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A model of movement dysfunction provides a classification system guiding


diagnosis and therapeutic care in spinal pain and related musculoskeletal
syndromes: A paradigm shift—Part...

Article  in  Journal of bodywork and movement therapies · May 2008


DOI: 10.1016/j.jbmt.2007.04.006 · Source: PubMed

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Journal of Bodywork and Movement Therapies (2008) 12, 105–120

Journal of
Bodywork and
Movement Therapies
www.intl.elsevierhealth.com/journals/jbmt

CLINICAL PHYSIOLOGY

A model of movement dysfunction provides


a classification system guiding diagnosis
and therapeutic care in spinal pain and
related musculoskeletal syndromes:
A paradigm shift—Part 2
Josephine Key, Dip. Phys, PGD. Manip. Ther., Andrea Clift, B. App. Sc.
(Phys), Fiona Condie, Dip. Phys; Masters (Manip), Caroline Harley, MSc,
MACP, SRP

Edgecliff Physiotherapy Sports and Spinal Centre, Suite 505 Eastpoint Tower, 180 Ocean Street, Edgecliff,
N.S.W. 2027, Australia

Received 18 January 2007; received in revised form 14 April 2007; accepted 17 April 2007

KEYWORDS Summary An integrative functional model largely based upon the observation and
Clinical classification analysis of the more common features of neuromusculoskeletal dysfunction
LBP; encountered in clinical practice was presented as a working hypothesis in Part 1.
Diagnosis LBP; The functional inter relationships between these regional and general features
Neuromusculoskeletal and their contribution to the development and perpetuation of local and or referred
dysfunction; spinal pain syndromes was explored.
Movement Here we look more closely at clinical patterns of presentation.
dysfunction; A simple classification system of clinical subgroups with back pain and related
Back pain; disorders is offered. These more commonly observed dysfunctional postural and
Posture; movement strategies have been distilled into a number of dysfunction syndromes
Motor control which will have predictable consequences.
In beginning to provide a map of the tendencies towards, or actual, changed
postural and movement responses seen in people with spinal pain and related
disorders, this model provides a valuable reference for those working in the body
work and movement therapies realm. It is a practical and useful clinical tool to assist

Corresponding author. Tel.: +61 02 93261168; fax: +61 02 93281695.


E-mail address: edgecliffphysio@iprimus.com.au (J. Key).
URL: http://www.edgecliffphysio.com.au (J. Key).

1360-8592/$ - see front matter & 2007 Elsevier Ltd. All rights reserved.
doi:10.1016/j.jbmt.2007.04.006
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106 J. Key et al.

diagnosis and help better understand the development and perpetuation of most
spinal pain and related disorders. In so doing, more rational, functional and effective
therapeutic and research interventions can ensue.
& 2007 Elsevier Ltd. All rights reserved.

Introduction 3. Mixed Syndrome: demonstrates certain fea-


tures of both pelvic crossed syndromes with
Pelvic crossed syndromes a primary tendency to either APXS or PPXS.
4. The Shoulder Crossed Syndrome: described
Kendall et al. (1993, p. 72) maintain that ‘‘the by Janda (1988), is also apparent from
position of the pelvis is the key to good or faulty the lateral view. It is generally, although
postural alignment’’. They also state, ‘‘the centre variably apparent in both pelvic crossed
of gravity of the body is considered to be slightly syndromes.
anterior to the first or second sacral segment’ (p. (B) Anterior and posterior view of posture
12). The pelvis, in housing the centre of gravity of 5. Stratification Syndrome: described by Janda
the body, thus plays a central role in control of (1987a, b) encompasses the entire torso and
posture and movement—small shifts can effect big is a meld of the shoulder and pelvic crossed
changes throughout the body. syndromes and is usually apparent, albeit to
We have maintained in Part 1 that patients with a varying extent.
spinal pain and related disorders commonly demon- (C) Composite view
strate consistent underactivity of the deep system 6. Belted Torso Syndrome. This more fully
but show variable overactivity of the superficial describes the observed dysfunction around
system in the strategies they adopt for posture and the central torso and the body’s centre of
movement. How do we further see this? gravity.
Observing the habitual standing posture provides
a convenient ‘road map’ of the way in which the
patient has adaptively organised himself. Posterior Pelvic Crossed Syndrome—the
Essentially, we see that there are two principal pelvis is back!
spatial deviations of the pelvis from the ideal
sagittal alignment—it is either forward or back. Here the neuromuscular system is generally more
This changed pelvic alignment gives rise to The switched on but in an abnormal manner of relative
two primary pictures of dysfunction—the pelvic systemic global muscle system (SGMS) ‘overdrive’,
crossed syndromes. These paradigms have elabo- with patchy axial extensor hyperactivity and
rated Janda’s (1987a, b) model. related under activity of the deep system. In its
For conceptual clarity, these two and the other purest form it may be more common in males. The
related syndromes are seen as follows: patient ‘looks up’—the ‘pseudo warrior’ although
he is tense, unyielding, generally tight and stiff,
(A) Lateral view with poor selective control of movement within the
1. Posterior Pelvic Crossed Syndrome: (PPXS). torso.
This fairly much represents Janda’s original Characterised by (Fig. 1):
‘Pelvic or Lower Crossed Syndrome’.
2. Anterior Pelvic Crossed Syndrome: (APXS).  Pelvis—posterior shift with increased anterior
This appears to be more common. sagittal rotation or tilt.
These two syndromes form the basis of our  Trunk—anterior translation of the thorax via
simple clinical classification system. thoracolumbar ‘shunt’ from increased thoraco-
It is important to appreciate that only some lumbar extensor muscle activity creates a for-
patients will demonstrate the extreme pel- ward-loaded trunk and associated compensatory
vic picture. Some will show some tendency, anterior pelvic rotation. See Harrison et al.
and others will exhibit a variable mixture of (2002).
the two with a dominant tendency. Under-  Cursory glance shows they look ‘extended’ with
standing the features of each helps under- an increased lordosis. This is principally high
stand the patient in front of you—probably a lumbar and over the thoracolumbar junction.
mixed syndrome. Closer inspection reveals that the lower lumbar
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Figure 1 Schematic view: Posterior Pelvic Crossed


