infiltrated the neuromuscular dimension.
Mechanical and computer code ideals are applied to
motor control to explain musculoskeletal conditions.
These include looking at minute timing changes between muscle groups, an emphasis on singling out
particular muscles for rehabilitation or the identification of “weak muscle” or muscle imbalances. Corestability and spinal stabilization approaches are examples of this neuro-mechanistic model.
This PSB belief system also permeates other formsof manual therapy. In visceral osteopathy it manifests
as a focus on the movement of the organs and theiranatomical–mechanical relationship. In cranial approaches it appears as a focus on the position andmovement of cranial structures including the articulations between cranial bones and tension in dural
membranes. In many manual therapy disciplines
there is a belief that spinal misalignments(subluxations) can cause visceral conditions as wellas other health issues beyond the spine (Mirtz et al.,2009). In these disciplines, PSB factors are used tomake links between skeletal and non-skeletal body
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systems to explain the predisposing and maintaining
factors for the condition.
The outcome of these PSB examinations is an appreciation of the individual’s PSB status. This information is then used to explain why the patient is suffering from back pain. It also forms the rationale forthe treatment which may aim to mechanically/physically correct/change the observed misalignments or improve range. This is achieved through theuse of various manual therapy procedures (e.g., manipulation, muscle energy techniques, stretching andarticulation/mobilization) or specific exercises (e.g.,
McKenzie back exercise, core stability, Yoga, Pilates).
The basic premise is that an existing condition will
improve and future recurrences or chronicity can beprevented by correcting these PSB predisposing/maintaining factors.
However, the most important question is consistently being ignored—can a person’s physical shape/
posture/structure/biomechanics be the cause of theirlower back pain?

Is development of LBP associated with PSB factors?
In the last two decades the PSB model has beeneroded by clinical studies examining the relationshipbetween PSB factors and lower back pain (Fig. 1).

Trunk asymmetry, thoracic kyphosis and lumbar lordosis
in teenagers and developing LBP in adulthood.
Low muscle strength, low muscle endurance, or reduced
spinal mobility and erector spinea pairs imbalances during extension.
Variations in lumbar lordosis and thoracic kyphosis. Increased lumbar lordosis and sagittal pelvic tilt on backpain during pregnancy. Differences in regional lumbar
spine angles or range of motion.
Disc degeneration, spina bifida, transitional lumbar vertebra, spondylolysis and spondylolisthesis.
Pelvic obliquity and the lateral sacral base angle pelvic
asymmetry.
Hamstrings and psoas tightness.
Inflexibility of the lower extremities or leg length discrepancy.
Correcting foot mechanics have no effect on preventing
back pain.

Figure 1 — Many postural–structural–biomechanical (PSB) factors havefailed to show an association or to be the cause of lower back pain.

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Eyal Lederman
Prospective studies are particularly useful to examine the causal relationship between PSB factors
and LBP. In these studies groups of asymptomatic
individuals are assessed for PSB factors initially andtracked over several years noting the episodes of
LBP. Other less ideal studies compare subjects with
LBP to an asymptomatic group. However these studies can only be used to inform us about the changes
that are due to the condition but they cannot indicate
its cause, that is, the consequence of LBP is not necessarily its cause. This distinction is important clinically. Often the PSB assessment is made when thepatient is already in pain, once the individual/bodyhas reorganised to cope with the condition.
Spinal curves, asymmetry and motion

There was the lack of association between posturalspinal asymmetry, thoracic kyphosis and lumbar
lordosis in teenagers and developing LBP in adulthood (Papaioannou et al., 1982; Dieck, 1985; Poussa,
2005). Even obvious increases in lordosis and sagittal
pelvic tilt during pregnancy lack an association withback pain (Franklin & Conner-Kerr, 1998). Stronger
predictors of the development of back pain during
pregnancy were body mass index, history of hypermobility and amenorrhea, low socioeconomic class,previous LBP, posterior fundal location of placenta
and fetal weight to LBP with radiation to leg (Orvieto
et al., 1990; Mogren & Pohjanen, 2005).
In adults, the extent of lumbar lordosis as well as
the presence of scoliosis failed to show an association
with back pain (Dieck, 1985; Norton, 2004; Haefeli etal., 2006; Christensen & Hartvigsen, 2008, syst. rev.).
Also differences in regional lumbar spine angles orrange of motion between the segments failed to show
an association with the future development of LBP(Hellsing, 1988b; Burton & Tillotson, 1989; Hambergvan Reenen, 2007, syst. rev.; Mitchell et al., 2008).
Segmental pathomechanics

