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KINETIC CONTROL . .

The Management of Uncontrolled Movement

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ELSEVIER

Churchill.Livingstone is an imprinr of Elsevier

Elsevier Australia. ACN 001 002 35 7 (a division of Reed Intemational Books Australia Pty Ltd) Tower L 475 Victoria Avenue, Chacswood, NSW 2067

il> 2012 Elsevier Australia

This publication is copyright. f.xcept as expressly provided in the Copyright Act 1968 and the Copyright Amendmem (Digital Agenda) Act 2000, no pan of this publicaon may be reproduced, stored in any rerriev;il sysrem or rransmitted by any means (including electronic, mechanical, microcopying, photocopying, recording or otherwise) withom prior written permission from the publisher.

Every auempt has been made to trace and acknowledge copyright but in sorne cases this may not have been poosible. The publisher apologises for any accidental infringemem and would welcome any information to redress the situation.

This publication has been carefully reviewed and checked to ensure that the conrem is as accurate aod currem as possible ar time of publication. We would recommend, however, thac the reader verify any procedures, treatmencs, drug dosages or legal comem described in this book. Neither the author, the conrributors, nor the publisher assume any liability for injury andor damage to persons or property arising from any error in or omission from this publication.

!'fational Library of A\!Stralia C

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This book presents a comprehensive system for che assessment and reuaining of movemem control. lt has been in evolution for the last 25 vears.

Unconuolled movemem has a significant impaa on che. development of move-ment disorders and pain. The scienti.fic support for the process of the assessment and rerraining of unconrrolled movement has been steadily expanding panirularly in e.he last 10 years. The influence of uncontrolled rnovement on symptoms, especially pain, movemenc function, recurrence of symptoms and disability is now well established. We believe chat in the next 10 years the literature will support tl1at me presence of uncontrolled movement will also be recognised as a prediaor of injury risk and as having an influence on performance.

Uncontrolled movement can be idenrified by movement control tests. People wich pain demonsuate aberrant movement pattems during the performance of these movement control tests. A growing body of evidence supporu the use of movement control tests in the assessment and management of chronic and rerurrent pain. The identi.ficarion of uncontrolled movement in terms of the site, direction and threshold of movement impairment is a unique subdassification system of musruloskeletal disorders and pain. The movement testing process proposed enables the dassification of uncontrolled movement into diagnostic subgroups that can be used to develop dient-specific. retraining prograrns. This process can determine management priori-ties and optimise the management of musculoskeletal pain and injury recurrence. Subdassification is now recognised as being the comerstone of movemem assess-ment and the e'lidence fer subdassification of site, direction and threshold is growing. This book details a struaured system of testing, dinical reasoning and specific retrain-ing. This system

-Pref~~e Recurrent musculoskeletal pain has a significant impact on health care costs,

employment producvityand quality oflife. Unconuolled movement can be identi-fied by observation, and corrective reuaining of this unconrrolled movement may have an mtluence on onset and recurrence of symptoms. To date, outcome measures in terrns of changes in range and strength, have not influenced the onset and recur-rence of injury. The ability to assess for uncontrolled movemem and to retrain move-ment control is an essential skill for ali clinidans involved in the management of musculoskeletal pain, rehabifation, injury prevention, and those working in health promotion. sport and occupational environrnents. Preventing e.he recurrence of mus-culoskeletal pain can both influence quality of life and have an economic impact.

Movement control dysfunction represents muJtifaceted problems in the movement system. Skills are required to analyse movement, make a clinical diagnosis of move-ment faultS and develop and apply a patient-specific retraining program and manage-ment plan to

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:':JI Foreword

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approaches to musculoske_letal pain. The authors have organised the rationale and methods from these varying approaches inco a comprehensive approach. Comerford and Mott.ram have done a thorough job of desoibing ali aspects of what could be considered the 'psychobiosodal' model of analysis and trearmem of musculoskelecaJ pain. The timeliness of this book is reflected by the incorporation of their concepts to the lncemational Classification of Functioning, Disability, and Health. As stated previously this book has its particular value in the comprehensiveness and detailed desoiptions of possible tissue dysfunctions as reported in the literature, methods of analysis ami treatrnent The reader will be truly impressed by the many complexities of the movement systern and the rigorous analysis that is required to understand, diagnose and treat me dysfunctions lhat can develop and contribute to pain syn-dromes. The authors have rruly provided an outstanding te.xt in its inclusive and thorough discussion of !he tapie of movement dysfunction.

X

Shirley Sahrmann, PT, PhD, FAl7TA Professor Physical Therapy, Neurology, Cell Biology and Physiology

Washington Universiry School of Medicine - Se. Louis

The contem of this book has been a work in progress since 1988. The background to the developmem of the assessmem and reuaining of uncontrolled movement has been influenced by the work ofShirley Sahrmann, Vladami.r landa, Gwendolyn Jull, Paul Hodges, Carolyn Richardson and Maria Smkes. Since 1995 many colleagues w;thin Kinetic Control and Performance Stabilicy have helped with the development of !he dinical tests and the consolidarion of theoretical frameworks. Erik Thoomes comributed to the dinical reasoning process in Chapter l. We would ver much like to thank ali these people for their contribution through inspiration, advice, support or feedback. We both appredate the support of our family and friends a.nd in par-ticular Mark' s wife Selina, without whom he would not have found the time to devote to this projecc.

Technical Reviewer Prue Morgan M.App.Sc (Rosearch). B.App.sc (Physio) Grad Dip NeuroS

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Uncontrolled movement

The key w managing movement dysfunction is thorough assessment. This indudes the deter mination of any uncontro lled movement (UCM) and a comprehensive dinical reasoning process by the clinian to evaluare contribung factors which influence the development of UCM. This fiJst

Movement system

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Behavioural and affective 'yellow ftaos'

movement anxiety fear-avoidance peor coping skiils depression blame transference abnonnal pain beliefs exaggerated pain behaviour

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physiologicaVfuncticnal accessorytranslational afferent feedback

Links all sys!ems structure and support energy storage passive force transmission propoception and feedback

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motor control via sensory-motor integraon neurodynamics

....... --.. -- -- --

Figure 1.1 lmer-related components of the movement system

(Sahrmann 2002; O'Sullivan et al 2005) and control impairments (O'Sullivan et al 2005; Dankaerts et al 2009 ). Ali of these terms describe aspeas of movement dvsfunction, ianv of which are linked to UCM. , -

The focus of this text is co describe UCM and explore the relationship of UCM to dysfunction in the movement system (Comerrord & Mottram 2011 ). Movement dysfunction represents multi-faceted problems in the movement system and the therapist needs the tools to relate UCM and faults in the movemem system to symptoms, recurrence of symptoms and disability. Skills are required to analyse movement, make a dinical diagnosis of movemem faults and apply a patiem-specific retraining program and management plan to -

r'.J Kinetic Control: The management of uncomrolle movemem 1

Jette l994). Movement faults are related to disa-1 biliry. Fore.'

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/ Motor controrresearch

and training model {Hodges, Jull, Richardson) ~

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Force closure.model' {Mooney, Stoeckarf~

Vle~ming, ~ee)

Moef:~fol[nical'

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.l\iialysis and developmenlof Movement analysls model

lComerford ~ Mottram)

i .rnovemen~analyssand:

. movment-dysfunCtforndiagnosis . Sahrm~nrr (!Jirection,susceptible. iO'.motioo J

~comerford;&.Mbttralll'-.Kinetie:Contrct (Si!e.amf dr;cti6riofunoonroi1ect movem911t)

-. 0'Sullmand!Danliaerts. (;onirof inpairmeni)

---Figure 1.4 i he development o the movemem analysis model

clinical evidence (Emery et al 201_0; Rydeard et al 2006). Box l.l lsts sorne useful approaches to pain managemem and/or movement dysfunction to explore. i\fany e.xercise approaches have either stood the test of time or their popularity suggests that people who practise them feel or function better.

Whilst the various exercise concepts feature ds-tinctive elements that characterise their approach, there are features that are common co ali approaches (Box 1.2). These commou features may comribute to good function and warrant d oser nspection and further 'investigation. Breathing control is a key feature in many of these merapies. The link benveen respii atory disorders

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Box 1.1 Usefut alternative therapies in the management of movement dysfncton

Tai ciii The Mexander technique Yoga Pi lates ?hysio ball (Swiss. ball) feldenkrais tlilartal arts GYROTONIC-

Box 1.2 Common features in alternatve therapies.

Multi-joint movements Slow movements

low force movements large range movements Cocrdination and. control ot rotation Smooth transitiori. of concentric-eccentric. movement Awareness of gravity

Conceptof a 'core' Coordnated breathing Awareness of posture lnterinittent static hold of position Conuol ot the centre of mass of one body segment

v.~th respect to ~djacent segments Proximal control for distal mo~emenr

Positive memal artitude

and increased risk of developmem of back pain has recently been established (Smith et al 2009) and altered breathing patterns have been noted during lumbopelvic motor control tests (Roussel et al 2009c).

Effective intervention requires the therapist to have a thorough understanding of me mech-anisrns of aberrant movement pattems, an abilicy to condently diagnose and dassify the move-ment faults and to manage these dysfunctions. Guidelines far a comprehensive analysis of mave-ment dysfunction have been described with factors the therapist needs to consider in Box 1.3

Box' T.3 Procedure for analysix of movement dysfunction.

Uncontrolled movement: assessment and retraining guidelines l. Assess, dagnose and d~sify movementil'! terms o

pain and dysfunction froin a moior- coritrol and a biomechanical perspective.

2. Develop a !arge range ofmovement retrainng strategies to. estabfish optJmariunctional control.

3. Use a clinical_reasoning frameworR to.-prioritise the dinical dedsion-making challenges. experienced in concemporary d inical practice.