Syndrome. Figure 2 Pure Posterior Pelvic Crossed Syndrome: ante-
rior view.
levels in fact show some relative flexion and are
poorly controlled.
 Quick appraisal reveals big belly, bottom and calves
and bulky T/L extensor groups. Puffy superficial
tissues and poor definition over the low lumbar
levels and lumbosacral junction (Figs. 2–4).

Muscle hypoactivity/lengthened:

o Entire abdominal wall and pelvic floor.


o Lumbosacral multifidus.
o Iliacus in controlling anterior pelvic rotation at
the lumbosacral junction.
o Glutei Medius +.
o Inefficient diaphragm activity.

Hyperactivity/adaptive shortness:

o Thoracolumbar erector spinae +++.


o Anterior hip flexor groups primarily psoas.
o Piriformis.
o Hip internal rotators 4external rotators.

As a consequence we can expect or predict that


in movement:

 Patchy extensor synergies tend to dominate in Figure 3 Pure Posterior Pelvic Crossed Syndrome: lateral
most movements—particularly thoracolumbar view.
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108 J. Key et al.

Figure 5 Central posterior cinch: static.

Figure 4 Pure Posterior Pelvic Crossed Syndrome: poster-


ior view.

(T/L) extensors. Inhibition of the overactive


muscles can be difficult and they often cannot
let them go, e.g. in standing, forward bending,
T/L extensor muscle groups keep holding instead Figure 6 Central posterior cinch: active.
of eccentrically lengthening (Figs. 2–4).
 Trunk extension is generally reduced particularly in the important patterns of pelvic control are
through the thorax. In attempting extension, the lower abdominals (Tr.A; IO), pelvic floor
both poor spatial pre-positioning of the pelvis muscles; lumbar multifidus and, we believe,
and poor hip and thoracic extension leads to importantly the iliacus psoas synergy. Ideally,
further over activation of the extensor muscle we think, anterior pelvic rotation at the lumbo-
groups over thoracolumbar junction (T/L/J) and sacral junction relies a lot on iliacus contributing
upper lumbar levels. to anterior iliac rotation and so also indirectly,
 Thoracolumbar region becomes hyperstabilised nutation of the sacrum with coactivation of low
by overactive erector spinae groups/serratus lumbar multifidus (particularly when working
posterior inferior producing a ‘‘central posterior with a reversed origin and insertion on a fixed
cinch’’ (CPC). This over-anchors the lower femur). Instead, sagittal pelvic rotation control
thorax, further reducing movement within the is indirectly attempted by abnormal SGMS
thorax and over the thoracolumbar junction activity—anterior rotation primarily from the
to the upper lumbar spine. This then creates thoracolumbar extensors and the anterior pel-
a compensatory functional ‘‘break’’ in the vic-femoral muscles—particularly psoas. The
mid /low lumbar spine—these levels become apparent anterior pelvic rotation is not con-
relatively over stressed in movement with poor trolled at the lumbosacral junction.
intersegmental control (Figs. 5 and 6).  Decreased hip extension because of tight/over-
 Poor control of the pelvis in space, on the active psoas/anterior hip muscles and related
lumbar spine and hips in posture and movement underactive glutei. Active hip extension move-
because of reduced systemic local muscle system ments are associated with increased thoraco-
(SLMS) activity. The deep muscles most involved lumbar activity. The poor contribution and
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Therapeutic care in spinal pain and related musculoskeletal syndromes: Part 2 109

