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

Bodywork and

Journal of

Movement Therapies

CLINICAL PHYSIOLOGY

A model of movement dysfunction providesa classification system guiding diagnosisand therapeutic care in spinal pain andrelated 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

KEYWORDSClinical classificationLBP;Diagnosis LBP;Neuromusculoskeletaldysfunction;Movementdysfunction;Back pain;Posture;Motor control

Summary An integrative functional model largely based upon the observation andanalysis of the more common features of neuromusculoskeletal dysfunctionencountered in clinical practice was presented as a working hypothesis in Part 1.

The functional inter relationships between these regional and general featuresand their contribution to the development and perpetuation of local and or referredspinal pain syndromes was explored.

Here we look more closely at clinical patterns of presentation.A simple classification system of clinical subgroups with back pain and related

disorders is offered. These more commonly observed dysfunctional postural andmovement strategies have been distilled into a number of dysfunction syndromeswhich will have predictable consequences.

In beginning to provide a map of the tendencies towards, or actual, changedpostural and movement responses seen in people with spinal pain and relateddisorders, this model provides a valuable reference for those working in the bodywork and movement therapies realm. It is a practical and useful clinical tool to assist

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

�Corresponding author. Tel.: +61 02 93261168; fax: +61 02 93281695.E-mail address: [email protected] (J. Key).URL: http://www.edgecliffphysio.com.au (J. Key).


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

Introduction

Pelvic crossed syndromes

Kendall et al. (1993, p. 72) maintain that ‘‘theposition of the pelvis is the key to good or faultypostural alignment’’. They also state, ‘‘the centreof gravity of the body is considered to be slightlyanterior to the first or second sacral segment’ (p.12). The pelvis, in housing the centre of gravity ofthe body, thus plays a central role in control ofposture and movement—small shifts can effect bigchanges throughout the body.

We have maintained in Part 1 that patients withspinal pain and related disorders commonly demon-strate consistent underactivity of the deep systembut show variable overactivity of the superficialsystem in the strategies they adopt for posture andmovement. How do we further see this?

Observing the habitual standing posture providesa convenient ‘road map’ of the way in which thepatient has adaptively organised himself.

Essentially, we see that there are two principalspatial deviations of the pelvis from the idealsagittal alignment—it is either forward or back.This changed pelvic alignment gives rise to Thetwo primary pictures of dysfunction—the pelviccrossed syndromes. These paradigms have elabo-rated Janda’s (1987a, b) model.

For conceptual clarity, these two and the otherrelated syndromes are seen as follows:

(A) Lateral view1. Posterior Pelvic Crossed Syndrome: (PPXS).

This fairly much represents Janda’s original‘Pelvic or Lower Crossed Syndrome’.

2. Anterior Pelvic Crossed Syndrome: (APXS).This appears to be more common.These two syndromes form the basis of oursimple clinical classification system.It is important to appreciate that only somepatients will demonstrate the extreme pel-vic picture. Some will show some tendency,and others will exhibit a variable mixture ofthe two with a dominant tendency. Under-standing the features of each helps under-stand the patient in front of you—probably amixed syndrome.

3. Mixed Syndrome: demonstrates certain fea-tures of both pelvic crossed syndromes witha primary tendency to either APXS or PPXS.

4. The Shoulder Crossed Syndrome: describedby Janda (1988), is also apparent fromthe lateral view. It is generally, althoughvariably apparent in both pelvic crossedsyndromes.

(B) Anterior and posterior view of posture5. Stratification Syndrome: described by Janda

(1987a, b) encompasses the entire torso andis a meld of the shoulder and pelvic crossedsyndromes and is usually apparent, albeit toa varying extent.

(C) Composite view6. Belted Torso Syndrome. This more fully

describes the observed dysfunction aroundthe central torso and the body’s centre ofgravity.

Posterior Pelvic Crossed Syndrome—thepelvis is back!

Here the neuromuscular system is generally moreswitched on but in an abnormal manner of relativesystemic global muscle system (SGMS) ‘overdrive’,with patchy axial extensor hyperactivity andrelated under activity of the deep system. In itspurest form it may be more common in males. Thepatient ‘looks up’—the ‘pseudo warrior’ althoughhe is tense, unyielding, generally tight and stiff,with poor selective control of movement within thetorso.