4. Develop ar assessment. frameworit-that addresses the four key criteria ielevant to dysfnctional movenient a. diagnosis of movement dysfunction

. site and direction of uncontrolled movement ii: uncontrolled transfatfort ' - -

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iii. uncontrolled range of. motion. -iv. niyofascial and articular restrcton v. aberrant guarding respooses-

b. diagnosis of pain-sensitive tissue(s)-i. patho-anatomical structure

c. diagnosis of pain mechanisms i. peripheral nociceptive (inflammatory ar

mechanicat) ii. neurogenlc sensitisation

d. identification o relevantcontextuaf ractors (Verbrugge & Jette 1994)

environmental factocs. (extra-individual). (e.g. physical and social context\

(Comerford & Mottram 2011)

ii. personal iactors (intra-individual) {e. g: lifestyte anctbeh?viouial changes, psydiosocial: attrilMs, 'Pin~ ~li ills) .

5. Make. finks. 6etween. uncontrolled; movement arid pain and other sYmptoms, dy_siunction. reeurrence,. risk of iniury and performance.

6. Mal

\ n Kinetic Control: The managemem of uncontrolled movemenc )

(Comerford & Mouram 2011). An understanding ) of the inter-rclationship of the elemems of the

movemem is needed alongside an understanding 1 of faoors relating to normal movement, function

and dysfunction (Chapcer 2). A sound dinical 1

reason ing process underpins this process lO ) optimise the assessmem and retraining strategy.

This process is described in the fo llowing ) section .

The efficient and effecve managemem of UCM 1 in relation ro symptoms, disability, dysfuncton,

recurrence, risk of injury and performance is dependent on a comprehensive assessmem. This

should lead to a specifi.c action plan for the J individual patiem. E.xerse protocols do have a place in the management of musculoskeletal

) disorders. However, because of differences in presentation and diagnostic subgroups, effective

1 managemem is dependent on assessment analy-) sis and managemenc planning. E.-

- Kineti;c Contr~l: The: managemenr of unconu:oued"';ovement -=--~. Table 1.3 Example ol uncontrolled movement and restrictons at the shoulder girdle

Unconuolled lntersegmental Range movement translation

Uncontrolled anterior Uncontrolled translanon at the sea pula glenohume,al 101nt '.orwaro ;ilt

Restriaion Articular Myofascial Postenor uanslaaon ~esuic:mn o at glenohumeral 01nt medial rotation

(infraspinatus/ :eres m1nor)

Table 1.4 Example of uncontrolled movement and restrictions at the lumbar spine

Uncontro/led lntersegmental Range movement translation

Uncontrolled Uncorurolled 1ntersegmental lumbar flex1on translation {e.g. at L4 or lSJ

Re.stricrion Articular Myofascial Resttiction of Restr1ction 1n hio 1ntersegmental flexion (hamsmngs, translation superficial gluteus

max1mus)

w;th shoulder pain (Morrissey 2005), as can uncomrolled range. illustrated:withCnconrrolled fotward tilt (Lin et al 2005, 2006). lmerestingly, this uncontrolled forward tilt (and loss of back- ~ ward tilt) corresponds to a decrease in serrarus anterior activity, which confinns the role of ser-racus in produdng backward til ting of the sea pula (and controlling forward tilting).

Table 1.4 provides e.xamples of UCM in terrns of translation and range at the lumbar spine. UCM in the lumbar spine has been described in terms of uncontroJJed lumbar lexion (Dankaerts et al 2006a; Luomajoki et al 2008; Sahrmann 2002; Vibe fersum et al 2009). UncontroJJed lumbar tle:cion has been associated with either uncontrolled range of lumbar flexion relative to hip tlexion, or abnormal segmemar initiation of lumbar motion during forwa rd bending and other fle'lhoraac~~(e.9.

Retrain site and diredion o unconlrolfed movemen! t

~n et'..eocafsarnl!Js an:air tn coolrol ai;!aior lit

and::rodooe po...r posencrglde at 11>1

glenohumarol joinl)

Regain exiellSIOiity of global mobility musde system and eddress any neural sansi1ivir

R~aln exlensibilily ofiffa;pinarus

Figure 1 .6 The management plan developed fer a person with snoulder pain and unccntrolled scapula f01Ward nlt

6 Relate pain mechanisms to presentation Pain mechanisms can have a significant intluence on movement control and consideration of changes v.;thin. the nervous system is a key com-ponem of the dinical reasonjng process (for more decailsee Breivik & Shipley2007; Butler & Moseley 2003). fr is essential to consider the intluence of mechanical nociceptive or inflammatory pain in

movementcontrol (e.g. the influence on proprio-ception, allodynia and motor control). Useful screening too Is for neuropathic pain could indude the S-IANSS (Bennen et a! 2005) or the pain DETECT questionnaire (Freynhagen et al 2006), while the McGill Pain Questionnaire (Melzack 1975; Melzack & Katz 1992) also evaluares the affective aspeas of pai.n for a patient.

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~ Ki netic ConttoL The managemem of uncontrolled movement )

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Taige1loca! muscle system Taryat gkloal musoe system Retrainin9 ol lhe lumbill global s1allili1y mu$Cles to

retraincontrol olrange,(e.g. reaain etllciency o/

supen\cial mul:l~ijus and

Retrainingot le lwnllar spine leca! stability muscles

10 retrain oonlrol of 1ranslatioo {e.g. ihe

inlegrated inner ~ide1,. lransversus abdominis,

segmenial lumbar mui~dus, Retrain sile and direction oi spinaJis :o conlrol naxlon and

uncontrolled movement produce eJml!lsion)

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posteriot !ascicuiof pscas, dial>hragm. palvic oor)

Manual !etapy

j Micular motiisalion otjoint ~1rlc:ions j R29ain sxtens:birity of global mobiity lllllscle

sysiem al(f address any neural sens11Mty Regain exiensibi6ty oi hamsMgs ano.

superlicial gluteus maxlmus

) Figure 1. 7 The managemeru plan developed for a person wrth back pain and unconuolled lumoar flex1on

' 7 Consideration of tissues or structures contributing to symptoms The site and direction of UC.M may match the pathology identified. For example, people with a shoulder impingernem demonstrate UCM at the

l scapula (Morrissey 2005). AbnonnaJ qualicy of 1 rnotion in spinal lumbar segmems has been dem-

onsrrated to be associated with spondylolisthesis ! pathology (Schneider eral 2005). The link

berween tissue stress resulti.ng in B,athology and J abnormal range or quality of movemem is becom-

ing more evidenL The therapist needs to find a link berween the UCM and any presenting~ pathology.

8 Assess for environmental and personal factors Personal factors ( e.g. lifestyle and behavioural changes. psychosocial attributes, coping and activity accommodations) and environmental faa ors ( e.g. medica! care and rehabilication, med-icado os and other therapeutic regimens, externa! suppons. physical and social environment) should also be assessed. Personal factors com-monly assessed within che come.xt of physical

) cherapy indude items sud1 as depression. anxiety, coping sllls and cogn.ition. These can be

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objeaively assessed (and reassessed) with valid and reliable questionnaires such as the Pain Coping Invencory ( PCl; Kraaimaat & Evers 2003 ), Tampa Scale of Klnesiophobia (TSK Swinkels-Meewisse et al 2003; Vlaeyen et al 1995), Fear Avoidance Beliefs Questionnaire (FABQ; Waddell 1998) and the Pain Self-Efficacy Questionnaire (PSEQ; Ncholas 2007; Nicholas et al 2008).

Once the site and direction of UCM have been established, effecve rehabilitation should ensure that rnovernent dysfunction is addressed ilirough-outfunctional tasks. Control ofmovememduring functional acvities, and awareness of the UCM during posture, daily activities. spon and training prograrns should be promoted_ For examp!e, a person with uncontrolled scapula downward rotation needs to be aware of this rnovement fault during daily acvities such as reaching for a cup in a cupboard. A person with uncontrolled lumbar tlexion needs to be aware of this move-ment fault when bending forwards to tie up their shoelaces.

9 lntegrate other approaches or modalties There are many other cherapeutic modalities that can influence the correction of moveme.nt faults. Table 1.5 details sorne examples. This is not imended to be an exhaustive list but illustrates

Unconuo~ed movement u;;. 1 1 1 11 Table 1.5 Examples of therapeutic modalities that can influence the correction of movement faults

OTHER THERAPEUTIC EXAMPLES APPROACHES Palhophysiological approaches Ice. heat, elearotherapy, medicat1on Articular approacnes Jo1nt mobliisation and manipulat10n (Maitland et al 2005; Cyriax 1980;

Kaltenborn et al 2003) : rgonomic and environmental factors Work place assessment. postura! advice Neurodynamic approacnes Neurodynam1c mobdisation (Butler 2000; Shaddock 2005) Sensory-mmor oo~roaches Neuromuscular acilitauon (Rood 1n Gotf 1972), !!obath 'nonnal movement'

(Bobath 1990), neurofunCtJonal training (Carr & She;herd 1998), neurc~nsory approach (Homs-.al 2009)

Sof'. tissue approaches Massage trierapy (Cha11ow 2003) Psycnosocial aporoaches 3e~vioura1 evaluation and the1aoy (Waaden 1998; Wocy et al 2008) Biomechanical approacnes T;ping, orthotics, brac1ng

useful adjuvam modalities in recraining UC.M, managing pain. mobilising restria ions or treating pathology.

10 Consider prognosis Although the management of sympwms has been the prirnary aim in the treatment oi musculoskel-etal disorders, research has also demonsuated links becween UCM and dysfuncon, disability and the recurrence of symptoms. lt is there.fore appropriate that dysfunction and disabiliry are also considered, atongwith symptoms. when pro-viding a prognosis for recovery in the manage-ment of musculoskeletal disorders. The timeframe for expected improvemem in symptorns should be considered independently of the timeframes for recovery of dysfunction and disabilicy when making prognostic judgments for recovery.