control of the lumbosacral region towards ante-


rior pelvic rotation/low lumbar lordosis to
support hip extension is interesting. Psoas is
overactive in synergy with thoracolumbar ex-
tensors, and iliacus seemingly underactive we
feel. This observed imbalance between psoas
and iliacus activity in this group will hopefully be
confirmed by future primary research.
 Important standing forward bending pattern.
The pelvis is already posteriorly shifted and
anteriorly rotated, and so contributes reason-
ably to hip flexion. However reduced control of
anterior iliac rotation and sacral nutation at
lumbosacral junction is compensated by in-
creased thoracolumbar extensor activity. This
leads toy
 Relatively increased intersegmental flexion over
the mid/low lumbar levels during spinal flexion
(and other movements) as the thoracolumbar
contribution to movement is reduced from
overactive CPC. This becomes exacerbated by
the frequent therapeutic misdirective to ‘tuck
the tail under’ in a misguided attempt to
decrease thoracolumbar extensor hyperactivity.
 Abnormal axial rotation—lack of general and
rotary mobility in the thorax and over the
thoracolumbar junction because of CPC and a Figure 7 Schematic view: anterior pelvic crossed syn-
‘dome’ (see Part 1), plus poor spatial pelvic drome.
control, means any rotation imposed on the
system is forced to occur abnormally in the mid/
low lumbar spine.
 Dysfunctional breathing patterns—inefficient  Trunk (thorax) backward loaded—posture that of
diaphragm activity because of CPC which also more general flexion; adaptive shortening and/
reduces posterior basal expansion. Possible or overactivity of the upper abdominals. Flexion
hypertonus of diaphragm in those with a barrel of lumbar spine.
chest where the attachments of the diaphragm  Hips in extension with adaptively tight posterior
are part of the muscular bracing seen around the hip structures.
thoracolumbar junction.  Quick appraisal shows no buttocks, forward
loaded head posture, thoracic kyphosis—thorax
collapsed/pulled down towards pelvis, poor calf
Anterior Pelvic Crossed Syndrome—the development.
pelvis is forward!  Rely more on passive structures for support
(O’Sullivan et al., 2006a)—hang on iliofemoral
Here, the neuromuscular system is more ‘switched ligaments, adopt wide base of support, knees
off’—both the deep and the superficial systems. hyperextended (Figs. 8–10).
However, while less dominant, the superficial system
is still abnormally used though more intermittently. Muscle hypoactivity/lengthened (Fig. 7):
Those with generally low muscle tone fall into this
group. In its purest form, it is probably more
common in females. The patient appears somewhat o Lower abdominal group and pelvic floor.
collapsed and exhausted while ‘up’. o Lumbar multifidus—particularly over lower
Characterised by (Fig. 7): levels.
o Diaphragm—reduced excursion ++.
o Iliacus, psoas.
 Pelvis—anterior shift with increased posterior o Glutei—reduced postural and movement
rotation or tilt. demand and often adaptively shortened.
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Figure 8 Pure Anterior Pelvic Crossed Syndrome: ante- Figure 10 Pure Anterior Pelvic Crossed Syndrome:
rior view. posterior views.

Hyperactivity/adaptive shortness:

o Hamstrings.
o Piriformis.
o Upper abdominal group including lateral internal
oblique.
o Hip external rotators 4 internal rotators.
o +/ T/L erector spinae (Figs. 8–10).

As a consequence we can expect that in move-


ment:

 Patchy flexor synergies tend to dominate in


movement—e.g. upper abdominals with pector-
als in antigravity trunk flexion.
 Generalised loss of extension through spine is
marked—more in the thorax followed by lumbar
spine. Loss of lordosis is marked through lumbar
spine. Most active extension is achieved by
intermittent thoracolumbar extensor activity
and/or further swaying pelvis forward and
extending hips to compensate.
 Thoracolumbar junction hyperstabilised in flex-
ion. Upper abdominal overactivity or cinch
creates a ‘‘central anterior cinch ‘‘(CAC) which
Figure 9 Pure Anterior Pelvic Crossed Syndrome: lateral holds the anterior thorax down, inhibiting
view. good descent of the diaphragm, increasing the
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thoracic kyphosis and ‘dome’ and further


