Manual Therapy Journal - Volume 14, Issue 1, Pages 1-116 (February 2009)

VOLUME 14 NUMBER 1 PAGES 1–116 February 2009 Editors International Advisory Board Ann Moore PhD, GradDipPhys, FCSP, C...

Author: Editors: Ann Moore and Gwen Jull

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VOLUME 14 NUMBER 1 PAGES 1–116 February 2009

Editors

International Advisory Board

Ann Moore PhD, GradDipPhys, FCSP, CertEd, FMACP Clinical Research Centre for Health Professions University of Brighton Aldro Building, 49 Darley Road Eastbourne BN20 7UR, UK Gwendolen Jull PhD, MPhty, Grad Dip ManTher, FACP Department of Physiotherapy University of Queensland Brisbane QLD 4072, Australia

K. Bennell (Victoria, Australia) K. Burton (Huddersfield, UK) B. Carstensen (Frederiksberg, Denmark) M. Coppieters (Queensland, Australia) E. Cruz (Setubal Portugal) L. Danneels (Maríakerke, Belgium) S. Durrell (London, UK) S. Edmondston (Perth, Australia) J. Endresen (Flaktvei, Norway) L. Exelby (Biggleswade, UK) D. Falla (Aalborg, Denmark) J. Greening (London, UK) C. J. Groen (Utrecht,The Netherlands) A. Gross (Hamilton, Canada) T. Hall (West Leederville, Australia) W. Hing (Auckland, New Zealand) M. Jones (Adelaide, Australia) S. King (Glamorgan, UK) B.W. Koes (Amsterdam,The Netherlands) J. Langendoen (Kempten, Germany) D. Lawrence (Davenport, IA, USA) D. Lee (Delta, Canada) R. Lee (London, UK) C. Liebenson (Los Angeles, CA, USA) L. Maffey-Ward (Calgary, Canada) E. Maheu (Quebec, Canada) C. McCarthy (Coventry, UK) J. McConnell (Northbridge, Australia) S. Mercer (Queensland, Australia) D. Newham (London, UK) J. Ng (Hung Hom, Hong Kong) S. O’Leary (Queensland, Australia) L. Ombregt (Kanegem-Tielt, Belgium) N. Osbourne (Bournemouth, UK) M. Paatelma (Jyvaskyla, Finland) N. Petty (Eastbourne, UK) A. Pool-Goudzwaard (The Netherlands) M. Pope (Aberdeen, UK) G. Rankin (London, UK) D. Reid (Auckland, New Zealand) A. Rushton (Birmingham, UK) C. Shacklady (Manchester, UK) M. Shacklock (Adelaide, Australia) D. Shirley (Lidcombe, Australia) V. Smedmark (Stenhamra, Sweden) W. Smeets (Tongeren, Belgium) C. Snijders (Rotterdam,The Netherlands) R. Soames (Dundee, UK) P. Spencer (Barnstaple, UK) M. Sterling (St Lucia, Australia) P. Tehan (Victoria, Australia) M. Testa (Alassio, Italy) M. Uys (Tygerberg, South Africa) P. van der Wurff (Doorn,The Netherlands) P. van Roy (Brussels, Belgium) B.Vicenzino (St Lucia, Australia) H.J.M. Von Piekartz (Wierden,The Netherlands) M. Wallin (Spanga, Sweden) M. Wessely (Paris, France) A. Wright (Perth, Australia) M. Zusman (Mount Lawley, Australia)

Associate Editor’s Darren A. Rivett PhD, MAppSc, (ManipPhty) GradDipManTher, BAppSc (Phty) Discipline of Physiotherapy Faculty of Health The University of Newcastle Callaghan, NSW 2308, Australia E-mail: [email protected] Tim McClune D.O. Spinal Research Unit. University of Huddersfield 30 Queen Street Huddersfield HD12SP, UK E-mail: [email protected]

Editorial Committee Deborah Falla PhD, BPhty(Hons) Department of Health Science and Technology Aalborg University Fredrik BajersVej 7, D-3 DK-9220 Aalborg Denmark Email:deborahfvhst.aau.dk Timothy W Flynn PhD, PT, OCS, FAAOMPT RHSHP-Department of Physical Therapy Regis University Denver, CO 80221-1099 USA Email: [email protected] Masterclass Editor Karen Beeton PhD, MPhty, BSc(Hons), MCSP MACP ex officio member Associate Head of School (Professional Development) School of Health and Emergency Professions University of Hertfordshire College Lane Hatfield AL10 9AB, UK E-mail: [email protected] Case reports & Professional Issues Editor Jeffrey D. Boyling MSc, BPhty, GradDipAdvManTher, MCSP, MErgS Jeffrey Boyling Associates Broadway Chambers Hammersmith Broadway London W6 7AF, UK E-mail:[email protected] Book Review Editor Raymond Swinkels MSc, PT, MT Ulenpas 80 5655 JD Eindoven The Netherlands E-mail: [email protected]

Visit the journal website at http://www.elsevier.com/math

Available online at www.sciencedirect.com

Manual Therapy 14 (2009) 1 www.elsevier.com/math

Editorial

New Year wishes Welcome to the 14th volume of Manual Therapy Journal and a Happy 2009 to all our readers. This year sees the expansion of our Editorial Board to now include Tim Flynn who takes on responsibility for ‘‘review’’ and ‘‘systematic review’’ articles and Deborah Falla who has taken up an Associate Editor role. In 2008 we said goodbye to Darren Rivett who had served on the Editorial Board of Manual Therapy Journal for ten years, but whose professional/academic role at the University of Newcastle, Australia had left him little time to work on Manual Therapy Journal matters. We would like to thank Darren, particularly for all his valuable and sustained work for Manual Therapy Journal over the ten-year period. He will be sorely missed, but he has agreed to take a very active role as an Editorial Advisory Board member. 2008 also saw the resignation of Marina Wallin and Venke Smedmark from the Editorial Advisory Board of the Journal. They had both been on the Editorial Advisory Board since the Journal was created in 1995 and we thank them both for their advocacy for the Journal over this fifteen-year period. We would like to express a warm welcome to all new Editorial Advisory Board members. Time now for all readers to look forward to the next range of international conferences: - the Kinetic Control and MACP Movement Dysfunction conference to be held in Edinburgh in 2009,

1356-689X/$ - see front matter Ó 2008 Published by Elsevier Ltd. doi:10.1016/j.math.2008.12.002

- The World Congress of Physical Therapy to be held in Amsterdam in 2011 and; - IFOMT to be held in 2012 in Quebec, Canada. So time to plan attendance at these events now and think about what new research findings you will have to present at these conferences and what CPD opportunities you might take up from the conference programmes. It is interesting now to think what issues will be on the international agenda for Manual Therapists over the next four years, for example: public health, obesity, chronic diseases? and what the balance of research presentations will be in relation to qualitative and quantitative research. Hopefully we will be seeing a rise in cost effectiveness studies and also studies which explore the patient’s experience as well as more studies that underpin our choice of frequency and dosage in relation to treatment applications. We may also see more pedagogic research to underpin how Manual Therapists are educated in Higher Education and in practice. As usual, all the conferences will offer a wonderful opportunity for meeting up with old colleagues, making new friends and acquaintances and forming collaborations across the World. We wish you a very Happy and Prosperous 2009. Ann Moore* Gwendolen Jull *Tel./fax: þ44 1273 643766. E-mail address: [email protected]



List of reviewers 2008 J. Haxby Abbott Caroline Alexander Trevor Allen Caroline Appel Jeff Baghurst Chris Barnett David Baxter Iain Beith Kim Bennell Jon Blacktop Elizabeth Bryant Barbara Cagnie Melinda Cairns Dawn Carnes Elizabeth Cheek Thomas Chiu Jacek Cholewicki Michael Cibulka Ann Cools Michel Coppieters Duncan Critchley Wim Dankaerts Lieven Danneels Anna Dawson Krysia Dziedzic Steven J. Edmondston Jorge Esteves David Evans Darrell Evans Linda Exelby Cesar Fernandez de las Penas Laura Finucane Timothy Flynn Jamie French Angela Glynn Anita Gross Toby Hall Michelle Harms Emma Healey Nicola Heneghan Lee Herrington

1356-689X/$ - see front matter doi:10.1016/j.math.2008.12.001

Jonathan Hill Di Hopper Ian Horsley Alan Hough Anne Jackson Susan Jeno Kajsa Johansson Venerina Johnston Andrew Kerr Roger Kerry Mike Kondracki Birgit Kristensen Raija Kuisma Jennifer Langworthy Mark Laslett Diana Lawrence-Watt Janine Leach Diane Lee Raymond Lee Jeremy Lewis Jiu Jenq Lin Gail Louw Nick Lucas Mary Magarey Dennis Martin Tom McCarron Chris McCarthy Jenny McConnell Suzanne McDonough Alison McGregor Chris Mercer Stephan Milosavljevic Robert Moran Lorimer Moseley Donald Murphy Joseph Ng Shaun O’Leary Neil Osborne Peter Osmotherly Kieran O’Sullivan Johan Pel

Nick Penny Jan Pool Annelies Pool-Goudzwaard Louise Potter Christopher Powers Gabrielle Rankin Kathryn Refshauge Barbara Richardson Colette Ridehalgh Darren Rivett Alison Rushton Paddy Searle-Barnes Michael Shacklock Gary Shum Julius Sim Helen Slater Andrew Smith Suzanne Snodgrass Tina Souvlis Meena Sran Michele Sterling Graham Stew Mark Stigant Maria Stokes Jenny Strong Britt Stuge Annette Swinkels Grace Szeto Paul Tofts Julia Treleaven Michael Troke Neil Tuttle Bill Vicenzino Benedict Wand Hsing-Kuo Wang Peter Watt Chris Wright Jo Zamani Max Zusman


Manual Therapy 14 (2009) 3e12 www.elsevier.com/math

Masterclass

From acute musculoskeletal pain to chronic widespread pain and fibromyalgia: Application of pain neurophysiology in manual therapy practice Jo Nijs a,b,*, Boudewijn Van Houdenhove c b

a Department of Human Physiology, Faculty of Physical Education and Physiotherapy, Vrije Universiteit Brussels, Belgium Division of Musculoskeletal Physiotherapy, Department of Health Care Sciences, University College Antwerp, Van Aertselaerstraat 31, B-2170 Merksem, Belgium c Faculty of Medicine, Katholieke Universiteit Leuven, Belgium

Received 4 December 2007; accepted 9 March 2008

Abstract During the past decade, scientific research has provided new insight into the development from an acute, localised musculoskeletal disorder towards chronic widespread pain/fibromyalgia (FM). Chronic widespread pain/FM is characterised by sensitisation of central pain pathways. An in-depth review of basic and clinical research was performed to design a theoretical framework for manual therapy in these patients. It is explained that manual therapy might be able to influence the process of chronicity in three different ways. (I) In order to prevent chronicity in (sub)acute musculoskeletal disorders, it seems crucial to limit the time course of afferent stimulation of peripheral nociceptors. (II) In the case of chronic widespread pain and established sensitisation of central pain pathways, relatively minor injuries/trauma at any locations are likely to sustain the process of central sensitisation and should be treated appropriately with manual therapy accounting for the decreased sensory threshold. Inappropriate pain beliefs should be addressed and exercise interventions should account for the process of central sensitisation. (III) However, manual therapists ignoring the processes involved in the development and maintenance of chronic widespread pain/FM may cause more harm then benefit to the patient by triggering or sustaining central sensitisation. Ó 2008 Elsevier Ltd. All rights reserved. Keywords: Fibromyalgia; Central sensitisation; Whiplash; Chronic fatigue syndrome

1. Introduction The 1990 American College of Rheumatology criteria for the classification of fibromyalgia (FM) define chronic widespread pain as a history of at least 3 months of axial skeletal pain, pain in the right and left sides of the body, and pain above and below the waist (Wolfe * Corresponding author. Division of Musculoskeletal Physiotherapy, Department of Health Care Sciences, University College Antwerp, Van Aertselaerstraat 31, B-2170 Merksem, Belgium. Tel.: þ32 3 6418265; fax: þ32 3 641827. E-mail address: [email protected] (J. Nijs). 1356-689X/$ - see front matter Ó 2008 Elsevier Ltd. All rights reserved. doi:10.1016/j.math.2008.03.001

et al., 1990). In addition to the presence of chronic widespread pain, pain in 11 of 18 tender point sites must be present on digital palpation with an approximate force of 4 kg (Wolfe et al., 1990). FM is classified as a rheumatic illness and is often treated by manual therapists. In the United States, patients with FM are frequently seen in chiropractic practice. Studying the health-care use of 402 patients from a university-based clinic, it was found that nearly 56% of the patients fulfilling the diagnostic criteria for both FM and the related chronic fatigue syndrome visited chiropractors, and 32% of the primary FM subjects consulted chiropractors (Bombardier and Buchwald, 1996). Trigger point

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J. Nijs, B. Van Houdenhove / Manual Therapy 14 (2009) 3e12

injections, joint manipulation, and myofascial release techniques are among the more commonly used modalities in the treatment of FM (Clauw, 2007). Although these treatment modalities are currently not evidencebased, this does not imply that manual therapy cannot benefit people with FM. The question arises, however, which rationale can be formulated for applying manual therapy to people with chronic widespread pain/FM? During the past decade, scientific research has provided new insights into the development from an acute, localised musculoskeletal disorder (e.g. a whiplash trauma) towards chronic widespread pain/FM. Understanding these processes might enable manual therapists to develop a theoretical rationale for using manual therapy in the prevention of chronicity and for the treatment of chronic widespread pain/FM. The present manuscript intends to provide such a theoretical framework. The development from an acute, localised musculoskeletal pain problem towards chronic widespread pain/FM is explained and applied to the practice of manual therapy, to explore how manual therapy might be able to influence this process in three different ways. (I) Manual therapy, when applied successfully to acute musculoskeletal disorders, might have the capacity to prevent chronicity. Conversely, when manual therapists ignore the processes involved in the development and maintenance of chronic widespread pain/FM, then they may cause more harm than benefit to the patient. (II) The manuscript explores how the application of manual therapy to (sub)acute musculoskeletal disorders should account for the processes involved in the chronicity of pain. (III) Finally, the manuscript explains that besides its role in primary prevention of chronicity, manual therapy might have its place in the comprehensive management of those with chronic widespread pain/FM. In the next section, the neurophysiology of central sensitisation is briefly introduced. The body of the manuscript consists of six sections each dealing with a different aspect of manual therapy in those at risk of/with chronic widespread pain and FM.

2. Theoretical background: central sensitisation It is important to understand that not all nociceptive signals are perceived as pain, and not every pain sensation originates from nociception. Nevertheless, acute pain almost always originates from nociceptors in somatic or visceral tissue. However, when the nociceptors keep on ‘firing’ nociceptive impulses, the dorsal horn neurons may become hypersensitive (Baranauskas and Nistri, 1998; Staud and Smitherman, 2002). This increased neuronal responsiveness is accomplished by neurotransmitters like glutamate, aspartate and substance P, which modulate the postsynaptic electric discharges

with further transmission to supraspinal sites (thalamus, anterior cingulate cortex, insular cortex, and somatosensory cortex) via ascending pathways (Staud and Smitherman, 2002). The neurotransmitters initiate increased postsynaptic responses by triggering hyperexcitability of N-methyl-D-aspartate (NMDA) receptor sites of second-order neurons in the dorsal horn (Fig. 1). This mechanism is related to temporal summation of second pain or wind-up. Wind-up refers to the progressive increase of electrical discharges from the second-order neuron in the spinal cord in response to repetitive Cfibre stimulation, and is experienced in humans as increased pain (Mendell and Wall, 1965; Gracely et al., 2004; Staud et al., 2007). Wind-up is part of the process known as central sensitisation (Meeus and Nijs, 2007). When manual therapists apply hands-on techniques, and by doing so elicit identical nociceptive stimuli to the skin, muscles or joint capsules more often than once every 3 s, they are likely to trigger this mechanism of pain amplification. Central sensitisation is defined as ‘‘an augmentation of responsiveness of central pain-signalling neurons to input from low-threshold mechanoreceptors’’ (Meyer et al., 1995). While peripheral sensitisation is a local phenomenon, central sensitisation means that central pain processing pathways localised in the spinal cord and the brain are sensitised. Indeed, the process of central sensitisation is neither limited to the dorsal horn, nor to pain amplification of afferent impulses. Central sensitisation encompasses altered sensory processing in the brain and malfunctioning of pain-inhibitory mechanisms. Coding of the mechanism of wind-up involves multiple brain sites, including somatosensory (thalamus, anterior insula, posterior insula, primary somatic sensory cortex, and secondary somatic sensory cortex), cognitiveeevaluative/affective (anterior cingulate cortex and prefrontal cortex), and pain-modulating regions (rostral anterior cingulate cortex) (Staud et al., 2007). The elevated central nervous system reactivity inhibits functioning of regulatory pathways for the autonomic, endocrine and the immune system (Bell et al., 1998). Activation of certain regions of the midbrain activates extremely powerful descending pain-modulating pathways that project, via the medulla, to neurons in the dorsal horn that control the ascending information in the nociceptive system (Purves et al., 1997). These pain-inhibitory pathways arise mainly from the periaqueductal grey matter and the rostral ventral medulla in the brainstem (Purves et al., 1997). One function of the descending inhibitory pathway is to ‘‘focus’’ the excitation of the dorsal horn neurons by suppressing surrounding neuronal activity (Woolf and Salter, 2000), a role attributed to the ‘‘diffuse noxious inhibitory controls’’ phenomenon (Le Bars and Villaneuva, 1988). In the case of central sensitisation and chronic widespread pain these descending pain-inhibitory pathways are malfunctioning (Fig. 1)


5

brain: malfunctioning of central pain inhibitory pathways arising from periaquaductal gray matter and rostral ventral medulla in brainstem

PAIN

brain: cognitive-emotional sensitisation brain: sensory-motor conflict

overactive ascending pain fascilatory pathways

malfunctioning of descending pain-modulating pathways dorsal horn: hyperexcitability of NMDA-receptor sites of second-order neurons & progressive increase in discharges from second-order neurons

spinal cord

injury / trauma / arthritis peripheral tissues: enhanced responsiveness of nociceptive endings Fig. 1. Anatomical localisations of hyperexcitability of peripheral and central pain pathways.

(Staud et al., 2001; Price et al., 2002; Banic et al., 2004). Malfunctioning of central pain-inhibitory pathways in people with chronic pain becomes particularly apparent to clinicians during exercise interventions: both isometric and aerobic exercises activate endogenous opoid and adrenergic pain-inhibitory mechanisms in healthy subjects, while it increases experimental pain ratings in patients with FM (Staud et al., 2005) and chronic fatigue syndrome (Whiteside et al., 2004). So how do we account for the process of central sensitisation during manual treatment of those with musculoskeletal pain? This will be discussed in the following sections.