Physiological tissue repair timelines have been well researched and are reasonably well de.fined. In more acute (Tess than 6 weeks) conditions, these provide a useful guideline. ln more chrnic (more than 12 weeks) conditions, other prognos-tic factors become more important. A systematic review on prognostic factors in whipfash-associated disorders established that factors related to poor recovery induded: female gender; a low leve! of education; high initial neck pain; more severe disability; higher levels of somatisa-tion and sleep difficulties (Hendriks et al 2005; Scholten-Peecers et al 2003). >ieck pain intensity

and work disability proved w be the most consistem predictors for poor recovery in these srudies.

The relative influence of faaors beyond physi-ological processes is a contemporary research subject and there is a growing body of evidence indicating that sodo-demographic, physical and psychological factors strongly a.ffea short- and long-term outcomes. These faaors must be taken into consideration when establishing a real istic timeframe fo r when dysfunction, symptoms and disability could be expected to improve and by how much.

As noted in Box 1.3, when a patiem presems wich neuromusculoskeletal pain and dysfunction. it is good cl inical pracce to assess and identify four key cri teria: 1. diagnosis of movement dysfunction 2. diagnosis of pain-sensitive or pain-generad ng

structures 3. diagnosis of presenting pain mechanisms

- peripheral nodceptive and neurogenic sensitisation

4. evaluation and consideration of contextual factors.

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1 Diagnosis of movement dysfunction (site and direction of uncontrolled motion) The initial priority is to identify the site and direc-tion ofUCM that best correlates with the patient's presenting mechanical sympt0ms. In complex presemations, there is frequently more than one site of UCM. When chis is the case, it is useful t0 identify whether one site is the site of primary dysfunaion and whether che other site is com-pensming for the primary one. If there are obvious restriaions i:hat are causing

compensatory UCM, it is very effecve for the therapist to work t0 achieve nonnal mobility of these resuictions early in the management plan (see Chapter 4).

The therapist should also identify if there is a priority to retrain local stability musde funaion early or if chis can be reuained later in che reha-bilitation process. Similarly, che cherapist should identify any concributing musde mbalance issues related to che dysfunction, such as altered length and recruitment relationships berween mono-articular stabiliser muscles and multi-articular mobiliser musdes. [f the:se: imbalance:s are: idemi-fied, the global stabiliser muscle recruitmem effi-dency should be retrained to recover aaive control through the full available range of motion, and the gfobal mobility musde exrensibiliry should be restored.

2 Clinkal diagnosis of pain-sensitive or pain-generating sttuctufe(s) The therapist should idemify the struaure o tissue that is the source of the symptoms or pain that the patient complains o.f. Patients who presem 'l'lith a chronic or recurrem condition fre-quently repon more than one tissue conuibuting to the pain experience. The dinical reasoning process that identifies a variety of pain-sensitive tissues requi res a thorough understanding of tissue anatomy and physiology, a know[edge of the mechanism of injury (if there is one) and an understanding of the rypical responses of differ-ent tissues to stress and strain and injury. All avail-able therapeutic skills, tools or modalities can be utilised t0 best provide an optima! environmem lo allow and promote tissue healing and to control or manage the presenting signs and ~ympwms. Contemporary dinical reasoning in patients

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with chronic pain suggests it is more appropriale to e.'C]) lore factors affecting impairment of func-tion and partidpation than to attempt lo diag-nose specific strucrures or tissues as a source of nodception.

3 Clinical diagnosis of presenting pain mechanisms lt is essemial to have an understanding of ch~ relevant pain mechanisms contributing to any individual's pain pres.entation. In a person with chronic or recurrent pain it is common lo find differem mechanisms contributing w their sy,mp-loms. Melzack's ( 1999) neuromatrix theory of pain proposes that pain is a multidimensional experience produced by characteristic 'neurosig-narure' pattems of nerve impulses generated by a widely distributed neural nerwork in the brain. 1t proposes that che output pattems of the neu-romatrix acrivate perceptual, homeostatic, and behaviouraL responses after injury, pathology or chronic stress. The resultant pain expeence is produced by the output of a widely distribmed neural network in i:he brain rather than solely by sensory input evoked by injury, iuflammation or other pathology (Moseley 2003). Therefore, pain is a multi-system output that is produced when a conical pain neuromatrix is acrivated.

Ideally, an attempt should be made t0 deter-mine the reJevant proportions of these mech-anisms; that is, the degree t0 which peripheral nodceptive (mechanical/ inflamrnatory) elements contribute t0 the pain e.'C])erience and the degree to which neurogenic sensitisation is present. Behavioural, social and psychosomatic influences further comribute to the multdimensional nature of chronic and recurrent pain. The dominant mechanisms need to be addressed as a prforizy. A multidisdplinary and multidi-mensional approach can be more effeaive in managing symptoms, both in the shon and long term.

4 Evaluation and consideration of contextual factors The therapist should assess for the intluence of contextual' factors - both personal and environ-mental - on the patient's signs and symptoms and e..'Cplore how these might rela ce tO UCM (Figure 1.8).

Four key criteria witbin clinlcalreasoning framework t . Diagnosis of movementdysiunction

~ - sita am! dfrection of unccntrol!ed motion. ~ : 2: Diagnosis oi pansensitive tissue(s) (linked to pathology.). . 3, Diagnosis.o pain mecllanisms _

- . peripheral oociceptive 7 - - - neurogeriic sensitiSation. '

D . Kinetic-Control: T,he managemem of uncor~tr~ll:~.~oveui~nt ~\

Figure 1.11 he rehabilitation problem solving iorm, odapted from Steiner et al 2002

facilitates the analysis of patient problems, focus-ing on specific targets. and relating saliem disa-bilities w relevant and modifiable variables.

This form can indude the diagnostic criteria within the dinical reasoning framework described in Figure 1.8 in order w assess the key criteria that relate to the funaional lif,l}itations. This

) process identifies links berween"fadors .in the diagnostic framework and subsequent funaional

) limitations so that the mechanism behind the dysfunction can be addressed to.optimise efficacy

) of imervemion. The form in Figure l.11 can include the dagnostic framework as described in

} Figure 1.8. The essence of both the ICF model of function-

) ing and disabiliry and the RPS form is that an ) individual's ( dys-)functioning or disability repre-

sents an interaaion berween the health condition ) ( e.g. diseases, disorders, injuries, traumas and all

factors in the diagnostic framework) and the con-) textual factors (i.e. 'environmental factors' and

'personal fadors'). The interadio.ns of the com-) ponents in the model are two-way, and interven-

tions in one componem can pocentially modify ) one or more other components. ) ) 18

In the !CF model !he horizontal dimension of a health status or profile is Lllustrated as being influenced bv elements in !he vertical dimension. The lCF mode! could be considered a method of dassification, describing a heal!h condition at a particular moment, such as a picture or 'freeze frame'. In contrast, the disablement process rep-resents constructs within the ICF model under !he constant influence of risk factors and hence could be described as more like a 'film'.

To summarise, 'health' can be described in cerms of.

health condition (using !CF temlinology) course (normal or aberrant) prognostic profile patient's perspective.

Clnica! decision-making should start from the patiem's perspective and intervenons sh0uld be primarily aimed at those aspem of impairment !hat have a direct bearing on disabiliry and/or fundional limitations. In the subjeaive e.xamina-tion, the patiems wili define !heir perspecve- in terms of disability and functional limitaons: for example, !he inability (dueto low back pain) w bend over from standing to tie shoelaces or the inability (due to shoulder pain) to reach into a cupboard above!he shoulders. These self-reponed syrnptoms are explored further within the phy-sical examination to inform the dinical decision-making process. For example, if patients Nilh low back pain are unable to actively control movemems of the low back, especially fle.xion control while performing a waiters' bow (Luoma-joki 2008), lhen clinicians should direa their imervention towards correaing the neuromus-cular impairment underpinning this. Similarly, if patients with shoulder pain are unable to actively control the (re-) positioning of the scapula during fundional movements (Tate et al 2008; von Eisenhart-Rothe 2005), then clinidans should aim their imervention strategy at reganing this control. ;rherapists should not solely focus on addressing an isolated pathology, but use frame-works such as !he disablement assessment model w facilitate effective intervention. The link between specific movement retraining and improvement in functiona1 tasks is now well supported by evidence (Jull et al 2009; Roussel et al 2009b ).

Praaitioners need to have the skills to identilY and recrain movement faults. These skills should be imegrated into current practice and !he patient

.-_ w~~0n;rl1ea movement fi.fiUIM 1., 1 11 managed in a holistic way with consideration of ali asperu of the human motion system, and the influence of bo!h intra- and extra-individual factors. An understanding ofhow UCM can influ. ence pain is essential in the management of

neuromusculoskeletal disorders. To assist in this reasoning process the anatomical and physiologi-cal principies are reviewed in Chapter 2 and how pain, dysfunction and pathology can effect UCM is explored in Chapter 3.

Bellamy, N . Buchanan, W.W., Coldsmith, C.H . Campbell, J., Stin. l.W., 1988. Validation srudv of W01'vlAC: a health status ~crumem for measuring d inically irnponam patiem ;elevanl outcomes co antirheumac drug therapy in patiencs with osceoartllritis of the hio or !mee. Journal of Rheumatology 15 ( l2), 1833-1840.

Sennen. M.I.. Smlb, B.H .. Torrance. N., Poner, /., 2005. The S-L-\NSS score for dentifying pain of predo'minany neuropathic origin: validation for use in cUnical and postal research. Journal of Pain 6 (3), 149- 1513.

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Solton, f.E., Humphreys, B.K. 2002. The Boumemouth Questionnare: a shortform comprehensive ouccome measure. !f. Psychometric propenies in neck pan paciems. Joumal of Manpulative and Physiological Therapeutics 25 (3), 141- 148.

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Buder: D., Moseley, L. 2003. 6.xplain pain. NO! C'ublications, Adelaide. ,'\uscralfa.

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Chaitow, L . 2003. Modern neuromuscular techniques -advanced soft tissue techrques. Churchill Llvingscone, Edinburgh.

Comerford, M./., Mottram. S.L.. 200la. Functional srnbility rmainiog: principies and suategies for managing mechanical dysfunction. .\.Janual Therapy 6, 3-14.

