Manual Therapy Journal - Volume 11, Issue 2, Pages 91-166 (May 2006)

VOLUME 11 NUMBER 2 PAGES 91–166 MAY 2006 Editors International Advisory Board Ann Moore PhD, GradDipPhys, FCSP, CertE...

Author: Editors: Ann Moore and Gwen Jull

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VOLUME 11 NUMBER 2 PAGES 91–166 MAY 2006

Editors

International Advisory Board

Ann Moore PhD, GradDipPhys, FCSP, CertEd, FMACP Clinical Research Centre for Healthcare Professions University of Brighton Aldro Building, 49 Darley Road Eastbourne BN20 7UR, UK

K. Bennell (Victoria, Australia) K. Burton (Hudders¢eld, UK) B. Carstensen (Frederiksberg, Denmark) E. Cruz (Setubal Portugal) L. Danneels (Mar|¤ akerke, Belgium) S. Durrell (London, UK) S. Edmondston (Perth, Australia) J. Endresen (Flaktvei, Norway) L. Exelby (Biggleswade, UK) 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 (Hung Hom, Hong Kong) C. Liebenson (Los Angeles, CA, USA) L. Ma¡ey-Ward (Calgary, Canada) C. McCarthy (Coventry, UK) J. McConnell (Northbridge, Australia) S. Mercer (Queensland, Australia) E. Maheu (Quebec, Canada) D. Newham (London, UK) J. Ng (Hung Hom, Hong Kong) 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) M. Rocabado (Santiago, Chile) 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) M. Sterling (St Lucia, Australia) R. Soames (Leeds, UK) P. Spencer (Barnstaple, UK) P. Tehan (Victoria, Australia) M. Testa (Alassio, Italy) M. Uys (Tygerberg, South Africa) 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)

Gwendolen Jull PhD, MPhty, Grad Dip ManTher, FACP Department of Physiotherapy University of Queensland Brisbane QLD 4072, Australia Editorial Committee Karen Beeton MPhty, BSc(Hons), MCSP (Masterclass Editor) MACP ex o⁄cio member Department of Allied Health Professions—Physiotherapy University of Hertfordshire College Lane Hat¢eld AL10 9AB, UK Je¡rey D. Boyling MSc, BPhty, GradDipAdvManTher, MAPA, MCSP, MErgS (Case reports & Professional Issues Editor) Je¡rey Boyling Associates Broadway Chambers Hammersmith Broadway LondonW6 7AF, UK Tim McClune D.O. Spinal Research Unit. University of Hudders¢eld 30 Queen Street Hudders¢eld HD12SP, UK Darren A. Rivett PhD, MAppSc, MPhty, GradDip ManTher, BAppSc (Phty) (Case reports & Professional Issues Editor) Discipline of Physiotherapy Faculty of Health The University of Newcastle Callaghan, NSW 2308, Australia Raymond Swinkels MSc, PT, MT (Book Review editor) Ulenpas 80 5655 JD Eindoven The Netherlands

Visit the journal website at http://www.intl.elsevierhealth.com/journals/math doi:10.1016/S1356-689X(06)00058-0

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Manual Therapy 11 (2006) 91–92 www.elsevier.com/locate/math

Editorial

The systematic review of systematic reviews has arrived! April saw the publication of Ernst and Canter’s (2006) paper, ‘‘A systematic review of systematic reviews of spinal manipulation’’. The summary statement concluded that ‘‘considering the possibility of adverse effects this review does not suggest that spinal manipulation is a recommendable treatment’’. The media hype in the United Kingdom rose to a deafening crescendo with most of the media focus on osteopathy and chiropractic, even though the review has included a number of studies incorporating manipulative physiotherapy. Systematic reviews are usually regarded as the peak of evidence to judge the efficacy of an intervention. Thus it is disappointing to be able to detect fundamental problems in this review, considering its impact in the popular press. The paper Ernst and Canter (2006) includes systematic reviews focusing on a heterogeneous

dizziness, and a paper on any condition!). Reviews were selectively chosen from the years 2000 to May 2005. The paper included no reference to a methodological approach used in the appraisal in the systematic reviews contained within the article and did not go back to source. No critical appraisal of the pre-existing systematic reviews was offered. In addition, the interventions were poorly described and defined and were heterogeneous i.e., the reviews included a range of manual therapy techniques, although the article title referred to spinal manipulation only. The authors comments on the included systematic reviews unfortunately appeared to be selectively biased. One is left asking the question why? As mentioned we know that the accepted hierarchy of evidence as it is held currently in the health arena, shows systematic reviews to be the gold standard level of