Characterised by (Fig. 1):

� Pelvis—posterior shift with increased anteriorsagittal rotation or tilt.� Trunk—anterior translation of the thorax via

thoracolumbar ‘shunt’ from increased thoraco-lumbar extensor muscle activity creates a for-ward-loaded trunk and associated compensatoryanterior pelvic rotation. See Harrison et al.(2002).� Cursory glance shows they look ‘extended’ with

an increased lordosis. This is principally highlumbar and over the thoracolumbar junction.Closer inspection reveals that the lower lumbar

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levels in fact show some relative flexion and arepoorly controlled.� Quick appraisal reveals big belly, bottom and calves

and bulky T/L extensor groups. Puffy superficialtissues and poor definition over the low lumbarlevels 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 atthe 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 thatin movement:

� Patchy extensor synergies tend to dominate inmost movements—particularly thoracolumbar

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Figure 1 Schematic view: Posterior Pelvic CrossedSyndrome. Figure 2 Pure Posterior Pelvic Crossed Syndrome: ante-

rior view.

Figure 3 Pure Posterior Pelvic Crossed Syndrome: lateralview.

Therapeutic care in spinal pain and related musculoskeletal syndromes: Part 2 107


(T/L) extensors. Inhibition of the overactivemuscles can be difficult and they often cannotlet them go, e.g. in standing, forward bending,T/L extensor muscle groups keep holding insteadof eccentrically lengthening (Figs. 2–4).� Trunk extension is generally reduced particularly

through the thorax. In attempting extension,both poor spatial pre-positioning of the pelvisand poor hip and thoracic extension leads tofurther over activation of the extensor musclegroups over thoracolumbar junction (T/L/J) andupper lumbar levels.� Thoracolumbar region becomes hyperstabilised

by overactive erector spinae groups/serratusposterior inferior producing a ‘‘central posteriorcinch’’ (CPC). This over-anchors the lowerthorax, further reducing movement within thethorax and over the thoracolumbar junctionto the upper lumbar spine. This then createsa compensatory functional ‘‘break’’ in themid /low lumbar spine—these levels becomerelatively over stressed in movement with poorintersegmental control (Figs. 5 and 6).� Poor control of the pelvis in space, on the

lumbar spine and hips in posture and movementbecause of reduced systemic local muscle system(SLMS) activity. The deep muscles most involved

in the important patterns of pelvic control arethe lower abdominals (Tr.A; IO), pelvic floormuscles; lumbar multifidus and, we believe,importantly the iliacus psoas synergy. Ideally,we think, anterior pelvic rotation at the lumbo-sacral junction relies a lot on iliacus contributingto anterior iliac rotation and so also indirectly,nutation of the sacrum with coactivation of lowlumbar multifidus (particularly when workingwith a reversed origin and insertion on a fixedfemur). Instead, sagittal pelvic rotation controlis indirectly attempted by abnormal SGMSactivity—anterior rotation primarily from thethoracolumbar extensors and the anterior pel-vic-femoral muscles—particularly psoas. Theapparent anterior pelvic rotation is not con-trolled at the lumbosacral junction.� Decreased hip extension because of tight/over-

active psoas/anterior hip muscles and relatedunderactive glutei. Active hip extension move-ments are associated with increased thoraco-lumbar activity. The poor contribution and

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Figure 4 Pure Posterior Pelvic Crossed Syndrome: poster-ior view.

Figure 5 Central posterior cinch: static.

Figure 6 Central posterior cinch: active.

J. Key et al.108


control of the lumbosacral region towards ante-rior pelvic rotation/low lumbar lordosis tosupport hip extension is interesting. Psoas isoveractive in synergy with thoracolumbar ex-tensors, and iliacus seemingly underactive wefeel. This observed imbalance between psoasand iliacus activity in this group will hopefully beconfirmed by future primary research.� Important standing forward bending pattern.