Comerrord, M.J . .\.Jonran1, S.L, 200l b. Movement and stabilicy dysfunction. Manual Therapy 6, 15- 26.

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Coppieters, .\-1. W.., Stappaens, KH., Everaen. D.G . Staes, EE, 2001. Addition of test components dwing neurodynamic testing: effect on range of motion and sensory responses. Joumal of Onhopaedic and Sports Physical Therapy 31 (5), 226- 235.

Coppierers, M .. Stappaens, K, Janssens, K. Jull, C., 2002. Reliabiiicv of detecting 'onset of pain' an'd

'submaxim~l pain' during neura! provocation testing of the upper quadrant Physiotherapy Research Intemational 7 (3), 146- 156.

Cyriu J.H., 1980. Textbook of onhopaedc medicine. vol. 2. t reaunem by manipulation, massage and injection. Balliere Tfndall. London.

Dankaerts. W., O'Sullivan, P.B .. Straker, r . M . Bumen. A.F., Skouen. J.S., 2006a. The incer-e.'(aminer reliablicv of a dassifi~acion method for ' non-specific chronic low back pain paems with motor conuol mpairmenL Manual Therapy ll ( 1 ), 28- 39.

Dankaens, W., O'SuUivan, P .. Bumen,. A.., Straker, L.. 2006b. Altered panems of supertidai trunk musde aaivation duri ng sitting in nonspecfic c.hronic low back pain patiencs: importance of

subdassification. Spine 31 (17), 2017- 2023.

Dankaerts, W, O'SulliV3n, P., Bumett A .. Straker, L.. Davey, P., Cupta, R., 1009. Discriminating healthy controls and cwo dinical subgroups of nonspt:dfic chronic low bac.k pain pacients using trunk musde activation and lumbosacral kinematics of postures and movements: a statistical dassilication model. Spine 34 (15), l 6!0- 1618.

Edgar. D . Jull, C., Sunon, S .. . !994. The relacionship between upper trapezius muscle len.gth and upper quadram neural tissue extensibilicy. Australian foumal o Physiotherapy 40, 99- 103.

t!vey. R.L., 1995. Peripheral neuropadiic dsorders and neuromusculoskeleta! pain. In: Shacklock M (Ed. ), Moving in on pain. Bunerwonh Heinemann. Sydney.

Emery, K, De Serres, S.f., Mc.Millan. A., Ct, J.N., 2010. The dfects of a Pilares training program on arm-trunk posture and movemenL Clinical Biomechanics 25 (2). 124-130.

Escalante, ,-\., del Rincon, l.. 2002. The disablemem process in rheumatoid arthritis. Arthritis and Rheumatism 4 (3). 333- 342.

Fairbank, J.C.. Couper. J., Davies. J.B., O'Brien, f. l'., 1980. The Oswescrv [ow back pain disabiiity questionnai~e Physiotherapy 66 (8), 2il - 273.

fairbank J.C.T.. Pynsent; P.B., 2000. The Oswestry disabliy index, Spne 25 (22), 2940- 2953.

Falla, D., Bilenkij, C., Jull, G., 2004. Patients with chronic neck pain demomtrate altered pattems of musde actiV3tion during performance of a funaional upper limb cask. Spine 29, 1436- 1440.

Falla, D .. Farina. D., 2008. Neuromuscular adaptation in e.xperimental and clinicaJ ner:k pain.

19

Kineuc Control: The- management of unconttolted movement.

Joumal of Elearomyography and Kinesiology 18 (2), 255-261':

Fersum, K.V., Dankaerts, W., o sullivan, P.B., et al., 20!0. fmegration of subci:assification strategies in randomised controlled ciinical trials evaluating manual therapy treatrnent and e.xercise therapy fer non-specific chronic low back pain: a systematic review. British Joumal of Spons Medicine 44 (14), 1054- 1062.

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Coff. B., 1972. The application of recent advances in neurophysiology to Miss R Rood's concept of neuromuscular facilitation. Physiotherapy 58 (2), 409-HS.

Gombano. S.P., Collins, D.R., Sahrmann, S.A., Engsberg, J.R.. Van Dillen, L R., 200'7. Paneras of lumbar region movemem during mmk lateral bending in 2 subgroups of people with low badc pain. Physical Therapy S7 (4), 441- 454.

Heald. 5.L., Riddle, D.L .. lamb, R.L . 199. The shoulder pain and disabilicy inde.-c t:he construct validicy and responsiveness of a region-spedfic disabilicy measure. Pnysical Therapy 77 (10), 109- -1089.

Hen.dri.ks, E.J., Scholten-Peetei:s, C.G., van der Windt. D.A., Neelemen-van der Steen, C. w., Oostendorp, R.~-\. , Verhagen, A.P., 2005. Prognosti factora fer peor recovery in acute whiplash paciems. Pain 114 (3), 408-416.

Hides, J.A, Richardson. C.A. Jull, C.A.; 1996. Multi6dus muscie recovery is not automatic after resolurioo of acute. lirst-episode low back pai.n. Spine 21 (23), 2763-2769.

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Hodges, P.W., Cholewiclti, J.. 2007.

20

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Llvingstone, Edinburgh, pp. 489- 512.

Hodges, P.W., Riciiardson, C.A., l996. Inefficient muscular stabilisation of he lumbar spine associated A'ith low back pai~: a motor conuol e-.'aluation of uansversus abdominis. Spine 2 (22), 2640- 2650.

Homst0I. G.M., Homst0l, B.O ... 2009. Changes in rnechanosensitiviry due to lumbopelvic ;ind ankle positioning. 3rd lnternational Conference on Movemem Dysfunctcn, E.dinburgb, Uf

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back pain? Joumal of Pain LO (8), 876-886.

Steiner. WA. Ryser, L, Hube~, E . Uehelhan, D .. Aesclllimann, A., Stucki. C., 2002. Use of the fCF model as a clnica! problem-solving tool in physical tlierapy and rehabilitation medicine. PhysicaJ Therapy 82 ( 11 ), 1098- 1107.

Sruge. B .. Veierod. M.8., Laerum, E.., Vollestad, N., 2004. The efficacv of a treatmem program Ol'\Jsing o; specitic stabilizing e.~ercises for pelvic girdle pain after pregnancy: a two-year follow-up of a randomized dinical aial. Spine 29 ( LO). El97- E203.

Swinkels-Meewisse. E.J .. Swinkels. R.A .. Verbeek. A.L. Vlaeyen. J.W .. Ostendorp. R.A .. 2003. Psychometric properries of 1he Tampa scale for kinesiophobia and the fear-avoidance beliefs questionnaire in acute low back oain. Manual Thernpy 3 (! ), 29- 36.

Tate, A.R .. McClure. P.W .. Kareha, S., lrwin, O., 2008. Effecr o the scaoula reposition test on shou!der impingemem symnoms and elevation strcngth in overhead athletes. Journal of Onhopaedic and Sports Physical Therapy 38 ( l ). 4-11.

van Dillen, LR., ~laluf, KS .. Sahrmann. S.A .. 2009. Further e.~ination of

) 22

modifying patient-preferred movernen1 and alignment strniegies in patients with low back pain during 5)1!Ilptomatic tests. Manual Therapy 14 ( t), 52- GO.

Verbrugge. L M., /ette. A.M .. 1994. The disablement orocess. Social Science and Medidn~ 33 (l}, 1- 14.

Vemon, H .. Mior. S., 1991. Tiie nec.1< disabilicy index: a study of reliabilicy and validicy. JournaJ of Manipulative and Physiological Tnerapeutics 14 (7). 409- 415.

Vibe Fersum, K. O'Sullivan, P.B.. Kvle. A .. Skouen. J.S .. 2009. lnter-exarniner reliabilicy of a dassificarion svstem for paticnts with non-specifi l0eapular positioning correlates with humeral head centering. C!inical Orthopaedic.~ and Related Research 433, 82-89.

Von I..iral control function'

3. to eccemrically lengthen under tensi'on to decelerate motion and control e.xcessive range of motion. which will betermed 'stability function'

4. to provide afferenc proprioceptive feedback to the central nervous system (CNS) fer coordination and regulation of musde stiffuess and cension.

Stabiliser and mobiliser function Rood, in Goff (1972), Janda (1996) and Sahrmann (2002) have described and developed funetionaL muscle testing based on sr.abillser and mobiliser musde roles. Table 2.1 describes sta-biliser and mobiliser musde role characteristics.

Sorne musd es are more efficient at one o these roles and less efficient in the other role. For e.xample: lacissimus dorsi is a powerful multi-joim medial rotator of the shouJder co accelerate the arm in the sagittil plane during chr01'1ing

23

Table 2.1 Characteristics of muscles witn stabiliser and mobiliser roles

STABILITY MUSCLE ROLE CHARACTERISTICS One-joint (monoarncular) Deep (snort lever and short moment am) Bread 3poneurotic insertJons {:o distnbute and absorb

force and load) leveraqe or load ma1ntenance, stauc ~oldinq and

,01m compressiOll Posrural nolding role associated wrth eccentncally

aecelerating or resist1ng momentum (especially in the axial plane - rotat1onl

EXAMPLES OF STABILISER MUSCLES Externa! oblique lnternal oblique Semisp1nalis Deep gluteus maximus SubsGJoularis

actions. l atissimus dorsi is biomechanically suited to large range, high speed. high force move-mem at che shoulder. This muscle obviously has a power ro le acting as a mobiliser or sagittal plane movement accelerator. Conversely, subscapularis co-activates synergistically but its co-activation force aas to stabilise the humeral head from excessive translation, while the arm is medially rotating in a throwing action. Subscapularis, with its shon lever, small momenc arm and capsular anachments, is best suited to non-fatiguing, func-tional movements in posrural control tasks. lt. is also ideally placed to resistor decelerate excessive lateral rotation of the shou1der . . 'Fhis musde has a greater stabilisation role and is less suited biome-chanically to a power movement role. A musde's role must also be customised to its function.