reducing contribution of thorax in movement
(Figs. 11–13).
 Decreased hip flexion due to tight posterior
pelvic/hip muscles and hamstrings. This is
compensated by further increased lumbar flex-
ion in movement.
 Important pattern of forward bending in stand-
ing. Initiated more from overactivity of the
upper abdominals (CAC) rather than from poster-
ior shift and anterior rotation of pelvis on
hips into flexion with associated controlled
lumbar lordosis. Resultant over flexion of lumbar
segments.
 Poor spatial control of the pelvis, pelvis on the
hips and lumbar spine because of under active Figure 12 Central anterior cinch: chronic picture.
SLMS synergies. Pelvis is placed forward in
spatial relationship of ‘reduced SLMS demand’
as they hang off the iliofemoral ligaments. There
is poor spatial pre-positioning of pelvis to
support lower limb movement. We feel that
both psoas and iliacus are more under-active in
concert with Multifidus, Lower IO and Transver-
sus, creating difficulty in anteriorly rotating the
pelvis and controlling the low lumbar lordosis.
So-called ‘‘Instability’’ syndromes of the lumbar
spine and S.I.J. become predictable.

Figure 13 Central anterior cinch: chronic picture.

 Relatively increased intersegmental flexion over


low lumbar levels seen due to poor lumbopelvic
control as well as compensation for associated
posterior hip and pelvic tightness. Lumbar joints
and intersegmental structures including the disc
are used in untenable, more unstable and
vulnerable end range flexion. Disc, facet and
the plethora of other various ‘‘diagnoses’’ are a
predictable consequence over time.
 Abnormal axial rotation—a general reduction in
extension and rotation because of CAC and
thoracic ‘dome’, plus deficient lumbo-pelvic
control, means any imposed rotation will abnor-
mally occur in the lumbar spine.
 Dysfunctional breathing Patterns—CAC greatly
hampers diaphragmatic breathing and basal
expansion—increasing upper chest breathing
with sympathetic dominance. Related upper
body tension and cervical pain syndromes occur.
Figure 11 Central anterior cinch: acute presentation.  Important to Note: when attempting to be ‘up’,
Note predominance of general flexion synergies. performing certain movements or trying too hard,
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112 J. Key et al.