3. Manual therapy to prevent hypersensitivity of pain pathways in (sub)acute musculoskeletal pain An important and ongoing source of pain is required before the process of peripheral sensitisation can establish central sensitisation. It seems crucial to limit the time course of afferent stimulation of peripheral nociceptors: tissue injury healing and focal pain recovery should occur within a period of approximately 3 months to prevent development of chronic widespread pain/FM (Vierck, 2006). Progression towards chronic widespread pain is associated with injuries to deep tissues which do not heal within several months (Vierck, 2006). Consequently, appropriate and effective manual therapy in those with (sub)acute musculoskeletal disorders is important to prevent evolvement from an acute, localised

musculoskeletal pain problem to complex clinical cases, characterised by chronic widespread pain and even symptoms outside the musculoskeletal system such as increased sensitivity to bright lights, auditory loudness, odours, and other sensory stimuli. Pain due to damage or inflammation of peripheral tissues is clearly capable of causing chronic widespread pain/FM (Clauw, 2007). 15e20% people with whiplash injuries develop chronic pain and disability (Spitzer et al., 1995; Radanov and Sturzenegger, 1996; Coˆte´ et al., 2001). Regardless of whether FM is present in chronic whiplash, altered central pain processing and central sensitisation is evident (Curatolo et al., 2001; Sterling et al., 2002, 2003, 2006; Banic et al., 2004). Moreover, altered central pain processing rather than impaired motor control has been identified as one of the prime prognostic factors for developing chronic whiplash (Sterling et al., 2003, 2006). Another example of a local musculoskeletal disorder associated with FM and frequently seen in manual therapy practice is arthritis (rheumatoid arthritis and osteoarthritis), possibly causing continuous activation of local nociceptors that initiate or sustain central sensitisation (Yunus, 2007). Thus, effective manual therapy in (sub)acute cases of arthritis should be able to limit the (time course of) afferent barrage of noxious input to the central nervous system and thus prevent chronicity. In addition, manual therapy aimed at improving motor control in symptomatic regions/joints is likely to have its place in the prevention of chronicity. Indeed, a sustained mismatch between motor activity and

6


sensory feedback is able to serve as an ongoing source of nociception inside the central nervous system. There is evidence that a mismatch between motor activity and sensory feedback can elicit pain and sensory perceptions in healthy pain-free volunteers (McCabe et al., 2005) and exacerbate pain and sensory perceptions in patients with FM (McCabe et al., 2007), suggesting a possible aetiological role for sensoryemotor incongruence in the development of (chronic) pain. The role of the motor control system in the brain is to manage the relationship between motor commands and sensory feedback (proprioception, vision). In case of inaccurate execution of movements due to deconditioning or joint tissue damage (and consequent altered proprioception), an incongruence between motor activity and sensory feedback is likely to occur. The motor control system may alert the individual to the abnormality in information processing by generating warning signals (i.e. pain or other sensory changes like temperature change or a feeling of peculiarity) (McCabe et al., 2005). Apart from manual therapy skills targeting local musculoskeletal disorders, manual therapy in its broader sense (including stress management, pain physiology education, etc.) has its place in the prevention of chronic widespread pain and FM. These issues are explained below, together with the explanation of the role of manual therapy in those with established hypersensitivity of central pain pathways.

any adverse reactions to the interventions immediately and to adapt their (home) exercises accordingly (Fig. 2). 4.1. Myofascial treatment Anecdotally, muscles and fascia often become hypertonic and develop trigger points in people with chronic widespread pain/FM. Soft-tissue mobilisation is required to free up restrictions and restores local blood flow. However, it is important not to increase pain during treatment. The vicinity of myofascial trigger points differs from normal muscle tissue by its lower pH levels (i.e. more acid), increased levels of substance P, calcitonin gene-related peptide, tumour necrosis factor-a and interleukine-1b, each of which has its role in increasing pain sensitivity (Shah et al., 2005). Sensitised muscle nociceptors are more easily activated and may respond to normally innocuous and weak stimuli such as light pressure and muscle movement (Shah et al., 2005). Therefore, starting the soft-tissue mobilisation superficially with well-tolerated strokes along the length of the muscle fibres (referred to as ‘stripping’ in Benjamin and Tappan, 2005) and progressing towards deeper strokes that go perpendicular to the soft-tissue fibres is recommended (Table 1). Aggressive ways of treating trigger points (e.g. by using ischaemic pressure) are usually not welltolerated and therefore not recommended. 4.2. Motor control training

4. Manual therapy targeting local problems in patients with central sensitisation In cases of hypersensitivity of central pain pathways, relatively minor injuries/trauma at any locations are likely to sustain the process of central sensitisation (Vierck, 2006). In these patients, local musculoskeletal problems are more than epiphenomenona and serve as a continuous source of afferent painful barrage (Nijs et al., 2006). Appropriate manual physiotherapy is unlikely to cure the chronic widespread pain, but can still resolve the localised musculoskeletal pain problem and thus decrease afferent barrage (Nijs et al., 2006). However, clinicians should be aware of the consequences of central sensitisation (i.e. a marked reduced sensory threshold) and adapt their hands-on techniques and exercise programs accordingly. Any therapeutic interventions triggering more pain will serve as a new peripheral source of nociceptive barrage and thus will sustain the process of central sensitisation, as evidenced by the study in patients with FM showing that altered central pain processing is further augmented by isometric exercise (Staud et al., 2005). Likewise, treatments triggering more pain serve as a physical stressor attacking the already deregulated stress response system, thereby initiating a vicious cycle. It is therefore crucial to educate the patient to report

In line with the findings in those with phantom limb pain (Flor et al., 2001), it seems plausible to improve appropriate sensory feedback by using local motor control training to account for the sensoryemotor conflict capable of exaggerating local FM symptoms (McCabe et al., 2005, 2007). Local motor control training is the core feature of the treatment of joint hypermobility. Since FM primarily affects the central nervous system, joint treatment is secondary. Still, there is consistent evidence that generalised joint hypermobility is more prevalent in people with FM compared to healthy controls (AcususoDiaz and Collantes-Estevez, 1998; Hudson et al., 1998; Karaaslan et al., 2000). Combining the prevalence rates of the various studies generates a prevalence rate of 21% (Nijs, 2005), supporting the notion that at least a subgroup of FM has generalised joint hypermobility (Fitzcharles, 2000). Hypermobility has been suggested to account, at least in part, for the widespread pain in FM patients (Gedalia et al., 1993; Fitzcharles, 2000). Impaired motor control in end-range movements might lead to recurrent microtrauma and consequent widespread pain in hypermobile patients (Fitzcharles, 2000). In line with this view, generalised joint hypermobility and its repetitive microtrauma might trigger or sustain central sensitisation (Staud, 2004). Joint hypermobility might even lead to a sensoryemotor incongruence and consequent


7

patient with musculoskeletal pain nature of complaint? acute/subacute pain

chronic localised pain

inappropriate beliefs?

inappropriate beliefs?

no treat local problem with MT*

yes address beliefs + treat local problem with MT below pain threshold

no

yes

treat local address problem beliefs + with MT treat local below pain problem with threshold MT below pain threshold

chronic widespread pain when appropriate: treat local problems with MT below pain threshold pain neurophysiology education treat hypermobility below pain threshold aerobic exercise allowing muscle (re)perfusion, below pain threshold & without post-exertional symptom increase

Fig. 2. Proposed treatment options accounting for central hyperexcitability of central pain pathways. MT, manual therapy.

pain exaggeration. However, there is currently no evidence in support of an association between pain complaints and generalised joint hypermobility in those with FM (Nijs, 2005). In the absence of such evidence, it is recommended to search for such an association on an individual basis. If the manual therapist suspects a role for joint hypermobility in a particular FM case, then a treatment consisting of end-range stabilisation exercises, postural advice, movement advice, self-management strategies and the application of protective and supportive devices is recommended (Nijs, 2005).

5. Changing inappropriate beliefs in an attempt to desensitise the central nervous system Although the dysfunctional descending paininhibitory mechanism as seen in those with chronic widespread pain/FM is primary biological, it is influenced by inappropriate cognitions, emotions and behaviour like catastrophizing, hypervigilance, avoidance behaviour, and somatisation. In case of more intense pain levels, pain catastrophizing is associated with decreased activity in brain regions involved in top-down Table 1 Practical guidelines for hands-on manual therapy skills in those with hypersensitive pain pathways -Educate patient to report adverse reactions during treatment -Do not elicit identical nociceptive stimuli > once every 3 s -Adopt techniques to reduced sensory threshold -Do not increase nociceptive barrage -Initiate soft-tissue mobilisation with superficial stripping techniques -Progress soft-tissue mobilisation with deeper cross-fibre techniques -Careful with ischaemic compression

pain suppression like the dorsolateral prefrontal cortex and the medial prefrontal cortex (Seminowicz and Davies, 2006). In addition to catastrophizing, avoidance behaviour and somatisation may result in sensitisation of dorsal horn spinal cord neurons (through inhibition of descending tracts in the central nervous system e Fig. 1), or alternatively, may be the result of central sensitisation (Zusman, 2002). Sustained arousal is likely to maintain sensitisation of the neurobiological loops (Ursin and Eriksen, 2001). It is important for clinicians to recognise that pain cognitions such as fear of movement and catastrophizing are not only of importance to chronic pain patients, but may even be crucial at the stage of acute/subacute musculoskeletal disorders (Swinkels-Meewisse et al., 2006). So how do you screen for this in daily practice? Screening patients for maladaptive beliefs and subsequently changing them should not be limited to multidisciplinary settings applying cognitive behavioural therapies. Instead, all practitioners can use easy-administered questionnaires (e.g. the pain vigilance and awareness questionnaire, the pain catastrophizing scale) to screen their patients with (sub)acute/chronic musculoskeletal pain for maladaptive beliefs. In the case of hypervigilance, catastrophic beliefs about pain (i.e. helplessness, rumination and magnification) or passive coping strategies like avoidance behaviour, intensive education about the exact nature of chronic widespread pain is likely to clear the path for effective manual physiotherapy (including exercise interventions). Pain neurophysiology education aims at reconceptualising pain, and was found to be effective in reducing pain catastrophising in those with chronic low back pain (Moseley et al., 2004) and chronic widespread pain (Meeus et al., submitted for publication). In

8


addition, educating people with FM about central sensitisation of pain pathways was part of a successful rehabilitation program (Mannerkorpi et al., 2000, 2002). If pain cognitions can be changed by educating patients, increased exposure to activity is allowed, leading to increased performances (Watson et al., 1997). Altered pain beliefs leads to increased confidence, which in turn leads to increased activity levels (Moseley, 2005). From the explanation above, it is clear that pain neurophysiology education should be included in the initial phase of rehabilitation in those patients who have inappropriate beliefs about their pain complaints. If not, a poor understanding of pain may lead to the acquisition of maladaptive attitudes, cognitions and behaviour (Geisser and Roth, 1998) and a consequent poor compliance to any active treatments such as exercise interventions.

6. Changing inappropriate beliefs to improve movement performance It seems plausible that improving beliefs like pain catastrophizing is important not only for enabling proper functioning of the central pain-inhibitory pathways, but to improve movement performance as well. In cases where motor control training appears very difficult in those with chronic widespread pain/FM, changing inappropriate beliefs might solve the problem (Moseley, 2005). Indeed, inappropriate cognitions appear closely related to movement performance. In patients with chronic widespread pain, pain catastrophizing is strongly related to physiological exercise variables (Nijs et al., 2008). In subjects with chronic pain, pain physiology education and consequent altered pain beliefs are directly associated with improved movement performance, even if there is no opportunity to be physically active (Moseley, 2004, 2005). These observations make more sense when interpreted in relation to evidence from brain studies: healthy subjects display a relationship between pain catastrophizing and brain activity in regions involved in motor response and motor planning (i.e. thalamus, putamen, and premotor cortex) (Seminowicz and Davies, 2006). In spite of an increasing amount of research in this area, an in-depth understanding of the bidirectional painemotor interaction is still far from being achieved (Le Pera et al., 2007), but has important messages for manual therapy.

7. Stress management to counteract abnormal pain processing We believe that manual therapy in its broader sense (i.e. treatment modalities including relaxation, breathing exercises and stress management) is able to prevent chronicity in many acute/subacute musculoskeletal

pain problems, and has its place in the comprehensive management of chronic widespread pain/FM (Table 2). The available evidence suggests that in FM the stress response system, notably the hypothalamicepituitarye adrenal (HPA) axis and the sympathetic nervous system, is deregulated (Okifuji and Turk, 2002; Crofford et al., 2004; Adler and Geenen, 2005). Some authors have proposed that this might imply a neurobiological ‘switch’ from hyper(re)activity to hypo(re)activity of the stress system, based on functional or even structural receptor changes, and followed by a cascade of disturbances in neurotransmitter functions, immunological and central pain processing mechanisms (Van Houdenhove and Egle, 2004; Fries et al., 2005). More specifically, deficient HPA-axis functioning might foster pathological immune activation with release of pro-inflammatory cytokines (Raison and Miller, 2003) provoking a so-called ‘sickness response’ (lethargia and malaise, social withdrawal, flulike symptoms, mood lowering, concentration difficulties and generalised pain hypersensitivity), all of which characterise the symptom picture of FM (Wallace et al., 2001). Even in healthy fit subjects with reduced baseline HPA-axis activity, decreasing the physical activity level can trigger symptoms (pain, fatigue) (Glass et al., 2004), suggesting a role for the stress system in the development of symptoms in case of reduced activity (McLean et al., 2005). In this respect, it has recently been shown that HPA-axis hypo-function predicted Table 2 Potential treatment goals and treatment modalities for those with chronic widespread pain and FM Treatment goal

Treatment modality

Decrease afferent nociceptive barrage of trigger points

Soft-tissue mobilisation

Improve appropriate sensory Motor control training feedback to prevent sensorye motor conflict Address joint hypermobility

Motor control training þ movement advice þ self-management strategies

Improve inappropriate beliefs (Pain neurophysiology) education (e.g. catastrophizing) Stress management/stress reduction

Relaxation þ stress self-management techniques þ breathing exercises

Decrease fear of movement

Exposure in vivo or low to moderate intensity exercise below pain threshold

Improve exercise capacity

Low to moderate intensity exercise below pain threshold

Improve effort tolerance


Improve symptoms and daily functioning


Improve muscular blood flow Low to moderate intensity exercise below pain threshold


the development of chronic widespread pain in a group of psychologically ‘at risk’ subjects (McBeth et al., 2007). In line with the patients’ history, this abnormal functioning of the stress system seems to occur mostly in the aftermath of a long period of overburdening by physical and/or emotional stressors and to be precipitated by an additional trigger in the form of an acute physical or emotional event (McLean et al., 2005). In those with chronic widespread pain/FM, the inability of the central nervous system to activate the descending pain-inhibitory pathways is likely to be related to the stress system (i.e. the initial stress response to the collision during whiplash trauma and via behavioural changes that occur in response to the trauma) (McLean et al., 2005). The stress system is capable of influencing pain processing via dorsal horn glucocorticoid receptors (receptors having pain-inhibitory capacity) (McLean et al., 2005). However, many unsolved questions remain about the precise role of stress and stress system disturbance in FM (Cleare, 2004).

8. Exercise therapy accounting for central sensitisation There is evidence to support specific exercise therapies as a cornerstone in the comprehensive management of FM (McCain et al., 1988; Isomeri et al., 1993; Burckhardt et al., 1994; Martin et al., 1996; Buckelew et al., 1998; Mannerkorpi et al., 2000; Nijs and Van Parijs, 2004). The evidence from randomised clinical trials is underscored by the conclusions of a systematic literature review (Karjalainen et al., 2000). In relation to the use of exercise therapy, various treatment goals of potential relevance to those with chronic widespread pain and FM can be identified (Table 2) including effort tolerance rather than low effort capacity (Van Houdenhove et al., 2007). However, clinicians should be cautious not to sustain or even amplify the process of central sensitisation. As outlined above, isometric and aerobic exercises activate endogenous opoid and adrenergic pain-inhibitory mechanisms in healthy subjects, while it increases experimental pain ratings in patients with FM (Staud et al., 2005). Thus, people with FM are increasingly susceptible to activation of nociceptors during exercise. As is the case with hands-on manual therapy skills, exercise interventions that are too vigorous are likely to activate muscle and joint nociceptors and thus cause afferent painful barrage. Altered central pain processing is further augmented by isometric exercise (Staud et al., 2005). Post-exertional complaints should be prevented and closely monitored, if not aversive consequences of exercise therapy can arise and may be a deterrent to compliance with the intervention (Dupree Jones et al., 2006; Vierck, 2006). In those with FM, post-exertional complaints are more pronounced than the well documented delayed

9

onset muscle soreness experienced by healthy deconditioned persons without FM who engage in unfamiliar muscle activity. Post-exertional complaints are typically seen in exercise programs using higher intensities, higher impact movements and those where subjects cannot selfadjust exercise intensity (Dupree Jones et al., 2006). Exercises that are too vigorous might trigger immune activation with release of pro-inflammatory cytokines provoking a so-called ‘sickness response’ (Maier and Watkins, 1998), possibly explaining a variety of postexertional complaints. Therefore, low to moderate intensity exercise (approximately 50% of maximum heart rate) of any types has lower attrition and better symptom improvement than those with the higher intensity (Dupree Jones et al., 2006). Further support in favour of mild to moderate exercise over vigorous exercise interventions comes from the study showing a blunted increase in muscular vascularity in response to both dynamic and static contractions (Elvin et al., 2006). This can result in diminishing blood flow towards the working muscles both during and following exercises (Elvin et al., 2006). These data are in line with other observations pointing to widespread muscular ischaemia in patients with FM (reviewed in Vierck, 2006). Since muscle nociceptors are highly sensitive to ischaemia, exercise interventions should account for the widespread muscular ischaemia and blunted increase in muscular vascularity in response to muscle contractions. If not, exercise is likely to increase afferent painful barrage and thus sustain or accelerate the process of central sensitisation. Apart from using mild to moderate exercise intensity, aerobic exercises using multiple recovery periods (to allow muscular reperfusion) within training sessions might be beneficial (Fig. 2). If available, hydrotherapy in warm water, known to be beneficial to those with FM (Mannerkorpi et al., 2000), might even be able to account for the decreased muscle perfusion during exercise (Vierck, 2006).

9. Conclusion Chronic widespread pain/FM is characterised by sensitisation of central pain pathways. An important and ongoing source of pain is required before the process of peripheral sensitisation can establish central sensitisation. Ongoing nociceptive barrage results in adaptation of dorsal horn neurons, and the process of central sensitisation encompasses altered sensory processing in the brain and malfunctioning of pain-inhibitory mechanisms as well. There is evidence that a stress response system dysfunction may play a role in central sensitisation. Moreover, inappropriate cognitions, emotions and behaviour may have a negative impact on the descending pain-inhibitory mechanisms. In order to

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prevent chronicity in acute or subacute musculoskeletal disorders, it seems crucial to limit the time course of afferent stimulation of peripheral nociceptors. In line with this view, it is suggested that manual therapy might have the capacity to prevent chronicity. In the case of chronic widespread pain and established sensitisation of central pain pathways, relatively minor injuries/trauma at any locations are likely to sustain the process of central sensitisation and should be treated appropriately with manual therapy accounting for the decreased sensory threshold. In addition, generalised joint hypermobility might lead to recurrent microtrauma and consequently sustain the process of central sensitisation. Thus, manual therapy appears to have its place in the comprehensive management of those with chronic widespread pain/FM. The role of manual therapy in such patients may not be limited to localised joint and muscle treatment, but encompasses improvement of pain beliefs and exercise therapy as well. Exercise interventions should take the process of central sensitisation into account by using low to moderate intensity, aerobic exercises using multiple recovery periods. Also stress management techniques such as relaxation and breathing exercises may be useful in some cases. However, manual therapists unaware of, or ignoring the processes involved in the development and maintenance of chronic widespread pain/FM, may cause more harm then benefit to the patient by triggering or sustaining central sensitisation. Finally, it should be noted that the proposed role of manual therapy in the management of chronic widespread pain/FM is based on a theoretical framework rather than on evidence from randomised clinical trials. References Acususo-Diaz M, Collantes-Estevez E. Joint hypermobility in patients with fibromyalgia syndrome. Arthritis Care and Research 1998;11:39e42. Adler GK, Geenen R. Hypothalamicepituitaryeadrenal and autonomic nervous system functioning in fibromyalgia. Rheumatic Disease Clinics of North America 2005;31:187e202. Banic B, Petersen-Felix S, Andersen OK, Radanov BP, Villiger PM, Arendt-Nielsen L, et al. Evidence for spinal cord hypersensitivity in chronic pain after whiplash injury and in fibromyalgia. Pain 2004;107:7e15. Baranauskas G, Nistri A. Sensitization of pain pathways in the spinal cord: cellular mechanisms. Progress in Neurobiology 1998;54:349e65. Bell IR, Baldwin CM, Schwartz GE. Illness from low levels of environmental chemicals: relevance to chronic fatigue syndrome and fibromyalgia. American Journal of Medicine 1998;105:74Se82. Benjamin PJ, Tappan FM. Tappan’s handbook of healing massage techniques. Classic, holistic, and emerging methods. New Jersey: Pearson Prentice Hall; 2005. p. 127. Bombardier CH, Buchwald D. Chronic fatigue, chronic fatigue syndrome, and fibromyalgia. Disability and health-care use. Medical Care 1996;34:924e30. Buckelew SP, Conway R, Parker J, Deuser WE, Read J, Witty TE, et al. Biofeedback/relaxation training and exercise interventions

for fibromyalgia: a prospective trial. Arthritis Care and Research 1998;11:196e209. Burckhardt CS, Mannerkorpi K, Hedenberg L, Bjelle A. A randomized, controlled clinical trial of education and physical training for women with fibromyalgia. Journal of Rheumatology 1994;21: 714e20. Clauw DJ. Fibromyalgia: update on mechanisms and management. Journal of Clinical Rheumatology 2007;13:102e9. Cleare AJ. Stress and fibromyalgia e what is the link? Journal of Psychosomatic Research 2004;57:423e5. Coˆte´ P, Hogg-Johnson S, Cassidy JD, Carroll L, Frank JW. The association between neck pain intensity, physical functioning, depressive symptomatology and time-to-claim-closure after whiplash. Journal of Clinical Epidemiology 2001;54:275e86. Crofford LJ, Young EA, Engleberg C, Korszun A, Brucksch CB, McClure LA, et al. Basal circadian and pulsatile ACTH and cortisol secretion in patients with fibromyalgia and/or chronic fatigue syndrome. Brain, Behavior, and Immunity 2004;18:314e25. Curatolo M, Petersen-Felix S, Arendt-Nielsen L, Giani C, Zbinden AM, Radanov BP. Central hypersensitivity in chronic pain after whiplash injury. Clinical Journal of Pain 2001;17:306e15. Dupree Jones K, Adams D, Winters-Stone K, Burckhardt CS. A comprehensive review of 46 exercise treatment studies in fibromyalgia (1988e2005). Health and Quality of Life Outcomes 2006;4:67. doi:10.1186/1477-7525-4-67. Elvin A, Sio¨steen A-K, Nilsson A, Kosek E. Decreased muscle blood flow in fibromyalgia patients during standardised muscle exercise: a contrast media enhanced colour Doppler study. European Journal of Pain 2006;10:137e44. Fitzcharles M-A. Is hypermobility a factor in fibromyalgia? Journal of Rheumatology 2000;27:1587e9. Flor H, Denke C, Scha¨fer M, Gru¨sser S. Sensory discrimination training alters both cortical reorganisation and phantom limb pain. Lancet 2001;357:1763e4. Fries E, Hesse J, Hellhammer J, Hellhammer DH. A new view on hypocortisolism. Psychoneuroendocrinology 2005;30:1010e6; Gracely RH, Grant MA, Giesecke T. Evoked pain measures in fibromyalgia. Best Practice and Research in Clinical Rheumatology 2003;17:593e609. Gedalia A, Press J, Klein M, Buskila D. Joint hypermobility and fibromyalgia in schoolchildren. Annals of Rheumatic Diseases 1993; 52:494e6. Geisser ME, Roth RS. Knowledge of and agreement with chronic pain diagnosis: relation to affective distress, pain beliefs and coping, pain intensity and disability. Journal of Occupational Rehabilitation 1998;8:73e88. Glass JM, Lyden AK, Petzke F, Stein P, Whalen G, Ambrose K, et al. The effect of brief exercise cessation on pain, fatigue, and mood symptom development in healthy, fit individuals. Journal of Psychosomatic Research 2004;57:391e8. Gracely RH, Geisser ME, Giesecke T, Grant MAB, Petzke F, Williams DA, et al. Pain catastrophizing and neural responses to pain among persons with fibromyalgia. Brain 2004;127:835e43. Hudson N, Fitzcharles MA, Cohen M, Starr MR, Esdaile JM. The association of soft-tissue rheumatism and hypermobility. British Journal of Rheumatology 1998;37:382e6. Isomeri R, Mikkelson M, Latikka P, Kammonen K. Effects of amitriptyline and cardiovascular fitness training on pain in patients with primary fibromyalgia. Journal of Musculoskeletal Pain 1993;1:253e60. Karaaslan Y, Haznedaroglu S, O¨ztu¨rk M. Joint hypermobility and primary fibromyalgia: a clinical enigma. Journal of Rheumatology 2000;27:1774e6. Karjalainen K, Matmivaara A, van Tulder M, Roine R, Jauhiainen M, Hurri H, et al. Multidisciplinary rehabilitation for fibromyalgia and musculoskeletal pain in working age adults (Cochrane Review). Cochrane Database of Systematic Reviews 2000;2.