Generating high force may be detrimental in sorne instances. For example: rectus abdominis is a fle.xor of the lumbar spine. If it is over-trained and inappropriately strengthened it contributes to pain-related changes in the movement system. It is often over-trained in a misguided belief that ir is imponam to strengthen the abdominals to stabilise and protect the low back or to acquire an abdominal 'six pack'. However, if chis musde becomes excessively dominant in comparison to the lateral abdominal musdes it increases flexion and compression forces on the fl.lmbar spine and ro tation stress and strain is inadequately control-led. This imbalance between rectus abdominis and the lateral abdominal st.abilisers has been

24

MOBILITY MUSCLE ROLE CHARACTERISTICS Two..oint (biarticular or mulnsegmental) Superficial (longer lever. 'arger moment arm and greatest

bulk) Uniirect.ional bres or :endinous insertions (to direct

force to Jroduce movement) Leverage ior range and soeed and joint distraCtTon

Repetitiv or rapid movemem role and high stra1nlforce loading

EXAMPLES OF MOBILISER MUSCLES Rectus femos Peaoralis rnajor Levator scapula Reaus abdominis

identified as a common movement-related change in people with low back pain (O'Sullivan et al 1997).

lmplications of stabiliser-mobiliser characteristics 1. Musdes with predominantly stability role

characteristics ( one-joint) optimally assist posrural holding/anti-gravity/stability and comrol function. ~iusdes that have a stabilicy funaion (one-joint stabiliser) demonsuate a tendency to inhibition. excessive flexibility, laxity and wealmess in the presence of dysfunction (Kendall et al 2005). Janda (1983) desaibed these musdes as 'phasic' musdes.

2. Musdes with predominantly mobility role characteristics (multi-joint) optimally assist rapid/accelerated movemem and produce hlgh .force or power. Musdes that have a mobility function (two-joim or multi-joint mobiliser) demonstrate a tendency to overactiv.ity. loss of e.\.'tensibility and excessive stiffness in the presence of dysfunction (Kendall et al 2005). Janda (1983) described these musdes as 'postura!' musdes.

Local and global function Bergmark (1989) developed a model lO describe the muscle control of load transfer across the

Table 2.2 Local and global muscle system characteristics and general features

LOCAL MUSCLE SYSTEM CHARACTERISTICS Deeoest layer oi mu..

)

)

)

4. Global muse/e 'mrem': Lhe musdes that make up the global musde.system are responsible for the production and control of the range and the direction of movemem. The global musdes can change length significantly and therefore are the musdes of range of motion. The global musdes participate in. both non-fatiguing low load and fatiguing high load activities.

Both the local and global musde systems must work together for efficient normal function. :-Jeither systern in isolarion can control the func-tional stability of body motion segmencs.

Functional efficiency The functlonal efficiency of a musde is related to its ability to generace cension. A musde's tension is not constant throughout a comraction, espe-ciatly if the musde is changing length to produce movement. Length and rension properties of a musde are closely related. The tension or force a muscle produces is the resultant force arising from a combination of both active and passive components of the musde. Tue active compo-nem of musde tension is deterrnined by the number of actin- myosin cross-bridges that are linked at any point in time. Tue passive tension property of musde is largely due to the elastic

tin filamems which anchor t.he myosin chain t0 the Z band. Other connective tissue suucrures INithin musde only contribute panially to passive tension. figure 2. l illusttates the actln-myosin filamem cross-bridges and titin attachmems.

The position in range (usually mid-range) where the anive length-tension curve is maximal is known as the muscle's resring \ength. In this position, the maximum number of actln-myosin cross-bridge links can be established. In a mus-de's shonened or inner range position, the passive elastic components do not contribute to musde tension. Passive tension only begins to play a role after a musde stans to lengthen or stretch in to the musde's outer range. beyond its resting length or mid-range posion. Musdes are most efficiem and generare optima! force when they functlon in a mid-range position near resting length. Muscles are less efficiem and appear functionally weak when they are required to contral"t in a shortened or lengthened range relative to their resng length because of physiologicaJ or mechanical insuffi-ciency (Figure 2.2).

Pbysiological insufficiency occurs when a musde actively shortens into its nner range where the actin filamencs overlap each other, thus reducing the number of cross-bridges that can link to t.he myosin fament. As the musde pro-gressively shonens, there are fewer cross-bridges

lnner range 'sl1011ened' Middle ranga neutral' orresting posilion

Ou1errange 'lengthened'

= ..2 ..

" ~

Physiolog:e

multi-joint mobilisers '!I:e not parricularly

proposed by various a~thors (Vleeming et al 2007). This training would be appropriate to help manage sacroiliac joint pain assoated with high load or high speed activities such as running or throwing because these t'\VO musdes are auwmatically recruited in these activities. However, for patients who have sacroiliac joim pain associated \vith non-fariguing funaional movemems ( e.g. normal gait) and postura! comrol activities ( e.g. scatic standing), this training is unlikely to be beneficia!. There is often an assumption that the musdes used in strength training will be used in ali funl"tional activities. However, this is not me case as there is minirnal automatic activation of latissimus dorsi in mese low load activities.

Another example of measuremem discrepancy occurs following the assumption that psoas major is a hip fle.wr. Biomechanical modelling of psoas major often assumes that it is a fusiform musde wilh a straight line of action from the upper lumbar. spine to the femur. This is not the case. Psoas major is a pennate musde vlith obliquelv oriemated libres .. A more detailed mechanical evaluation of its pennate orientation (Gibbons 2007) suggests thar its maxmum shortening potential is approximmely 2.25 cm. This is insufficient to produce the fle.'Cion range of motion of me hip. The posterior fascia of psoas major is anchored to che anterior rim of the pelvis (Gibbons 2007). This attachment would produce posterior tilt of the pclvis. Posterior tik of the pelvis is a conjoinei movemem with hip fle.xon, and interestingly the range_. of movement of the pelvis at the psoas anachmem poim during posterior tilt perfectly matches the prediaed range of shortening of psoas major.

2. Misinterpretaton of measured features; for example, upper trapezius, lower c:rapezius, psoas major, vastus medialis obliquus_ Upper trapezus has been assumed to elevate the shoulder because it demonstrates high revels of EMG activity during scapular elevation tasks. fohnson et al (1994) demonstrate that 90% of the contractile fibres of upper trapezius inserr on the ligam~ntum nuchae below C6 and are horizontally orientated (the venical libres are predomlnam ly fuscial and connective tissue}. They state that the

1 30

upper uapezius musde cannot elevate the scapula above C6. [t is suggested that the reason for the high levels of EMG activation may be to assist the clavicular rotation (necessary for ful! shoulder elevation), or an atternpt to st.abilise the cervical spine during arrn load activities.

Similarly, vastus medialis obliquus demonstrates high levels of EMC activity in terminal e.nension of the knee. Lieb & Perry (1968) demonstrated that vastus medialis obliquus has no biomechanical potendal to extend the knee in this last 30. The high, leve! of vastus medialis obliquus recruitment is best explained by its role of maimaining alignment tracking of the patella during the last 30 of ful! e.xtension.

3. The muscle is designed to participate in more than one primary functional rofe; for example, Hodges (2003) suggests that a musd e may have three functional roles: (i) control of inter-segmemal motion (ii) control of posture and alignment {iii} to produce and control movement. Sorne musdes can effectively perfonn ali three of these functional ro les_ Gluteus maximus is an example of a muscle that multitasks ali three functional roles (Gibbons 2007). Gluteus maximus has deep sacra[ fibres that run from the inferior lateral comer of the sacrum to the posterior inferior ischal spine. lt is believed thai: these fibres perform a local stabiliry role and have the funl'tion of controlling intersegmental translation at the sacroiliac joint. Gluteus maximus also has fibres that run from the medial aspea of the ileum to the gluteal trochamer on the femoral nec.k. These deep tibres constitute the one-oint part of a musde that performs a global stability role at the hip joint. 1he most superficial fibres of gluteus maximus run from the iliac crest and anach imo the posterior aspect of the iliotibial band and evemually insert on the anterior aspect of the lateral tibiaI condyie, below the knee. This multi-joint part of gluteus maximus has a global mobiliser role and produces movemenr at the hip joint and the knee joim.

For many of the musdes that thcrapists work with on a regular basis mere. is currently insuffi-cient infoanation on ali four of these features

(seeTable 2.4) to enable thorough understanding of the primary function or role of these musdes ( e.g. serratus anterior, ad ductor magnus, subscapularis ).

Identifying a musde's primary role is not always simple. Sorne musdes appear to have a single, very specific primary role (single task/specific muscle) while other musdes appear to be more versatile and contribute t0 more than one primary role (multitasking musde).

Single task-specific muscles Single rask muscles have a specific task orientated role associated with having only a local stabiliser role e e.g. transversus abdominis, vastus medial is obliquus ), a global stabiliser role ( e.g. extemal obLiquus abdominls) ora global mobiliser role e e.g. reaus abdominis, hamstrings, iliocostalis lurnborum ). In the presence of pathology and/or pain,

very specific dysfunctions can develop and are associated with the recognised specilic primary role. These dysfunctions are consistent and predictable.

Very specific reuaining or correction has been advocated in crearment of this dysfunction (Hodges & Richardson 1996, 1997; Hodges & Richardson 1999; full 2000; O'Sullivan 2000; Hides et al 1996, 2001). This spefic training or corrective imervention is typically non-functonal ahd as such is designed to corree! very specilic elemems of dysfunction. This spefic retraining or correction may or may not integrate into normal functional activity. There s currendy no method to predict or dinically measure automatic integration into normal function. In many patients this integration has to be facilitated.