The pelvis is already posteriorly shifted andanteriorly rotated, and so contributes reason-ably to hip flexion. However reduced control ofanterior iliac rotation and sacral nutation atlumbosacral junction is compensated by in-creased thoracolumbar extensor activity. Thisleads toy� Relatively increased intersegmental flexion over

the mid/low lumbar levels during spinal flexion(and other movements) as the thoracolumbarcontribution to movement is reduced fromoveractive CPC. This becomes exacerbated bythe frequent therapeutic misdirective to ‘tuckthe tail under’ in a misguided attempt todecrease thoracolumbar extensor hyperactivity.� Abnormal axial rotation—lack of general and

rotary mobility in the thorax and over thethoracolumbar junction because of CPC and a‘dome’ (see Part 1), plus poor spatial pelviccontrol, means any rotation imposed on thesystem is forced to occur abnormally in the mid/low lumbar spine.� Dysfunctional breathing patterns—inefficient

diaphragm activity because of CPC which alsoreduces posterior basal expansion. Possiblehypertonus of diaphragm in those with a barrelchest where the attachments of the diaphragmare part of the muscular bracing seen around thethoracolumbar junction.

Anterior Pelvic Crossed Syndrome—thepelvis is forward!

Here, the neuromuscular system is more ‘switchedoff’—both the deep and the superficial systems.However, while less dominant, the superficial systemis still abnormally used though more intermittently.Those with generally low muscle tone fall into thisgroup. In its purest form, it is probably morecommon in females. The patient appears somewhatcollapsed and exhausted while ‘up’.

Characterised by (Fig. 7):

� Pelvis—anterior shift with increased posteriorrotation or tilt.

� Trunk (thorax) backward loaded—posture that ofmore general flexion; adaptive shortening and/or overactivity of the upper abdominals. Flexionof lumbar spine.� Hips in extension with adaptively tight posterior

hip structures.� Quick appraisal shows no buttocks, forward

loaded head posture, thoracic kyphosis—thoraxcollapsed/pulled down towards pelvis, poor calfdevelopment.� Rely more on passive structures for support

(O’Sullivan et al., 2006a)—hang on iliofemoralligaments, adopt wide base of support, kneeshyperextended (Figs. 8–10).

Muscle hypoactivity/lengthened (Fig. 7):

o Lower abdominal group and pelvic floor.o Lumbar multifidus—particularly over lowerlevels.

o Diaphragm—reduced excursion ++.o Iliacus, psoas.o Glutei—reduced postural and movementdemand and often adaptively shortened.

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Figure 7 Schematic view: anterior pelvic crossed syn-drome.



Hyperactivity/adaptive shortness:

o Hamstrings.o Piriformis.o Upper abdominal group including lateral internaloblique.

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 inmovement—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 lumbarspine. Loss of lordosis is marked through lumbarspine. Most active extension is achieved byintermittent thoracolumbar extensor activityand/or further swaying pelvis forward andextending hips to compensate.� Thoracolumbar junction hyperstabilised in flex-

ion. Upper abdominal overactivity or cinchcreates a ‘‘central anterior cinch ‘‘(CAC) whichholds the anterior thorax down, inhibitinggood descent of the diaphragm, increasing the

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Figure 8 Pure Anterior Pelvic Crossed Syndrome: ante-rior view.

Figure 9 Pure Anterior Pelvic Crossed Syndrome: lateralview.

Figure 10 Pure Anterior Pelvic Crossed Syndrome:posterior views.

J. Key et al.110


thoracic kyphosis and ‘dome’ and furtherreducing contribution of thorax in movement(Figs. 11–13).� Decreased hip flexion due to tight posterior

pelvic/hip muscles and hamstrings. This iscompensated by further increased lumbar flex-ion in movement.� Important pattern of forward bending in stand-

ing. Initiated more from overactivity of theupper abdominals (CAC) rather than from poster-ior shift and anterior rotation of pelvis onhips into flexion with associated controlledlumbar lordosis. Resultant over flexion of lumbarsegments.� Poor spatial control of the pelvis, pelvis on the

hips and lumbar spine because of under activeSLMS synergies. Pelvis is placed forward inspatial relationship of ‘reduced SLMS demand’as they hang off the iliofemoral ligaments. Thereis poor spatial pre-positioning of pelvis tosupport lower limb movement. We feel thatboth psoas and iliacus are more under-active inconcert with Multifidus, Lower IO and Transver-sus, creating difficulty in anteriorly rotating thepelvis and controlling the low lumbar lordosis.So-called ‘‘Instability’’ syndromes of the lumbarspine and S.I.J. become predictable.