One important area to examine is whether the profound biomechanical changes brought about by segmental pathologies can give rise to lower back symptoms.
A systematic review from 1997 suggests an association between disc degeneration and nonspecific
low back pain (van Tulder et al., 1997, syst. rev.).
However, it might not be the cause of it—there isstrong evidence that X-ray and MRI findings have nopredictive value for future LBP or disability (Waddell& Burton, 2001, review). Several studies since havefailed to show a clear relationship between spinal/

disc degeneration and LBP (Savage et al., 1997;
Borenstein et al., 2001; Carragee et al., 2005; Jarvik etal., 2005; Kanayama et al., 2009; Kalichman et al.,2010). In a population-based study of 34,902 Danish
twins 20-71 years of age, there were no meaningful
differences in the frequency in LBP between younger
and older individuals (Leboeuf-Yde et al., 2009), although greater degenerative changes are expected inolder individuals.
In studies that show some relationship between
disc degeneration and LBP it has been suggested thatthe genes that play a part in the heritability of backpain also play a part in disc degeneration, that is,pain may not be due to the mechanical changes in thespine but to shared biological factors (Battie et al.,2007). These hereditary factors are not associatedwith the shape of the back but linked to variations in
the collagen and immune-repair system/processes
between individuals (Paassilta et al., 2001; Valdes etal., 2005; Battié et al., 2009; Videman, 2009a). It wasdemonstrated in twins that as much as 47%–66% ofspinal degeneration is due to hereditary and sharedenvironmental factors, whereas only 2%–10% of thedegeneration can be explained by physical stresses
imposed by strenuous occupations or sporting activities (Battié, 1995; Battié et al., 2009; Videman et al.,2006, 2007).
No association has been found between congenitalabnormalities in the lumbar spine and pain in thatarea (spina bifida, transitional lumbar vertebra,
spondylolysis and spondylolisthesis; van Tulder etal., 1997, syst. rev.; Luoma et al., 2004; Brooks et al.,2009). Although spina bifida and transitional vertebra
may not be the cause of LBP, they may determine thepain levels (Taskaynatan et al., 2005, weaker study).
Another popular and enduring biomechanicalconcept is the spinal “neutral zone”. It claims to berelated to stability and LBP (Panjabi, 1992a,b, 2003;
Suni et al., 2006). This mechanical concept is derived
from mathematical models and cadaver experiments
on which an extensive amount of spinal joint damage
had to be inflicted before the findings could fit themodel (Gracovetsky, 2005). Since its inception three
decades ago, no study exists to show a correlation
between mechanical changes in the neutral zonechanges and LBP (Leone et al., 2007, review).
The disparity between pathomechanics and symptomatology can be observed in other segmental conditions. For example, in a MRI study of patients withnerve root pain it was found that the degree of discdisplacement, nerve root enhancement or nerve compression did not correlate with the magnitude of thepatients’ subjective pain or level of functional disabil-

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Fall of PSB model in manual and physical therapies
ity (Karppinen et al., 2001; see also Beattie et al.,2000). However there is a strong association between
severe nerve compression, disc extrusion and distal
leg pain (Beattie et al., 2000).
Non-spinal structures