Multitasking muscles Sorne muscles appear Iess specilic and seem to particpate in a variety of roles without demon-strating dysfunction. They appear to have a mul-draslting funaion associated with the potential to perform more than one role. That is, there is good

evidence to support che musde having both a local role and a global role, or the evidence may suppon the musde having a contribution to both stability and mobility ro les ( e.g. gluteus maximus, infraspinatus and pelvic floor). Such musdes appear to be able to contribute to combinations of local stabiliser, global srabiliser and global mobiliser rofes when required in normal function. In the presence of pathology and/or pain, a

variery of different dysfunaions may develop. These dysfunaions can be identified as being associated with either or all of the multitasking roles and are related to the 'weak links' in an indvidual's integrated stabiltry system. Because- these con tribute to more than one functional role, differem dysfunctions can presem with pain_ Therefore, dysfunction in these musdes is not predictable and a more detailed assessmem is required with a dinical reason.ing process.

Treatment and rerraining has to address me particular dysfunction that presents, usually needs to be mu[tifactorial and should emphasise imegration imo 'normal' function.

As well as a considcration of che macro function( s) and role(s) of the musde, the therapist should consider me physiological or micro basis of the musde with respect to its potential for recruit-ment in single or multifunction roles.

The motor unit A single motor unit consists of the motor neurone plus the musde libres it innervates. Ali musde fibres in a single motor unit are of the same libre rype. Ali skeleral muscle fibres do not have the same mechancal and metabolic characteristics. Ali human musdes are composed of different motor unit rypes Lnterspersed with each other. The maximal contraction speed, strength and fad-guability of each musde depend on che propor-tions of fibre cypes (Widmaier et al 2007).

Most musdes are composed predominantly of t'\.YO different types of motor unitso (Figure 2.4). There are slow low thresho[d motor units (SMU) and fast hgh thresho[d motor units {FMU). Other

31

Fgure 2.4 Slow and 'ast motor units (with permission of KC lnternatlonall

Table 2.5 Summary of slow and fast motor unit characterstcs

FUNCTION Conuac'JOn ~ Conuacnon force Recr1.11tment dominance

Recruitment threshola

Fati9uab1lit:y

SLOW MOTOR UNITS S!cw

low

Primarily recruited a1 fow % of maximum volumary conuaCtJon (MVC) ( 40+% MVC) or if plan to perorm a fast movemem High hresho/a (insensiuve) - requires h19her stimulus

Fast fatiguing Role Conrrcl of normal non-fatiguing

'.uncticnal movements ano Ullloaded postura! control tasks

Rapid or accelerated movement and high load activity

rypes of motor units have been identified. but this basis dassification is useful for rehabilitation pur poses (Lieber 2009).

Slow motor units have a low lhreshold of acti-vation, slow speed of contraction, a low contrae tion force and are fatigue resistanc. Fast motor units have a high threshold of activation. fast speed of contraaion. a high contraaion force and fatigue quickly (see Table 2.5 for review). Slow motor units are predominantly'recruited during normal non-fatiguing daily aaivities (Monster et al 1978).

32

Table 2.6 summarises functio nal activities thar stimulate dominant slow and fast motor unit recruitment paneros.

Recruitmenc is modulated by the higher central nervous system (CNS) and is powerfully influ-enced by the afferent proprioceptive system along with various psychosocial factors. Hyperrrophy, however, is a peripheral strucrural adapration in

Postural sway Maimained postura! pos1tions Non-fatiguing rnovements of the unloaded limbs and

uunk ac a natural comfortable spet?d

musde. in response to d.emand along with CNS adaptation and is lhe result of overload rraining (Widmaier et al 2007).

Hodges (2003) argues chat high threshold mengthening of lhe global musdes of range and force potential and low threshold motor control training of deeper (force ineffidenr) local musdes are two distinctly separate processes, bolh of which are required to perfonn to high levels of activity such as competitive spon. One analogy for chis is co chink of the musculoskeletal system as a computer:

Hfgh sp~d or high. load strength training:chariges muscle::structure (hypertropnyi and can bedikened to upgraing, tlie computer's hardware. This ~ai m'a~~ .thecomputerworl< fasterand ruii',m0re:c0mple{ programS-. :Upgrading the hardware d0es not-'requfre speific. cognitive retraining - the same software. iS'

used:b~more efficiently. _ , tovJ threshofd motor control trainng does: not da!lge

t!Teelipheial musde structure-ttl any great extent, but ir.w..ad improves the central nervous sjstem's.. recruinentof musdes to fioe-l'Jne musde coordfation ano fmprcve the efficiency of m~emenl Tliis: cari !je likened to upgradinq the software n a . coinputer !E} perform its task~ more. eJfioentiy/and to getthemost out of the hardwareafrea'fP.reser}t "

liJ~gradi'ng tfle software. thouqh. always requires -cogoitive eierator training and familiadsatlor.r.. .. . lo this.anal(igy~ paln is.best represented'as a ~or.iptJter . -~fru{whidi primarly affectS. the software, casing tne computer to run slowly and crash more- often~ in. ihe buman _body. pain has more cor.sistent effeds.oa the. morar control aspects of movement rather !han. dire:tlyaffect1ng musde structwe.

Accelerated movement Rapid movement Large or sudden shift in the cenue of gravit:y High force or heavy Joads Conscious maxrmal contraa1on

Stabillty functlon: antl-gravity

postura! control

Stabiliser muscles

1 Racru1tment of

sf(1H motor wids (1ow weshold SlimulusJ

Functional role oractivity

/a e al muscle

/eaJ 1eauilmen1

Mobility function: rasistad or

fast movement

Mob11iser muscles

1 Reau1tment of

sbw- !ast motor UJ1its (kw rlveshold stimulusl

Figure 2.5 The relanonsnip betwe0 the ot0mechamcal and ohysiolog1cal cnaracteristia of muscfes in nab1ity and mob11ity function

[n an ideal or nonnal situation, a one-omt musde perfonning a non-fatiguing anti-gravity or postura! holding function and possessing stabil iser characteristics demonstrates greater recruit: ment of slow motor units (Figure 2.5). Slow motor unirs are sensitive to low threshold stimuli and should react effidently to Iow force loading situaons such as postura! sway. maimenance of postural positions and normal funaional move-mencs of the unloaded limbs or trunk

Similarly, fo c a fase, repetive movement or power function. muscles with mobiliser charac-teristics would demonstrate greater recruiunent of fast motor units ( although the slow motor units are also still recruited). fast momr units are less sensitive, have higher recruitment thresholds and aaivate more effi.ciently in response to high force Joading such as accelerated movement, rapid movemem. a large or sudden shft of the cenue

33

-

)

)

)

) ) ,

)

) )

)

) ) ) )

)

) )

of gravity, high force Qr heavy loads and con-scious maximal contraCtion.

Functional implications of recruitment within stabiliser and mobiliser roles Stabiliser roles and slow motor unit recruitment

Dynarnic postura! control and normal low load functional movement is primarily a function of slow motor unit (tonic) recruitment.

Functionally, effient recruitment of slow motor units will optimise postural holding/ anti-gravity and stability function.

Normal postural control and functional movemem of the unloaded limbs and trunk should ideally demonstrate efficiem recruiunent of deeper, segmentally anaching musdes that provide a stability role.

Mobiliser roles and fast motor unit recruitment

Functionally, efficient recruitmenr of fast mowr units will optimise rapid/accclerated rnovemem and the production of high force or power.

High load activiry or strength training ( endurance or power overload craining) is a function of both slow ( tonic) and fast (phasic) motor unit recruitment.

High load or high speed activfties normally dernonstrate a dominance of recruitrnent of more superfial, multi-joint musdes that a1e biomechanically advamaged for high load. large range and high speed.

Musde spindles have both sensory and mowr functions and are sensitive to changes both in length and in force (Figure 2.6). The information from muscle spndles contributes to propriocep-tion. This allows the central nervous system to be aware of the position of joints,~how far L'iey are moving. how fast they are moving, how much force is being used, and relates to the sensation of effon requ ired for panicular activities. Musd e

34

Gamma motor

Extrafusal dbres

Figure 2.6 Musde spindle (with permission of KC lmernationaJ)

spindles play a primruy role in propriocepcion and afferent feedback for motor control but also contribute significantly to the regulaon and control of musde stiffness and therefore segmen-ta! stabiliry_

The dinical imerpretation of 'stiffness' is orren poruayed as a negative outcome. Clinically, 'stiffness' often refers to a loss of motion or func-tion. Biomechanical 'stiffness' on the other hand usually describes a process of providing streng!h and SUP,port. A simple but appropriate way of describing stiffness biomechanically relates to the pass.ive or active tension that may resise a displac-ing force. .

Muscle stiffness (i.e. the ratio of force change to length change) consists of two componems: intrinsic muscle stiffness and ret1ex mediated muscle stiffness (Johansson et al 1991). 1. lntrinsic muscle stiffness is dependent on the

viscoelastic properties o[ musde and the existing actin- myosin aoss-bridges. This can

be affected by hypertrophy or strength training. Hypertrophy, which increases musde size. musde fibres in parallel and also increases musde connective tissue. resuhs in increased musde stiffness which in turn provides increased resistance to displacement and a mechanism of resisting UCM. This mechanism. nowever, is largely passive and does not provide dynamic responses to movemem challenges.

2. Reflex mediated stiffness is determined by the e.xtability of the alpha motor neurone pool. which in tum is dependent on descending commands and refle.xes which are fadl itated by the musde spindle afferem input (refer again to Figure 2.6). This mechanism is dynam.ic and provides refle.x automatic activarion of musdes to provide dynamic responses to postural displacement. For example, in sitting or standing, du.ring activies of leaning forwards at the trunk, the posterior paraspinal Slabiliser musdes ( multifidus) up-regulate their activation in response to postural foading. During forward leaning, the position of the trunk creales a tkxion loading force on t:he lumbar spine whch, in order to maintain spinal neutral alignment, must be resisted by posterior musdes such as multifidus. Likewise, when the trunk rerurns to an upright position ( vertically aligned above the peJv;s) the flexion loading force on the lumbar spine is reduced and the posterior musdes down-regulate their activity because they are no longer required to work as hard to resist or stabilise the spine against flexion loading.