the tendency is for the patient to flip to using a that this is probably the more common under-
more primitive gross extensor synergy—princi- lying clinical presentation (O’Sullivan et al.,
pally utilising the thoracolumbar extensors (CPC) 2006a).
in association with their retained upper abdom-  Posterior Pelvic Crossed Syndrome shows fea-
inal CAC pattern. The lower thorax then becomes tures in common with his Extension Pattern.
functionally converted to a cone shape. We have  We see that O’Sullivan’s other directional pat-
termed this a ‘‘central conical cinch’’ (CCC) terns are variations on these basic two patterns
whereby the anterior, posterior and lateral at differing stages of neuromusculoskeletal
thoracolumbar junction becomes hyperstabilised. dysfunction.
Control of the pelvis is attempted from this
habitual thoracolumbar strategy. The reflex re-
active response becomes the postural set from Mixed Syndrome: display features of
which they move. APXS and PPXS—usually with a dominant
Van Wingerden et al. (2004) presented a study
tendency towards one or the other
that supports the concept of the two Pelvic
Crossed Syndromes. They examined forward
Clinically, this is perhaps the more common
bending motion patterns of the lumbar spine
presentation. Appreciating each syndrome sepa-
and pelvis in patients with chronic pelvic girdle
rately helps see the composite presentation and
pain and chronic low back pain (CLBP). They
the relative dominance of one.
found those with pelvic girdle pain demonstrated:
We are finding that the effects of some of the
increased posterior rotation of the pelvis; a
currently popular yet poorly conceived and admi-
decreased lumbar lordosis in standing and when
nistered exercise programmes (therapeutic, gyms,
forward bending, used more lumbar flexion than
personal trainers, Pilates and some forms of Yoga)
hip flexion, i.e. APXS. Those with low back pain:
are further creating and compounding this picture
maintained more lordosis when forward bending,
of dysfunction.
i.e. they could not let their extensors (? thor-
The combination of features of a CPC in PPXS
acolumbar), lengthen. They clearly belong to the
with those of a CAC seen in APXS creates a CCC (see
PPXS group. Predictably we can expect symptoms
above) in posture and movement function.
to differentially occur in both groups over time.
Common to all is the tendency to posturally align
O’Sullivan (2005, 2006) proposes three broad
and move predominantly in the more primitive,
clinical subgroups of CLBP patients, based on
gross, bilateral flexion/extension synergies which
the mechanism underlying the disorder. Within
disallow:
one of these groups he proposes an underlying
defective motor control problem—primarily as
either movement impairments or control impair-
 Appropriate patterns of axial setting and control
to support limb movement.
ments. Under the control impairments subgroup
he further defines his five clinical directional
 The important rotary and lateral shifts and
adjustments needed for weight shift and to
patterns based on subjective history and symp-
maintain axial alignment and equilibrium and
tom behaviour. (O’Sullivan P.B., 2000; O’Sullivan,
control.
2004, 2005; Dankaerts et al., 2006a.)
There is a close affinity between our approach
and that of O’Sullivan. We feel our two primary
pelvic syndromes provide a simpler yet elegant, Shoulder Crossed Syndrome (Janda
integrated understanding of the underlying in- 1980, 1988)
herent tendency to dysfunction in us all, and
importantly, the commonly observed, magnified, Common to all three pelvic syndromes is the
motor control dysfunctions seen in CLBP. We see variable coexistence of this syndrome.
that movement and control impairments coexist It is an expression of the typical changes in
though in different proportions, depending on the posture and movement function seen in the upper
primary underlying pelvic postural and movement torso. It will also affect related function in the
syndrome and the presenting stage of the lower torso.
disorder. Importantly however, we observe similar It is characterised by:
patterns of clinical presentation (O’Sullivan P.,
2000; Dankaerts et al., 2006b, c) namely:  Altered posture—round shoulders; increased
 Anterior Pelvic Crossed Syndrome shows features upper thoracic kyphosis including a ‘‘dome’’;
in common with his Flexion Pattern. We agree forward drawn head.
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 Increased activity and tightness of—the anterior drome and upper body tension. Cervical pain
chest and shoulder muscles, long cervico-thor- syndromes inevitable.
acic extensors, sternocleidomastoid and scaleni.  Neuromuscular patterns triggered in response to
 Related hypoactivity of—the deep neck flexor stress, tension and anxiety (cringing, protection)
group, the lower scapular stabilisers and related are more upper body global muscle system
spinal intersegmental muscles (Figs. 14 and 15). dominant and associated with disturbed breath-
ing (see Hanna, 1988).
Contributing factors to this syndrome are vari-
 Most occupations require sustained forward arm
use in predominant flexor synergies e.g. manual
able combinations of the following:
physiotherapist, computer operator.
 Adverse training effect, e.g. poorly conceived gym
 Dysfunctional breathing patterns. and exercise routines which over emphasise
J Breath holding and central cinch in posture contemporary aesthetics over function—the de-
and movement (either CAC, CPC or CCC). sire for ‘good pecs’ and ‘a six pac’ abdominals
J Adaptive SGMS strategy of upper chest which further stiffen the thorax and reinforce the
breathing in both low and high demand tendency to dominant upper body flexor synergies.
situations. Related Hyperventilation Syn-  Overuse of upper limb ‘fixing strategies’ (parti-
cularly in the elderly) to compensate for
decreased lumbo-pelvic control and equilibrium
reactions within the body. Watch even young
people in the train clinging and hanging off the
bars instead of resolving the perturbations
through the legs and trunk!

Stratification or Layer Syndrome (Janda


1987a, b)

The prescence and related effects of this syndrome


explains the frequent coexistence of cervical and
lumbar pain syndromes in many patients.
Janda (1980) saw this as ‘‘another muscular
syndrome’’, yet ‘‘this layer syndrome is a sign of a
severely and deeply fixed central motor dysregula-
tion accompanied by very bad movement pat-
Figure 14 Schematic view of Shoulder Crossed Syn- terns’’. It is surprising how many of our spinal
drome. patients display features of this!
In describing the general dysfunction seen in the
torso, our elaborated construct of the APXS enables
the layer syndrome to better demonstrate the
combined effects of the pelvic crossed syndromes
and the Shoulder Crossed Syndrome. In particular it
helps us see the proclivity for patchy ‘banding’ of
coarse flexor and extensor activity. This pattern of
trunk muscle activity consistently plays out in all
movements, e.g. reaching up. Predictably, in time,
this more obligatory pattern of muscle activity
causes some regions of the axial skeleton to become
hyper-stabilised and stiff while other regions become
under-controlled and relatively mobile (Fig. 16).
Viewing the patient’s torso from the front and
particularly from behind, we see layers or bands of
overactive and hence bulky muscles alternating
with regions of under active muscles with flattened
Figure 15 Actual view of Shoulder Crossed Syndrome. contours. This provides clues to the probable
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114 J. Key et al.