Studies have also failed to identify an association
between other structures beyond the spine and backpain. For example, there is no correlation between
pelvic obliquity/asymmetry and the lateral sacralbase angle and lower back pain (Dieck, 1985; Levangie, 1999a,b; Fann, 2002; Knutson, 2002).
Leg length differences as a cause for back pain has
been debated for the last three decades. It is estimated that about 90% of the population has a leg
length inequality with a mean of 5.2 mm. The evidence suggests that for most people anatomic leglength inequality is not clinically significant(Papaioannou et al., 1982; Grundy & Roberts, 1984;
Dieck, 1985; Fann, 2002; Knutson, 2005, review), until
the magnitude reaches approximately 20 mm(Gurney, 2002, review; Knutson, 2005, review). Although some earlier studies comparing people experiencing back pain with asymptomatic controls
suggest a correlation (Giles & Taylor, 1981; Friberg,
1983, 1992), more relevant are prospective studies inwhich no correlation was found between leg length
inequality and LBP (Hellsing, 1988a; Soukka et al.,
1991; Nadler, 1998).
Patients who have acquired their leg length differences later in life as consequence of disease or surgery may also help to shed light on the relationshipbetween pathomechanics and LBP. Individuals whodeveloped a shorter leg due to Perthe’s disease had apoor correlation between leg-length inequality, lumbar scoliosis and low-back disorders, assessed several
decades after the onset of the condition (Yrjönen etal., 1992). In studies of patients who had marked
changes in leg length due to hip fractures or replacement, such changes were not associated with backpain assessed several years after surgery (Gibson etal., 1983; Edeen et al., 1995; Parvizi et al., 2003).
One of the arguments in favour of an association
between leg length differences and LBP is the supposed success of heel lifts in reducing back pain
(Giles & Taylor, 1981; Gofton, 1985; Helliwell, 1985;
Friberg, 1983, 1992; Brady et al., 2003, review). However, all these studies failed to include controls or
sham heel lift (such as inefficient soft foam lift).
Prospective studies of inflexibility of the lower
extremities and hamstrings and psoas tightness also
fail to predict future episodes of LBP (Hellsing, 1988c;
Nadler, 1998).

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As for foot biomechanics there is strong evidence
that orthotic corrections have no effect on preventing
back pain (Sahar et al., 2007, syst. rev.).
Surprisingly even whole body changes such as
overweight/obesity have a low association with LBP(Leboeuf-Yde, 2000, syst. rev.). Contrary to common
beliefs, a recent study has shown that cumulative or
repetitive loading due to higher body mass (nearly 30
pounds on average) was not harmful to the discs. The
study found a slight delay in disc desiccation (L1–L4)
in the heavier men when compared with their lighter
twin brothers (Videman, 2009b).
Neuromuscular factors

Although not fully within the scope of this article,
motor control of the trunk is relevant in relation tomuscle function and posture. Certain neuromuscularcomponents also failed to show a clear association
with LBP.
Although earlier studies demonstrated an association between muscle endurance and LBP (BieringSørensen, 1984; Alaranta et al., 1995), a recent systematic review found strong evidence that low trunk
muscle endurance is not associated with LBP(Hamberg-van Reenen, 2007, syst. rev.). This review
found inconclusive evidence for an association between low trunk muscle strength and LBP. Also there
is no association between erector spinae pairs imbalances during extension and LBP (Reeves et al., 2006;
Hamberg-van Reenen, 2007, syst. rev.; Van Nieuwenhuyse et al., 2009). Furthermore, no study to date has
shown that back pain is due to timing differences in
specific muscle such as transversus abdominis(Lederman, 2010b, see Discussion). These control
changes have been observed only in individuals whoalready have back pain. They probably represent theoutcome rather than the cause of back pain
(Lederman, 2010a, see Discussion).
Two studies using the same methodology appear
to demonstrate that in athletes a delayed reflex muscle response at the trunk could increase the risk oflower back as well as knee injury (Cholewicki et al.,2005; Zazulak et al., 2007). Unfortunately, the obvious
was not examined in these studies—the reflex response to a sudden perturbation of the trunk shouldhave been examined in other body areas (e.g., a control recording from the leg). This would have helped
establish whether the injuries are due to delayed
muscle onset-timing, specific to the trunk, or the alternative more plausible explanation that athleteswith sluggish muscle reaction times/reflexes may be
more susceptible to injury.

Eyal Lederman
Postural behaviour factors

An area that is often assessed in manual and physicaltherapy is how “correctly” a person is using their
body—their “postural behaviour”. It is believed that
prolonged postural stresses at work or sporting activities could be the cause of LBP. The results of recent systematic reviews challenge these widely held
beliefs. These studies demonstrate lack of association
between work-related posture and LBP. They include
postures such as prolonged standing, bending, twisting, awkward postures (kneeling or squatting) sitting
posture at work and prolonged sitting at work andleisure time (Hartvigsen et al., 2000, syst. rev.; Bakker
et al., 2009, syst. rev.; Chen et al., 2009, syst. rev.; Roffey et al., 2010, syst. rev.; Wai et al., 2010, syst. rev.).
Also physical leisure time activities such as sport orexercises, sitting and prolonged standing/walking
were found not to be associated with LBP (Bakker etal., 2009, syst. rev.). Heavy manual lifting is strongly
associated with LBP, however the effect size is considered to be modest (Waddell & Burton, 2001, review).
Prediction of back pain by PSB assessment

In a recent prospective study on young workers(n = 692) examined by physical therapists, PSB factors
failed to show a correlation with future developmentof LBP (Van Nieuwenhuyse et al., 2009). A number offactors were evaluated including iliac crest height
inequality, scoliosis, lumbar flexion, extension andlateral flexion, length of hamstring muscles andstrength testing in the motor distribution of L4/L5/
S1.