Evidence based authority –future ? ! Systematic reviews of meta-analyses Systematic reviews of systematic reviews Meta-analyses Systematic reviews Well designed non-randomised trials e.g. cohort, case-controlled Opinions:respected authorities based on clinical evidence

collection of problems (low back pain, neck pain, neck problems, chronic headache, non-spinal pain syndrome, dysmenorrhoea, infantile colic, asthma, cervicogenic 1356-689X/$ - see front matter r 2006 Published by Elsevier Ltd. doi:10.1016/j.math.2006.04.001

At least one RCT of appropriate size Well designed non-experimental studies from more than one centre

evidence, but in view of the recent developments how will the hierarchy will look in a few years time if we do not take stock now?

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Editorial / Manual Therapy 11 (2006) 91–92

It is worth reflecting on issues with the model in the current context. Systematic reviews are recognized as the highest level of evidence, but to be at this highest level they must include multiple, well designed randomized control trials. Hence the systematic review is only as good as the original studies it includes and the systematic reviewers interpretation of the studies. There are several additional known problems associated with systematic reviews. The primary studies do not necessarily reflect contemporary practice largely due to the time at which they were published and also due to the fact that the research base is evolving all the time. Frequently we see the pooled studies include heterogeneous patients, professions and interventions which are often poorly defined and described. The quality of interventional approach is never assessed in systematic reviews. The only assessment that takes place is with regards to the quality of the randomized control trial design. Following the CONSORT statement (Moher et al., 2001) can help to rectify this. Worryingly many of the author teams associated with systematic reviews do not include an expert in the interventions used, therefore the interpretation of randomized control trials including interventions with which the author team are not strictly familiar can be flawed if clear definitions of terms have not been included in the original randomized control trial write up. Generally speaking, the systematic review can for a number of reasons muddy the waters of understanding and foil attempts to get to the truth rather than clarifying the evidence base picture. The systematic review of systematic reviews is an untested methodology at best and might take us even further away from the truth. It has become popular in medicine but it is worth reflecting on the fact that many hard science subject areas, for example chemistry, believe that the systematic review itself is poor science.

If anything positive has come out of this new publication, it must be that it raises the need for all the professions engaged in manual therapy to do several things: Increase the amount of research in the field to include standardized data collection, qualitative, experimental and randomized control trial studies which are well designed. Refine and closely define the terms used in manual therapy so that techniques are not subject to misinterpretation. Clearly publish the probable and possible known effects and side effects of these individual techniques. Increase the development work on clinical subgrouping. Develop a system for assessing the quality of interventions included in randomized control trials. So lets get back to proper science and discover the real truth if we can. References Ernst E, Canter PH. A systematic reviews of systematic reviews of spinal manipulation. Journal of the Royal Society of Medicine 2006;99:189–93. Moher D, Schulz KF, Altman DG. The CONSORT Statement: revised recommendations for improving the quality of reports of parallel group randomised control trials. BMC Medical Research Methodology 2001;1(2):1186–97.

(Editors) Ann Moore, Gwen Jull University of Brighton, Clinical Centre for Health Professions, 49, Darley Road, Eastbourne BN20 7UR, UK E-mail address: [email protected] (A. Moore)

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Review

Methodological quality and outcomes of studies addressing manual cervical spine examinations: A review Dieter Hollerwo¨ger Am Exerzierfeld 11, 4060 Leonding, Austria Received 17 October 2004; received in revised form 15 August 2005; accepted 16 December 2005