Low threshold recruitment and timing The timi.ng of the automatic refle.x activation in response to movement and postura! displace-ment is influenced by the threshold ( or sensitiv-ity) of muscle recruitrnent. For example, during fonvard weight rransfer in normal gait the mul-tifidus musde on the rear leg side activates in response to loading. As weight shifts forwards (off the rear leg and towards the from foot) the pelvis on that side has to be supported from dropping dO'wn imo lateral tilt_ Multifidus and the lateral trunl< muscles on tha't side play a role in provid-ing pelvic stabilisation and suppon while that leg swings through. Tlle activation of multifidus on

1, U.ii.li 12 1 11

Figure 2.7 Palpation of muitifidus aaivation (rear ieg) durng weght transfer

the rear leg side during forwarcf weight transfer can be palpated by the therapisc or the patiem. [f multifidus is palpated when ful! weight is sup-poned on the rear leg, the muscle is unloaded and relaxed. Du.ring the transfer of body weight forwards onto the front leg (Figure 2.7) the multi-ndus musde on the rear leg sde will automati-cally activate as it is required to suppon the pelvis from dropping in preparation w li~ the rear leg for the swing phase of gait.

The timing of the onset of activation of multi-fidus is not always consistent. Sorne people dem-onstrate automatic activation early in weight transfer, while others demonstrate a delayed acti-vation response. [deally. the activation of multi-6.dus on the rear leg side should coincide with t.he iniation of weighc transfer, and irs onset activa-tion can be palpated as the weightshifts from the heel of the rear foot to the metatarsal heads of th.at same foot. If multi.fidus has sufficient low threshold recruitment it should activare before

35

any signiiicant weighl is. c:ransfeiTed to the front foot. lf efficient low threshold recruitment of multifidus is inhibited, multifidus does not pal-pably actvate until body weight is transferred to the front foot and body weight is unloaded from the rear foot. This observed delay in automatic recruitment is associated with altered low thresh-old activation. It is a very common observation that patients with a history of recurrent low back or pelvic girdle pain consistently demonsi:rate a timing delay in multifidus activation during forward weighl transfer compared to people who have no history of low back pain. This is not an issue of muscle weakness. as it is consistently observed in athletes with back pain who have hyperuophy of the parasplna[ musde groups due to suength and conditioning rraining programs. This delay may be related to a change in the threshold of automatic activation of low thresh-old slow motor units.

Recruitmem is altered u the presence of pain. Pain affeas slow motor -wJ:it -recnlitment more significantly than fast motor unit recruiunent. Pain does not appear to significantly limit an athlete's ability lO generate power and speed, so long as they can mentally 'put the pain aside'. It has been suggested anecdotally that up to 90% of sponing world records are broken by athletes with a chronic or recurrent musculoskeletal pain problem. .,.

In the pain-free state, reseaich (Hodges & Mosefey 2003; Moseley & Hodges 2005) indicat)S that the brain and the central nervous svstem (CNS) are able to utilise a variezy of motor c~ntrol strategies to perform functional tasks and main-tain control of movement, equilibrium and joint stability. However, in the pain state, the opons available to the CNS appear to become limited. These altered ( or limited) motor control strate gies present as consistent co-conuaction pattems usually with exaggerated recruirmern: of the multi-joim rnusdes over the deeper segmenta! muscles.

Recem research on musculoskeletal pain has focused on motor control changes assocated with the pain state. This researCh has provided importam new information regarding chronic or recurrent musculoskeletal pain. A large nurnber

36

of independent research groups are ali reporting a common finding (Lee 2011; Jull 2000; Sahr-mann 2002; Hodges 2003; Hodges & Moseley 2003; Rid1ardson et al 2004; Falla et al 2004a, b; Sterling et al 2001, 2005; Dankaerts et.al 2006; Moseley & Hodges 2006; O'Sullivan et al 2006; O'Leary et al 2001). They have ali consistemly observed that, in the presence of chronic or recur-rent pain, subjects change the patterns or suate-gies of synergistic recruiunent that are normall'y used to perforrn low load functional movements or poscures. They have demonsuated that these subjects employ srrategie.s or pattems of muscle recruiunent that are rlOrrnally rese.rved for ,high load function ( e.g. lifting. pushing, pulling, throwing, jumping. running, etc.) for normal postura! control and low threshold furictional activities. The common observation is that the multi-joint musdes with a primary mobility role for force and speed functions inappropriately become the dominant synergists in non-fatiguing normal funcrional movemems and for low thresh-old postura! control tasks. At the same time, the one-joim muscles that shouJd be dominant in non-fatiguing function and postural conuol. demonsuate down-regulation of their activation and are less active than controls with no pain history. Figure 2.8 illustrates graphically the dif-ferences in recruitment patterns of stabiliser and mobilser synergists in the pain-free state and the chronic: pain stat~

These pain-related changes in the pattems or the thresholds of recruiunem between one-joint stabilisers and their multi-joim mobiliser syner-gists can only be demonstrated during unloaded or low threshold testing. Under high load or high threshold function it is normal, in both the pain-free state and in the presence of pain, to demon-strate mobiliser dominance ('lith respect to stabiliser activation). Therefore, tests based on strength or endurance cannot consistently iden-tify if there is a pain-related change in recruitmem thresholds or pattems of recruitment.

These altered strategies or pattems have been described in the research and clinical literature as 'substitution suategies', 'compensatory move-ments', 'muscle imbalance' berween inhibited/ lengthened stabilisers and shortened/overactive mobilisers, ' faulty movements', 'abnormal domi-nance of the mobiliser synergists', 'co-contraction rigidir.y' and 'control impairmem.s'. The inconsist-ent terminology used in the dinical and academic literature has contributed to a lack of universal

Pain-freelnormaUideal

Low High load load

Chronic musculoskeletal pain

100 90 so

Low High load load

Mobiliser

~ Stahilisar

11 Mobiliser [] S!aoiliser

figure 2.8 Graphical representaticn of iecruitment differences re!ated to chronic or recurrem musculoskeletal pain

recogniton of this consistent and almost predict-able change related to pain.

Inhibition and dysfacilitation can. be dentfied as abnormal alteration of normal recruitment (Table 2.7). Inhibition relates to a process of neural dis-charge being actively suppressed by another neural influence. This process fs pan of normal movementbut it may beco me abnormal in certain.

Table 2.7 Recruitment changes associat ed with uncontrol led movement

With uncontrolled movemenr (UCM), inhibition and dysfacilitation presentas: Poor recruitment under low

threshold stimulus - ineiic1ent slow motor unit (SMU)

lnhibition and dysfacilitation

" 'off' recUitmem " 'weak' - (evidence in both the local

and global musde systems) Delayed recruitment timing

- (evidence in me local muscle sys1em)

Altered recruitment sequencing (evidence in the global muscle system)

situations. Dvsfacilitation relates to the utilisation of altered mwr conrrol strategies. These altered strategies contribute to changes in thresholds of facilitation and inefficient pauem of muscle activation. Example 1: Pain causes active inhibition ofSMU recruitment The pain may resolve and the mec.hanism of inhibition may be removed, but dysfadlitaon may persist. Example 2~ Stress (fear/ anxiety) can cause active inhibition of SMU recruitment. Central fatigue contributes to dysfadlitation.

Clinically, one-joint stabiliser muscles demon-strate a recruitment problem. They appear to increase their threshold, become less responsive to Iow load stimulus and respond best when the load becomes greater (Figure 2.9). Therefore the stability muscles respond mainly to higher load activities such as accelerated movement, rapid movernent, high force and a large shift of the centre of gravity.

As a consequence, the multi-joint mobilisers take over the stability role. They appearto decrease their threshold and become more reactive to a Iow load stimulus. Therefore the mobilising muscles appear to respond to low load activities such as postura! sway, maintained posrural posi-tion and slow movement of the unloaded limb (figure 2. LO). The qecrease in threshold and

37

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)

)

) ) ) ) ) ) ) )

) ) ) )

)

)

) ) )

1 Stability funclion: ., Mobility functon: anti-gravity resisted or

postura! control fast movemenl .;.

Stabiliser muscies '- Monillsa: mu.scle:;

~ ... less responsive lo low esponds efficiently threshold but responds ;o a low lhresnolo efficiently to a high

.;timUhJS lhreshold smulus

Figure 2.9 Dysfunc-Jonal stabiliser 1ecruitment - down-regulation, inh1biiion and dysfacilitation

Stability unction; Mobility fun-ction:. anii-gravity_ resisied or.

+. posturalcontrol fast movemenl

Stabliser musdes

V / Mobiliser musc!es

becomes more K r~sponds primanly to responsive to a low a high thresncld threshold stimulus stimL:lus

Figure 2.1 o Oysunctional mobiliser recruitment -up-regulation and overactivity

increased tonic aLi.ivity of SMU recruiunem in mobiliser musdes conaibutes to their observed dominance in posrural control (O'Sullivan et al 1998; ful! 2000; Sahrmann 2002).

./

The concept of 'sensation of effort' has significant relevance to e.he dincal assessment of threshold changes in recruiunent functions and subsequenr implications for the re-assessmem of recruitment after exercise intervemions. The sense of effon has been defined as ajudgrnem on the effon required to generare a force (Enoka & Stuan 1992). This is processed in higher centres in the cenaal ner-vous system and relates to the mental challenge required to perfonn a task in the periphery.

The relative recruitrnent of s]O\V and fast motor units in sustained volumary contraction is panly due to the intluence of proprioceptive activity

) 38

(Grimby & Hannerz 1976). [ndeed, propriocep tive information from e.he primary muscle spindle endings ( especially the gamma spindle system loops) is essential for efficient facilitation of tonic or slow motor unit recruitment (Ecdes et al 1957; Grimby & Hannerz 197 6).

Grimby & Hannerz ( 1976) reponed that when proprioceptlon is dimin ished, the sense of effort necessary fo r efficient activation of slow motor units is increased. That is. during low load activity, the subject feel.s c.hat c.hey must try harder ( even if it feels like maximum effort) to achieve tonic recruiunent of slow motor units. It feels much easier to contract the same musde against high loador resistance (where fast motor unit recruit-ment is significant).