J. Nijs, B. Van Houdenhove / Manual Therapy 14 (2009) 3e12 Le Bars D, Villaneuva L. Electrophysiological evidence for the activation of descending inhibitory controls by nociceptive afferent pathways. Progress in Brain Research 1988;77:275e99. Le Pera D, Brancucci A, De Armas L, Del Percio C, Miliucci R, Babiloni C, et al. Inhibitory effect of voluntary movement preparation on cutaneous heat pain and laser-evoked potentials. European Journal of Neuroscience 2007;25:1900e7. Maier SF, Watkins LR. Cytokines for psychologists: implications of bidirectional immune-to-brain communication for understanding behavior, mood, and cognition. Psychological Review 1998;105:83e107. Mannerkorpi K, Nyberg B, Ahlmeń M, Ekdahl C. Pool exercise combined with an education program for patients with fibromyalgia syndrome. A prospective, randomized study. Journal of Rheumatology 2000;27:2473e81. Mannerkorpi K, Ahlmeń M, Ekdahl C. Six- and 24-month follow-up of pool exercise therapy and education for patients with fibromyalgia. Scandinavian Journal of Rheumatology 2002;31:306e10. Martin L, Nutting A, Macintosh BR, Edworthy SM, Butterwick D, Cook J. An exercise program in the treatment of fibromyalgia. Journal of Rheumatology 1996;23:1050e3. McBeth J, Silman A, Gupta A, Chiu Y, Ray D, Morris R, et al. Psychological risk factors are moderated through dysfunction of the hypothalamic pituitary adrenal stress axis in the onset of chronic widespread musculoskeletal pain. Arthritis and Rheumatism 2007;56:360e71. McCabe CS, Haigh RC, Halligan PW, Blake DR. Simulating sensoryemotor incongruence in healthy volunteers: implications for a cortical model of pain. Rheumatology 2005;44:509e16. McCabe CS, Cohen H, Blake DR. Somaesthetic disturbances in fibromyalgia are exaggerated by sensoryemotor conflict: implications for chronicity of the disease? Rheumatology 2007;46:1587e92. McCain GA, Bell DA, Mai FM, Halliday PD. A controlled study of effects of a supervised cardiovascular fitness training program on the manifestations of primary fibromyalgia. Arthritis and Rheumatism 1988;31:1135e41. McLean SA, Clauw DJ, Abelson JL, Liberzon I. The development of persistent pain and psychological morbidity after motor vehicle collision: integrating the potential role of stress response systems into a biopsychosocial model. Psychosomatic Medicine 2005; 67:783e90. Meeus M, Nijs J. Central sensitization: a biopsychosocial explanation for chronic widespread pain in patients with fibromyalgia and chronic fatigue syndrome. Clinical Rheumatology 2007;26:465e73. Meeus M, Nijs J, Van Oosterwijck J, Van Alsenoy V, Truijen S. Pain neurophysiology education improves pain beliefs in patients with chronic fatigue syndrome: a randomised clinical trial, submitted for publication. Mendell LM, Wall PD. Responses of single dorsal cord cells to peripheral cutaneous unmyelinated fibres. Nature 1965;206:97e9. Meyer RA, Campbell JN, Raja SN. Peripheral neural mechanisms of nociception. In: Wall PD, Melzack R, editors. Textbook of pain. 3rd ed. Edinburgh: Churchill Livingstone; 1995. p. 13e44. Moseley GL, Nicholas MK, Hodges PW. A randomized controlled trial of intensive neurophysiology education in chronic low back pain. Clinical Journal of Pain 2004;20:324e30. Moseley GL. Evidence for a direct relationship between cognitive and physical change during an education intervention in people with chronic low back pain. European Journal of Pain 2004; 8:39e45. Moseley GL. Widespread brain activity during an abdominal task markedly reduced after pain physiology education: fMRI evaluation of a single patient with chronic low back pain. Australian Journal of Physiotherapy 2005;51:49e52. Nijs J. Generalized joint hypermobility: an issue in fibromyalgia and chronic fatigue syndrome? Journal of Bodywork and Movement Therapies 2005;9:310e7.

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Nijs J, Meeus M, De Meirleir K. Chronic musculoskeletal pain in chronic fatigue syndrome: recent developments and therapeutic implications. Manual Therapy 2006;11:187e91. Nijs J, Van Parijs M. Long-term effectiveness of pool exercise therapy and education in patients with fibromyalgia. Journal of Chronic Fatigue Syndrome 2004;12:73e9. Nijs J, Van de Putte K, Louckx F, Truijen S, De Meirleir K. Exercise performance and chronic pain in chronic fatigue syndrome: the role of pain catastrophizing. Pain Medicine 2008. doi:10.1111/j.15264637.2007.00368.x. Okifuji A, Turk DC. Stress and psychophysiological dysregulation in patients with fibromyalgia syndrome. Applied Psychophysiological and Biofeedback 2002;27:129e41. Price DD, Staud R, Robinson ME, Mauderli AP, Cannon R, Vierck CJ. Enhanced temporal summation of second pain and its central modulation in fibromyalgia patients. Pain 2002;99:49e59. Purves D, Augustine GJ, Fitzpatrick D, Katz LC, LaMantia A-S, McNamara. In: Purves D, Augustine GJ, Fitzpatrick D, Katz LC, LaMantia A-S, McNamara, editors. Neuroscience. Pain 1997:167. Sunderland: Sinauer Associations, Inc. Radanov BP, Sturzenegger M. The effect of accident mechanism and initial findings on the long-term outcome of whiplash injury. Journal of Musculoskeletal Pain 1996;4:47e60. Raison CL, Miller AH. When not enough is too much: the role of insufficient glucocorticoid signaling in the pathology of stress-related disorders. American Journal of Psychiatry 2003; 160:1554e65. Seminowicz DA, Davies KD. Cortical responses to pain in healthy individuals depends on pain catastrophizing. Pain 2006;120:297e306. Shah JP, Philips TM, Danoff JV, Gerber LH. An in vivo microanalytical technique for measuring the local biochemical milieu of human skeletal muscle. Journal of Applied Physiology 2005; 99:1977e84. Spitzer WO, Skovron ML, Salmi LR, Cassidy JD, Duranceau J, Suissa S, et al. Scientific monograph of the Quebec task force on whiplash-associated disorders: redefining ‘‘whiplash’’ and its management. Spine 1995;20:S1e73. Staud R. Fibromyalgia pain: do we know the source? Current Opinion in Rheumatology 2004;16:157e63. Staud R, Robinson ME, Price DD. Isometric exercise has opposite effects on central pain mechanisms in fibromyalgia patients compared to normal controls. Pain 2005;118:176e84. Staud R, Smitherman ML. Peripheral and central sensitization in FM: pathogenic role. Current Pain and Headache Reports 2002;6:259e66. Staud R, Vierck CJ, Cannon RL, Mauderli AP, Price DD. Abnormal sensitization and temporal summation of second pain (wind-up) in patients with fibromyalgia syndrome. Pain 2001;91:165e75. Staud R, Craggs JG, Robinson ME, Perlstein WM, Price DD. Brain activity related to temporal summation of C-fiber evoked pain. Pain 2007;129:130e42. Sterling M, Treleaven J, Edwards S, Jull G. Pressure pain thresholds in chronic whiplash associated disorder: further evidence of altered central pain processing. Journal of Musculoskeletal Pain 2002;10:69e81. Sterling M, Jull G, Vicenzino B, Kenardy J. Sensory hypersensitivity occurs soon after whiplash injury and is associated with poor recovery. Pain 2003;104:509e17. Sterling M, Jull G, Kenardy J. Physical and psychological factors maintain long-term predictive capacity post-whiplash injury. Pain 2006;122:102e8. Swinkels-Meewisse IEJ, Roelofs J, Schouten EGW, Verbeek ALM, Oostendorp RAB, Vlaeyen JWS. Fear of movement/(re)injury predicting chronic disabling low back pain: a prospective inception cohort study. Spine 2006;31:658e64. Ursin H, Eriksen HR. Sensitization, subjective health complaints, and sustained arousal. Annals of the New York Academy of Sciences 2001;933:119e29.

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Van Houdenhove B, Egle UT. Fibromyalgia: a stress disorder? Piecing the biopsychosocial puzzle together. Psychotherapy and Psychosomatics 2004;73:267e75. Van Houdenhove B, Verheyen L, Pardaens K, Van Wambeke P. Rehabilitation of decreased motor performance in patients with chronic fatigue syndrome: should we treat low effort capacity or reduced effort tolerance? Clinical Rehabilitation 2007; 21:1121e42. Vierck CJ. Mechanisms underlying development of spatial distributed chronic pain (fibromyalgia). Pain 2006;124:242e63. Wallace DJ, Linker-Israeli M, Hallegua D, Silverman S, Silver D, Weisman MH. Cytokines play an aetiopathogenetic role in fibromyalgia: a hypothesis and pilot study. Rheumatology (Oxford) 2001;40:743e9. Watson PJ, Booker CK, Main CJ. Evidence for the role of psychological factors in abnormal paraspinal activity in patients

with chronic low back pain. Journal of Musculoskeletal Pain 1997;4:41e56. Whiteside A, Hansen S, Chaudhuri A. Exercise lowers pain threshold in chronic fatigue syndrome. Pain 2004;109:497e9. Wolfe F, Smythe HA, Yunus MB, Bennett RB, Bombardier C, Goldenberg DL, et al. The American College of Rheumatology 1990 criteria for the classification of fibromyalgia: report of the multicenter criteria committee. Arthritis and Rheumatism 1990;33:160e72. Woolf CJ, Salter MW. Neuronal plasticity: increasing the gain in pain. Science 2000;288:1765e9. Yunus MB. Fibromyalgia and overlapping disorders: the unifying concept of central sensitivity syndromes. Seminars in Arthritis and Rheumatology 2007;36:330e56. Zusman M. Forebrain-mediated sensitization of central pain pathways: ‘non-specific’ pain and a new image for MT. Manual Therapy 2002;7:80e8.



Original article

Motion analysis study of a scapular orientation exercise and subjects’ ability to learn the exercise Sarah L. Mottram a,*, Roger C. Woledge b, Dylan Morrissey c a KC International, Lower Mill Street, Ludlow, SY8 1BH, UK Centre for Applied Biomedical Research, King’s College London, London SE1 1UL, UK c Centre for Sports and Exercise Medicine, Queen Mary University of London, Mile End Hospital, London E1 4DG, UK b

Received 17 August 2006; received in revised form 25 July 2007; accepted 30 July 2007

Abstract Exercises to retrain the orientation of the scapula are often used by physiotherapists to optimise shoulder girdle function. The movements and muscle activity required to assume this position have not yet been quantified. Further, patients often find this a difficult exercise to learn accurately, with no data being available on the accuracy of repeated performance. The primary objective of this study was to quantify the movements occurring during a commonly used scapular orientation exercise. The secondary objective was to describe the ability of subjects to learn this position after a brief period of instruction. A group of normal subjects (13 subjects; mean age 32, SD¼9) were taught the scapular orientation exercise. Measurement of the position and muscle actions were made with a motion analysis system and surface electromyography. Further comparison was made of the accuracy of repeated trials. The most consistent movements were upward (mean¼4 , SEM¼0.9 ) and posterior rotation (mean¼4 , SEM¼1.6 ). All parts of the trapezius muscle demonstrated significant activity in maintaining the position while latissimus dorsi did not. Repeated trials showed that subjects were able to accurately repeat the movement without guidance. The key movements of, and immediate efficacy of a teaching approach for, scapular orientation have been established. Ó 2007 Elsevier Ltd. All rights reserved. Keywords: Scapula; Motion analysis; Muscle activity; Exercise

1. Introduction Abnormal scapular movement and muscle function have been shown to be important factors associated with shoulder impingement syndrome (Lukasiewicz et al., 1999; Ludewig and Cook, 2000). Exercises to retrain shoulder function are routinely used by physiotherapists as part of a treatment package for patients with scapular dysfunction (Dickens et al., 2005). One such exercise commonly used is teaching scapular orientation with the arm by the side (Mottram, 1997, 2003). The movements and muscle activity required to assume this position have not yet been quantified. * Corresponding author. E-mail address: [email protected] (S.L. Mottram). 1356-689X/$ - see front matter Ó 2007 Elsevier Ltd. All rights reserved. doi:10.1016/j.math.2007.07.008

The primary objective of this study was to quantify the movements occurring during a scapular orientation exercise (SOE) and normal subjects’ ability to reproduce the position. The secondary objective was to measure the activity in specific muscles in maintaining this movement, particularly the components of the trapezius muscle. 2. The scapular orientation exercise The SOE or previously described as scapula setting (Mottram, 1997, 2003) is taught by physiotherapists in a variety of postures, initially with the arm by the side. It has been described as dynamic orientation of the scapula in order to optimise the position of the glenoid (Mottram, 1997). It is the scapular neutral (mid range)

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position in which there is minimal support from the passive osteo-ligamentous system with the position being maintained by the myofascial structures. A description of this exercise may be of value to the clinician planning the rehabilitation of scapular movement and is necessary in order to evaluate the relationship of this exercise to what is already known about scapular movement faults. Many clinicians find the SOE difficult to teach. A clear description of, and evaluation of a teaching schedule for, scapular orientation will give clinicians a clearer picture of the movements involved and help them adopt a suitable strategy for retraining.

3. Methods 3.1. Subjects The Royal National Orthopaedic Hospital Trust ethics committee granted ethical approval and each subject gave written informed consent. Thirteen subjects were recruited (nine females, four male) aged between 18 and 43 (mean 32, SD 9). All subjects were right handed. Subjects with a history of spinal or upper limb problems that had required treatment or time off work, or any known bony abnormality of the spine (such as a fracture or congenital deformity) were excluded. 3.2. Data collection A motion analysis system, CODA MPX 30 (Charnwood Dynamics, Rothley, UK) was used to collect the motion data. Studies have shown that skin mounted motion sensors are suitable to measure scapula rotation and translation (Johnson and Anderson, 1990; Ludewig and Cook, 2000; Karduna et al., 2001; Lin et al., 2005; Morrissey et al., 2007). The accuracy of all skinmounted marker-tracking systems is inherently limited but satisfactory for the purposes of this study. The CODA uses active infrared LED markers to measure positions within a 223 m3 volume. The translational precision of the instrument has been shown to be within 0.5 mm in each direction, while rotational accuracy is within 1 , determined using factory calibration experiments. Marker positions were captured at 100 Hz. Markers were attached to the thorax (T1, T3, T6), the root of the spine of the scapula, scapula inferior angle and posterior-lateral acromion therefore allowing construction of axis systems in line with ISB recommendations (Karduna et al., 2001). EMG was recorded using a multi-channel EMG system (MA 300 DTU, Motion Lab Systems, Bolton Rouge, LA, USA). Pairs of self-adhesive gelled surface electrodes 1 cm in diameter at 2 cm distance were used.

Preamplifiers were mounted directly over these electrodes and a reference electrode placed over the contra-lateral acromion. EMG was recorded within a bandwidth of 0.2e5.0 kHz and integrated over 5 ms intervals. The resultant values were collated on computer by infrared telemetry at 200 Hz interleaved with the operation of the infrared motion analysis system. The subject was asked to hold the orientated position for 5 s. Records were examined to determine 2 s when the least movement occurred. Scapula position and muscle activity in the orientated position was extracted by the average position or muscle activity during this 2 s period. Scapula movement was defined in relation to the thorax co-ordinate system, using a ZYX Eulerian transform in accordance with ISB recommendations (Karduna et al., 2000). This procedure effectively removed confounding thoracic movement from the results. Translation of the scapula were measured in millimetres and described as lateral (in the frontal plane), ventral (in the sagittal plane) and superior (in the horizontal plane). Rotations of the scapula were measured in degrees and described as upward rotation (in the coronal plane), external rotation (in the transverse plane) and posterior rotation (in the sagittal plane). For movement data, comparison was made between the resting and scapular orientated positions (unassisted). For data pertaining to the accuracy of positioning, comparison was made with the assisted position data (therapist assisting the new scapula positioning). EMG electrode pairs were attached over the upper trapezius centred 2 cm lateral to the midpoint between the seventh cervical vertebrae and the lateral end of the acromion (Jensen et al., 1993); the middle trapezius on the mid point of a line from the acromion to the end of the spinous process of the seventh cervical vertebra (Guazzelli et al., 1991); the lower trapezius 3 cm lateral to the spine at the level of the inferior angle of the scapula (Cherington, 1968); and finally the latissimus dorsi 4 cm below the inferior angle of the scapula (Basmajian and DeLuca, 1985). The electrode placements were in line with the fibre direction for each muscle.

4. Procedure The right shoulder was used in each subject. Subjects were seated on a stool with the feet supported and spine in a neutral position. The subject was taught the SOE by an experienced physiotherapist (primary author). The procedure for teaching the SOE in this experiment has been previously described and is described below (Mottram, 1997, 2003). The SOE position was determined in each individual. In each subject this was judged to be the mid position

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between their available range of upward and downward rotation, external and internal rotation and posterior and anterior rotation (posterioreanterior tilting) of the scapula. The SOE position was established by active movements by the subject assisted by the therapist. The movements required to achieve the SOE (as judged by the therapist) were then explained to the subject and visual, auditory and kinaesthetic cues were used. Different cues were used for different subjects in order to achieve the objective of positioning the scapula actively in the mid neutral region as subjects respond differently to a given cue. Examples of cues included passive/assisted movements into the SOE position, tactile feedback with gentle pressure on the acromion to encourage upward rotation, recognition of a feeling of widening the chest to encourage posterior tilt, demonstration of common wrongly directed movements, demonstration and verbal feedback. The exact instructions given by the therapist were dependent on the judgement of the relaxed position of the scapula, the movement required to achieve the SOE position and the response of the patient to visual, auditory and kinaesthetic cues. A maximum of 5 min was used for the teaching procedure. A record of EMG activity was made as the subjects raised their arm through 150 in the scapular plane. The arm was raised over a 3 s period and lowered over a 3 s period. This produced a clear burst of activity at all four recording sites. Maximum activity within any 0.1 s interval during this movement was used as the standard for normalisation purposes. The normalisation of EMG activity with reference to recording during another movement has been used in other studies (Hungerford et al., 2003; Lehman et al., 2004). All EMG signals were rectified and then averaged over the 2 s period and then divided by the normalisation standard. At rest, markers were attached to the bony landmarks described above and their position recorded. The experimenter next positioned the subject in the orientated position for remarking of the scapular landmarks as described above (assisted). A maximum of 5 min was required for this. Following a recording in this position the subject returned to the resting position. Immediately following this (within 2 min), motion data recordings were taken while the subject made three further attempts to

return to, and hold for 5 s, the scapula orientated position (unassisted). A rest period of 30 s was allowed between these attempts. EMG recording was made on the first unassisted repositioning attempt only. All EMG signals were rectified and then averaged over the 2 s period and then divided by the normalisation standard.