Summary points:• Postural and structural asymmetries cannot
predict back pain and are unlikely to be its
cause.
• Local and global changes in spinal biomechanics are not demonstrably the cause of back pain.
• A PSB model is not suitable for understanding
the causes of back pain.

Biological not mechanical dimension
There seems to be a disparity between pathomechanics of the body and the experience of a low back condition. Why does the body, which in essence appears
so mechanical (joints, levers), behave symptomatically in such a non-mechanical and perhaps unexpected way?
This paradox arises from the way in which people
are educated to perceive the musculoskeletal system—primarily as a mechanical entity and only minimally as a biological entity. In this biomechanicalmodel the musculoskeletal system is seen as a precision engine where every system, organ and cellworks in perfect harmony within itself and otherbody systems. All joints and body masses are in someanatomically ideal relationship to each other. Muscles
are in anatomical–physiological–functional balancewith motoneurons firing synchronously in perfectharmony. Injury, damage, “disease” or the experience of a back “condition” are seen as the consequence of some disturbance in this harmonious relationship. However, this sequence of events is notevident in the body/spine. Unlike mechanical systems the causation and experience of a spinal condition seem to be unrelated to PSB factors. They seemto largely reside within the biological dimension and

Figure 2—Differences between mechanical and biological systems in regards to biological reserve and tolerance.
A. Mechanical system often has a set range with little tolerance before failure. B. Biological systems and processes often have a wide physiological range, less defined end range and a large potential adaptive range. C. In
mechanical systems events that exceed the system’s range and tolerance often result in damage and progressive
failure. In biological systems overloading can result in two possibilities: D. Acute overloading will result indamage and eventual repair, or permanent damage but without loss of function or symptomatology. E. Chronic
overloading often results in adaptation and expansion of the physiological range.

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Fall of PSB model in manual and physical therapies

Figure 2—Continue

6Eyal Lederman

Figure 2—Continue
hence, the disparity between PSB factors such discdegeneration and LBP.
Within a biological dimension the structure(spine) is capable of self-repair and is able to adapt
and change according to needs and demands (Fig. 2).
But crucially, being a human with a highly evolved
nervous system means that the structure is within theawareness. It is also under the influence of our emotions as well as the will and the actions taken. Therefore a person’s cognitions and behaviour will haveimportant implications to their recovery from LBP(Lederman, 2010a, see Discussion). Humans are also
capable of experiencing pain and suffering—something a washing machine cannot do (yet). This
has led to the emergence of a biopsychosocial modelfor LBP replacing the traditional PSB model.
Biological reserves and tolerance

The mechanical view of the body contains also anatomical and functional ideals—a form of utopian
view of the body. The utopian view gives rise to the
expectation that, like machines or computers, thebody has to work in perfect precision/synchrony.
The question that arises is does it really matter ifthese PSB factors or minor control changes exist andwould they cause some catastrophic failure in themusculoskeletal system? It was apparent from thestudies discussed above that the spine can undergo
profound physical changes that are well tolerated
without the development of a symptomatic condition. What is observed here is that biological systems
contain reserve capacity to accommodate for loss
without failure/symptoms.
So does it matter, for example, that patients with
CLBP may have localised wasting of the multifidus at
L4–L5 (Hides et al., 2008)? Probably not, during
standing and walking the trunk muscles are minimally activated (Andersson, 1996). In standing thedeep spinal erectors, psoas and quadratus lumborum
are virtually silent. In some subjects there is no detectable EMG activity in these muscles. During walking rectus abdominis has an average activity of 2%
maximal voluntary contraction (MVC) and external
oblique 5% MVC (White & McNair, 2002). During
standing “active” stabilisation is achieved by very
low levels of co-contraction of trunk flexors and extensors, estimated at < 1% MVC rising up to 3% MVC
when a 32-kg weight is added to the torso. A backinjury is estimated to raise these values by only 2.5%
MVC for the unloaded and loaded models(Cholewicki et al., 1997). During bending and lifting aweight of about 15 kg co-contraction increases by
only 1.5% MVC (van Dieen et al., 2003). This meansthat an individual will have to lose substantial mus-7