Abstract The aims of this review were, first to rate the methodological quality of studies which investigate the reliability of manual tests for cervical spine dysfunctions by applying a new quality assessment tool; secondly to compare the outcomes of these studies. The literature search included databases of CINAHL, MEDLINE, AMED, AMI, and SPORT DISCUS, the Cochrane Library, the Physiotherapy Evidence Database (PEDro), the National Library of Medicine (PubMed), Factiva, the EBSCOT HOST Research Database, online journal databases of ELSEVIER Science periodicals, LIPPINCOTT WILLIAMS & WILKINS, ELSEVIER Science @ Direct, THIEME ONLINE, and BLACKWELL SYNERGY. The application of the Quality Assessment of Diagnostic Accuracy Studies tool (QUADAS) to the 15 studies which met the inclusion criteria showed methodological weaknesses such as not considering an independent reference standard, or a representative study population. The studies demonstrated methodological strength in describing selection criteria and in interpreting results. The studies’ outcomes make the claim to be able to detect segmental cervical dysfunction based on a manual assessment only questionable. Further improvements in quality, uniform study designs, and a valid reference standard would be necessary in order to obtain more reliable data in the future. r 2006 Elsevier Ltd. All rights reserved. Keywords: Cervical spine; Reliability; Manual assessment; Review

1. Introduction An important part in the interpretation of musculoskeletal disorders is the evaluation of the amount and quality of segmental movement. This is achieved by a number of different manual examination techniques, depending on education and individual preferences. Even if these techniques differ in their approach to the topic because of different assessment and treatment philosophies, all their proponents claim that findings are reliable, if performed by an experienced examiner. Following Bruton et al. (2000), measurements are reliable if the results are consistent or repeatable. In case of studies which compare two or more examiners with each other, the term reproducibility would be more Tel.: +43 732 770199.

E-mail address: [email protected]. 1356-689X/$ - see front matter r 2006 Elsevier Ltd. All rights reserved. doi:10.1016/j.math.2005.12.001

appropriate. But as most of the reviewed articles use reliability, this term is used here exclusively. While interexaminer reliability assesses the agreement of findings between two or more examiners, the intraexaminer reliability assesses the agreement in findings by one examiner. The aim of this review is first the quality assessment of studies which investigated the reliability of manual cervical spine examination, and second to compare their outcome to obtain some indications regarding the accuracy of certain examination approaches. To compare outcome, studies are divided into an estimation of quality and/or range of segmental motion group, and a palpation of tender or painful segmental levels group. To the best of the author’s knowledge and based on the literature search, this review is the first one addressing the reliability of cervical spine examination.

ARTICLE IN PRESS D. Hollerwo¨ger / Manual Therapy 11 (2006) 93–98

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2. Methods 2.1. Inclusion and exclusion criteria Inclusion criteria were studies published between January 1, 1966 and December 31, 2004 which assessed the reliability of manual examination techniques within one observer, between two or more observers, or between one or more observers against an independent reference standard. No limitations were made regarding their level of evidence. Exclusion criteria were unpublished studies, studies published in other languages than English or German and studies of manual assessment on manikins. 2.2. Search strategy The search strategy was designed to conduct a detailed search of relevant literature addressing the two study questions: ‘‘What is the quality of studies which investigate the reliability of manual tests for cervical spine dysfunctions?’’ and ‘‘Is there an agreement regarding the outcome?’’ To search CINAHL, MEDLINE, AMED, AMI and SPORT DISCUS databases, the topic was divided into four categories with relevant keywords for each category. The subdividing into categories was used to limit the hits between 50 and 250 per database. Categories and keywords used were: Anatomic region:

Method: Nature of inquiry:

Examination tool:

‘‘Cervical spine’’, ‘‘Cervical vertebrae’’, ‘‘Cervical vertebra’’, ‘‘Cervical region’’, ‘‘Neck’’, ‘‘Atlanto axial joint’’, ‘‘Atlanto occipital joint’’ ‘‘Diagnosis’’, ‘‘Examination’’, ‘‘Investigation’’, ‘‘Assessment’’ ‘‘Trial’’, ‘‘Randomized’’, ‘‘Outcome’’, ‘‘Comparison’’, ‘‘Reliability’’, ‘‘Intertester’’, ‘‘Intratester’’, ‘‘Interobserver’’, ‘‘Intraobserver’’, ‘‘Interexaminer’’, ‘‘Intraexaminer’’ ‘‘Physical therapy’’, ‘‘Manual therapy’’, ‘‘Osteopathy’’, ‘‘Chiropractic’’, ‘‘Manipulative therapy’’

For the Cochrane Library database, the Physiotherapy Evidence Database (PEDro), the National Library of Medicine (PubMed), Factiva Database, the EBSCOT HOST Research Database and the online journal databases from ELSEVIER Science periodicals, LIPPINCOTT WILLIAMS & WILKINS, ELSEVIER Science @ Direct, THIEME ONLINE and BLACKWELL SYNERGY, the keywords applied were ‘‘cervical spine’’, ‘‘reliability’’, ‘‘intertester’’, ‘‘intratester’’, and combinations of these words due to a less sophisticated search software.