5. Statistical methods All statistics were performed using Sigma Stat 2 (Jandel Scientific, CA, USA). The distribution of the data was tested for normality using the KolmogoroveSmirnov test. Specifically, the Pearson correlation analysis was used for repeated movements, t-tests were used to derive the p-values for the difference between the resting and SOE position and ANOVA for muscle action with Tukey post hoc tests. The level of significance was set at p GPs Manipulative Physiotherapists > GPs Physiotherapists, Manipulative Physiotherapists, Chiropractors, and Osteopaths > GPs Physiotherapists, Manipulative Physiotherapists, and Chiropractors > Musculoskeletal Medical Practitioners Physiotherapists and Manipulative Physiotherapists > Chiropractors or Osteopaths Physiotherapists and Manipulative Physiotherapists > Chiropractors, Osteopaths, GPs, or Musculoskeletal Medical Practitioners Physiotherapists and Manipulative Physiotherapists > Chiropractors, Osteopaths, GPs, or Musculoskeletal Medical Practitioners Chiropractors, Osteopaths, and Musculoskeletal Medical Practitioners > GPs Physiotherapists and Manipulative Physiotherapists > Chiropractors, Osteopaths, GPs, or Musculoskeletal Medical Practitioners Chiropractors, Osteopaths, and Musculoskeletal Medical Practitioners > GPs Physiotherapists, Manipulative Physiotherapists, Chiropractors, and Osteopaths > GPs Physiotherapists, Chiropractors, and Osteopaths > Musculoskeletal Medical Practitioners Physiotherapists, Chiropractors, and Osteopaths > GPs or Musculoskeletal Medical Practitioners Chiropractors and Osteopaths > Manipulative Physiotherapists Physiotherapists, Manipulative Physiotherapists, Chiropractors, and Osteopaths > GPs or Musculoskeletal Medical Practitioners Manipulative Physiotherapists > Musculoskeletal Medical Practitioners

Lateral flexion Rotation ROM Combined movement McKenzie side-glide

Repeated movement Visual postural analysis Leg length discrepancy

Quadrant/Kemp’s Test

Sacroiliac joint movement

Sacroiliac joint pain

Straight leg raise Slump Neurological testing (Myotomes, dermatomes, reflexes, etc.) Muscle strength testing Applied Kinesiology BieringeSorensen Test Muscle stabilisation

Stabilising pressure biofeedback Janda

Muscle length

Soft tissue palpation Bony landmark palpation Passive joint movement Tenderness palpation

P.M. Kent et al. / Manual Therapy 14 (2009) 88e100

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Table 5 (continued ) Technique

Significant between-discipline differences in the use of NSALBP assessments (pair-wise ManneWhitneyeU comparisons p < 0.003)

Motion palpation

Chiropractors and Osteopaths > Physiotherapists, Manipulative Physiotherapists, GPs, or Musculoskeletal Medical Practitioners Physiotherapists > GPs Osteopaths > all other disciplines Chiropractors > Physiotherapists, Manipulative Physiotherapists, GPs, or Musculoskeletal Medical Practitioners Physiotherapists > GPs No between-discipline differences Physiotherapists and Manipulative Physiotherapists > Chiropractors, Osteopaths, GPs, or Musculoskeletal Medical Practitioners Chiropractors, Osteopaths, and Musculoskeletal Medical Practitioners > GPs Physiotherapists > Chiropractors, GPs, or Musculoskeletal Medical Practitioners Manipulative Physiotherapists > GPs Musculoskeletal Medical Practitioners > Physiotherapists, Chiropractors, or Osteopaths Manipulative Physiotherapists > Osteopaths Physiotherapists and Manipulative Physiotherapists > GPs Physiotherapists > Chiropractors Physiotherapists, Manipulative Physiotherapists, and Musculoskeletal Medical Practitioners > Osteopaths Physiotherapists, Manipulative Physiotherapists, Chiropractors, and Musculoskeletal Medical Practitioners > GPs Physiotherapists, Manipulative Physiotherapists, and Chiropractors > Osteopaths Physiotherapists, Manipulative Physiotherapists, Chiropractors, and Musculoskeletal Medical Practitioners > Osteopaths Physiotherapists, Manipulative Physiotherapists, and Chiropractors > GPs Physiotherapists > Osteopaths and GPs Manipulative Physiotherapists > Chiropractors and Musculoskeletal Medical Practitioners No between-discipline differences No between-discipline differences Musculoskeletal Medical Practitioners > all other disciplines Physiotherapists and Manipulative Physiotherapists > Osteopaths No between-discipline differences Musculoskeletal Medical Practitioners > Osteopaths or GPs Manipulative Physiotherapists > Osteopaths No between-discipline differences Chiropractors > all other disciplines Chiropractors more frequently > all other disciplines Osteopaths > Manipulative Physiotherapists Physiotherapists > Chiropractors, Osteopaths, GPs, or Musculoskeletal Medical Practitioners Manipulative Physiotherapists > GPs or Musculoskeletal Medical Practitioners Physiotherapists > Chiropractors, Osteopaths, GPs, and Musculoskeletal Medical Practitioners Manipulative Physiotherapists, Chiropractors, Osteopaths, and Musculoskeletal Medical Practitioners > GPs Manipulative Physiotherapists > Chiropractors or Musculoskeletal Medical Practitioners

Craniosacral rhythm

Pain description Pain drawing

Verbal pain scales Visual pain scales Numerical pain scales McGill pain scale Oswestry Disability Questionnaire

RolandeMorris Disability Questionnaire Quebec Disability Questionnaire Patient-Specific Scale LB Outcome Score Short Form 12 or 36 Waddell’s Non-organic Signs Modified Core LBP Questions Fear-avoidance Questionnaire Distress & Risk Assessment Visual X-ray analysis X-ray line drawing CT MRI

be perceived as novel and/or clinicians may consider themselves inadequately trained to assess the effects of health conditions on other domains. For example, only recently in Australia have insurers actively promoted the reporting of activity limitation and participation outcomes (Australian Physiotherapy Association, 2003; Transport Accident Commission, 2003; Victorian WorkCover Authority, 2004). The movement towards more comprehensive patient assessment reflects a growing awareness of the role that a range of factors play in recovery from LBP. For instance, there is evidence that some psychosocial factors are associated with LBP outcome (Pincus et al., 2002).

It is possible that clinicians believe that levels of physical impairment and pain are strongly associated with performance in other domains such as activity limitation. Assessment of activity limitation and psychosocial function might therefore be perceived as providing information that does not warrant the time commitment required to collect and utilise these data. However, there is evidence that assessments in different domains measure different aspects of the patient’s presentation and that measurements in one domain are not good substitutes for measurements in another domain. Measurements taken at a single time consistently display a relatively weak linear relationship between domains (Deyo, 1986;

98


Fig. 2. Assessment of acute NSLBP across health domains. The proportion of clinicians who assess NSLBP using any technique from these assessment domains. Note: the width of the 95% confidence intervals have been adjusted (Tryon, 2001) such that where no visual overlap occurs between confidence intervals for any particular comparison, a difference between these proportions can be observed with 95% confidence.

Onoyama-Ball, 1992; Waddell et al., 1992; Rainville et al., 1994; Johannsen et al., 1995; Lindstrom et al., 1995; Schonheinz, 1995; Gronblad et al., 1997; Riddle, 1997; Kuukkanen and Malkia, 2000; Sullivan et al., 2000; Mannion et al., 2001; Kovacs et al., 2004). It also may be that the focus of assessment in the first few consultations of acute NSLBP is on gathering information that informs immediate treatment decisions. Clinicians may believe that the favourable short term prognosis of most acute LBP pragmatically constrains the need to assess more than physical impairment and pain. While it is possible that other assessments used to monitor progress or determine outcome are obtained during later consultations, without baseline measurement such monitoring is likely to be under-informed. Routine assessment across domains may be advantageous, but clinicians may need to be convinced that it influences NSLBP management and improves patient outcomes. Currently, evidence of this is sparse. The recognition that aspects of activity limitation and psychosocial function are associated with NSLBP outcomes may not change clinician behaviour while clinicians remain uncertain regarding effective interventions signalled by these findings. This uncertainty may stem from inflexible beliefs and practices, limited relevant empirical research, limited knowledge of best practice or a lack of therapeutic resources.

The strengths of this survey design and results are: (1) these data form a historical record to benchmark acute NSLBP assessment practice, (2) data were gathered from a representative sample of primary care clinicians responsible for the treatment of NSLBP in Australia. The weaknesses of this survey design and results are: (1) a nonrespondent bias could not be determined for the 40% of clinicians who did not return completed questionnaires; (2) the data were based on clinician self-report, not observation of actual behaviour; and (3) caution may be required in generalising these results to other countries.

5. Conclusions Primary care clinicians report that they commonly assess symptoms and signs in acute NSLBP from the domains of physical impairment and pain. The assessment of symptoms and signs from the domains of activity limitation and psychosocial function was less common, although there is evidence that this information can be prognostically important and useful for outcome assessment. There were differences between professional disciplines in the use of particular assessments. Adoption of greater standardisation of assessment by clinicians


may require demonstration of the capacity of this standardisation to improve patient outcomes. One pathway to promote standardisation would be further research to determine if the identification of subgroups of NSLBP based on clusters of symptoms and signs does result in better patient outcomes, or whether simple generic assessments provide adequate clinical information.

Competing interests The authors declare they have no competing interests.

Acknowledgements Elements of this work were supported by Faculty of Health Sciences (La Trobe University), Joint Coal Board Health & Safety Trust (Australia), Musculoskeletal Physiotherapy Association (Victoria). Peter Kent is supported by grant number 348366 from the National Health and Medical Research Council of Australia.

Appendix 1. Supplementary data Supplementary data associated with this article can be found, in the online version, at doi:10.1016/ j.math.2007.12.006.

References Accident Compensation Commission. New Zealand acute low back pain guide. Wellington, New Zealand: Accident Compensation Commission; 1999. Altman DG. Practical statistics for medical research. London, England: Chapman and Hall; 1991. p. 1e611. Australian Acute Musculoskeletal Pain Guidelines Group. Evidencebased management of acute musculoskeletal pain: a guide for clinicians. 1st ed. Bowen Hills, Australia: Australian Academic Press; 2004. p. 66. Australian Physiotherapy Association. Clinical justification and outcome measures e APA position statement. Melbourne, Australia: Australian Physiotherapy Association; 2003. p. 1e3. Battie´ MC, Cherkin DC, Dunn R, Ciol MA, Wheeler KJ. Managing low back pain: attitudes and treatment preferences of physical therapists. Physical Therapy 1994;74(3):219e26. Bigos S, Bowyer O, Braen G. Acute low back problems in adults. Clinical practice guidelines No. 14: AHCPR Publication No. 95-0642. Rockville, MD: Agency for Health Care Policy and Research, Public Health Service, U.S. Department of Health and Human Services; 1994. Binkley J, Finch E, Hall J, Black T, Gowland C. Diagnostic classification of patients with low back pain: report on a survey of physical therapy experts. Physical Therapy 1993;73(3):138e55. Bogduk N. Evidence-based guidelines for the management of acute low back pain. NHMRC website; 2000a. Bogduk N. What’s in a name? The labelling of back pain. Medical Journal of Australia 2000b;173:400e1.

99

Brennan GP, Fritz JM, Hunter SJ, Thackeray A, Delitto A, Erhard RE. Identifying subgroups of patients with acute/subacute ‘‘nonspecific’’ low back pain e results of a randomized clinical trial. Spine 2006;31(6):623e31. Childs JD, Fritz JM, Flynn TW, Irrgang JJ, Johnson KK, Majkowski GR, et al. A clinical prediction rule to identify patients with low back pain most likely to benefit from spinal manipulation: a validation study. Annals of Internal Medicine 2004;141:920e8. Cochrane WG. Sampling techniques, 3rd ed. New York: John Wiley & Sons; 1977. Delitto A, Erhard RE, Bowling RW. A treatment-based classification approach to low back syndrome: identifying and staging patients for conservative treatment. Physical Therapy 1995;75(6):470e89. Deyo RA. Comparative validity of the sickness impact profile and shorter scales for functional assessment in low-back pain. Spine 1986;11(9):951e4. Deyo RA, Battie M, Beurskens AJ, Bombardier C, Croft P, Koes B, et al. Outcome measures for low back pain research. A proposal for standardized use. Spine 1998;23(18):2003e13. Deyo RA, Phillips WR. Low back pain: a primary care challenge. Spine 1996;21(24):2826e32. Deyo R, Rainville J, Kent D. What can the history and physical examination tell us about low back pain? Journal of the American Medical Association 1992;268(6):760e5. Flynn T, Fritz JW, Whitman M, Wainner RS, Magel J, Rendeiro D, et al. A clinical prediction rule for classifying patients with low back pain who demonstrate short-term improvement with spinal manipulation. Spine 2002;27(24):2835e43. Foster NE, Thompson KA, Baxter GD, Allen JM. Management of non-specific low back pain by physiotherapists in Britain and Ireland. A descriptive questionnaire of current clinical practice. Spine 1999;24(13):1332e42. Fritz JM, George SZ, Delitto A. The role of fear-avoidance beliefs in acute low back pain: relationships with current and future disability and work status. Pain 2001;94(1):7e15. Gracey J, McDonough S, Baxter G. Physiotherapy management of low back pain e a survey of current practice in Northern Ireland. Spine 2002;27(4):406e11. Grimmer K, Sheppard L, Pitt M, Magarey M, Trott P. Differences in stakeholder expectations in the outcome of physiotherapy management of acute low back pain. International Journal for Quality in Health Care 1999;11(2):155e62. Gronblad M, Hurri H, Kouri J. Relationships between spinal mobility, physical performance tests, pain intensity and disability assessments in chronic low back pain patients. Scandinavian Journal of Rehabilitation Medicine 1997;29(1):17e24. Haggman S, Maher CG, Refshauge KM. Screening for symptoms of depression by physical therapists managing low back pain. Physical Therapy 2004;84(12):1157e66. Hahne AJ, Keating JL, Wilson SC. Do within-session changes in pain intensity and range of motion predict between-session changes in patients with low back pain? Australian Journal of Physiotherapy 2004;50(1):17e23. Hall H, McIntosh G, Melles T. A different approach to back pain diagnosis: identifying a pattern of pain. Canadian Journal of CME 1994:31e41. Indahl A. Good prognosis for low back pain when left untampered: a randomized clinical trial. Spine 1995;20(4):473e7. Indahl A, Kaigle A, Reikera˚s O, Holm S. Five-year follow-up study of a controlled clinical trial using light mobilization and an informative approach to low back pain. Spine 1998;23(23):2625e30. Jette AM, Smith K, Haley SM, Davis KD. Physical therapy episodes of care for patients with low back pain. Physical Therapy 1994; 74(2):101e15. Johannsen F, Remvig L, Kryger P, Beck P, Warming S, Lybeck K, et al. Exercises for chronic low back pain: a clinical trial. Journal of Orthopaedic and Sports Physical Therapy 1995;22(2):52e9.

100


Kent PM, Keating J. Do primary-care clinicians think that nonspecific low back pain is one condition? Spine 2004;29:1022e31. Kent PM, Keating JL. Classification in non-specific low back pain e what methods do primary care clinicians currently use? Spine 2005;30:1433e40. Kovacs FM, Abraira V, Zamora J, Gil Del Real M, Llobera J, Fernandez C, et al. Correlation between pain, disability, and quality of life in patients with common low back pain. Spine 2004; 29(2):206e10. Kuukkanen T, Malkia E. Effects of a three-month therapeutic exercise programme on flexibility in subjects with low back pain. Physiotherapy Research International 2000;5(1):46e61. Leboeuf-Yde C, Lauritsen J, Lauritzen T. Why has the search for causes of low back pain largely been inconclusive? Spine 1997; 22:877e81. Lindstrom I, Ohlund C, Nachemson A. Physical performance, pain, pain behavior and subjective disability in patients with subacute low back pain. Scandinavian Journal of Rehabilitation Medicine 1995;27(3):153e60. Long A, Donelson R, Fung T. Does it matter which exercise? A randomized control trial of exercise for low back pain. Spine 2004; 29:2593e602. Maitland G. Vertebral manipulation, 5th ed. London, England: Butterworth-Heinemann; 1986 [chapter 7, p. 215e42]. Mannion A, Junge A, Taimela S, Muntener M, Lorenzo K, Dvorak J. Active therapy for chronic low back pain e Part 3. Factors influencing self-rated disability and its change following therapy. Spine 2001;26(8):920e9. McCarthy CJ, Arnall FA, Strimpakos N, Freemont A, Oldham JA. The biopsychosocial classification of non-specific low back pain: a systematic review. Physical Therapy Reviews 2004;9:17e30. McKenzie R. Prophylaxis in recurrent low back pain. New Zealand Medical Journal 1979;89:22e3. McKenzie R. Mechanical diagnosis and therapy for low back pain: toward a better understanding. In: Twomey L, Taylor J, editors. Physical therapy of the low back. New York, NY, USA: Churchill Livingstone; 1987. p. 157e73. Newton W, Curtis P, Witt P, Hobler K. Prevalence of subtypes of low back pain in a defined population. Journal of Family Practice 1997;45(4):331e6. Onoyama-Ball M. The relationship of impairments and function in patients with back pain. Unpublished MSc thesis, Boston, Massachusetts: NGH Institute of Health Professionals; 1992. p. 1e76, p3. Petersen T, Laslett M, Thorsen H, Manniche C, Ekdahl C, Jacobsen S. Diagnostic classification of non-specific low back pain. A new system integrating patho-anatomic and clinical categories. Physiotherapy Theory & Practice 2003;19(4):213e37. Philips HC, Grant L. Acute back pain: a psychological analysis. Behaviour Research and Therapy 1991;29(5):429e34. Phillips RB, Frymoyer JW, Mac Pherson BV, Newburg AH. Low back pain: a radiographic enigma. Journal of Manipulative and Physiological Therapeutics 1986;9(3):183e7. Pincus T, Burton A, Vogel S, Field A. A systematic review of psychological factors as predictors of chronicity/disability in prospective cohorts of low back pain. Spine 2002;27(5):E109e20. Quebec Task Force on spinal disorders. Scientific approach to the assessment and management of activity-related spinal disorders e a monograph for clinicians. Spine 1987;12(7):1e59.

Rainville J, Sobel JB, Hartigan C. Comparison of total lumbosacral flexion and true lumbar flexion measured by a dual inclinometer technique. Spine 1994;19(23):2698e701. Riddle D. Relationships between disability and physical impairment in patients with low back pain. Unpublished PhD thesis, Richmond, VA, USA: Virginia Commonwealth University; 1997. p. 1e142, p8. Riddle DL. Classification and low back pain: a review of the literature and critical analysis of selected systems. Physical Therapy 1998; 78(7):708e37. Royal College of General Practitioners. Clinical guidelines for the management of acute low back pain. London, England: Royal College of General Practitioners, Chartered Society of Physiotherapy, Osteopathic Association of Great Britain, British Chiropractic Association, National Back Pain Association; 1999. Schonheinz N. Relationship of impairments to function in assessing back pain. Unpublished MSc thesis. Boston, MA, USA: MGH Institute of Health Professions; 1995. p. 1e83, p3. Spengler DM, David DP. Industrial low back pain: a practical approach. In: Wiesel SW, editor. Industrial low back pain: a comprehensive approach. Charlottesville, VA, USA: The Michie Company; 1985. p. 869e71. Spitzer RL, Williams JB, Kroenke K, Linzer M, deGruy F, Hahn SR, et al. Utility of a new procedure for diagnosing mental disorders in primary care e The PRIME_MD 1000 study. Journal of the American Medical Association 1994;272(22):1749e56. Sullivan MS, Shoaf LD, Riddle DL. The relationship of lumbar flexion to disability in patients with low back pain. Physical Therapy 2000;80(3):240e50. Transport Accident Commission. Clinical justification flowchart. Melbourne, Australia; 2003. p. 1e2. Tryon WW. Evaluating statistical difference, equivalence, and indeterminancy using inferential confidence intervals: an integrated alternative method of conducting null hypothesis statistical tests. Psychological Methods 2001;6(4):371e86. van Tulder MW, Assendelft WJ, Koes BW, Bouter LM. Spinal radiographic findings and nonspecific low back pain. A systematic review of observational studies. Spine 1997;22(4):427e34. Victorian WorkCover Authority. Clinical framework for the delivery of physiotherapy services to injured workers. Melbourne, Australia: Victorian WorkCover Authority; 2004. p. 1e15. Waddell G, Somerville D, Henderson I, Newton M. Objective clinical evaluation of physical impairment in chronic low back pain. Spine 1992;17(6):617e28. Watkins MA, Riddle DL, Lamb RL, Personius WJ. Reliability of goniometric measurements and visual estimates of knee range of motion in a clinical setting. Physical Therapy 1991;71:90e7. World Health Organisation. International classification of impairments, disabilities and handicaps (ICIDH). Geneva, Switzerland: World Health Organisation; 1980. World Health Organisation. International classification of functioning, disability and health. Geneva, Switzerland: World Health Organisation; 2001. Youdas JW, Carey JR, Garrett RR. Reliability of measurements of cervical spine range of motion e comparison of three methods. Physical Therapy 1991;71:98e106. Zusman M. Structure-oriented beliefs and disability due to back pain. Australian Journal of Physiotherapy 1998;44(1):13e20.