Wherr maximum o, higti sen~tfon of effort i? needed to pecfomr a low loa& activity or movemenrtnen it.~ most -likelr tha! !:here is iilefficient facilitation .of stow. qotor 1.mit recruitment. and dysfunc-Jo1:1 of normal spn~le responses. ~ , - ' for tfie same reasons. tbougl't,.wllen. less. sensation-0f effort is needed to. perform that same low lo,a,i:l activlt1 or movement (ancJ. it feels easier), then it is lik.elll that there is better facilitation-islow motor unit remifrmerit. This.decrease in trie sense of effort.reqiced isa good fndicator of improvi119 motor control ~~bility funcf;

The sensation of high effort to perfonn a low load task may be due co: recruiunent dysfunaion (commo n, with

mu1tiple contributing factors), or disuse atrophy and weakness ( uncommon,

but if present, with wasting and functional deficits ) .

During low threshold motor control stability uaining it is permissible for the patient to 'feel' or experience the sensation that c.hey are working hard ( even maximally) during low load exercise so long as c.hey do not show signs of fatigue of the stability musde or substitme wic.h a differem musde. !t is not appropriate to progress the exer-cise until that low toad exercise feels easy. Peripheral fatigue occurs when a musde can

maintain a leve! of conaaction force for longer beca use of peripheral factors ( e.g. depleted musde glycogen, phosphagen, and caJcium) even though the CNS may be increasing neural discharge to the motor neurone pool. The muscle runs out of fuel. This is best improved by suength training programs.

Central fatigue relates to alterations in the way that the CNS drives che motor neurone pool. The musde has che ab ility (and fue!) to generate more force but an i.nadequate neural stimulus is provided by the CNS. This is a motor control issue.

. . - , , ._ ... ,,._

ISlinical differentation betweerr centraHatigue and peripheral fatigue --' ., ' ~ . - ' -

. .. lf added or increase

function are an indirect ~onsequence of recover-ing SivtU recruiunent thresholds and restoring more ideal pattems of recruitment. l ow thresh-old mo-ror control training strategies usually require practising a highly cognitive, very specific, non-funLLional movement skill until the activa-tion strategy feels more 'familiar' and less 'unnat ural' and has a low sensation of effort (feels easy) during its performance. Once this low threshold motor control recruitrnent skill has been estab-lished it can be progressed in several ways:

While rnaintaining the cognitive activation, progressively remove or decrease load facilitation (unloading). Por e..xample, the multifidus has increased load fudliiation in standing with forward leaning of the trunk. Load fadlitation is decreased by moving the trunk backwards over the pelvis in sitting and. is maximally unloaded by lying supported in prone.

While maintaining the cognitive activation. impose a low threshold (non-fatiguingj perturbation. This penurbation should consist of small range, low force, non-prediaable displacemencs. For example, this can be achieved while sirting upright on an unstable base (such as an inflatable disc or round balance board) while maintaining the trained cognitive activation.

High threshold recruitment dominance High threshold scrength craining a~fects struaure (hardware) of musde tiss(le ovr time. When musd e tissue is loaded and stressed it adapts to stress and hypertrophies and increases the potel1-tial to generate force and power. This structural change occurs over a timeframe of 6- 8 weeks or more:

Strength training is progressed by ;irogressively ina easing resistive load, using fase altemating movements or progressively increasing holding endurance to the point of fatigue.

Table 2.8 lists the key differences between low and high. threshold recruitment retraining suategies.

40

Table 2.8 Key threshcld differences between low and high threshold recruitment strateg ies

KEY THRESHOLD DIFFERENCES

Low threshold High threshold recruitment recruitment

Slow motor unit dorninant Fast motor unit dominant

Slow I Static Fast

and or

Sustained Fatiguing

(non-fatiguing, low load) (high load)

Retrainng low threshold recruitment dominance

'

ff the patient is a ble to perform an e.xercise or task slowly and consistently for 4 minutes or more without fatigue or needing recovery time, then at least the first 1-2 minutes of that exerd se or task will be performed with low threshold recruitrnent dominance.

Retraining high threshold recruitment dominance 1f the load of the exerdse or task is such that it cannot be performed continually for 2 minutes because lhe load is suffidem to cause fatigue then that exercise or task will be performed vvith high threshold recruitmem dominance. If an e.xercise or task is performed at high speed, then it will be perforrned with high threshold recruitmem dominance ( even if it is low foaq).

rn berween these two regions there is a 'grey' area that can be sigriificantly influenced by crain ing responses.

These aspects of physiology and musd e recru-ment function underpin the processes used in developing assessmem principies (Chapter 3). The application of this knowledge to the design and mplementation of retraining scrategies to address UCM and for the integration of low threshold motor control training into function is furtber explored and demonstrated in Chapter 4.

Bergmark, A.. 1989. Stability of the lumbar spine. A study in mechanicaJ engineering. Acta Orthopaedica Scandinavica 230 (60), 20-24.

Comerford. M.J .. Mottram. S.L 2001. Movement and stability dysfunction - contemporaxy developments. Manual Therapy 6, lS- 26.

Dankaens, W., O'Sullivan. P., Sumen, ,\., Suaker, L. 2006. i'J tered patterns of superficial uunk musde activation during sitting in nonspedfic chronic low back pain patiems: imponance of subd assication. Soine fPhiladelphia Pa 197G) 31 (17), 2017-2023.

Ecd es, J.C.. Eccles, R.M . Lundberg, A., 1957. The convergence of monosynaptic exdtatory afferems omo many differem species of alpha motorneurons. fournal of Physiology (London) 137, 22-50.

Enoka, R.M., Stuai:t. D.G., l992. .'le\lrobio!ogy of muscle fatigue. Joumal of Applied Physiology 72 (5), 1631- 1648.

falla. D .. ful!. G .. Hodges, P .. 2004a. Patiencs with neck pain dernonsuate reduced e!earomyographic aai,ity of the deep cervical tle.~or muscles during performance of the craniocervical tlexion cesL Spine 29, 2108- 2114.

Falla, D., Bilenkij, G., Jul!. G . 1004b. Paencs with chwnic neck pain demonsuace altered patters of musde activation during performance of a fu11cr.ional upper limb iask. Spine 29. l436- l440.

Gibbons, S .. 2007. Clinical anatomy and function of psoas major and deep sacra! g!uteus maximus. In: Vleeming.. A .. Mooney, V., Sroed

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plasticiry. l ippincon William~. and Wilkins, Baltimore.

\.lcCill. S.M., 2007. The painful and unstable lumbar saine: a foundation and approach for iestabization. In: Yleeming, A.. Mooney, v .. Stoeckan. R. (Eds.), MovemenL stability and lumbopelvic pain. Elsevier, E.dinburgh. ch. 35.

Monster. /\.W., ChaJ1, H .. O'Connor, D .. 1978. Activity parrems of human skeletal muscles: relation to muscle fiber cype composition. Sdence 200 (4339 ), 314- 317.

Moseley. G.L, Hodges. P.W., 2005. Are che changes in posmral control associated with low back pain caused by pain interferencel Clnica! Joumal of Pain 21 (4), 323-329.

Moseley, C.L. Hodges. P.W. 2006. Reduced ariabilicy of posrural su:ategy prevenis normalization of motor d'1anges induced by bac.!( paio: a risk factor for chronic trouble? Behavioral Neurosciencc l20 (2), 474-476.

O'Leary, S .. Falla. D .. Jull. G ... 201 L The relationship between superficial musde acth~ry during me cranio ceP.ical fle.'J lison, G.T .. 1998. Altered abdominal musde reauiunent in patienis with chronk back pain following a spedfic exercise imervention. /oumal of Orthopaedic and Sporu Physicru Therapy.

Panjabi. M.M., l992. The stabiiising svstem of che spine. Pa re l. fonction. clysfunction ad~ption. and enhancement. fournal of Spinal Disorders 5, 383- 389.

Reeves, N.P .. Chole-.,i cki, / .. 2010. fapanding our iew of the spine syslem. European Spine foumal DOf: !0.1007/s00586009-1220-5.

:!'

Ridmdson, C., lull, G., Hodges, P., Hides, f.. l 998. Therapeuc e."

Kinetic Control: The managemem ot' unconuolled movement

Box 3. 1 Classification of siJbgroups based on non-specific mechanical pain related to movement dysfunction

Subgroups within non-specific musculoskeletal pain 1. Site and direction of uncontrolled movement (a) Site and direct1on of uncontrolled mouon (Comerford

& 'Aottram 2001al. (b) ) irec:ion suscepuble :o motion (Sanrmann 2002). {e) Control impa1rmems ano movement 1moairmencs

{O'Sullivan 2005). 2. Recruitment efficiency of local muscle stabil ity system {a) Changes in feedfor.vard mecnanism, for example:

(i) transversus abdomirus. multrfious, pelvi< :loor, diachragm (Richarescn et al 2004)

(li) deep neclc lex Oufl et al 20081 (iii) upper ttapezius (Wadsworm & Bullock Saxton

1997). (bl Recn11trnent efficiency dianges:

(i) ceep 'led flex (Jull et al 2008) (ii) psoas, subscaoula:;, upper crapeiius, lower

trapez1us. posterior nerJ< ext. (G1bbons 2007: Comericrd & Mottram 2010)

(iiO deep sacral glut. max. (Gibbons 2007) (iv) dinical rating system (Comerford & Mot"am

2011). (e) Ultrasound changes:

(i) rransversus abdominis (Richardson et al 20041 [IQ multiidus (Sto~es e 21 1992: H1des et al 2008)

dvsfunctions indude the evaltii1tion of the si.te and direction of unconcrolled movemenc (UCM), reauitrnenc effiency oflocal musde stability sy;tem, musde imba1ance, paltems of movement prov0cation ancl relief wilh postura! positioning. positional diagnosis, patterns of symptom relief assodated with manual mobilisaon. Box 3.1 illuscrates sorne of