Hits out of each database were as a first step checked for doubles. As a second step the abstracts of the studies which addressed the study questions just partly or not at all were eliminated. After having checked the full text versions of the remaining articles to see if they met the inclusion criteria, their references were crosschecked for new articles which were likely to meet the inclusion criteria. This procedure was applied until no new articles were found. 2.3. Quality assessment tool For the methodological quality assessment, the Quality Assessment of Diagnostic Accuracy tool (QUADAS) by Whiting et al. (2004) was applied (see Table 1). First published by Whiting et al. in 2003, the evidence for the development of QUADAS is based on three systematic reviews, which produced a list of 28 possible items. For the development itself, a panel of nine experts in the field of diagnostic accuracy agreed in four rounds on the 14 items finally included. The tool contains a background document which clarifies terms and indicates how the 14 items should be scored by YES, NO or UNCLEAR. QUADAS does not incorporate a quality score. 2.4. Comments on the application of the QUADAS tool Item 1 was answered NO in papers where the study population consisted of symptomatic as well as asymptomatic subjects. For this review, the assessment of a randomly chosen first examiner was added in Item 4, as the likelihood of changes in symptoms after a manual examination is evident. Following the explanation of how to score QUADAS items (Whiting et al., 2004), Items 5 and 6 were not considered here due to their relevance mainly for diagnostic cohort studies. Item 10 was rated NO in addition when marked palpation points had been used, or findings were rated as positive for more than one segmental level. Marked palpations points bisect the error in comparison to studies where the examiner had to state the symptomatic level by individual counting. 2.5. Appraisal procedure The studies were assessed by the author of this review only. Prior to assessment, copies of full text versions of the studies were put together in one pile, shuffled and then picked up with closed eyes, to guarantee a random order of assessment. A first reading was used to get an overview of the articles content. The following second reading was focused on answering the items of the QUADAS tool. If there were doubts concerning how to


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Table 1 QUADAS tool by Whiting et al. (2004) Item Item Item Item

1 2 3 4

Item Item Item Item Item Item Item Item Item Item

5 6 7 8 9 10 11 12 13 14

Was the spectrum of patients representative of the patients who will receive the test in practice? Were selection criteria clearly described? Is the reference standard likely to classify the target condition correctly? Is the period between reference standard and index test short enough to be reasonably sure that the target condition did not change between the two tests? Did the whole sample or a random selection of the sample, receive verification using a reference standard diagnosis? Did patients receive the same reference standard regardless of the index test results? Was the reference standard independent of the index test (i.e. the index test did not form part of the reference standard? Was the execution of the index test described in sufficient detail to permit replication of the test? Was the execution of the reference standard described in sufficient detail to permit its replication? Were the index test results interpreted without knowledge of the results of the reference standard? Were the reference standard results interpreted without knowledge of the results of the index test? Were the same clinical data available when the test results were interpreted as would be available when the test is used in practice? Were uninterpretable/intermediate results reported? Were withdrawals from the study explained?