Fall of PSB model in manual and physical therapies
cle mass and force production ability before suchdaily activities will be adversely affected. However,the biological reserve allows for such losses without anegative effect on spinal function or the developmentof a condition. Indeed, men tend to naturally lose
25% of their muscle mass between the ages 50 and 75
years without any detrimental effect. It is estimatedthat when the loss of this muscle reserve reaches 30%
it will limit normal function in an older individual(Marcell, 2003).
Biological reserve is likely to explain why footmechanics, leg length differences, pelvic torsion timing delays or any other PSB factors do not result in a
symptomatic spinal condition. The system is capableof tolerating and compensating for these factors
within the available surplus.
This reserve capacity can be seen elsewhere in the
body. For example, partial or full thickness rotator
cuff tears are found in a third of asymptomatic individuals over the ages of forty (Sher et al., 1995). These
structural losses are not associated with pain or lossof shoulder function. In an evaluation of 100 asymptomatic volunteers (19–88 years) acromioclavicular
joint osteoarthrosis were present in three-fourths ofthe shoulders, one-third had subacromial spurs. Also
found were changes in the peribursal fat plane andthe presence of fluid in the subacromial–subdeltoid
bursa. Joint fluid was observed in nearly all subjects(Needell et al., 1996). Furthermore, pathomechanicsof the gleno-humeral joint was found to be similar inboth symptomatic and asymptomatic individuals(Yamaguchi et al., 2000). We can assume that thesepathomechanical changes would also be associatedwith profound neuromuscular changes, yet without
giving rise to symptoms or functional loss. It is intriguing why some individuals develop a symptomatic condition while others remain asymptomatic.
Conflict within the PSB model

There is also a logical conflict within a PSB model. If
persistent PSB factors lead to injury/damage/pain noone would ever recover from a simple back pain condition, whether acute, recurrent or chronic. Under a
PSB model they would be expected to progressively
get worse to the point of total disability; in the same
way that damaged/unsynchronized machines gradually fail. Within a mechanical model, for example, theback condition of a person with leg length inequality
would be expected to deteriorate over time. However, this does not seem to be a common occurrence.
The symptomatology of LBP is variable and individuals may experience extended pain-free periods

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without progressive worsening or increase in thefrequency of their condition (Streiner, 2001; Carragee
et al., 2006; Hartman, 2009). This logical conflict applies to all PSB factors described so far including motor control, proprioceptive and muscular changes(See Discussion in Lederman, 2010a).
The utopian view of the body raises several morequestions. Is there ever a perfect PSB balance anddoes it matter? Do individuals develop/experience a
condition when this balance is affected? Should we
try to fix everybody even if they are not symptomatic? Where do we start, how do we decide which
imbalance/asymmetry is more important?
Concession to the PSB model

Perhaps there is a critical level where PSB factors will
exceed the reserve of the system. This can be either
from gross PSB asymmetry/imbalance or in extreme
physical demands. For example, there may be an
association between severe scoliosis and back pain or
substantial nerve root compression and leg pain
(Beattie et al., 2000; Haefeli et al., 2006). In sports,
extreme physical demands combined with underlying PSB factors may increase the likelihood for LBP(Ogon et al., 2001; Iwamoto et al., 2004). However
this leaves us with the question of what to do withthese findings in sports: correct the PSB factors or
introduce better management of training and gameschedule?
There is a catch with this concession in regards toclinical management. If the asymmetry/imbalance issevere it is unlikely that manual therapy or even exercise can substantially modify it (see below). On theother hand if the asymmetry/imbalance is minor ormoderate it is unlikely to contribute to the patient’s
LB condition.
Summary points:• The experience of a condition or disease is organised within the biological–psychologicaldimensions of the individual. The contributionof biomechanical factors is not clear.
• Body systems seem to have reserve capacity toallow for asymmetry and imperfections to exist
without failure or symptoms.