� Relatively increased intersegmental flexion overlow lumbar levels seen due to poor lumbopelviccontrol as well as compensation for associatedposterior hip and pelvic tightness. Lumbar jointsand intersegmental structures including the discare used in untenable, more unstable andvulnerable end range flexion. Disc, facet andthe plethora of other various ‘‘diagnoses’’ are apredictable consequence over time.� Abnormal axial rotation—a general reduction in

extension and rotation because of CAC andthoracic ‘dome’, plus deficient lumbo-pelviccontrol, means any imposed rotation will abnor-mally occur in the lumbar spine.� Dysfunctional breathing Patterns—CAC greatly

hampers diaphragmatic breathing and basalexpansion—increasing upper chest breathingwith sympathetic dominance. Related upperbody tension and cervical pain syndromes occur.� Important to Note: when attempting to be ‘up’,

performing certain movements or trying too hard,

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Figure 11 Central anterior cinch: acute presentation.Note predominance of general flexion synergies.

Figure 12 Central anterior cinch: chronic picture.

Figure 13 Central anterior cinch: chronic picture.



the tendency is for the patient to flip to using amore primitive gross extensor synergy—princi-pally utilising the thoracolumbar extensors (CPC)in association with their retained upper abdom-inal CAC pattern. The lower thorax then becomesfunctionally converted to a cone shape. We havetermed this a ‘‘central conical cinch’’ (CCC)whereby the anterior, posterior and lateralthoracolumbar junction becomes hyperstabilised.Control of the pelvis is attempted from thishabitual thoracolumbar strategy. The reflex re-active response becomes the postural set fromwhich they move.Van Wingerden et al. (2004) presented a studythat supports the concept of the two PelvicCrossed Syndromes. They examined forwardbending motion patterns of the lumbar spineand pelvis in patients with chronic pelvic girdlepain and chronic low back pain (CLBP). Theyfound those with pelvic girdle pain demonstrated:increased posterior rotation of the pelvis; adecreased lumbar lordosis in standing and whenforward bending, used more lumbar flexion thanhip flexion, i.e. APXS. Those with low back pain:maintained more lordosis when forward bending,i.e. they could not let their extensors (? thor-acolumbar), lengthen. They clearly belong to thePPXS group. Predictably we can expect symptomsto differentially occur in both groups over time.O’Sullivan (2005, 2006) proposes three broadclinical subgroups of CLBP patients, based onthe mechanism underlying the disorder. Withinone of these groups he proposes an underlyingdefective motor control problem—primarily aseither movement impairments or control impair-ments. Under the control impairments subgrouphe further defines his five clinical directionalpatterns based on subjective history and symp-tom behaviour. (O’Sullivan P.B., 2000; O’Sullivan,2004, 2005; Dankaerts et al., 2006a.)There is a close affinity between our approachand that of O’Sullivan. We feel our two primarypelvic syndromes provide a simpler yet elegant,integrated understanding of the underlying in-herent tendency to dysfunction in us all, andimportantly, the commonly observed, magnified,motor control dysfunctions seen in CLBP. We seethat movement and control impairments coexistthough in different proportions, depending on theprimary underlying pelvic postural and movementsyndrome and the presenting stage of thedisorder. Importantly however, we observe similarpatterns of clinical presentation (O’Sullivan P.,2000; Dankaerts et al., 2006b, c) namely:� Anterior Pelvic Crossed Syndrome shows features

in common with his Flexion Pattern. We agree

that this is probably the more common under-lying clinical presentation (O’Sullivan et al.,2006a).� Posterior Pelvic Crossed Syndrome shows fea-

tures in common with his Extension Pattern.� We see that O’Sullivan’s other directional pat-

terns are variations on these basic two patternsat differing stages of neuromusculoskeletaldysfunction.

Mixed Syndrome: display features ofAPXS and PPXS—usually with a dominanttendency towards one or the other

Clinically, this is perhaps the more commonpresentation. Appreciating each syndrome sepa-rately helps see the composite presentation andthe relative dominance of one.

We are finding that the effects of some of thecurrently popular yet poorly conceived and admi-nistered exercise programmes (therapeutic, gyms,personal trainers, Pilates and some forms of Yoga)are further creating and compounding this pictureof dysfunction.

The combination of features of a CPC in PPXSwith those of a CAC seen in APXS creates a CCC (seeabove) in posture and movement function.