Original article

Reduction of experimental muscle pain by passive physiological movements Michael Møller Nielsen a, Anne Mortensen a, Jakob Kierstein Sørensen a, Ole Simonsen b, Thomas Graven-Nielsen c,* a

College-of-Health, Aalborg, Department of Physiotherapy, Selma Lagerloefs Vej 2, 9220 Aalborg East, Denmark b Aalborg Hospital and Nordic Orthopaedic Division, Sdr. Skovvej 11, 2, 9000 Aalborg, Denmark c Center for Sensory-Motor Interaction (SMI), Laboratory for Experimental Pain Research, Aalborg University, Fredrik Bajers Vej 7D-3, DK-9220 Aalborg East, Denmark Received 22 September 2006; received in revised form 24 October 2007; accepted 2 December 2007

Abstract The analgesic effects of passive movements on deep-tissue pain have not been sufficiently explored in human studies. The purpose of this study was to examine the effect of passive physiological movements (PPMs) on deep-tissue pain sensitivity. Seventeen healthy subjects were included in this randomised crossover study. In one session an electrically driven bicycle performed 30 min PPM of the knee joint. Another session without PPM served as control. The effect of PPM on experimental muscle pain was assessed. Muscle pain was induced by i.m. injection of hypertonic saline into the tibialis anterior muscle and the pain intensity was scored on an electronic visual analogue scale (VAS). The pressure pain sensitivity was assessed by recording of pressure pain thresholds (PPTs). McGill Pain Questionnaire (MPQ) was used to describe the quality of the induced pain. Compared with the control session PPM demonstrated: (1) a reduction of the experimental muscle pain intensity (VAS area and peak) and duration (17e31%, P < 0.03), (2) lower MPQ score and a change in quality profile of experimental muscle pain (25%, P < 0.01) and (3) an increased PPT (17%, P < 0.0005). The present study demonstrated that PPM produced an immediate analgesic effect on deep-tissue pain indicating a possible involvement of neural inhibitory mechanisms. Ó 2008 Elsevier Ltd. All rights reserved. Keywords: Manual therapy; Joint mobilization; Passive physiological movements; Experimental muscle pain

1. Introduction Musculoskeletal physiotherapy is a keystone in the field of physiotherapy and its focus is mainly on identifying dysfunctional structures/mechanisms and attempting to correct any related subsequent biomechanical/ functional deficits (Shacklock, 1995; Maitland et al., 2002; Maitland, 2003). Basic assumptions and hypotheses in musculoskeletal physiotherapy are therefore often

* Corresponding author. Fax: þ45 98 15 40 08. E-mail address: [email protected] (T. Graven-Nielsen). 1356-689X/$ - see front matter Ó 2008 Elsevier Ltd. All rights reserved. doi:10.1016/j.math.2007.12.008

based on clinical empirical knowledge with an attempt to rationalise these within existing biomedical theories (Rivett, 2004). Recently, manual physiotherapy has been criticised for not implementing an evidence-based approach in the examination and treatment of patients (Shacklock, 1995; Maitland et al., 2002; Zusman, 2002, 2004; Maitland, 2003; Rivett, 2004). In the last decade clinical and experimental studies in spinal manipulative therapy (SMT) have indicated possible neurophysiological effects for mobilization induced analgesia (Skyba et al., 2003; Souvlis et al., 2004; Sluka et al., 2006; Moss et al., 2007). Several studies have shown that both manipulation and mobilizations of

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M.M. Nielsen et al. / Manual Therapy 14 (2009) 101e109

the spine produce a hypoalgesic mechanism measured by pressure pain thresholds (PPTs), visual analogue scale (VAS) and neural provocation test (Hayek et al., 1995; Vicenzino et al., 1996, 1998a,b; Herzog et al., 1999; Dishman and Bulbulian, 2000; Sterling et al., 2001; Mohammadian et al., 2004; Devocht et al., 2005). Vicenzino and others investigated whether the hypoalgesia produced by SMT could be explained by opioid mediated descending inhibition. In general, an opioid antagonist (naxolone) did not influence the hypoalgesic response by SMT (Zusman et al., 1989; Souvlis and Wright, 1997; Paungmali et al., 2004). Other studies have shown involvement of the sympathetic nervous system with SMT with skin conductance, skin temperature, heart rate, respiratory rate and blood pressure as outcome parameters (Petersen et al., 1993; McGuiness et al., 1997; Vicenzino et al., 1998a; Knutson, 2001). Driven by these findings there has been a focus on SMT and potential involvement of the dorsal part of the periaqueductal grey matter (dPAG) in the mesencephalon. The PAG plays an important role for behavioural responses to pain, stress and other stimuli by coordinating responses of a number of systems including the nociceptive system, the autonomic nervous system (ANS) and motor system (Fanselow, 1991; Lovick, 1991; Morgan, 1991). Low threshold mechanoreceptors from joint and muscles project to the dPAG and therefore non-noxious afferent input as SMT might be an adequate stimulus to activate key regions of PAG and mediate a non-opioid analgesia (Yezierski, 1991; Shacklock, 1995; Simon et al., 1997; Vicenzino et al., 1998a,b, 2001; Sterling et al., 2001; McLean et al., 2002; Paungmali et al., 2003; Mohammadian et al., 2004; Mulligan, 2004; Zusman, 2004). To date, few studies have characterised the effects of peripheral joint mobilization techniques on pain responses. Skyba et al. (2003) showed that peripheral mobilization of hyperalgesic knee joints in rats increased the mechanical withdrawal threshold; i.e. an anti-hyperalgesic effect. The reduced sensitivity was intact after spinal blockade of opioid or GABAA receptors and potentially due to descending inhibitory mechanisms that utilize serotonin and noradrenalin via corticospinal projections from the PAG (Skyba et al., 2003). Sluka and Wright (2001) showed that mobilizing the rat knee joint for 9 min reversed mechanical hyperalgesia induced by intra-articular injection of capsaicin in the ankle joint (Sluka and Wright, 2001). Recently, a study using similar design showed that mobilization of the knee joint caused a bilateral increase in mechanical withdrawal threshold in conditions of acute muscle inflammation and chronic muscle and joint inflammation (Sluka et al., 2006). A human study on patients with osteoarthritis showed that 9 min of accessory joint mobilization of the knee joint was sufficient to induce an increased threshold for mechanical pressure both locally and

distant from the treated joint (Moss et al., 2007). Several studies have used Mulligan’s ‘‘Mobilizations with Movement’’ (MWM) for the treatment of patients with long-lasting lateral epicondylalgia and found an immediate sympathoexcitatory effect, a change in motor activity and pain relief (Simon et al., 1997; Vicenzino et al., 1998a,b, 2001; Paungmali et al., 2003; Mulligan, 2004). The aim of this study was to assess the efficacy of passive physiological movements (PPMs) on experimental muscle pain (saline-induced and pressure pain) in a randomised crossover study including healthy subjects. The hypothesis was that PPM of joints decreases pain sensitivity localised in the same neurological segment.

2. Material and methods 2.1. Subjects Seventeen healthy subjects (six males and 11 females) were recruited among physiotherapy students (mean age: 23.9 years, SD 2.5) by verbal and written announcement. The exclusion criteria were pain, a trauma or injury in the last month causing pain for more than 7 days, known degenerative conditions in the limbs, pelvis or spine, surgery in limbs, pelvis and spine, psychological and/or neurological diseases, pregnancy and known severe allergy. The criteria were ensured based on questionnaires, short interviews and palpation of the relevant muscles. All subjects received both verbal and written information before signing a consent form for participating. The study was approved by the local ethical review board (VN 2004/64) and was conducted in accordance with the Helsinki Declaration. 2.2. Experimental procedure This randomised crossover study included a control session and an intervention session separated by at least a 1-week interval. It was not possible to blind subjects or assessors to the specific intervention in each sessions but subjects were blinded to the hypothesis tested in the current study. The subjects were positioned in a supine position (Fig. 1). In the intervention session PPMs of the knee joint were performed for 30 min by an electrical bicycle. In the control session subjects lay relaxed on the plinth with their feet positioned in the bicycle (Fig. 1). The experimental assessments were similar in both sessions. Pressure pain thresholds (PPTs) were recorded before and 15, 25 and 35 min after start of PPM on both the left and right m. tibialis anterior (Fig. 2). The assessment site on m. tibialis anterior (muscle belly) was determined by palpation of the muscleetendon junctions and the midpoint in-between these was estimated and used for assessment. Fifteen minutes after the start of PPM

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avoid any therapeutic touch (Gagne and Toye, 1994; Gordon et al., 1998) and to ensure reproducibility of the technique performed. PPM in this study was set to 30 rpm and with a rotation movement equal to midrange of the knee joints physiological range. 2.4. Experimental muscle pain

Fig. 1. Illustrating the position of subjects during the experiment. During experimental muscle pain the subjects continuously regulated the VAS manually and the computer sampled data. PPMs were performed by an electrical bicycle at 30 rpm. The bicycle was stopped during assessment of PPTs.

(immediately after the PPT assessment) experimental muscle pain was induced in the right tibialis anterior by injection of hypertonic saline (2 cm distal to the site for PPT assessment). The injection was performed at the same time for all subjects and the experimental muscle pain intensity was scored continuously on an electronic VAS only interrupted by the recording of PPTs at 25 and 35 min after start of PPM. The PPM was started immediately after the injection. The bicycle was stopped (typically less than 3 min) when PPTs were assessed. 2.3. PPM The PPM was performed by an electrical bicycle (Reck Motomed Viva, RECK Technik, Germany) to

15 min. PPM/rest

Experimental muscle pain was induced by i.m. injection of 1 ml 5.8% sterile hypertonic saline into the tibialis anterior muscle. The muscle pain intensity was scored on a 10 cm electronic VAS where 0 cm indicated ‘‘No pain’’ and 10 cm ‘‘Maximum pain’’. The VAS scores were sampled every 2 s and recorded for 900 s. The maximum pain (VAS peak), the duration of pain and the area under the VAS-time curve (VAS area) were extracted. Upon resolution of pain the subject filled in a body chart marking all areas of pain. This was later digitized (ACECAD D9000þ, Taiwan) and the pain areas were estimated. Referred pain was defined as being pain isolated and distinct from the local pain caused by injection. Quality of the pain was assessed by completion of a Danish MPQ (Drewes et al., 1993). The MPQ data were analysed according to the total score of the 20 word groups. Words chosen by more than 30% of subjects were included in the statistics (Graven-Nielsen et al., 1997a). 2.5. PPTs PPT was measured in the middle of the belly of the m. tibialis anterior, according to palpated landmarks (Kendall et al., 1993), with a handheld pressure algometer equipped with a 1 cm2 probe (Somedic Produktion AB, type 2, Sollentuna, Sweden). Pressure was applied with approximately 50 kPa/s in a simple, continuous ascending series. The subject was instructed to press a button at the moment the pressure stimulation elicited ‘‘just noticeable’’ pain. The mean of three measurements defined the PPT. Pressure algometry was performed by

10 min. PPM/rest

10 min. PPM/rest

VAS scale in use

Baseline PPT

PPT 1 and injection of hypertonic saline

VAS scale in use

PPT 2

PPT 3

Fig. 2. Schematic illustration of the experimental protocol. PPTs were recorded at baseline, just before injection of hypertonic saline (PPT1), 15 min after injection (PPT2), and at the end of the study (PPT3, 10 min after PPT2). PPMs are only performed in the intervention session. In the control session the subjects rest in a supine position. VAS was continuously recorded after the injection and only interrupted by PPT measurements.

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the same investigator throughout the experiment and prior to the study intensive training sessions were performed to increase accuracy (Fischer, 1987; Ohrbach and Gale, 1989; Vanderweeen et al., 1996; Smidt et al., 2002; Ylinen et al., 2007). During and post-intervention recordings were normalized to baseline recordings (100%). 2.6. Statistics Data are presented as mean values and standard deviation (SD). VAS, MPQ and pain area data were analysed by two-way mixed-model ANOVA with factors ‘condition’ (repeated: control and PPM) and ‘sequence’ (between group: PPM at first session or PPM at second session). PPT data were analysed by a four-way mixedmodel ANOVA with factors ‘condition’ (repeated: control and PPM), ‘side’ (repeated: left and right), ‘time’ (repeated: baseline, 15, 25 and 35 min) and ‘sequence’ (between group: PPM at first session or PPM at second session). When the ANOVA was found significant the NewmaneKeuls (NK) test was used for post-hoc analysis and to correct for multiple comparisons. The limit for significance was defined as P < 0.05.

3. Results 3.1. Experimental muscle pain The VAS scores were lower during PPM than during the control session (Fig. 3). The VAS-time curve identified two maxima: the first appearing immediately after the injection and the second maximum appears

during the final assessment of PPT. In the intervention session VAS peak was significantly lower, the VAS area (0e600 s) was significantly smaller and the duration of pain was significantly shorter during PPM than during the control session (Table 1; ANOVA: df ¼ 1; F > 4.64; P < 0.048). The area and distribution of pain were not significantly decreased in the PPM session (Fig. 4, Table 1). The MPQ data were significantly lower in the PPM session than in the control session (Table 1). In both sessions at least 30% of the subjects described the pain as ‘‘drilling, tingling, taut and tight’’. In the control session 47% used the word ‘‘miserable’’ whereas in the PPM session 41% chose the word ‘‘annoying’’ (lowest score) in the same word category. 3.2. Pressure algometry In one subject, PPTs were not reached before the maximum pressure limit (2000 kPa) and data were incomplete for two subjects. As a consequence 14 subjects were included for further analysis. The ANOVA showed an effect of condition (ANOVA: df ¼ 1; F ¼ 24.2; P ¼ 0.0004) which, however, was dependent on an interaction between the condition and time factors: left and right side PPTs during (15 and 25 min) and after (35 min) the PPM intervention increased significantly compared with baseline recordings and similar time points in the control session (Fig. 5; ANOVA: df ¼ 3; F ¼ 8.16; P ¼ 0.0003; NK: P < 0.001). The PPTs were 20 23% higher in the PPM study compared with baseline and 17 18% higher when compared with the control session (Fig. 5).

4. Discussion 5

4

VAS (cm)

The present study showed that the pain induced by intramuscular injection of hypertonic saline in m. tibialis anterior was reported lower with PPM of the knee joint. Moreover, in the intervention session some subjects experienced a characteristic change in pain quality expressed by the weaker word ‘‘annoying’’ in comparison to the stronger word ‘‘miserable’’ used in the control study. Throughout the intervention study PPT was increased compared with the baseline level and the control

Control PPM

3

2

1

Table 1 Mean (SD) VAS parameters after saline-induced muscle pain

0 0

5

10

15

20

25

Time (min) Fig. 3. The mean VAS-time curve after injection of hypertonic saline into the tibialis anterior muscle in the control (light grey) and PPM (solid) sessions. The injection was performed after 15 min with PPM. The VAS scores in the PPM session are clearly reduced compared with the control session.

VAS area0e600 (cm s) VAS area600e900 (cm s) VAS peak (cm) VAS duration (s) Pain area (A.U.) MPQ score

PPM

Control

P-value

1344.3 858.5 112.2 206.7 4.40 2.57 815.6 279.8 2.43 1.95 3.12 1.07

1950.4 1091.7 400.6 629.5 5.28 2.42 1016.1 299.2 2.97 2.23 4.15 1.97

0.03 NS 0.02 0.02 NS 0.01

NS: not significant; A.U.: arbitrary units.


105

Fig. 4. The pain distribution (ventral and dorsal view) after injection of hypertonic saline into the right tibialis anterior muscle in the control and PPM sessions.

session. These data therefore indicate that PPM results in hypoalgesia of deep tissue.

4.1. Experimental muscle pain The intramuscular injection with hypertonic saline caused a moderate to high muscle pain intensity associated with referred pain, and a quality of pain described as ‘‘drilling, tingling, taut and tight’’ which is similar to observations previously reported (Graven-Nielsen et al., 1997a,b, 1998, 2003; Gibson et al., 2006). The intensity and duration of experimental pain in the PPM session were on average scored approximately 1 cm lower and 200 s less compared with the control session. This might be explained by an inhibitory mechanism caused by PPM.

Similar findings have been shown in animal studies where joint mobilization reduced secondary hyperalgesia due to intra-articular injection of capsaicin; mobilization of the knee joint for more than 9 min diminished the withdrawal threshold to mechanical stimuli and the analgesia lasted for at least 30 min (Sluka and Wright, 2001; Skyba et al., 2003). Moreover, mobilization of the knee joint caused bilateral increases in mechanical withdrawal threshold in conditions of acute and chronic muscle inflammation, and chronic joint inflammation (Sluka et al., 2006). A similar study on patients with osteoarthritis reported that 9 min mobilization of the knee joint provided a significant local and widespread hypoalgesia when measured by PPT (Moss et al., 2007). Recently, however, a MWM intervention in healthy controls with experimentally induced lateral epicondylalgia did not reduce pain intensity (Slater et al., 2006).

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M.M. Nielsen et al. / Manual Therapy 14 (2009) 101e109 150

PPT (% of baseline)

Control PPM

∗

125

∗

∗

100

75

50 Baseline

10

20

30

40

Time (min) Fig. 5. Mean PPT (SD, N ¼ 14) as a percentage of baseline at baseline and during 35 min with PPMs. Hypertonic saline is injected after the assessment at 15 min. *Significantly different from baseline and control recordings at same time point (NK: P < 0.0005).

These contradictory results may be due to the use of a sustained mobilization procedure as opposed to rhythmical mobilizations as described previously (Mulligan, 2004; Moss et al., 2007). Treatment technique and duration might also be of importance for the reported differences. Other studies have advocated that repetitive movement rather than sustained pressure for a critical amount of time is a key factor in initiation of mechanisms related to the hypoalgesia (Sluka and Wright, 2001; Moss et al., 2007). In the present study only a tendency for reduced local and referred pain areas were found although the pain intensity was significantly decreased. The diffuse characteristics of muscle pain combined with the complex mechanisms involved in referred pain is likely to reduce the sensitivity of pain area assessment and therefore explain the present non-significant effects on pain distribution (Graven-Nielsen, 2006). Furthermore memory bias could account for a possible inaccuracy in reporting the pain area (Edwards et al., 1995; Kikuchi et al., 2006). 4.2. Deep-tissue pressure pain sensitivity The present results demonstrate that 15 min of PPM evoked a significant increase in bilateral PPTs compared with baseline levels and the control session. The increased PPT was consistently found throughout the PPM experiment. In the control session the PPT assessments were not significantly increased compared with baseline. It should be noted that the assessor was not blinded to the experimental intervention and therefore the PPT results could be biased (Ohrbach et al., 1998).

However, the saline-induced muscle pain shows the same hypoalgesic effects of PPM as pressure algometry (see above). The saline-induced muscle pain method has no direct assessor influence indicating that the confounding effect of the non-blinded assessor for pressure algometry is limited. The fourth and final PPT assessment in the control condition was not significantly decreased compared with baseline assessment although it approached significance. In case this reaches significance the decrease might be explained by peripheral sensitisation due to repeated pressure assessments (Lauersen et al., 1997a,b; Kosek and Hansson, 2002). Interestingly, the saline-induced pain did not induce muscle hyperalgesia as also reported previously in numerous studies (Graven-Nielsen, 2006) suggesting that the inhibitory mechanism is not dependent on conditions of hyperalgesia. Recent studies have reported that manual therapy of painful joints causes a significant increase in the levels of PPT measurements in line with these experimental findings (Vernon et al., 1990; Vicenzino et al., 1998a,b, 2001; Sterling et al., 2001; Paungmali et al., 2003). 4.3. Potential mechanisms of joint mobilization analgesia Previous studies have suggested that the dPAG in the mesencephalon is important for the analgesic effects of manual therapy due to activation of the sympathetic nervous system as seen in a number of studies (McGuiness et al., 1997; Simon et al., 1997; Sterling et al., 2001; Paungmali et al., 2003; Skyba et al., 2003; Souvlis et al., 2004; Moulson and Watson, 2006). It is proposed that descending pathways from dPAG influence the activity of inhibitory interneurons at the spinal level and thereby induce analgesia specific to mechanical stimulations (Shacklock, 1995; Vicenzino et al., 1998a,b, 2001; Sterling et al., 2001; Skyba et al., 2003). Skyba et al. (2003) reported that mobilization of rat knee joints did not induce hypoalgesia due to spinal opioids or segmental mechanisms due to release of GABAA, but more likely due to descending inhibitory mechanisms that utilize serotonin and noradrenalin via corticospinal projections from dPAG. Low threshold mechanoreceptors from joint and muscle have been shown to project to the PAG and a non-noxious afferent input (e.g. SMT), might be an adequate stimulus to activate the key regions of the PAG (Yezierski, 1991; Shacklock, 1995; Vicenzino et al., 1998a,b, 2001; Sterling et al., 2001; McLean et al., 2002; Paungmali et al., 2003; Mohammadian et al., 2004; Souvlis et al., 2004; Zusman, 2004). In the present study a reduction of sensitivity for mechanical stimuli (increase in PPT) was found. This could probably be related to the continuous performance of PPM stimulating Ab mechanoreceptors bilaterally and thereby activating key regions of PAG (and other


midbrain nuclei) to induce a hypoalgesic mechanism (Pickar, 2002; Souvlis et al., 2004). Interestingly, bilateral and extra-segmental hypoalgesia to pressure have also been found during voluntary submaximal isometric muscle contraction, suggesting a generalized inhibitory mechanism initiated by muscle afferent fibre activity or by increased release of blood b-endorphins due to muscle contraction (Kosek and Lundberg, 2003).

107

Acknowledgments We would like to thank Hanne Lisby, Physiotherapist, Master of Ethics and Values in Organisations, ‘‘Collegeof-Health, Aalborg’’, Department of Physiotherapy, for her kind support and advice during the development of this study.

4.4. Study limitations References In the present study the muscle activity was not monitored but a previous study report only sporadic muscle activity at a very low level during passive bicycling (Christensen et al., 2000). Therefore it is unlikely that the hypoalgesic mechanisms are due to muscle activity. Furthermore, blood flow/circulation was not monitored during the experiment and therefore a hypothetical risk of wash out of the i.m. hypertonic saline during PPM is present. In the present study only minimal plantar/dorsal movement occurred at the ankle joint which is the m. tibialis anterior primary function and it is not likely to account for the decreased saline-induced muscle pain during PPM. Another possible confounding factor that pertains to all experimental pain research is a shift of attention during pain. In the present study the laboratory was organized so that a minimum of disturbing elements and communication were interfering. 4.5. Perspectives Previous studies propose a link between range of motion and duration of treatment and the analgesic effect (Katawich, 1999; Sluka and Wright, 2001; Moss et al., 2007). Thus, it is possible that an intervention with PPM close to maximum range of motion could produce an adequate hypoalgesic mechanism within a shorter timeframe. The specific pain reduction of approximately 1 cm on a VAS is clinically relevant as indicated by the Cochrane Library where 1 cm pain reduction is identified as being clinically relevant (Gross et al., 2002). Therefore it is reasonable to assume that PPM can be used as a method for analgesia in clinical settings.

5. Conclusion The present study showed that PPM performed at the knee joint had a significant analgesic effect on deeptissue pain sensitivity in line with the hypothesis of the current study. Further studies are needed to clarify the exact neurophysiological mechanisms involved in this type of manual treatment and its analgesic effects.