The three clinical hurdles
The PSB model introduces unnecessary complexityand hurdles to practice. The first hurdle to overcomein the PSB model is the inability to identify/define
the critical level where PSB factors contribute to theindividual’s back pain. This critical level is impossible to predict on an individual basis.

Eyal Lederman
If we were to overlook this obstacle, the next hurdle to overcome is the reliability of assessing PSB
factors. It is now well established that many of theexaminations that assess PSB factors are either low onvalidity or reliability, in particular, the more precise/minute examinations such as leg length differences,tissue textures, pelvic angles and individual vertebral
positions (McCaw & Bates, 1991; Mannello, 1992;
Panzer, 1992; Levangie, 1999a,b; Hestbaek & LeboeufYde, 2000, syst. rev.; Dunk et al., 2004; Seffinger et al.,
2004; van Trijffel et al., 2005; Hollerwöger, 2006; May
et al., 2006; Paulet & Fryer 2009).
Even if we were to overlook the two former hurdles, there is yet a third one to overcome—are manual techniques or specific exercise effective in modifying inherent PSB factors? Can foot mechanics, leg
length differences, pelvic tilts, vertebral positions andspinal curves be permanently changed, solely, bythese clinical tools?
Permanent adaptive musculoskeletal changes require physical overloading well above the person’s
default daily use (See Discussion in Lederman, 2005).
Such an adaptation depends on the length and frequency of exposure to overloading. For example,
strength training requires overloading by progressive
increase in resistance and duration/frequency; an
improvement in running endurance is achieved byrunning further and often, and so on (Henriksson &Hickner, 1996). Conversely, a cessation of exercise
will result in rapid reversal of these training gains. In
the context of PSB factors, it is expected that tremendous forces, well above the daily physical stresses,
would be required to reposition/adjust/correct any
structural misalignments. These would have to be
applied on a daily basis over several months or evenyears. A termination of treatment is likely to result in
rapid reversal of PSB gains, unless the individual isable to self-maintain them by specific exercise. The
winner in this competition-in-adaptation is ultimately the one most practised, that is, the default PSB
state/behaviour of the individual (See Discussion in
Lederman, 2005, 2010a).
There are no known studies that examine the influence of manual techniques on PSB factors in themedium- or long-term, in particular at the cessationof the treatment. In essence, tensional forces (e.g.,
stretching) are required in order to induce adaptive
connective tissue or muscle length changes. Thesecan be applied within different time scales, as a sudden tensional force such as in spinal manipulation orforces applied from several seconds to minutes, suchas in manual stretching or exercise. Sudden application pulse of tension as in manipulation is only likely

to produce transient tissue lengthening (creep deformation), lasting no more than a few minutes (Light etal., 1984; Roberts & Wilson, 1999). Manual stretchingof muscles or exercise for several minutes will have atransient lengthening effect lasting up to an hour
(Magnusson, 1998; Magnusson et al., 1995). Longerterm stretching over several weeks will activate andmaintain specialized cellular processes in muscle andconnective tissues that account for permanent tissueelongation (Williams et al., 1986; Goldspink et al.,
1992; Arnoczky et al., 2002; Bosch et al., 2002). However, these tissue lengthening processes tend to revert
to the default-use at the cessation of treatments(Harvey et al., 2002). For example, a break of fourweeks completely abolishes the gains of six weeks ofstretching (Willy et al., 2001).
Orthodontic braces to correct the bite are an example of the enormity of the task required to produce
permanent PSB changes. A teenager is expected towear the fixed braces for several years. It is followed
by wearing a night brace for several more years toprevent the adaptation to revert back to the default.
Similarly, spinal curves are determined by the shapeof the vertebra and discs as well as every other tissue
connected to them (Lonstein, 1999; Marks & Qaimkhani, 2009). Therefore, a spinal brace worn daily formany years slightly straightens scoliosis, but the
curves tend to gradually regress when the brace isremoved (Maruyama, 2008, syst. rev.; Maruyama etal., 2008).
It would require a herculean effort to modify
many of the inherent PSB factors discussed so far. As
such, the therapeutic investment in correcting PSB
factors is irrational, in particular, as it is unlikely to
influence the course of the patient’s condition.
Summary points:• A PSB model introduces unnecessary complexity at a conceptual level and in clinical assessment.
• Observational or physical assessments of PSB
factors have no value in elucidating the causes
for back pain.
• Clinical assessment of PSB factors assessed bymanual and visual means may be unreliable.
• Such assessments are likely to be redundantand can be safely removed from clinical practice. This excludes assessment that aim to identify serious pathologies.
• PSB factors are unlikely to change in the longterm by manual techniques or even exercise,unless rigorously maintained (exercise).
• A PSB model may introduce an element oftherapeutic failure as the aims and goals of thisapproach may not be attainable by manual therapy or even exercise.