Common to all is the tendency to posturally alignand move predominantly in the more primitive,gross, bilateral flexion/extension synergies whichdisallow:

� Appropriate patterns of axial setting and controlto support limb movement.� The important rotary and lateral shifts and

adjustments needed for weight shift and tomaintain axial alignment and equilibrium andcontrol.

Shoulder Crossed Syndrome (Janda1980, 1988)

Common to all three pelvic syndromes is thevariable coexistence of this syndrome.

It is an expression of the typical changes inposture and movement function seen in the uppertorso. It will also affect related function in thelower torso.

It is characterised by:

� Altered posture—round shoulders; increasedupper thoracic kyphosis including a ‘‘dome’’;forward drawn head.

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� Increased activity and tightness of—the anteriorchest and shoulder muscles, long cervico-thor-acic extensors, sternocleidomastoid and scaleni.� Related hypoactivity of—the deep neck flexor

group, the lower scapular stabilisers and relatedspinal intersegmental muscles (Figs. 14 and 15).

Contributing factors to this syndrome are vari-able combinations of the following:

� Dysfunctional breathing patterns.J Breath holding and central cinch in posture

and movement (either CAC, CPC or CCC).J Adaptive SGMS strategy of upper chest

breathing in both low and high demandsituations. Related Hyperventilation Syn-

drome and upper body tension. Cervical painsyndromes inevitable.

� Neuromuscular patterns triggered in response tostress, tension and anxiety (cringing, protection)are more upper body global muscle systemdominant and associated with disturbed breath-ing (see Hanna, 1988).� Most occupations require sustained forward arm

use in predominant flexor synergies e.g. manualphysiotherapist, computer operator.� Adverse training effect, e.g. poorly conceived gym

and exercise routines which over emphasisecontemporary aesthetics over function—the de-sire for ‘good pecs’ and ‘a six pac’ abdominalswhich further stiffen the thorax and reinforce thetendency to dominant upper body flexor synergies.� Overuse of upper limb ‘fixing strategies’ (parti-

cularly in the elderly) to compensate fordecreased lumbo-pelvic control and equilibriumreactions within the body. Watch even youngpeople in the train clinging and hanging off thebars instead of resolving the perturbationsthrough the legs and trunk!

Stratification or Layer Syndrome (Janda1987a, b)

The prescence and related effects of this syndromeexplains the frequent coexistence of cervical andlumbar pain syndromes in many patients.

Janda (1980) saw this as ‘‘another muscularsyndrome’’, yet ‘‘this layer syndrome is a sign of aseverely and deeply fixed central motor dysregula-tion accompanied by very bad movement pat-terns’’. It is surprising how many of our spinalpatients display features of this!

In describing the general dysfunction seen in thetorso, our elaborated construct of the APXS enablesthe layer syndrome to better demonstrate thecombined effects of the pelvic crossed syndromesand the Shoulder Crossed Syndrome. In particular ithelps us see the proclivity for patchy ‘banding’ ofcoarse flexor and extensor activity. This pattern oftrunk muscle activity consistently plays out in allmovements, e.g. reaching up. Predictably, in time,this more obligatory pattern of muscle activitycauses some regions of the axial skeleton to becomehyper-stabilised and stiff while other regions becomeunder-controlled and relatively mobile (Fig. 16).

Viewing the patient’s torso from the front andparticularly from behind, we see layers or bands ofoveractive and hence bulky muscles alternatingwith regions of under active muscles with flattenedcontours. This provides clues to the probable

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Figure 14 Schematic view of Shoulder Crossed Syn-drome.

Figure 15 Actual view of Shoulder Crossed Syndrome.



habitual activation response of various musclegroups.

Observed from behind, we may see ‘banding’ inactivity 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, abdominalweakness particularly transversus and rectus abdo-minis.

Appreciating this pattern of response in muscleactivity presents a significant challenge to effectivetherapeutic movement control. Attempts to facil-itate activity of one hypoactive group will invari-ably risk early and over activation of the alreadydominant muscles, e.g. gaining activation oflumbar multifidus or lower scapular stabiliserswithout dominance of thoracolumbar extensorsand/or cervico thoracic extensors.