Christensen LO, Johannsen P, Sinkjaer T, Petersen N, Pyndt HS, Nielsen JB. Cerebral activation during bicycle movements in man. Experimental Brain Research 2000;135(1):66e72. Devocht JW, Pickar JG, Wilder DG. Spinal manipulation alters electromyographic activity of paraspinal muscles: a descriptive study. Journal of Manipulative and Physiological Therapeutics 2005; 28(7):465e71. Dishman J, Bulbulian R. Spinal reflex attenuation associated with spinal manipulation. Spine 2000;25(1):2519e25. Drewes AM, Helweg-Larsen S, Petersen P, Brennum J, Andreasen A, Poulsen LH, et al. McGill pain questionnaire translated into Danish: experimental and clinical findings. Clinical Journal of Pain 1993;9:80e7. Edwards LC, Pearce SA, Beard RW. Remediation of pain-related memory bias as a result of recovery from chronic pain. Journal of Psychosomatic Research February 1995;39(2):175e81. Fanselow MS. The midbrain periaqueductal gray as a coordinator of action in response to fear and anxiety. In: Depaulis A, Bandler R, editors. The midbrain periaqueductal gray matter. New York: Plenum Press; 1991. p. 151e73. Fischer AA. Pressure algometry over normal muscles. Standard values, validity and reproducibility of pressure threshold. Pain 1987; 30:115e26. Gagne D, Toye RC. The effects of therapeutic touch and relaxation therapy in reducing anxiety. Archives of Psychiatric Nursing 1994;8(3):184e9. Gibson W, Arendt-Nielsen L, Graven-Nielsen T. Delayed onset soreness at tendonebone junction and muscle tissue is associated with facilitated referred pain. Experimental Brain Research 2006; 174(2):351e60. Graven-Nielsen T, Arendt-Nielsen L, Svensson P, Jensen TS. Quantification of local and referred muscle pain in humans after sequential i.m. injections of hypertonic saline. Pain 1997a;69:111e7. Graven-Nielsen T, McArdle A, Phoenix J, Arendt-Nielsen L, Jensen TS, Jackson MJ, et al. In vivo model of muscle pain: quantification of intramuscular chemical, electrical and pressure changes associated with saline-induced muscle pain in humans. Pain 1997b;69:137e43. Graven-Nielsen T, Babenko V, Svensson P, Arendt-Nielsen L. Experimentally induced muscle pain induces hypoalgesia in heterotopic deep tissues, but not in homotopic deep tissues. Brain Research 1998;787:203e10. Graven-Nielsen T, Jansson Y, Segerdahl M, Kristensen JD, Mense S, Arendt-Nielsen L, et al. Experimental pain by ischaemic contractions compared with pain by intramuscular infusions of adenosine and hypertonic saline. European Journal of Pain 2003;7:93e102. Graven-Nielsen T. Fundamentals of muscle pain, referred pain, and deep tissue hyperalgesia. Scandinavian Journal of Rheumatology. Supplement 2006;122:1e43. Gordon A, Merenstein JH, D’Amico F, Hudges D. The effects of therapeutic touch on patients with osteoarthritis of the knee. Journal of Family Practice 1998;47(4):271e7.

108


Gross AR, Hoving JL, Haines TA, Goldsmith CH, Kay T, Aker P, et al. Manipulation and mobilisation for mechanical neck disorders. The Cochrane database of systematic reviews. The Cochrane collaboration; 2002. p. 1541e48. Hayek R, Austin S, Pollard H. An electromyographic study of the intramuscular effects of the chiropractic adjustment. A pilot study. Australian Chiropractic & Osteopathy 1995;4(1). Herzog W, Scheele D, Conway PJ. Electromyographic responses of back and limb muscles associated with spinal manipulative therapy. Spine 1999;24(2):146e52. Katawich L. Neural mechanisms underlying manual cervical traction. The Journal of Manual & Manipulative Therapy 1999;7: 20e5. Kendall FP, McCreary EK, Provance PG. Muscles testing and function. 4th ed. Lippincott Williams & Wilkins; 1993. p. 200e1. Kikuchi H, Yoshiuchi K, Miyasaka N, Ohashi K, Yamamoto Y, Kumano H, et al. Reliability of recalled self-report on headache intensity: investigation using ecological momentary assessment technique. Cephalalgia November 2006;26(11):1335e43. Knutson GA. Significant changes in systolic blood pressure post vectored upper cervical adjustments vs resting control groups: a possible effect of the cervicosympathetic and/or pressor reflex. Journal of Manipulative and Physiological Therapeutics 2001; 24:101e9. Kosek E, Hansson P. The influence of experimental pain intensity in the local and referred pain area on somatosensory perception in the area of referred pain. European Journal of Pain 2002;6: 413e25. Kosek E, Lundberg L. Segmental and plurisegmental modulation of pressure pain thresholds during static muscle contractions in healthy individuals. European Journal of Pain 2003;7:251e8. Lauersen RJ, Graven-Nielsen T, Jensen TS, Arendt-Nielsen L. Referred pain is dependent on sensory input from the periphery: a psychosocial study. European Journal of Pain 1997a;1:261e9. Lauersen RJ, Graven-Nielsen T, Jensen TS, Arendt-Nielsen L. Quantification of local and referred pain in humans induced by intramuscular electrical stimulation. European Journal of Pain 1997b;1:105e13. Lovick TA. Interactions between descending pathways from the dorsal and ventrolateral periaqueductal gray matter in rats. In: Depaulis A, Bandler R, editors. The midbrain periaqueductal gray matter. New York: Plenum Press; 1991. p. 101e20. Maitland GD, Hengeveld E, Banks K, English K. Vertebral manipulation. 6th ed. Oxford: Butterworth & Heinemann; 2002 [chapter 1]. Maitland GD. Peripheral manipulation. 3rd ed. Oxford: Butterworth & Heinemann; 2003 [chapter 1e2]. McGuiness J, Vicenzino B, Wright A. The influence of a cervical mobilisation technique on respiratory and cardiovascular function. Manual Therapy 1997;2(4):216e20. McLean S, Naish L, Reed L, Urry S, Vicenzino B. A pilot study of the manual force levels required to produce manipulation induced hypoalgesia. Clinical Biomechanics 2002;17:304e8. Mohammadian P, Gonsalves A, Tsai C, Hummel T, Carpenter T. Areas of capsaicin induced secondary hyperalgesia and allodynia are reduced by a single chiropractic adjustment. Journal of Manipulative Therapy 2004;27:381e7. Morgan MM. Differences in antinocioception evoked from dorsal and ventral regions of the caudal periaqueductal gray matter. In: Depaulis A, Bandler R, editors. The midbrain periaqueductal gray matter. New York: Plenum Press; 1991. p. 139e50. Moss P, Sluka K, Wright A. The initial effects of knee joint mobilization on osteoarthritic hyperalgesia. Manual Therapy 2007;12(2): 109e18. Moulson A, Watson T. A preliminary investigation into the relationship between cervical snags and sympathetic nervous system activity in the upper limbs of an asymptomatic population. Manual Therapy 2006;11:214e24.

Mulligan B. Manual therapy ‘‘NAGS’’, ‘‘SNAGS’’, ‘‘MWM’’ etc. 5th ed. New Zealand: Plane View Services; 2004 [chapter 1]. Ohrbach R, Gale EN. Pressure pain thresholds, clinical assessment and differential diagnosis: reliability and validity in patients with myogenic pain. Pain 1989;39:157e69. Ohrbach R, Crow H, Kamer A. Examiner expectancy effects in the measurements of pressure pain thresholds. Pain February 1998; 74(2e3):163e70. Paungmali A, Vicenzino B, Smith M. Hypoalgesia induced by elbow manipulation in lateral epicondylalgia does not exhibit tolerance. Physical Therapy 2003;4:448e54. Paungmali A, O’Leary S, Souvlis T, Vicenzino B. Naxolone fails to antagonize initial hypoalgesic effect of a manual therapy treatment for lateral epicondylia. Journal of Manipulative and Physiological Therapeutics 2004;23(3):180e5. Petersen NP, Vicenzino B, Wright A. The effects of a cervical mobilisation technique on sympathetic outflow to the upper limb in normal subjects. Physiotherapy Theory and Practice 1993;9: 146e9. Pickar JG. Neurophysiological effects of spinal manipulation. The Spine Journal 2002;2:357e71. Rivett J. Clinical reasoning for manual therapists. 1st ed. London: Butterworth & Heinemann; 2004 [chapter 1e2]. Shacklock M. Moving in on pain: Conference proceedings. 2. Printing. 1st ed. Australia: Butterworth & Heinemann; 1995 [chapter 1e3]. Simon R, Vicenzino B, Wright A. The influence of an anteroposterior accessory glide of the glenohumeral joint on measures of peripheral sympathetic nervous system function in the upper limb. Manual Therapy 1997;2(1):18e23. Smidt N, Van Der Windt DA, Assendelft WJ, Mourits AJ, Deville WL. Interobserver reproducibility of the assessment of severity of complaints, grip strength, and pressure pain threshold in patients with lateral epicondylitis. Archives of Physical Medicine and Rehabilitation 2002;83(8):1145e50. Skyba DA, Radhakrishnan R, Rohlwing JJ, Wright A, Sluka KA. Joint manipulation reduces hyperalgesia by activation of monoamine receptors but not opioid or GABA receptors in the spinal cord. Pain 2003;106:159e68. Slater H, Arendt-Nielsen L, Wright A, Graven-Nielsen T. Effects of manual therapy technique in experimental lateral epicondylia. Manual Therapy 2006;11:107e17. Sluka KA, Skyba DA, Radhakrishnan R, Leeper BJ, Wright A. Joint mobilization reduces hyperalgesia associated with chronic muscle and joint inflammation in rats. The Journal of Pain 2006;7(8): 602e7. Sluka KA, Wright A. Knee joint mobilisation reduces secondary mechanical hyperalgesia induced by capsaicin injection into the ankle joint. European Journal of Pain 2001;5:81e7. Souvlis T, Vicenzino B, Wright A. Neurophysiological effects of spinal manual therapy. In: Boyling JD, Jull GA, editors. Grieve’s modern manual therapy. 3rd ed. UK: Churchill Livingstone; 2004. p. 367e79. Souvlis T, Wright A. The tolerance effect: its relevance to analgesia produced by physiotherapy interventions. Physical Therapy Reviews 1997;2:227e37. Sterling M, Jull G, Wright A. Cervical mobilisation: concurrent effects on pain, sympathetic nervous system activity and motor activity. Harcourt Publishers Ltd. Manual Therapy 2001;6(2):72e81. Vanderweeen L, Oostendorp RA, Vaes P, Duquet W. Pressure algometry in manual therapy. Manual Therapy 1996;1(5):258e65. Vernon HT, Aker P, Burns S, Viljakaanen S, Short L. Pressure pain threshold evaluation of the effect of spinal manipulation in the treatment of chronic neck pain: a pilot study. Journal of Manipulative and Physiological Therapeutics 1990;13(1):13e6. Vicenzino B, Collins D, Wright A. The initial effects of a cervical spine manipulative treatment on the pain and dysfunction of lateral epicondylalgia. Pain 1996;68:69e74.

M.M. Nielsen et al. / Manual Therapy 14 (2009) 101e109 Vicenzino B, Collins D, Cartwright T, Wright A. Cardiovascular and respiratory changes produced by lateral glide mobilization of the cervical spine. Manual Therapy 1998a;3:67e71. Vicenzino B, Collins D, Benson H, Wright A. An investigation of the interrelationship between manipulation therapy-induced hypoalgesia and sympathoexcitation. Journal of Manipulative and Physiological Therapeutics 1998b;21(7):448e53. Vicenzino B, Paungmali A, Buratowski S, Wright A. Specific manipulative therapy treatment for chronic lateral epicondylalgia produces uniquely characteristic hypoalgesia. Manual Therapy 2001;6(4): 205e12. Yezierski RP. Somatosensory input to the periaqueductal gray: a spinal relay to a descending control center. In: Depaulis A, Bandler R,

109

editors. The midbrain periaqueductal gray matter. New York: Plenum Press; 1991. p. 365e86. Ylinen J, Nyka¨nen M, Kautiainen H, Ha¨kkinen A. Evaluation of repeatability of pressure algometry on the neck muscles for clinical use. Manual Therapy 2007;12:192e7. Zusman M, Edwards B, Donaghy A. Investigation of a proposed mechanism for the relief of spinal pain with passive joint movement. Journal of Manual Medicine 1989;4:58e61. Zusman M. Forebrain-mediated sensitisation of central pain pathways: non-specific pain and new image of MT. Manual Therapy 2002;7(2):80e8. Zusman M. Mechanisms of musculoskeletal physiotherapy. Physical Therapy Reviews 2004;9:39e49.



Technical and measurement report

Head repositioning accuracy to neutral: A comparative study of error calculation Robert Hill, Pa˚l Jensen, Tor Baardsen, Kristian Kulvik, Gwendolen Jull, Julia Treleaven* Division of Physiotherapy, The School of Health and Rehabilitation Sciences, The University of Queensland, Brisbane 4072, Queensland, Australia Received 28 February 2007; received in revised form 6 February 2008; accepted 28 February 2008

Abstract Deficits in cervical proprioception have been identified in subjects with neck pain through the measure of head repositioning accuracy (HRA). Nevertheless there appears to be no general consensus regarding the construct of measurement of error used for calculating HRA. This study investigated four different mathematical methods of measurement of error to determine if there were any differences in their ability to discriminate between a control group and subjects with a whiplash associated disorder. The four methods for measuring cervical joint position error were calculated using a previous data set consisting of 50 subjects with whiplash complaining of dizziness (WAD D), 50 subjects with whiplash not complaining of dizziness (WAD ND) and 50 control subjects. The results indicated that no one measure of HRA uniquely detected or defined the differences between the whiplash and control groups. Constant error (CE) was significantly different between the whiplash and control groups from extension ( p < 0.05). Absolute errors (AEs) and root mean square errors (RMSEs) demonstrated differences between the two WAD groups in rotation trials ( p < 0.05). No differences were seen with variable error (VE). The results suggest that a combination of AE (or RMSE) and CE are probably the most suitable measures for analysis of HRA. Ó 2008 Elsevier Ltd. All rights reserved. Keywords: Joint position error; Measurements; Whiplash; Neck pain; Head repositioning accuracy

1. Introduction Patients with neck pain of both traumatic and insidious onset have deficits in cervical joint position error or head repositioning accuracy (HRA) (Revel et al., 1991; Heikkila¨ and A˚stro¨m, 1996; Loudon et al., 1997; Kristjansson et al., 2003; Treleaven et al., 2003). HRA to neutral (Revel et al., 1991) is most commonly used as it has been the most reliable test for determining differences between neck pain and control subjects (Kristjansson et al., 2003). Nevertheless whilst disturbances in HRA to neutral have been

* Corresponding author. E-mail address: [email protected] (J. Treleaven). 1356-689X/$ - see front matter Ó 2008 Elsevier Ltd. All rights reserved. doi:10.1016/j.math.2008.02.008

consistently reported in whiplash cohorts (Heikkila¨ and Wenngren, 1998; Treleaven et al., 2003), results are less uniform in patients with neck pain of insidious onset (Rix and Bagust, 2001; Lee et al., 2005). Comparison between studies to understand these differences is difficult because of different measurement instruments, methodologies and properties of error used. The interest in this study was properties of error. Previous studies have used absolute error (AE) (Heikkila¨ and A˚stro¨m, 1996; Loudon et al., 1997; Kristjansson et al., 2003; Treleaven et al., 2003), constant error (CE) (Revel et al., 1991; Michaelson, 2004; Lee et al., 2006), variable error (VE) (Michaelson, 2004; Lee et al., 2006; Strimpakos et al., 2006) and/or root mean square error (RMSE) (Lee et al., 2006). The AE

R. Hill et al. / Manual Therapy 14 (2009) 110e114

describes the average AE (Schmidt and Lee, 1999). CE includes both the under and overestimations of the target position and represents the average magnitude and direction of the errors (Schmidt and Lee, 1999). The VE measures the variability in the results and is thought to reflect the effect of noise in the sensorimotor system (Clark et al., 1995). RMSE represents an overall measure of how successful the subject was in achieving the target (Schmidt and Lee, 1999). Recently it has been proposed that the CE and/or VE may be more suitable than AE to assess HRA (Michaelson, 2004). Studies comparing individuals with and without lumbar or thoracic pain have used more than one measurement of error (Brumagne et al., 2000; Koumantakis et al., 2002). While arguments might be mounted for the use of each particular error measurement, no study has compared these different calculations of HRA to neutral to determine whether one or more methods are better able to discriminate between control and neck pain subjects. This study compared the four measures of error between a control group and subjects with whiplash both complaining and not complaining of dizziness. 2. Methods

111

extensions. The 3-Space Fastrak system (Polhemus, Navigation Science Division, Kaiser Aerospace, Vermont) measured the positions of two sensors (one at the forehead and one at C7) relative to a source and the difference between the starting (zero) and position on return was calculated in degrees. The error in the primary plane of movement was used as the measure for HRA as directed by our previous research (Treleaven et al., 2003). 2.3. Procedure The starting position for the HRA tests was in sitting with the head in the neutral resting position. Subjects were blindfolded and were asked to perform the test neck movement within comfortable limits returning as accurately as possible to the starting position. Subjects indicated verbally when they had returned and this was marked electronically. The examiner, guided by realtime display, manually repositioned the subject’s head back to the original starting position before each trial. Three trials (as directed by our previous research) were performed for each movement (Treleaven et al., 2003). The subjects were able to visually re-centre their starting position prior to each new movement direction (Treleaven et al., 2003, 2006).

2.1. Subjects 2.4. Data management and statistical analysis The data set from a previous study (Treleaven et al., 2006) was used and consisted of 100 whiplash subjects with persistent pain, at least 3 months post-injury. Fifty subjects reported symptoms of dizziness or unsteadiness at least once per week (subjects with whiplash complaining of dizziness e WAD D) and 50 did not (subjects with whiplash not complaining of dizziness e WAD ND). Data from 50 control subjects (40 reported in Treleaven et al., 2006 and 10 additional subjects) were also used. The whiplash groups were comparable with respect to age (WAD D mean 35.5 SD (8.1) years, WAD ND group mean 35.0 SD (9.5) years) and mean time since injury (WAD D 1.4 range 0.35e3 years, WAD ND 1.6 range 0.3e3 years). The control subjects had no history of whiplash, neck pain, headache or dizziness. The mean age was 29.5 SD (8.3) years. Approval for the study was gained from the Institutional Medical Ethics Committee. All participants provided their informed consent. 2.2. Instrumentation and measurements As described previously (Treleaven et al., 2006) the subject’s HRA to the natural head posture was tested following active cervical left and right rotations and

VE ¼

The four different methods of presenting HRA for each movement direction were calculated as follows: AE: the mean of the total deviation from the starting point over the three trials, ignoring positive (overshoot) and negative (undershoot) values, i.e. (Treleaven et al., 2003): AE ¼ ðabsolute of raw error trial 1Þ þ ðabsolute of raw error trial 2Þ þ ðabsolute of raw error trial 3Þ=3: CE: the mean of the raw error over the three trials incorporating the positive and negative values in each trial, i.e. (Lee et al., 2006): CE ¼ ðraw error trial 1Þ þ ðraw error trial 2Þ þ ðraw error trial 3Þ=3: VE: the square root of the mean of the difference between the raw error and the calculated CE (as above) squared, i.e. (Lee et al., 2006):

rffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffi ffi ðraw error trial 1 CEÞ2 þ ðraw error trial 2 CEÞ2 þ ðraw error trial 3 CEÞ2 =3:

112


RMSE: the square root of the sum of the CE squared and the VE squared, i.e. (Lee et al., 2006): RMSE ¼

qffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffiffi 2 CE þ VE2 :

(Table 1, Fig. 3). Against the trend of other results, in CE the WAD ND group was significantly more accurate than controls (Fig. 3).

4. Discussion The data from each movement were analysed for between group differences with a generalized linear multivariate model, using SPSS statistical software. A preliminary analysis showed a significant age difference between the control group and the whiplash groups thus age was included as a co-variate to ensure that this could not account for any differences seen between the groups.

3. Results 3.1. Extension CE demonstrated significantly greater means between both the WAD D and controls and between the WAD ND and controls (Table 1, Fig. 1). There were no differences in CE between WAD D and WAD ND and no between group differences in any of the other measures. 3.2. Left rotation CE demonstrated significant differences between WAD D and controls and WAD D and WAD ND (Table 1, Fig. 2). Differences in AE and RMSE were also seen between the controls and WAD D. 3.3. Right rotation Both AE and RMSE distinguished between both the whiplash groups and between the WAD D and controls

The results of this study indicated that no one measure of HRA uniquely detected or defined the differences between the whiplash and control groups. The results suggest that a combination of AE and CE are probably the most suitable measures for analysis of HRA when assessing patients with whiplash. The RMSE mirrored exactly the AE findings and thus the use of both measures may be superfluous. The value of the measure of VE in the test of return to the natural head posture will be discussed. An argument can be mounted in support of the use of both AE and CE in future studies of HRA in patients with neck disorders. The AE indicates the accuracy of the deviation from neutral and demonstrated that the WAD D were, on average, further from the neutral target than healthy control subjects from rotation which is in accordance with other studies (Heikkila¨ and Wenngren, 1998; Treleaven et al., 2003). However, AE did not detect these differences in return from extension. The CE is a measure of the direction and deviation of the end position. It has benefits over AE and RMSE, which do not consider direction (Schmidt and Lee, 1999). Heikkila¨ and A˚stro¨m (1996) and Treleaven et al. (2003) counted overshoots and undershoots rather than calculating the CE, and showed subjects with whiplash overestimated whilst control subjects under estimated neutral. Similar results were reflected in this current analysis. The CE detected differences between controls and both whiplash groups in return from extension and also detected the overshooting of WAD D

Table 1 The differences in joint position error (degrees) between groups in the primary planes of movement for each measure and the p values for between group analysis Movement

Measure

Control

WAD ND

Ext

CE VE AE RMSE

Mean (SE) 0.35 1.36 3.01 3.41

(0.5) (0.2) (0.3) (0.3)

Mean (SE) 1.09 1.58 2.84 3.14

(0.5) (0.1) (0.3) (0.3)

Rot (L)

CE VE AE RMSE

0.74 1.59 2.47 2.72

(0.5) (0.2) (0.4) (0.4)

0.70 1.57 3.07 3.40

(0.5) (0.2) (0.3) (0.3)

Rot (R)

CE VE AE RMSE

2.11 1.47 3.16 3.42

(0.6) (0.2) (0.4) (0.4)

0.43 1.65 2.93 3.24

(0.5) (0.2) (0.4) (0.4)

WAD D

WAD D vs C

ND vs D

C vs ND

Mean (SE)

p Value

p Value

p Value

1.24 1.61 3.61 3.94

(0.5) (0.1) (0.3) (0.3)

0.02* 0.28 0.17 0.23

0.82 0.89 0.06 0.06

0.04* 0.34 0.69 0.55

1.19 1.88 4.01 4.36

(0.5) (0.2) (0.3) (0.3)

0.01* 0.28 0.00* 0.00*

0.01* 0.20 0.05 0.05

0.96 0.90 0.24 0.19

1.83 1.99 4.55 4.87

(0.6) (0.2) (0.4) (0.4)

0.73 0.06 0.02* 0.02*

0.07 0.21 0.00* 0.00*

0.04* 0.51 0.69 0.76

WAD D ¼ subjects with whiplash complaining of dizziness, WAD ND ¼ subjects with whiplash not complaining of dizziness, CE ¼ constant error, AE ¼ absolute error, RMSE ¼ root mean square error, and VE ¼ variable error.