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Fall of PSB model in manual and physical therapies
Implications for practice
The lack of association between PSB factors and backpain has far-reaching implications for the way weconceptualize musculoskeletal conditions, the clinicalexamination and the goals/objectives of the techniques and the exercise prescribed.
From the evidence so far many of the clinical examinations assessing PSB factors have no obvious
values in explaining why the patient has developed
their back condition. It implies that the PSB modeland the related clinical examinations are mostly redundant. Furthermore, there is compelling evidence
that the PSB model may take us further away fromunderstanding back pain. It has been consistently
demonstrated that lower back pain recurrences,chronicity or disability can be better predicted fromassessing biological, psychological and social factors(Carragee et al., 2006). For example, about 45%–55%
of LBP conditions are attributed to hereditary factors(Battié, 1995; Paassilta et al., 2001; MacGregor et al.,
2004; Valdes et al., 2005; Videman et al., 2006,
2009a,b; Battié et al., 2007, 2009). Several studies haveshown that as much as 80% of serious LBP eventsand 93% of LBP disability events can be better predicted by biopsychosocial factors such as gender,
abnormal psychometric testing, smoking and compensation issues (Carragee et al., 2006). In contrast, it
is difficult to find any studies that identify predisposing structural factors for LBP, despite several decadesof research into this condition (Bakker et al., 2009,
syst. rev.).
The lack of association between PSB factors and
LBP has also important implications for what we aim
to achieve and for our choice of techniques and exercise used to manage the condition. We can no longer
justify the use of manual techniques to readjust, correct or balance-out the misaligned structure. There isan urgent need to redefine what the therapeutic goals
are, beyond relieving the patient’s symptoms, forexample, is there any value in providing long-term
maintenance/preventative treatments for asymptomatic individuals?
In a prospective study using MRI scans it wasdemonstrated that recurrences of back pain over a
period of five years were not associated with any
progressive spinal damage (Carragee et al., 2006).
Individuals were experiencing periods of pain andsymptomatic recovery although their spinal condition remained unchanged. This is a regular phenomenon where a condition will exhibit natural variation
around a certain symptomatic mean. At certain times
the individual will experience periods of symptomatic quiescence (Streiner, 2001; Hartman, 2009; see

10also Kongsted & Leboeuf-Yde, 2010). This implies
that the therapeutic ideal of a “cure” may not be possible, as the underlying condition could still be present but is asymptomatic. Perhaps research and treatment should be directed towards finding better approaches to provide symptomatic relief during periods of pain as well as increasing the patient’s participation in social, occupational and recreational activities (Waddell et al., 2008; Kendall et al., 2009). This attitude may be more realistic than the idealized clinicalaspiration to provide a permanent cure by correcting
PSB factors.
Finally and more complex is the therapists’ education in the various manual and physical therapies
where the PSB model is dominant. If this model isflawed what is the alternative clinical model and who
is capable of teaching it?
The alternative: a Process Approach

A clinical alternative to the PSB model is a Process
Approach model. The aim in this approach is to identify the processes underlying the patient’s conditionand provide the stimulation/signals/management/
care that will support/assist/facilitate change. Thisapproach has been extensively discussed in Lederman (2005) and will be discussed in a future article.

Summary and conclusion points• PSB asymmetries and imperfections are normal
variations—not a pathology.

• Neuromuscular and motor control variations arealso normal.

• The body has surplus capacity to tolerate such••••variation without loss to normal function or development of symptomatic conditions.
Pathomechanics do not determine symptomatology.
There is no relationship between the pre-existing
PSB factors and back pain.
Correcting all PSB factors is not clinically attainable and is unlikely to change the future course ofa lower back condition.
This conclusion may well apply to many common
musculoskeletal conditions elsewhere in the body(e.g., neck pain).

Acknowledgement
I would like to thank Tom Hewetson and Steve
Robson for their kind help in preparing this article.

Eyal Lederman
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