Belted Torso Syndrome

Here, we attempt to help further clarify torsodysfunction, with a schematic composite of the

more common static and active patterns of muscleaction as described in the Pelvic Crossed andStratification Syndromes. This representation is aclose up lens, which helps us to appreciate thedysfunction that occurs around the body’s centre ofgravity. It just so happens that the belt line seemsto be a functional demarcation line. We consis-tently see a difference in the muscle activationpatterns above and below the belt in all our

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Figure 17 Stratification Syndrome from behind: instanding.

Figure 18 Stratification Syndrome from behind in lyingprone.

Figure 16 Schematic view of Stratification Syndromeafter Janda.

J. Key et al.114


patients—hyper above and hypo below. The pa-tient’s presenting pattern will be a reflection of hisprimary pelvic dysfunction picture (Figs. 20–23):

(a) Hyperactivity/over-stabilising by the musclesacting 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 aninverted cone—CCC in the mixed syndrome.Harrison et al. (2002) in a normal study,demonstrated that sagittal forward andbackward translations of the thorax initiatedfrom thoracolumbar junction (T12) muscleactivity, created compensatory changes inalignment in the thorax, lumbar spine andpelvic tilt.Our understanding of the consistently clini-cally observed overactivation of musclesaround the body’s centre of gravity seen inour patients has been greatly assisted byHanna’s (1988) notion of the ‘‘Reflexes ofStress’’. Stress is a response to both goodthings and bad. It can be positive (eustress),negative (distress), or relate to trauma, and

causes a specific reflex response of theneuromuscular system. Eustress will invokeassertion, action and perhaps effort and is

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Figure 19 Stratification Syndrome from behind.

Figure 20 Schematic view Belted Torso Syndrome.

Figure 21 Belted Torso Syndrome—central conical cinchfrom primary APXS picture.



extensor dominant. Distress will invokeprotection, withdrawal, fear and is flexordominant. Trauma will invoke a protectiveresponse guarding against pain, e.g. trunklist. These are unconscious, involuntaryrapid reflex motor acts, which primarilyaffect the muscles around the body’s centreof gravity. They are normal adaptive reflexesessential to our survival, which engage theentire nervous system and musculature.However when repeatedly triggered in mod-ern man, they become habitual backgroundneuromuscular activity. The reflex responsebegins to become the postural set fromwhich they move.The effects of emotional state on postureand consequent movement are becomingincreasingly acknowledged (Vleeming, 2000;Mosely, 2004).

(b) Muscle hypoactivity/poor control of postureand movement below the beltAnteriorly:� Whole abdominal wall in PPXS; lower ab-

dominal wall in APXSPosteriorly:� Lumbar multifidus is generally under active,

particularly the deep fibres—over the lowerlevels in both PPXS and APXS and also overhigher levels in APXS.

Centrally:� The diaphragm ideally functions as a ‘central

piston’ across the centre of the body.Imbalanced action between the two musclesystems and above and below the belthampers its efficient action.� Iliacus and psoas function ‘‘at’’ the centre of

gravity of the body. Currently, neithermuscle appears to be ‘fashionable’, particu-larly iliacus. The function of psoas continuesto be debated in the literature (Penning,2000; Hansen et al., 2006). We feel that theimportant pattern of forward bending islargely achieved by ‘‘the iliopsoas syner-gy’’—iliacus anteriorly rotating the ilia on afixed femur and also indirectly helping thesacrum into associated nutation; psoas ex-tending the lumbar spine; the ‘inner unit’synergy. Of course the deep abdominals andmultifidus amongst others, also contribute tothis pattern. Andersson et al. (1995) showedindividual and task specific activation pat-terns between iliacus and psoas for stabilityand movement of the lumbar spine, pelvisand hip in healthy subjects. Clinically, wesee psoas and iliacus are under active in APXSor show imbalanced activity between the

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J. Key et al.116


two in PPXS (psoas over active; iliacus underactive). Future primary research should helpconfirm this.� The pelvic floor muscles function closely

with lower Tr. A. and I.O, iliacus and L.M.Given their common underactivity, it istempting to assume related pelvic floordysfunction to some extent. Control ofintrapelvic movement is fundamental tocontrolling the pelvis in space, on the lumbarspine and the hips.

Lee and Vleeming (2000) suggested imbalance inthe pelvic floor with a tendency to under-activationof the anterior pelvic floor and over activation ofthe posterior pelvic floor. This may be associatedwith ‘butt clenching’ and overactivity of theexternal rotators of the hip.