113

R. Hill et al. / Manual Therapy 14 (2009) 110e114 6

5 4

*

*

Control WAD ND

5

Control

*

*

*

* *

WAD D

WAD D

3

WAD ND

Degrees

Degrees

4 2 1 0 -1

Contant error

Variable error

Absolute error

Root mean square error

3

2

1

-2

Fig. 1. The results of the various measures of JPE from extension means and standard error for each group (*p < 0.05). WAD D ¼ subjects with whiplash complaining of dizziness and WAD ND ¼ subjects with whiplash not complaining of dizziness.

compared to the undershooting of the other groups in return from left rotation. The inability of AE and RMSE to detect such differences between the control (undershot) and WAD subjects (overshot) in return from extension is highlighted by the non-significance of these errors in extension trials. Nevertheless, the AE detects differences that CE will not when the scores are a scatter of positives (overshoot) and negatives (undershoot). The VE revealed no between group differences in measures from any movement directions indicating that all subjects were equally consistent between the three trials for each movement direction. The mean values calculated for VE (Figs. 1e3) were similar to studies performed by Lee et al. (2006) and Strimpakos et al. (2006). Yet our findings are in contrast to those

5

*

*

Control

*

*

Absolute error


WAD ND

4

WAD D

Degrees

3

2

1

0

-1 Contant error

Variable error

-2

Fig. 2. The results of the various measures’ means and standard error of JPE from left rotation for each group (*p < 0.05). WAD D ¼ subjects with whiplash complaining of dizziness and WAD ND ¼ subjects with whiplash not complaining of dizziness.

0 Contant error

Variable error

Absolute error


-1

Fig. 3. The results of the various measures’ means and standard error of JPE from right rotation for each group (*p < 0.05). WAD D ¼ subjects with whiplash complaining of dizziness and WAD ND ¼ subjects with whiplash not complaining of dizziness.

of Michaelson (2004) who found significant differences in the VE between a whiplash and control group. However, there were methodological differences in testing. These researchers used eight trials in each rotation direction and the subjects were instructed to perform movements as fast as possible. In contrast, procedures for the data set analysed in this study included use of a natural speed of movement and three trials. Thus it is difficult to determine the source of difference in the findings of VE and it would be premature to discard it on the basis of the negative findings in this current study. A potential limitation of this study is the use of a previous data set. The data used were from a population of neck pain subjects with whiplash injury and measurements were limited to HRA to neutral from extension and rotation. Future research should also consider the usefulness of the different error calculations in subjects with idiopathic neck pain, as it is in this group that more inconsistency in results has been observed (Rix and Bagust, 2001; Lee et al., 2005). It could also consider different methodologies and procedures for this specific test and the utility of the various mathematical calculations in other measures of cervical kinaesthetic sense such as movement detection thresholds (Taylor and McCloskey, 1988) and reproduction of active movement tasks (Kristjansson et al., 2004). It has been shown that the measure of AE in the test of HRA to neutral is sensitive to change with interventions either directed towards cervical impairments (Heikkila¨ et al., 2000; Jull et al., 2007) or sensorimotor deficits (Revel et al., 1994; Jull et al., 2007). Nevertheless, the results of this study overall would suggest that when assessing HRA in future studies, use of CE in

114


combination with AE (or RMS) might be justified given their different properties and evidence of differences in findings between groups and movement directions. References Brumagne S, Lysens R, Verschueren S, Swinnen S. The role of paraspinal muscle spindles in lumbosacral position sense in individuals with and without low back pain. Spine 2000;25:989e94. Clark FJ, Larwood KJ, Davis ME, Deffenbacher KA. A metric for assessing acuity in positioning joints and limbs. Experimental Brain Research 1995;107:73e9. Heikkila¨ H, A˚stro¨m PG. Cervicocephalic kinesthetic sensibility in patients with whiplash injury. Scandinavian Journal of Rehabilitation Medicine 1996;28:133e8. Heikkila¨ HV, Wenngren BI. Cervicocephalic kinesthetic sensibility, active range of cervical motion, and oculomotor function in patients with whiplash injury. Archives of Physical Medicine and Rehabilitation 1998;79:1089e94. Heikkila¨ H, Johansson M, Wenngren BI. Effects of acupuncture, cervical manipulation and NSAID therapy on dizziness and impaired head repositioning of suspected cervical origin: a pilot study. Manual Therapy 2000;5:151e7. Jull G, Falla D, Treleaven J, Hodges PW, Vicenzino B. Retraining cervical joint position sense: the effect of two exercise regimes. Journal of Orthopaedic Research 2007;25:404e12. Koumantakis GA, Winstanley J, Oldham JA. Thoracolumbar proprioception in individuals with and without low back pain: intratester reliability, clinical applicability, and validity. Journal of Orthopaedic and Sports Physical Therapy 2002;32:327e35. Kristjansson E, Dall’Alba P, Jull G. A study of five cervicocephalic relocation tests in three different subject groups. Clinical Rehabilitation 2003;17:768e74. Kristjansson E, Hardardottir L, Asmundardottir M, Gudmundsson K. A new clinical test for cervicocephalic kinesthetic sensibility:

‘‘the fly’’. Archives of Physical Medicine and Rehabilitation 2004; 85:490e5. Lee HJ, Nicholson LL, Adams D, Bae S. Proprioception and rotation range sensitization associated with subclinical neck pain. Spine 2005;30:E60e7. Lee H, Teng C, Chai H, Wang S. Testeretest reliability of cervicocephalic kinaesthetic sensibility in three cardinal planes. Manual Therapy 2006;11:61e8. Loudon JK, Ruhl M, Field E. Ability to reproduce head position after whiplash injury. Spine 1997;22:865e8. Michaelson P. Sensorimotor Characteristics in Chronic Neck Pain. Thesis Umea˚: University of Umea˚; 2004. Revel M, Andre-Deshays C, Minguet M. Cervicocephalic kinesthetic sensibility in patients with cervical pain. Archives of Physical Medicine and Rehabilitation 1991;72:288e91. Revel M, Minguet P, Gergory J, Vaillant Manuel L. Changes in cervicocephalic kinesthesia after a proprioceptive rehabilitation program in patients with neck pain: a randomized controlled study. Archives of Physical Medicine and Rehabilitation 1994;75:895e9. Rix GD, Bagust J. Cervicocephalic kinesthetic sensibility in patients with chronic, nontraumatic cervical spine pain. Archives of Physical Medicine and Rehabilitation 2001;82:911e9. Schmidt RA, Lee TD. Methodology for studying motor performance. In: Schmidt RA, Lee TD, editors. Motor control and learning: a behavioural emphasis. New York: Human Kinetics; 1999. p. 15e40. Strimpakos N, Sakellari V, Gioftsos G, Kapreli E, Oldham J. Cervical joint position sense: an intra- and inter-examiner reliability study. Gait and Posture 2006;23:22e31. Taylor J, McCloskey D. Proprioception in the neck. Experimental Brain Research 1988;70:351e60. Treleaven J, Jull G, Sterling M. Dizziness and unsteadiness following whiplash injury: characteristic features and relationship with cervical joint position error. Journal of Rehabilitation Medicine 2003;35:36e43. Treleaven J, Jull G, LowChoy N. The relationship of cervical joint position error to balance and eye movement disturbances in persistent whiplash. Manual Therapy 2006;11:99e106.



Diary of events 2nd World Congress on Manual Therapy and Sport Rehabilitation, The Spine II, in Roma Italy 6the8th of February 2009 www.newmaster.it Tel: þ3906 51600107 Fax: þ3906 51882443 MSc Conference Day Lifestyle, Physical Activity and Health Learn more about contemporary health promotion issues by attending this topical interactive conference day. The day will include topical presentations delivered by public health professionals including; managers and strategists, clinicians and researchers. Date: 23rd February, 2009 Venue: University of Hertfordshire, Hatfield, Herts, UK or virtual attendance from your home or workplace via Elluminate. Cost: £120 or £60 for virtual attendance Details and bookings contact: Jane Simmonds j.1.simmonds @herts.ac.uk or Karen Wells [email protected] Back and beyond Theme The lumbar spine and pelvis Dates Sat 28e29th March 2009 Venue East Midlands Conference Centre, Nottingham For more details visit www.physiofirst.org.uk NZMPA biennial scientific conference, Heritage Hotel, Rotorua, New Zealand 28, 29 & 30 August 2009.

1356-689X/$ - see front matter doi:10.1016/S1356-689X(08)00178-1

The theme is ‘Striving for Excellence in OMT’ & also celebrating 40 years of Manual Therapy in New Zealand. The conference co-coordinator is Vicki Reid, Phone 0800 646 000 or 09 476 5353 Fax 09 476 5354 e-mail: [email protected] Website: www.nzmpa.org.nz NOI International conference UK and Ireland Nottingham UK e April 15e17, 2010 Dublin IRELAND April 21e23, 2010 For further details www.noi2010.com Fax þ 3906 51882443 Janet G. Travell, MD Seminar Series, Bethesda, USA For information, contact: Myopain Seminars, 7830 Old Georgetown Road, Suite C-15, Bethesda, MD 20814-2432, USA. Tel.: þ1 301 656 0220; Fax: þ1 301 654 0333; website: www.painpoints.com/seminars.htm E-mail: [email protected] If you wish to advertise a course/conference, please contact: Karen Beeton, Associate Head of School (Professional Development), School of Health and Emergency Professions, University of Hertfordshire, College Lane, Hatfield, Herts AL10 9AB, UK. E-mail: [email protected] There is no charge for this service.


Manual Therapy 14 (2009) e1ee2 www.elsevier.com/math

Letter to the Editor

Response to Butler and Coppieters 2007, Letter to the Editor: Clinical neurodynamics e Throwing the baby out with the bath water I agree entirely with the comments by Butler and Coppieters (2007) that central mechanisms are relevant in neurodynamic testing (Shacklock, 1995) and, of late, this has always been my position (Shacklock, 1999a,b). That is why I presented these aspects as forming the context in which neurodynamic movements are applied (Shacklock, 2005, p. 12). I have stated that neurodynamic tests are really psychophysical manoeuvres that can be modified by many things including the cognitive and contextual and, as such, I proposed clinical techniques to take this into account (Shacklock, 2005, p. 113e114). So on this aspect we agree. However, I have no problem with focusing on an aspect of neurodynamics and to do so constitutes no statement that other aspects are not involved. To say that to omit these aspects left the Editorial lacking was to miss the point of the Editorial which was to make certain specific statements about neurodynamics and plenty of modern evidence in support was presented. There is too little space to discuss Butler’s and Coppieter’s comments in detail but their statement that responses to structural differentiation may have little to do with mechanical alterations in neural tissue I feel throws the baby out with the bath water. Structural differentiation is the key means by which we determine neurodynamic influences in diagnosis and, in my opinion, this should remain the case. In some regions of the body, there is good evidence for the mechanical validity of differentiation, e.g. in cadavers and with realtime ultrasound imaging (McLellan and Swash, 1976; Shacklock and Wilkinson, 2001; Coppieters et al., 2006a). Furthermore, Coppieters et al. (2005, 2006b) showed that it may be used to good effect in differentiation of muscle and nerve, at least in acute experimental

DOI of original article: 10.1016/j.math.2007.01.001. 1356-689X/$ - see front matter doi:10.1016/j.math.2008.01.002

muscle pain. Interestingly, these latter studies did not involve measurement of central or psychosocial mechanisms. Nevertheless, without structural differentiation we have no decent clinical evidence of a neurodynamic mechanism above musculoskeletal or others. Hence, to say that the response could be due to psychosocial or central mechanisms is fine, once we have a response that shows a neurodynamic mechanism. From a clinical methods point of view, as soon as the test response is likely to involve neurodynamics (i.e. positive with differentiation) we may then ask if it involves mainly psychosocial or physical mechanisms or combinations of both, weighing up the balance of the evidence. But unless we do structural differentiation as a natural and routine part of neurodynamic testing, we cannot even be sure if we have specifically a neurodynamic test to work with. And in the end, many of our patients do have physical problems that need specific mechanical evaluation and treatment. References Butler D, Coppieters M. Neurodynamics in a broader perspective [Letter to the Editor]. Manual Therapy 2007;12(1):e7e8. Coppieters M, Alshami A, Babri A, Souvlis T, Kippers V, Hodges P. Strain and excursion of the sciatic, tibial, and plantar nerves during a modified straight leg raising test. Journal of Orthopaedic Research 2006a;24(9):1883e9. Coppieters M, Alshami A, Hodges P. An experimental pain model to investigate the specificity of the neurodynamic test for the median nerve in the differential diagnosis of hand symptoms. Archives of Physical Medicine and Rehabilitation 2006b;87(10):1412e7. Coppieters M, Kurz K, Mortensen T, Richards N, Skaret I, McLaughlin L, Hodges P. The impact of neurodynamic testing on the perception of experimentally induced muscle pain. Manual Therapy 2005;10(1):52e60. McLellan D, Swash M. Longitudinal sliding of the median nerve during movements of the upper limb. Journal of Neurology, Neurosurgery and Psychiatry 1976;39:556e70. Shacklock M. Neurodynamics. Physiotherapy 1995;81:9e16.

e2

Letter to the Editor / Manual Therapy 14 (2009) e1ee2

Shacklock M. Central pain mechanisms; a new horizon in manual therapy. Australian Journal of Physiotherapy 1999a;45:83e92. Shacklock M. The clinical application of central pain mechanisms in manual therapy. Australian Journal of Physiotherapy 1999b;45:215e21. Shacklock M. Clinical neurodynamics. Oxford: Elsevier; 2005. Shacklock M, Wilkinson M. Can nerves be moved specifically? In: Proceedings of the 11th biennial conference of the musculoskeletal physiotherapists’ association of Australia, Adelaide, Australia; 2001.

Michael Shacklock 118 King William Street, 6th Floor, Adelaide SA 5000, Australia Tel.: þ61 8 8212 4886; fax: þ61 8 8212 8028. E-mail address: [email protected] 4 December 2007


Manual Therapy 14 (2009) e3 www.elsevier.com/math

Book review Movement, Stability & Lumbopelvic Pain, Vleeming A, Mooney V, Stoeckart R. Churchill Livingstone (2007). 658 pp., price £59.99, ISBN: 9780443101786 This multi-author book (48 contributors) claims, as the editors stated in the preface, to provide the latest evidence-based relevant new data on the lumbopelvic area. However, the results of scientific research evolve so quickly that for some parts of this book the evidence is already out of date. In comparison to the first edition this second edition has been enlarged considerably. The book is now divided into six parts. The first part begins with biomechanical, clinicaleanatomical and evolutionary aspects in 13 chapters separated into two sections. Part II considers insights in function and dysfunction of the lumbopelvic region, and involves six chapters. In part III diagnostic methods are discussed in three sections containing nine chapters. The first section debates mainly the imaging of the sacroiliac joint and in the last chapter the relation of the pelvic girdle with the lumbar spine is discussed. In part IV the editors address in three chapters the European guidelines concerning prevention, acute and chronic LBP and finally diagnosis and treatment of pelvic girdle pain. Part V includes effective training and treatment which is described in seven chapters distributed over three sections. In the first two sections psychological, social and motivational aspects as well as motor control features are described while in the third section different views on effective treatment and training are discussed. Part VI integrates in two chapters’ different views and opinions when dealing with a complex system as the lumbopelvic region. One of the critical remarks on the first edition was the absence of the relationship between pelvic pain and low


back complaints. The editors have attempted to reduce this deficiency, however, they succeed only to a limited level. The first and second chapter of part III about differential diagnosis of low back pain and the asymmetrical overload syndrome does not reflect modern opinions in relation to pelvic and low back pain problems. For example, the current tendency for classifying pelvic and low back pain into subgroups of which pelvic girdle pain could be an evident example is lacking entirely. Another critical note about the previous edition was the strongly impairment-related approach to the management of lumbopelvic pain. In part V of the present edition a timorous attempt is made to introduce the biopsychosocial model, however, it is only mentioned in a marginal way in the integrated section. The difference in level of the contributions leads to an unbalanced impression of the book. All chapters included in this book are more or less isolated. In part VI an attempt is made to integrate different views, opinions and the therapeutic approach to the treatment of pelvic girdle pain and described as a case report. However, a final contemplative chapter with a reflection of the presented knowledge and insights as well as an opinion of future developments about lumbopelvic pain in relation to low back pain would be more desirable. Despite of these limitations this book gives a comprehensive overview of lumbopelvic pain and I recommend it for clinicians more then for researchers. Peter van der Wurff, PhD, PT, MT Military Rehabilitation Centre, Doorn, The Netherlands Tel.: þ31 343 474 507. E-mail address: peterwurff@hotmail.com 7 January 2008



Book review Manual Therapy for the Peripheral Nerves, Barral Jean-Pierre, Croibier Alain. Churchill Livingstone, Elsevier (2007). 270 pp., price £ 29.99, ISBN: 9780443103070 The topic of this book is interesting. I think this area of clinical practice is somewhat on the fringe of ‘manual therapy’, so the writing style is not what you would expect from most modern health textbooks, i.e. not supported by references. The first three chapters describe in a fairly superficial way the general anatomy, physiology and functional faults that may occur in the peripheral nervous system. This is interesting, nicely aided by diagrams, but I was left wondering if the information given is up to date and completely believable, and with no references, I couldn’t check. Chapter 4 covers treatment of the peripheral nerves, a very small part of this textbook, which for a title suggesting an in-depth presentation of such, this was disappointing. In the following chapters 5e8, attention is given to the large groups of peripheral


nerves in the body: cervical plexus, brachial plexus, lumbar plexus and sacral plexus. These chapters are interesting and well designed with images and photographs to illustrate the information presented. I found this part of the book very useful as a revision aid to peripheral nerves, but I still struggled with the lack of references and evidence to support the text. I would like to explore some of the ideas brought up here more fully, but my own experience in clinical practice casts doubt on treatment of peripheral nerves in such a simplistic way? Unfortunately, I am not really reassured after reading this book; I would like more robust evidence to help me in these ‘grey’ areas of manual therapy. Tim McClune, D.O. Spinal Research Unit, University of Huddersfield, 30 Queen Street, Huddersfield HD1 2SP, UK E-mail address: [email protected] 17 January 2008



Book review Exercise therapy, prevention and treatment of disease, Gormley J, Hussey J. Blackwell Publishing (2005). 260 pp., price £ 25.99, ISBN: 1405105275 The aim of this book is to provide physiotherapists and undergraduate students with a useful reference text that informs about the application of exercise for various physical pathologies and diseases. This book is divided into two sections. The first section presents a general overview of the physiology of the cardiorespiratory and musculoskeletal systems, as well as cardiovascular adaptations to exercise. This section concludes with a chapter on exercise in diabetes and obesity. This first section is a concise summary of a wide area, but should not be considered a reference text for the physiology of exercise. Many of the reference texts used in this section are commonly used as required reading in undergraduate exercise physiology science courses. Therefore for the clinician this section should provide a nice summary for what they would have already learnt. The second section of the book moves into aspects of exercise testing and the basics of prescription. Further chapters in this section deal with


specific conditions such as cardiovascular disease, respiratory disease, stroke, as well as behavioural aspects of facilitating long term exercise adherence. The exercise focus of this section is weighted towards aerobic testing and prescription, and often refers the reader to texts such as the ACSM guidelines for exercise testing and prescription. The editors and authors of this book have provided a text with an incredibly wide scope in only 250 pages. In providing such a wide summary, some detail is missing, however, the intent of this book is to be as a reference text for clinicians who have already covered the source material, or undergraduates who are getting a general overview. In this context, the book can be considered to be a success. Paul Marshall Exercise Rehabilitation Clinic, Tamaki Campus, Private Bag 92019, Manukau City, Auckland, New Zealand Tel.: þ64 9 373 7599. E-mail address: [email protected] 4 February 2008