Table 2 Qualitative outcome Item 1 Item 2 Item 3 Item 4 Item 5 Item 6 Item 7 Item 8 Item 9 Item 10 Item 11 Item 12 Item 13 Item 14 Uitvlugt and Indenbaum (1988) Jull et al. (1988) Nansel et al. (1989) Hubka and Phelan (1994) Jull et al. (1994) Jull et al. (1997) Cattrysse et al. (1997) Strender et al. (1997) Fjellner et al. (1999) Suijlekom et al. (2000) Smedmark et al. (2000) Schoeps et al. (2000) Marcotte et al. (2002) Pool et al. (2004) Humphreys et al. (2004) Percentage of YES for each item

Y Y N N N N Y N N Y Y N Y Y N 47

Y Y Y Y Y Y Y Y Y Y Y Y U Y Y 93

Y Y N N Y N N N N N N N N N Y 27

U U Y Y U U Y Y Y Y Y U U Y U 53

Y Y N N Y N N N N N N N N N Y 27

Y Y N Y Y N Y Y Y N Y N Y Y N 67

Y Y N N Y N N N N N N N N N N 20

U U N N Y Y Y Y Y N Y Y N Y N 53

Y N N N Y N N N N N N N N N Y 20

U Y U U U U U Y U Y U U U U U 20

Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y 100

U U U U U U U U Y U Y U U U U 13

Y ¼ yes, N ¼ no, U ¼ unclear.

answer a certain item, the article was read a third time and compared with the assessment of this particular item in other studies.

3. Results Fifteen studies published between 1988 and 2004 are included in this review. Their sample size ranges from 3 (Marcotte et al., 2002; Humphreys et al., 2004) to 250 (Nansel et al., 1989). Eleven studies assess reliability of cervical spine examinations by comparing two or more examiners against each other without considering an independent reference standard and four studies assess one or more examiner against an independent reference standard. Reference standards used are radiographic images (Uitvlugt and Indenbaum, 1988; Humphreys

et al., 2004), diagnostic nerve blocks (Jull et al., 1988) and pain reported by the subjects (Jull et al., 1994). Table 2 illustrates the results of the QUADAS tool applied to the 15 studies investigated. Items 3, 7, 9, 11, 12 and 14 are considered in less than 30%, items 1, 4, 8 and 10 in between 30% and 70% and items 2 and 13 in more than 70%. The study carried out by Humphreys et al. (2004) was credited NO for Item 1 because, even if the subjects had vertebral fusions, they had been subjectively asymptomatic at the time of examination. For Jull et al. (1988), Item 11 was rated NO because in the second part the diagnostic nerve blocks were conducted exclusively at the side stated by the manual examiner. Since raw data of the studies investigated were not available to the author, the studies’ outcomes in the form of Kappa Coefficient and/or Percentage of Agreement were compared. Seven studies offered both


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prov (palpation of tender or painful segmental levels) mov (estimation of quality and/or quantity of segmental motion) Nansel et al 1989 prov mov Hubka et al 1994 prov mov Jull et al 1997 prov mov Cattrysse et al1997 prov mov Strender et al 1997 prov mov Fjellner et al 1999 prov mov Suijlekom et al 2000 prov mov Smedmark et al 2000 prov mov Schoeps et al 2000 prov mov Marcotte et al 2002 prov mov Pool et al 2004 prov mov Humphreys et al 2004 prov mov -1

-0.8

-0.6

-0.4

-0.2 0 0.2 Kappa Coefficent

0.4

0.6

0.8

1

Graph 1. Outcomes comparison in form of Kappa Coefficient.

prov (palpation of tender or painful segmental levels) mov (estimation of quality and/or quantity of segmental motion) Uitvlugt et al 1988 prov mov Jull et al 1988 prov mov Nansel et al 1989 prov mov Hubka et al 1994 prov mov Jull et al 1994 prov mov Cattrysse et al 1997 prov mov Strender et al 1997 prov mov Fjellner et al 1999 prov mov Smedmark et al 2000 prov mov Marcotte et al 2002 prov mov 0

10

20

30

40 50 60 Agreement in %

70

80

90

100

Graph 2. Outcomes comparison in form of Percentage of Agreement.

values and are therefore listed twice. Graph 1 presents the comparison of Kappa Coefficient, while Graph 2 shows the comparison of Percentage of Agreement. In both graphs the values are divided into estimation of

quality and/or quantity of segmental motion, and palpation of tender or painful segmental levels. For studies which presented more than one value, the lowest and the highest ones are shown as a range. According to