Pool-Goudzwaard and Stoeckart (2000) notedhypertonicity of the pelvic floor in certain patientpopulations complaining of low back and pelvicpain. Clinically, we are seeing some patients withdysfunction related to poor therapeutic interven-tions which have emphasised ‘‘pulling it up andholding on’’.

Clinically, we see a relationship between pelvicfloor dysfunction syndromes and CPC and CCCmuscle activation patterns which hyperstabilisethe thoracolumbar region, creating segmental jointdysfunction and resultant autonomic effects.

Adequate antigravity support for the torso comesfrom below via effective control of the pelvis onthe legs. We see that in the dysfunctional state,muscle activation patterns seem to be somewhatupside down. The lower torso is underactive andpoorly controlled on the legs while excess SGMSactivity occurs in the upper body, as the patientattempts to ‘‘hold himself up’’. Similarly, thebreathing pattern is upside down—inadequatediaphragmatic excursion and central expansionwith an excess of accessory muscle respirationand upper body tension.

O’Sullivan et al. (1997) partly observed thistendency in altered patterns of abdominal activa-tion in patients with CLBP—difficulty preferentiallyactivating the deep abdominals with a tendency tohigher levels of upper rectus abdominis activity.Therapeutically, he also cautions the importance ofcorrect and selective activation of the wantedpatterns without reinforcing faulty patterns ofmuscle recruitment. The current overemphasis onabdominal strengthening is misunderstood and mis-applied ‘‘core control’’. Particularly in those withAPXS where this potentially leads to: a further lossof the lordosis; further imprinting the tendency to aCAC; and disturbed breathing amongst other things.

Improving lumbo-pelvic-femoral control includ-ing better Diaphragmatic breathing will help lessenthe need for so much mid—upper body globalmuscle activity.

Interestingly, Urquhart (2004) reported transver-sus abdominis in a normal population, consists ofthree regions which differ structurally and function-ally. Activation of the middle and lower region wasindependent of the upper region, demonstratingindependent activation above and below the belt.

The entire neuromusculoskeletal system isaffected by the muscle system imbalance creatinga complex multi system dysfunction—‘a functionalpathology of the locomotor system’ (Lewit, 1985);Janda, 1978, 1982, 1984)—will result in alteredalignment and control of the joints which in timewill create:

� Segmental dysfunction resulting in local and orreferred pain syndromes—both somatic and/ordermatomal, e.g. back pain, hip pain, sciatica.� Altered quality of afferent information going to

the CNS, thus further changed efferent (motor)output.� The muscles supplied by those irritated segmen-

tal nerves will be affected in two basic ways:(i) Inhibition/weakness—principally of SLMS

muscles, e.g. lumbar multifidus (Hides et al.,1996)—most have segmental innervation.

(ii) Facilitation/increased tonus—principally ofSGMS muscles, e.g. hamstrings, thoracolum-bar erector spinae.

� We observe a tendency to patterns of tightnessand imbalance within the SGMS related to:(i) The primary pelvic crossed syndromes:� PPXS—psoas, rectus femoris, tensor fascia

lata, gastro soleus—i.e. over active/tightanterior pelvic, hip and thigh muscles.� APXS—hamstrings, piriformis—tight/over-

active posterior pelvic, hip and thighmuscles.

(ii) The shoulder crossed syndrome where theupper limb girdle flexors are generallystronger and tighter than the extensors.

The Neuro-myo-articular dysfunction becomesself-perpetuating.

Summary of inappropriate antigravityand axial control strategies

The patient, to a greater or lesser extent, adoptsmore primitive and stereotyped strategies for

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antigravity postures, stability and movement con-trol as follows:

� Changed timing of activation between the SLMSand SGMS—delayed and reduced activation fromthe SLMS (Hodges and Richardson, 1996; Hun-gerford et al., 2003). Early SGMS activity(Hungerford et al., 2003) providing poor axialalignment, control and stability, thus creating a‘yanking’ torque on various spinal tissues—par-ticularly in the cervical and lumbar spines.� Abnormal ‘feed forward’ postural presetting

prior to movement. It seems a habituated reflexovercontraction of the SGM’s around the body’scentre of gravity with associated disturbedbreathing, creates the abnormal postural set/stability strategy from which they attempt tomove.� Over-activation of the SGM’s around the body’s