Figure 16 Schematic view of Stratification Syndrome


after Janda.

habitual activation response of various muscle


groups. Figure 17 Stratification Syndrome from behind: in
Observed from behind, we may see ‘banding’ in standing.
activity of the extensor system (Figs. 17–19):
Overactive and/or tight—cervical erector spi-
nae, upper trapezius, levator scapulae, thoraco-
lumbar erector spinae, piriformis, hamstrings.
Underactive—lower scapular stabilizers, lumbo-
sacral multifidus, gluteus maximus.
Observing the front it is not quite as apparent,
however we may see ‘banding’ in flexor activity as:
Overactive and/or tight—sternocleidomastoid,
pectorals, oblique abdominals.
Underactive—Deep neck flexor group, abdominal
weakness particularly transversus and rectus abdo-
minis.
Appreciating this pattern of response in muscle
activity presents a significant challenge to effective
therapeutic movement control. Attempts to facil-
itate activity of one hypoactive group will invari- Figure 18 Stratification Syndrome from behind in lying
ably risk early and over activation of the already prone.
dominant muscles, e.g. gaining activation of
lumbar multifidus or lower scapular stabilisers more common static and active patterns of muscle
without dominance of thoracolumbar extensors action as described in the Pelvic Crossed and
and/or cervico thoracic extensors. Stratification Syndromes. This representation is a
close up lens, which helps us to appreciate the
dysfunction that occurs around the body’s centre of
Belted Torso Syndrome gravity. It just so happens that the belt line seems
to be a functional demarcation line. We consis-
Here, we attempt to help further clarify torso tently see a difference in the muscle activation
dysfunction, with a schematic composite of the patterns above and below the belt in all our
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Figure 20 Schematic view Belted Torso Syndrome.

Figure 19 Stratification Syndrome from behind.

patients—hyper above and hypo below. The pa-


tient’s presenting pattern will be a reflection of his
primary pelvic dysfunction picture (Figs. 20–23):

(a) Hyperactivity/over-stabilising by the muscles


acting above the belt either:
 Posteriorly as a CPC in PPXS.
 Anteriorly as a CAC in APXS.
 Combination of the above whereby the
inferior thoracic cage is functionally
‘squeezed’ becoming like the apex of an
inverted cone—CCC in the mixed syndrome.
Harrison et al. (2002) in a normal study,
demonstrated that sagittal forward and
backward translations of the thorax initiated
from thoracolumbar junction (T12) muscle
activity, created compensatory changes in
alignment in the thorax, lumbar spine and
pelvic tilt.
Our understanding of the consistently clini-
cally observed overactivation of muscles
around the body’s centre of gravity seen in Figure 21 Belted Torso Syndrome—central conical cinch
our patients has been greatly assisted by from primary APXS picture.
Hanna’s (1988) notion of the ‘‘Reflexes of
Stress’’. Stress is a response to both good causes a specific reflex response of the
things and bad. It can be positive (eustress), neuromuscular system. Eustress will invoke
negative (distress), or relate to trauma, and assertion, action and perhaps effort and is
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116 J. Key et al.