Haas (in Humphreys et al., 2004) the Kappa coefficient determines whether agreement in results exceeds chance. Kappa value o0.00 ¼ poor agreement, 0.01–0.20 ¼ slight agreement, 0.21–0.40 ¼ fair agreement, 0.41–0.60 ¼ moderate agreement, 0.61–0.80 ¼ substantial agreement, and 0.81–1.00 ¼ almost perfect agreement. 4. Discussion Interpreting quality by using the QUADAS tool (Whiting et al., 2004) raises several methodological issues. Studies investigated show methodological strength in describing selection criteria and in interpreting results. Weaknesses, however, are not stating withdrawals or considering an independent reference standard and incorporating clinical data like in practice. Working with a representative study population, descriptions of test procedures, a random order of first examiners and a blinded interpretation are partly considered. Concerning reference standards, it should be mentioned that physiological movements in a motion segment are based on the interplay of all participating elements. Joint partners as well as muscles, connective tissue, nerves and blood vessels may be a trigger for joint dysfunctions. This limits the validity of single reference standards, as stated, for example, by Giles and Crawford: ‘‘All imaging procedures only provide a shadow of the truthy’’ (in Giles and Baker, 1998, p. 14). In case of joint blocks, Hancock (in Thacker, 1998) argues that this may eliminate a non symptomatic input but not the actual source. In order to reach a more valid reference standard, an approach which incorporates several investigation procedures would be required. Independent of the chosen statistical analysis tool, the comparison of the studies’ outcomes reveals no significant difference in reliability between interpreting altered passive movements and looking for reproduction of symptoms. An increase in reliability would require taking subjective data like history and behaviour of symptoms into account. This would also address issues raised in the qualitative assessment above. Despite different examination techniques, any outcome interpretation has to be seen as well under the aspect of the variability in research design and methodology. For example, Marcotte et al. (2002) used a measurement tool to evaluate the amount of movement at different spinal levels and a positive finding on one spinal level correlated to a positive finding on the level below. Furthermore, the authors divided their findings into a ‘‘success of reproducibility’’ group and a ‘‘failure of reproducibility’’ group compared to an experienced chiropractor. Suijlekom et al. (2000) assessed global cervical movements, and they divided the cervical spine only into ‘‘High’’, ‘‘Mid’’ and ‘‘Low’’. Nansel et al. (1989), Hubka and Phelan (1994) and Humphreys et al. (2004) used marked palpation points

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on the skin to detect the most tender level. With such study designs one can of course expect a better interexaminer reliability than determining a specific spinal level without prior marking. The need to determine a certain spinal level independently doubles the chance of errors, because even if two examiners judge the same spot as tender, the interpretation of its level can be different. This is confirmed for example by O’Haire and Gibbons (2000) who assessed inter- and intra-examiner agreement on sacroiliac anatomical landmarks, or by Billis et al. (2003) who investigated the reproducibility of palpation of the spinous processes at C5, T6 and L5. In both studies the authors describe their outcome of the interexaminer reliability as poor. The limitations of this review are the non-implementation of three studies from the database search which were not available to the author in their full text versions (for their references see Appendix A) and that the studies have been reviewed by the author only. 5. Conclusion The application of the QUADAS tool (Whiting et al., 2004) demonstrated its capability to address studies of diagnostic accuracy. In future, design specific items such as the likelihood of certain examination protocols to detect dysfunctions, should be incorporated in the QUADAS tool. According to the outcomes interpretation of this review, the claim to be able to detect segmental cervical dysfunction based on manual assessment alone is questionable. Reaching higher reliability would require more practically orientated study designs, which most importantly should incorporate subjective data for interpreting segmental mobility or pain. To ensure better comparability future studies should also utilize pragmatic criteria such as uniform movement and pain scales, and an agreement on a uniform reference standard. Such a standard should at least incorporate two independent investigation procedures, like functional radiographs and joint blocks. However, further research will be necessary to obtain more reliable data. Acknowledgments Without the inspiration from Aude Steiner (Universiteé de Neuchaˆtel/Switzerland) and Dr. Karen Grimmer (University of South Australia/Australia) this paper would not have been possible. Appendix A. Studies not included Deboer et al. Reliability study of detection of somatic dysfunction in the cervical spine. Journal of Manipulative and Physiological Therapeutics 1985;8:9–16.