centre of gravity with hyperstabilisation of thethoracolumbar junction either as: CAC seen inAPXS; CPC seen in PPXS; or more often acombination of both—CCC intermittently inAPXS and in the Mixed Syndrome.� Breathing is affected by this central cinch that

disallows effective descent of the diaphragm andis associated with breath holding and poor basalexpansion. The patient utilises the accessorymuscles of respiration in low load situations andbecomes an upper chest breather. This createsunnecessary tension in the neck shoulder mus-cles, hyper stabilising the cervico-thoracic junc-tion and upper thorax with attendant effects onthe cervical spine and shoulders.� Relative mobility of lumbar spine and poor

lumbo-pelvic-femoral control because of re-duced deep system activity—patient attemptsto control pelvis in space from thoracolumbarfixing strategies using global muscles (CAC: CPC:CCC). This further stiffens the thoracolumbarjunction and thorax.� Active spinal extension is defective and

achieved unevenly and primarily from abnormalSGMS activity.� The patient finds it difficult to activate and

modulate activity between the deep flexors andextensors in order to align and control the spine.He frequently employs more primitive, globalsystem dominant flexor/extensor ‘holding pat-terns’. Stiffness, hyperstabilisation, lack ofmovement initiation and control from withinthe thorax means attempts to do so will tend toincrease thoracolumbar ‘shunt’ or ‘cinch’ e.g.attempts in trying to align spine and /or openchest will evoke a lower anterior rib thrust withor without anterior ‘cinch’.

� Reduced initiation and control of rotary pat-terns in the axial spine contributes to segmental‘blocks’, restricts movement transmission up thespine, as well as rendering some regions vulner-able in movement.� Increased use of the anterior chest shoulder and

arm muscles in abnormal gripping and ‘fixingstrategies’ as a response to perturbations in thesystem. This contributes to propagation of a‘dome’ and further stiffening of the thorax andcervico-thoracic problems.� The habitual neuromuscular strategy creates

the joint dysfunction over time, which in turninfluences and perpetuates the neuromuscularstrategy.

Much of the current over applied approachto core stability training risks becoming ‘corerigidity training’ and inducing further centralfixing behaviour around the body’s centre of gravitywith associated dysfunctional breathing patterns(O’Sullivan, 2005; Comerford, 2001b; Thompsonet al., 2004; Hanna, 1988).

Conclusion

This practical model endeavours to integrateclinical pattern recognition and analysis withcurrent research, and the influence of respectedthinkers in the field.

It invites primary research to further validate theclinical patterns commonly observed.

Appreciation of the model poses significantimplications for a shift in our thinking in the waywe approach assessment, diagnosis and therapeuticintervention in spinal pain and related disorders.

Diagnosis based upon local, regional and systemicfunctional neuromusculoskeletal deficits ratherthan structural changes and local symptoms alone,is more likely to lead to improved therapeuticoutcomes.

An improved understanding of the commondysfunctional neuromuscular patterns of responseand their effect on joint function helps delineatefundamental principles of therapeutic approach—

both manual and movement therapies—whichmovement patterns we want to facilitate and gainimproved control, and those which we need tomodify or avoid.

Unfortunately, it has been our experience thatmany of the programmes being offered in gyms andwork hardening programmes are in fact compound-ing the patient’s underlying dysfunction. Hopefully,

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this model helps us understand why, and predictwhy, some patients benefit and why many do not.

Posture and movement dysfunction is inherent inus all and occurs in a continuum over time, and willbe evident before the onset of pain syndromes. Weneed to question, do ‘normal’, ‘pain free’,‘healthy’ subjects, used as controls in researchdesign, move in an ‘‘ideal’’ way, or do they just nothave pain yet? O’Sullivan et al. (2006b), examiningmuscle activation patterns in different uprightsitting postures in a pain free population, is aninteresting study which by default, indicates theinherent tendency to altered, less ideal musclefunction in us all.

Evidenced-based practice is becoming de rigueur.However, to date, some of the outcomes have notbeen particularly impressive as shown by Ferreiraet al. (2006) in a systematic review of specificstabilisation exercise for low back and pelvic pain.

Appreciating the more common presenting pat-terns of dysfunction as described in this model, willhopefully facilitate more functionally relevant andclinically useful research design and so improvedoutcomes in the future.

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