extensor dominant. Distress will invoke


protection, withdrawal, fear and is flexor
dominant. Trauma will invoke a protective
response guarding against pain, e.g. trunk
list. These are unconscious, involuntary
rapid reflex motor acts, which primarily
affect the muscles around the body’s centre
of gravity. They are normal adaptive reflexes
essential to our survival, which engage the
entire nervous system and musculature.
However when repeatedly triggered in mod-
ern man, they become habitual background
neuromuscular activity. The reflex response
begins to become the postural set from
which they move.
The effects of emotional state on posture
and consequent movement are becoming
increasingly acknowledged (Vleeming, 2000;
Mosely, 2004).
(b) Muscle hypoactivity/poor control of posture
and movement below the belt
Anteriorly:
 Whole abdominal wall in PPXS; lower ab-
dominal wall in APXS
Posteriorly:
 Lumbar multifidus is generally under active,
Figure 22 Belted Torso Syndrome—central conical cinch particularly the deep fibres—over the lower
from primary APXS picture. levels in both PPXS and APXS and also over
higher levels in APXS.
Centrally:
 The diaphragm ideally functions as a ‘central
piston’ across the centre of the body.
Imbalanced action between the two muscle
systems and above and below the belt
hampers its efficient action.
 Iliacus and psoas function ‘‘at’’ the centre of
gravity of the body. Currently, neither
muscle appears to be ‘fashionable’, particu-
larly iliacus. The function of psoas continues
to be debated in the literature (Penning,
2000; Hansen et al., 2006). We feel that the
important pattern of forward bending is
largely achieved by ‘‘the iliopsoas syner-
gy’’—iliacus anteriorly rotating the ilia on a
fixed femur and also indirectly helping the
sacrum into associated nutation; psoas ex-
tending the lumbar spine; the ‘inner unit’
synergy. Of course the deep abdominals and
multifidus amongst others, also contribute to
this pattern. Andersson et al. (1995) showed
individual and task specific activation pat-
terns between iliacus and psoas for stability
and movement of the lumbar spine, pelvis
and hip in healthy subjects. Clinically, we
Figure 23 Belted Torso Syndrome—central conical cinch see psoas and iliacus are under active in APXS
from primary APXS picture. or show imbalanced activity between the
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two in PPXS (psoas over active; iliacus under Improving lumbo-pelvic-femoral control includ-
active). Future primary research should help ing better Diaphragmatic breathing will help lessen
confirm this. the need for so much mid—upper body global
 The pelvic floor muscles function closely muscle activity.
with lower Tr. A. and I.O, iliacus and L.M. Interestingly, Urquhart (2004) reported transver-
Given their common underactivity, it is sus abdominis in a normal population, consists of
tempting to assume related pelvic floor three regions which differ structurally and function-
dysfunction to some extent. Control of ally. Activation of the middle and lower region was
intrapelvic movement is fundamental to independent of the upper region, demonstrating
controlling the pelvis in space, on the lumbar independent activation above and below the belt.
spine and the hips. The entire neuromusculoskeletal system is
affected by the muscle system imbalance creating
Lee and Vleeming (2000) suggested imbalance in a complex multi system dysfunction—‘a functional
the pelvic floor with a tendency to under-activation pathology of the locomotor system’ (Lewit, 1985);
of the anterior pelvic floor and over activation of Janda, 1978, 1982, 1984)—will result in altered
the posterior pelvic floor. This may be associated alignment and control of the joints which in time
with ‘butt clenching’ and overactivity of the will create:
external rotators of the hip.
Pool-Goudzwaard and Stoeckart (2000) noted
 Segmental dysfunction resulting in local and or
hypertonicity of the pelvic floor in certain patient
referred pain syndromes—both somatic and/or
populations complaining of low back and pelvic
dermatomal, e.g. back pain, hip pain, sciatica.
pain. Clinically, we are seeing some patients with
 Altered quality of afferent information going to
dysfunction related to poor therapeutic interven-
the CNS, thus further changed efferent (motor)
tions which have emphasised ‘‘pulling it up and
output.
holding on’’.  The muscles supplied by those irritated segmen-
Clinically, we see a relationship between pelvic
tal nerves will be affected in two basic ways:
floor dysfunction syndromes and CPC and CCC
(i) Inhibition/weakness—principally of SLMS
muscle activation patterns which hyperstabilise
muscles, e.g. lumbar multifidus (Hides et al.,
the thoracolumbar region, creating segmental joint
1996)—most have segmental innervation.
dysfunction and resultant autonomic effects.
(ii) Facilitation/increased tonus—principally of
Adequate antigravity support for the torso comes
SGMS muscles, e.g. hamstrings, thoracolum-
from below via effective control of the pelvis on
bar erector spinae.
the legs. We see that in the dysfunctional state,  We observe a tendency to patterns of tightness
muscle activation patterns seem to be somewhat
and imbalance within the SGMS related to:
upside down. The lower torso is underactive and
(i) The primary pelvic crossed syndromes:
poorly controlled on the legs while excess SGMS
 PPXS—psoas, rectus femoris, tensor fascia
activity occurs in the upper body, as the patient
lata, gastro soleus—i.e. over active/tight
attempts to ‘‘hold himself up’’. Similarly, the
anterior pelvic, hip and thigh muscles.
breathing pattern is upside down—inadequate
 APXS—hamstrings, piriformis—tight/over-
diaphragmatic excursion and central expansion
active posterior pelvic, hip and thigh
with an excess of accessory muscle respiration muscles.
and upper body tension.
(ii) The shoulder crossed syndrome where the
O’Sullivan et al. (1997) partly observed this
upper limb girdle flexors are generally
tendency in altered patterns of abdominal activa-
stronger and tighter than the extensors.
tion in patients with CLBP—difficulty preferentially
activating the deep abdominals with a tendency to
higher levels of upper rectus abdominis activity. The Neuro-myo-articular dysfunction becomes
Therapeutically, he also cautions the importance of self-perpetuating.
correct and selective activation of the wanted
patterns without reinforcing faulty patterns of
muscle recruitment. The current overemphasis on
abdominal strengthening is misunderstood and mis- Summary of inappropriate antigravity
applied ‘‘core control’’. Particularly in those with and axial control strategies
APXS where this potentially leads to: a further loss
of the lordosis; further imprinting the tendency to a The patient, to a greater or lesser extent, adopts
CAC; and disturbed breathing amongst other things. more primitive and stereotyped strategies for
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118 J. Key et al.