Book review Physiotherapy for children, Pountney Teresa. Butterworth Heinemann, Elsevier (2007). 360 pp., price: £ 39.99, ISBN: 9780750 68886 4 The book aims at undergraduate students and qualified physiotherapists starting a career in paediatrics, in other words novices in the field of paediatric physiotherapy. All contributing authors work in the United Kingdom and are considered experts in their field. The book contains 8 parts (21 chapters) with the following titles: Working with children, Assessment and outcome measures, Neurology, Acquired brain injury, Musculoskeletal, Cardio-respiratory, Oncology and palliative care and Child and adolescent mental health, covering a large spectrum of clinical paediatrics. The chapters are structured similarly beginning with background information followed by a description of the clinical pattern, assessment strategies, interventions (multidisciplinary), and finishing with case studies and an extensive reference list. The case studies in each chapter are a strong didactic tool especially for physiotherapy novices. Except for the chapters that describe ‘delivery of care’ and ‘physiotherapy at the intensive care unit’, which focus specifically on the legal and professional situation in the UK, all other chapters are of a more generic nature and can be appreciated in physiotherapy


settings outside the UK as well. The chapters, although similar in set up differ considerable in content and detail, some are primarily symptom driven (e.g. cardio pulmonary section) while others are ‘diagnosis’ oriented (e.g. musculoskeletal section) or age related (neonatal section). Interventions are rather conventional (muscle stretching in musculoskeletal conditions) and lack innovations (e.g. (an-)aerobic exercise training in childhood chronic conditions). ‘Outcome measures and measurement techniques’ are extensive in ‘clinical gait analysis’ while e.g. muscle strength testing equipment e.g. handheld dynamometry are not addressed. Although extensive in some of its topics, the book never reaches the level of a textbook, at its best it is a well written selection of paediatric physiotherapy capita with a detailed, but conservative treatment approach. Janjaap van der Net Department of Paediatric Physiotherapy and Paediatric Exercise Physiology, University Children’s Hospital, University Medical Centre at Utrecht, Lundlaan 6, The Netherlands E-mail address: [email protected] 5 February 2008



Book review The physiology of the joints, Kapandji IA, Adalbert I. 6th ed. The upper limb, vol. 1. Churchill Livingstone Elsevier (2007). 361 pp., price £ 29.99, ISBN: 9780443103506 The books of Dr. Kapandji on ‘‘Physiologie articulaire’’, first published in French more than 30 years ago, rapidly became famous worldwide and were translated in 11 languages. This first volume of the sixth English edition concerns the upper limb and two more volumes will follow. Whereas the first five editions remained very similar, this new edition probably will be the start of a renewed longstanding success. The concept of the book remains unchanged, with simple but clear illustrations on the right page and the corresponding explanations on the left-hand page. For the first time the diagrams are printed in colour, but this is not the only, nor the main cosmetic change. Both text and illustrations have been largely reworked, new items were added, especially pronation, the supination, the biomechanics of the wrist and the movements of the thumb have been thoroughly revised. Clinical


and functional aspects have also been extended. The result is a book with over 150 new pages and dozens of new illustrations. Some terminology problems of the French edition due to the use of older French anatomical terminology have been corrected in the English translation by Dr. L. Honore´. The book ends with instructions to assemble a working cardboard model of the hand. Not easy! I am convinced this is a much improved and up to date edition which should rapidly replace the older editions. This book is a must for physicians, physiotherapists, manual therapists, osteopaths and all practitioners involved in rehabilitation. E. Barbaix Vrije Universiteit Brussel, Department of Human Anatomy, Brussels, Belgium E-mail address: [email protected] 5 February 2008


Manual Therapy 14 (2009) e8ee12 www.elsevier.com/math

Masterclass

Physical and psychological aspects of whiplash: Important considerations for primary care assessment, Part 2 e Case studies Michele Sterling a,b,* a

Centre of National Research on Disability and Rehabilitation Medicine (CONROD), The University of Queensland, Mayne Medical School, Herston Road, Herston, QLD 4066, Australia b Division of Physiotherapy, The University of Queensland, QLD 4072, Australia Received 20 March 2008; accepted 20 March 2008

Abstract Whiplash is a heterogenous and in many, a complex condition involving both physical and psychological factors. Primary care practitioners are often the first health care contact for individuals with a whiplash injury and as such play an important role in gauging prognosis as well as providing appropriate management for whiplash injured patients. It is imperative that factors associated with poor outcome are recognized and managed in the primary care environment at the crucial early acute stage post-injury. This paper presents 2 case studies of individuals with acute whiplash pain. The case studies illustrate the heterogeneity of the whiplash condition and the importance of clinical assessment that includes consideration of both physical and psychological manifestations. They also demonstrate the important role physiotherapists’ play in the management of people with whiplash, particularly in the early post-injury stage. Crown Copyright Ó 2008 Published by Elsevier Ltd. All rights reserved. Keywords: Whiplash associated disorders; Central hyperexcitability; Posttraumatic stress; Assessment

1. Introduction Whiplash is a common and costly consequence following a motor vehicle crash, with up to 60% of those injured reporting persistent neck pain and disability (Rebbeck et al., 2006; Sterling et al., 2006). In recent times, there has been an accumulation of research data demonstrating whiplash to be a heterogeneous and complex condition involving varying degrees of both physical and psychological manifestations. Importantly some of these features, for example, hyperalgesia, movement loss, posttraumatic stress symptoms, moderate/ * Centre of National Research on Disability and Rehabilitation Medicine (CONROD), The University of Queensland, Mayne Medical School, Herston Road, Herston, QLD 4066, Australia. Tel.: þ61 7 3365 5344; fax: þ61 7 3346 4603. E-mail address: [email protected]

severe levels of pain and disability are predictive of poor functional recovery (Scholten-Peeters et al., 2003; Rebbeck et al., 2006; Sterling et al., 2006). Musculoskeletal clinicians play an important role in the early management of whiplash injury, particularly in the primary care environment where many injured people will seek treatment for their condition. In the accompanying paper to this one, the heterogeneous clinical presentation of acute and chronic whiplash was outlined and suggestions made for the assessment of this condition. It was argued that some patients will present with a ‘less complex’ clinical presentation and these patients should respond well to shortterm physiotherapy interventions. In contrast and at the other end of the spectrum, there are the group of patients whose clinical presentation is complicated by the additional presence of widespread sensory hypersensitivity and symptoms of posttraumatic stress (Fig. 1). This

1356-689X/$ - see front matter Crown Copyright Ó 2008 Published by Elsevier Ltd. All rights reserved. doi:10.1016/j.math.2008.03.004

M. Sterling / Manual Therapy 14 (2009) e8ee12

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Fig. 1. An outline of factors that is indicative of 2 different clinical presentations of whiplash. It is argued that the ‘more complex’ presentation will require a more intensive and interdisciplinary approach to management.

group will likely require a more concerted approach to their management based on early identification of these factors and others associated with poor outcome. In order to illustrate the varied clinical presentation of whiplash and the assessment required, 2 case studies will be presented. Acute whiplash injury has been selected for the outline of these case studies, in order to emphasize the importance of this stage of the whiplash process and that effective assessment and management may help to prevent the development of chronicity in those at risk. In order to illustrate the ‘overall’ management of acute whiplash, in depth discussion of specific physical interventions is not provided, instead readers are provided with appropriate references with more detailed discussion of specific techniques.

2. Case studies 2.1. Case 1: ‘less complex’ whiplash presentation 2.1.1. Patient interview and history Jane, 30-year-old female; married; 1 child (3 years old). Work: Personal assistant to CEO of advertising company. History: Jane was on her way home from work 10 days ago when her car was rear-ended whilst stopped at a red traffic light. Jane felt slight pain in her neck at the time of the accident and after organising the car to be towed away she went home. That night she could feel her neck getting stiff. She went to bed early but

when she awoke the next morning, she could barely turn her neck. Jane managed to rest that day and her partner cared for their child. Jane took the following 2 days off work (sick leave). She then returned to work and reports that she ‘struggles’ through her day before collecting her child from childcare and returning home to rest as much as she can. Jane is usually very active and goes to gym classes 3 times a week as well as playing hockey on the weekends but has not been able to do so since the car accident due to neck pain. However, she has been able to ride a stationary bike at home for about 15 min at a time. Jane presents to the physiotherapist 10 days after the accident as she feels that her neck should be better by now and she is worried since her friend experienced a similar injury and was unable to play any sports for 12 months. Jane has not had any radiological investigations. She has taken Panadol as necessary with some reported relief. Jane’s sleep is not disturbed by pain and her pain is no worse with cold. Pain: left sided neck pain (VAS: 5/10); left sided frontal headache (VAS: 4/10). Patient Specific Functional Scale (PSFS) (Westaway et al., 1998): Picking up child: 4/10. Working at office desk (longer than 30 min): 6/10. Reading (longer than 30 min): 6/10. Neck Disability Index (NDI) (Vernon and Mior, 1991): 32/100. Impact of Events Scale (IES) (Horowitz et al., 1979): 7 (Note: the IES is preferred to the IES-R for clinical

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use as cut-off scores for levels of posttraumatic stress symptoms have been reported). General Health Questionnaire-28 (GHQ-28): 19 (just below threshold of 23/24) (Goldberg, 1978). Self-reported Leeds Assessment of Neuropathic Signs and Symptoms scale (S-LANSS) (Bennett et al., 2005): 6.

2.1.2. Physical examination Posture: can actively correct posture to good position when facilitated. Neck range of movement (measured using gravity dependent goniometer): left rotation: 50 ; extension: 30 . Right rotation and flexion: full. Cervical muscle control: tested using the craniocervical flexion test (Jull et al., 2007). Could achieve 24 mm Hg before loss of correct movement pattern and marked superficial muscle activity. Shoulder girdle muscle control: good control in prone lying, sitting and with arm movement (Jull et al., 2007). Postural control (Treleaven, 2007): joint position error e less than 3 all directions. Manual examination (Maitland et al., 2001): decreased movement and pain (VAS: 4/10) at C2/3 segment on the left side with localised hyperalgesia only. Clinical neurological examination (muscle power, reflexes, sensation): nothing abnormal detected. Brachial plexus provocation test (BPPT) (Elvey, 1997; Sterling et al., 2002): elbow extension 15 from 180 (bilaterally) at pain threshold (VAS: 1/10).

2.1.3. Key findings from the examination Moderate levels of pain and disability. Some psychological distress (GHQ-28 approaching threshold); anxiety about not being able to return to sport. No symptoms of posttraumatic stress: low scores on the IES. No evidence of central hyperexcitability (hyperalgesia is localised to the cervical spine and is not widespread; S-LANSS score is 12, likely neuropathic component to the pain). In both case studies it could be argued that additional questionnaires that aim to measure other psychological substrates could be included (for example, fear avoidance beliefs or catastrophisation). The above questionnaires have been included in view of their use in the investigation of whiplash.

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10); left, elbow extension 20 from 180 ) at pain threshold (VAS: 2/10). Allodynia of right arm. 2.2.3. Key findings from the examination Moderate levels of pain and disability. Moderate psychological distress (GHQ-28 above threshold). Moderate levels of posttraumatic stress symptoms; IES score of 30. Evidence of central hyperexcitability and/or neuropathic pain condition (constant pain; irritable condition; S-LANSS score of >12; allodynia; marked hypersensitivity to the BPPT on the right side and protective posture may indicate mechanosensitivity of peripheral nerve tissue although nerve conduction appears normal, Hall and Elvey, 1999). Indications of a complex presentation involving central hyperexcitability; possible peripheral nerve tissue involvement (mechanosensitivity) as well as moderate levels of distress, particularly posttraumatic stress.

2.2.4 Prognosis There are several adverse prognostic indicators associated with this clinical presentation. In addition to moderate/high levels of pain and disability, there is evidence of central hyperexcitability, marked neck movement loss and moderate levels of posttraumatic stress. Patricia is at risk of developing chronic pain and disability as a result of her injury. It is important that any treatment plans take this into account.

2.2.2. Physical examination Posture: right shoulder elevated, cradling right arm. Arm pain increases with shoulder depression. Neck range of movement (measured using gravity dependent goniometer): left and right rotations: 20 ; extension: 10 ; flexion: 10 . Cervical muscle control: poor pattern of craniocervical flexion; marked activity in superficial flexors (Jull et al., 2007). Unable to formally test with biofeedback unit due to the presence of allodynia. Shoulder girdle muscle control: not tested due to pain provocation with shoulder depression. Postural control (Treleaven, 2007): joint position error e unable to test due to lack of neck ROM. Balance e unsteadiness in tandem stance. Manual examination (Maitland et al., 2001): unable to effectively perform as neck is allodynic. Clinical neurological examination (muscle power, reflexes, sensation): generalized decrease in light touch sensation over right arm but not specific to a particular dermatome. BPPT (Elvey, 1997; Sterling et al., 2002): right, elbow extension 60 from 180 at pain threshold (VAS: 8/

2.2.5 Management plan This is a critical time period for Patricia’s condition. The complex nature of her condition indicates that an interdisciplinary approach to her management will be required. It is now 6 weeks post-injury and the patient is reporting moderate levels of posttraumatic stress symptoms. A psychological referral should be instigated such that further evaluation of the patient’s psychological status is undertaken. Guidelines recommend that trauma-focussed cognitive behavioural therapy delivered by a psychologist should be commenced (Forbes et al., 2007). The physiotherapist also plays a role and it is important that clear information is provided to the patient without further adding to her distress or catastrophising the condition. It is unlikely that a psychological approach to treatment alone will be sufficient to reduce pain (Blanchard et al., 2003), so it is also important that some pain relief is achieved via other means. Liaison with the GP would be indicated with the view to improve pain control via medication (Curatolo et al., 2006). Physical interventions such as active movement/exercises within pain limits, gentle manual therapy and modalities such as

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TENS may also assist in this regard (Skyba et al., 2003; Sluka et al., 2006). Whilst at this stage, treatment emphasis should be placed on the psychological and pain processing aspects of the condition, it is also important that treatment is directed to improving movement and function. This may take the form of advice and encouragement to commence gentle exercises of the neck as well as general activity as tolerated by pain (MAA, 2007), taking care not to overly provoke symptoms. The physiotherapist should also be aware that posttraumatic stress symptoms can influence activity levels of people with whiplash (Sterling and Chadwick, submitted for publication) and this should be taken into account. The physiotherapist may elect to defer more intensive rehabilitation (e.g., motor and postural control retraining) in order to decrease the burden on the patient until her posttraumatic stress symptoms improve. In this case, liaison with the treating psychologist would be essential such that the patient’s progress be monitored and more intensive physical treatment commenced at an appropriate time. Due the complexity of this whiplash presentation, it is clear that a more concerted approach to management is required. It is likely that the length of treatment time and the number of treatments will be greater than those required for case study 1. In both cases, progress should be monitored with validated outcome measures and treatment adapted in view of the individual patient’s progress. It can be seen that such an integrated approach to the management of this patient requires collaborative communication between the health care providers involved in her management. However, for this to occur the physiotherapist must consider the overall status of the patient and resist focusing on motor retraining only. 2.3. Summary These 2 distinct clinical presentations of acute whiplash injury highlight the importance of adequate and appropriate early assessment. Musculoskeletal clinicians play an important role in the assessment and management of both the physical and psychological aspects of this condition and are ideally placed to play a role in the co-ordination of care for patients such as this. References Bennett M, Smith B, Torrance N, Potter J. The S-LANSS score for identifying pain of predominantly neuropathic origin: validation for use in clinical and postal research. The Journal of Pain 2005; 6:149e58. Blanchard E, Hickling E, Devineni T, Veazey C, Galovski T, Mundy E, et al. A controlled evaluation of cognitive behaviour therapy for posttraumatic stress in motor vehicle accident survivors. Behaviour Research and Therapy 2003;41:79e96.

Curatolo M, Arendt-Nielsen L, Petersen-Felix S. Central hypersensitivity in chronic pain: mechanisms and clinical implications. Physical Medicine Rehabilitation Clinics of North America 2006;17: 287e302. Elvey R. Physical evaluation of the peripheral nervous system in disorders of pain and dysfunction. Journal of Hand Therapy 1997;10: 122e9. Forbes D, Creamer M, Phelps A, Bryant R, McFarlane A, Devilly G, et al. Australian guidelines for the treatment of adults with acute stress disorder and posttraumatic stress disorder. Australian and New Zealand Journal of Psychiatry 2007;41:637e48. Goldberg D. Manual of the general health questionnaire. Windsor: NFER-Nelson; 1978. Hall T, Elvey R. Nerve trunk pain: physical diagnosis and treatment. Manual Therapy 1999;4:63e73. Horowitz M, Wilner N, Alvarez W. Impact of event scale: a measure of subjective stress. Psychosomatic Medicine 1979;41:209e18. Jull G, Sterling M, Falla D, Treleaven J, O’Leary S. Whiplash, headache and neck pain: research based directions for physical therapies. Edinburgh: Elsevier; 2007. Kamper S, Rebbeck T, Maher C, McAuley J, Sterling M. Course and prognostic factors of whiplash: a systematic review and metaanalysis. Pain, in press. doi:10.1016/j.pain.2008.02.019. MAA. Guidelines for the management of whiplash associated disorders. Sydney: Motor Accidents Authority; 2007. p. 16. Maitland G, Banks K, English K, Hengeveld E, editors. Maitland’s vertebral manipulation. Butterworth Heinemann; 2001. Rebbeck T, Sindhausen D, Cameron I. A prospective cohort study of health outcomes following whiplash associated disorders in an Australian population. Injury Prevention 2006;12:86e93. Scholten-Peeters G, Verhagen A, Bekkering G, van der Windt D, Barnsley L, Oostendorp R, et al. Prognostic factors of whiplash associated disorders: a systematic review of prospective cohort studies. Pain 2003;104:303e22. Skyba D, Radhakrishnan R, Rohlwing J. Joint manipulation reduces hyperalgesia by activation of monoamine receptors but not opioid or GABA receptors in the spinal cord. Pain 2003;106:159e68. Sluka K, Lisi T, Westlund K. Increased release of serotonin in the spinal cord during low, but not high, frequency transcutaneous electric nerve stimulation in rats with joint inflammation. Archives of Physical Medicine and Rehabilitation 2006;87:1137e40. Sterling M, Chadwick B. Psychological processes in daily life with chronic whiplash: relations of post-traumatic stress symptoms and fear-of-pain to hourly pain and uptime, submitted for publication. Sterling M, Jull G, Kenardy J. Physical and psychological predictors of outcome following whiplash injury maintain predictive capacity at long term follow-up. Pain 2006;122:102e8. Sterling M, Jull G, Wright A. Cervical mobilisation: concurrent effects on pain, sympathetic nervous system activity and motor activity. Manual Therapy 2001;6:72e81. Sterling M, Treleaven J, Jull G. Responses to a clinical test of mechanical provocation of nerve tissue in whiplash associated disorders. Manual Therapy 2002;7:89e94. Stewart M, Maher C, Refshauge K, Herbert R, Bogduk N, Nicholas M. Randomised controlled trial of exercise for chronic whiplash associated disorders. Pain 2007;128:59e68. Treleaven J. Sensorimotor disturbances in neck disorders affecting postural stability, head and eye movement control. Manual Therapy 2007;13(3):262e75. Vernon H, Mior S. The neck disability index: a study of reliability and validity. Journal of Manipulative and Physiological Therapeutics 1991;14:409e15. Westaway M, Stratford P, Binkley J. The patient-specific functional scale: validation of its use in persons with neck dysfunction. The Journal of Orthopaedic and Sports Physical Therapy 1998;27: 331e8.

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Manual Therapy Journal - Volume 8, Issue 1, Pages 1-62 (February 2003)

Manual Therapy Journal - Volume 13, Issue 1, Pages 1-90 (February 2008)

Manual Therapy Journal - Volume 9, Issue 1, Pages 1-58 (February 2004)

Manual Therapy Journal - Volume 11, Issue 1, Pages 1-90 (February 2006)

Manual Therapy Journal - Volume 10, Issue 1, Pages 1-92 (February 2005)

Manual Therapy Journal - Volume 12, Issue 1, Pages 1-84 (February 2007)

Manual Therapy Journal - Volume 14, Issue 2, Pages 117-240 (April 2009)

Manual Therapy Journal - Volume 14, Issue 5, Pages 461-584 (October 2009)

Manual Therapy Journal - Volume 14, Issue 4, Pages 353-460 (August 2009)

Manual Therapy Journal - Volume 14, Issue 6, Pages 585-716 (December 2009)

Manual Therapy Journal - Volume 14, Issue 3, Pages 241-352 (June 2009)

Manual Therapy Journal - Volume 14, Supplement (October 2009)

Behavioral and Brain Sciences, Volume 32, Issue 1, February 2009

Manual Therapy Journal - Volume 13, Issue 2, Pages 91-180 (April 2008)

Manual Therapy Journal - Volume 13, Issue 4, Pages 277-372 (August 2008)

Manual Therapy Journal - Volume 8, Issue 2, Pages 63-128 (May 2003)

Manual Therapy Journal - Volume 12, Issue 4, Pages 297-396 (November 2007)

Manual Therapy Journal - Volume 10, Issue 4, Pages 239-304 (November 2005)

Manual Therapy Journal - Volume 8, Issue 3, Pages 129-192 (August 2003)

Manual Therapy Journal - Volume 8, Issue 4, Pages 193-270 (November 2003)

Manual Therapy Journal - Volume 12, Issue 3, Pages 199-296 (August 2007)

Manual Therapy Journal- Volume 13, Issue 6, Pages 475-564 (December 2008)

Manual Therapy Journal - Volume 12, Issue 2, Pages 85-198 (May 2007)

Manual Therapy Journal - Volume 10, Issue 2, Pages 93-174 (May 2005)

Manual Therapy Journal - Volume 9, Issue 2, Pages 59-120 (May 2004)

Manual Therapy Journal - Volume 13, Issue 3, Pages 181-276 (June 2008)

Manual Therapy Journal - Volume 10, Issue 3, Pages 175-238 (August 2005)

Manual Therapy Journal - Volume 9, Issue 3, Pages 123-182 (August 2004)

Manual Therapy Journal - Volume 11, Issue 3, Pages 167-240 (August 2006)

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