antigravity postures, stability and movement con-  Reduced initiation and control of rotary pat-
trol as follows: terns in the axial spine contributes to segmental
‘blocks’, restricts movement transmission up the
 Changed timing of activation between the SLMS spine, as well as rendering some regions vulner-
and SGMS—delayed and reduced activation from able in movement.
the SLMS (Hodges and Richardson, 1996; Hun-  Increased use of the anterior chest shoulder and
gerford et al., 2003). Early SGMS activity arm muscles in abnormal gripping and ‘fixing
(Hungerford et al., 2003) providing poor axial strategies’ as a response to perturbations in the
alignment, control and stability, thus creating a system. This contributes to propagation of a
‘yanking’ torque on various spinal tissues—par- ‘dome’ and further stiffening of the thorax and
ticularly in the cervical and lumbar spines. cervico-thoracic problems.
 Abnormal ‘feed forward’ postural presetting  The habitual neuromuscular strategy creates
prior to movement. It seems a habituated reflex the joint dysfunction over time, which in turn
overcontraction of the SGM’s around the body’s influences and perpetuates the neuromuscular
centre of gravity with associated disturbed strategy.
breathing, creates the abnormal postural set/
stability strategy from which they attempt to
move. Much of the current over applied approach
 Over-activation of the SGM’s around the body’s to core stability training risks becoming ‘core
centre of gravity with hyperstabilisation of the rigidity training’ and inducing further central
thoracolumbar junction either as: CAC seen in fixing behaviour around the body’s centre of gravity
APXS; CPC seen in PPXS; or more often a with associated dysfunctional breathing patterns
combination of both—CCC intermittently in (O’Sullivan, 2005; Comerford, 2001b; Thompson
APXS and in the Mixed Syndrome. et al., 2004; Hanna, 1988).
 Breathing is affected by this central cinch that
disallows effective descent of the diaphragm and
is associated with breath holding and poor basal
expansion. The patient utilises the accessory Conclusion
muscles of respiration in low load situations and
becomes an upper chest breather. This creates This practical model endeavours to integrate
unnecessary tension in the neck shoulder mus- clinical pattern recognition and analysis with
cles, hyper stabilising the cervico-thoracic junc- current research, and the influence of respected
tion and upper thorax with attendant effects on thinkers in the field.
the cervical spine and shoulders. It invites primary research to further validate the
 Relative mobility of lumbar spine and poor clinical patterns commonly observed.
lumbo-pelvic-femoral control because of re- Appreciation of the model poses significant
duced deep system activity—patient attempts implications for a shift in our thinking in the way
to control pelvis in space from thoracolumbar we approach assessment, diagnosis and therapeutic
fixing strategies using global muscles (CAC: CPC: intervention in spinal pain and related disorders.
CCC). This further stiffens the thoracolumbar Diagnosis based upon local, regional and systemic
junction and thorax. functional neuromusculoskeletal deficits rather
 Active spinal extension is defective and than structural changes and local symptoms alone,
achieved unevenly and primarily from abnormal is more likely to lead to improved therapeutic
SGMS activity. outcomes.
 The patient finds it difficult to activate and An improved understanding of the common
modulate activity between the deep flexors and dysfunctional neuromuscular patterns of response
extensors in order to align and control the spine. and their effect on joint function helps delineate
He frequently employs more primitive, global fundamental principles of therapeutic approach—
system dominant flexor/extensor ‘holding pat- both manual and movement therapies—which
terns’. Stiffness, hyperstabilisation, lack of movement patterns we want to facilitate and gain
movement initiation and control from within improved control, and those which we need to
the thorax means attempts to do so will tend to modify or avoid.
increase thoracolumbar ‘shunt’ or ‘cinch’ e.g. Unfortunately, it has been our experience that
attempts in trying to align spine and /or open many of the programmes being offered in gyms and
chest will evoke a lower anterior rib thrust with work hardening programmes are in fact compound-
or without anterior ‘cinch’. ing the patient’s underlying dysfunction. Hopefully,
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Therapeutic care in spinal pain and related musculoskeletal syndromes: Part 2 119

this model helps us understand why, and predict affect the sagittal lumbar spine, pelvic tilt, and thoracic
why, some patients benefit and why many do not. kyphosis? European Spine 11, 287–293.
Posture and movement dysfunction is inherent in Hides, J.A., Richardson, C.A., Jull, G.A., 1996. Multifidus muscle
recovery is not automatic following resolution of acute first
us all and occurs in a continuum over time, and will episode low back pain. Spine 21, 2763–2769.
be evident before the onset of pain syndromes. We Hodges, P.W., Richardson, C.A., 1996. Inefficient muscular
need to question, do ‘normal’, ‘pain free’, stabilisation of the lumbar spine associated with low back
‘healthy’ subjects, used as controls in research pain: a motor control evaluation of transversus abdominis.
design, move in an ‘‘ideal’’ way, or do they just not Spine 21, 2640–2650.
Hungerford, B., Gilleard, W., Hodges, P., 2003. Evidence of
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