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Mior et al. Intra- and interexaminer reliability of motion palpation in the cervical spine. Journal of the Canadian Chiropractic Association 1985;29:195–8. Tuchin et al. Interexaminer reliability of chiropractic evaluation for cervical spine problems: a pilot study. Australasian Chiropractic and Osteopathy 1996;5:23–9. References Billis EV, Foster NE, Wright CC. Reproducibility and repeatability: errors of three groups of physiotherapists in locating spinal levels by palpation. Manual Therapy 2003;8(4):223–32. Bruton A, Conway J, Holgate S. Reliability: what is it and how is it measured? Physiotherapy 2000;86(2):94–9. Cattrysse E, Swinkels R, Oostendorp R, Duquet W. Upper cervical instability: are clinical tests reliable? Manual Therapy 1997;2(2):91–7. Fjellner A, Bexander C, Faleij R, Strender L. Interexaminer reliability in physical examination of the cervical spine. Journal of Manipulative and Physiological Therapeutics 1999;22(8):511–6. Giles L, Baker P. Introduction. In: Giles L, Singer K, editors. Clinical anatomy and management of cervical spine pain. Oxford: Butterworth-Heinemann; 1998. p. 3–19. Hubka MJ, Phelan SP. Interexaminer reliability of palpation for cervical spine tenderness. Journal of Manipulative and Physiological Therapeutics 1994;17(9):591–5. Humphreys BK, Delahaye M, Peterson CK. An investigation into the validity of cervical spine motion palpation using subjects with congenital block vertebrae as a ‘gold standard’. BMC Musculoskeletal Disorders 2004;5(19). Jull G, Bogduk N, Marsland A. The accuracy of manual diagnosis for cervical zygophysial joint pain syndrome. The Medical Journal of Australia 1988;148:233–6. Jull G, Treleaven J, Versace G. Manual examination: is painful provocation a major cue for spinal dysfunction? Australian Journal of Physiotherapy 1994;40(3):159–65. Jull G, Zito G, Trott P, Potter H, Shirley D, Richardson C. Interexaminer reliability to detect painful upper cervical joint dysfunction. Australian Journal of Physiotherapy 1997;43(2):125–9.

Marcotte J, Normand M, Black P. The kinematics of motion palpation and its effect on the reliability for cervical spine rotation. Journal of Manipulative and Physiological Therapeutics 2002;25(7):E1–9. Nansel DD, Peneff AL, Jansen RD, Cooperstein R. Interexaminer concordance in detecting joint-play asymmetries in the cervical spine of otherwise asymptomatic subjects. Journal of Manipulative and Physiological Therapeutics 1989;12(6):428–33. O’Haire C, Gibbons P. Inter-examiner and intra-examiner agreement for assessing sacroiliac anatomical landmarks using palpation and observation: pilot study. Manual Therapy 2000;5(1):13–20. Pool JJ, Hoving JL, de Vet HC, van Mameren H, Bouter LM. The interexaminer reproducibility of physical examination of the cervical spine. Journal of Manipulative and Physiological Therapeutics 2004;27(2):84–90. Schoeps P, Pfingsten M, Siebert U. Reliability of manual examination techniques at the cervical spine. Study on quality assessment of manual diagnosis. Zeitschrift fuer Orthopaedie 2000;138: 2–7. Smedmark V, Wallin M, Arvidsson I. Inter-examiner reliability in assessing passive intervertebral motion of the cervical spine. Manual Therapy 2000;5(2):97–101. Strender L, Lundin M, Nell K. Interexaminer reliability in physical examination of the neck. Journal of Manipulative and Physiological Therapeutics 1997;20(8):516–20. Suijlekom HA, Vet HCW, Berg SGM, Weber WEJ. Interobserver reliability in physical examination of the cervical spine in patients with headache. Headache 2000;40:581–6. Thacker M. Whiplash—is there a lesion? In: Gifford L, editor. Topical issues in pain. Kestrel: NOI Press; 1998. p. 27–43. Uitvlugt G, Indenbaum S. Clinical assessment of atlanto axial instability using the Sharp-Purser Test. Arthritis and Rheumatism 1988;31(7):918–22. Whiting P, Rutjes AWS, Dinnes J, Reitsma JB, Bossuyt PMM, Kleijnen J. The development of QUADAS: a tool for the quality assessment of studies of diagnostic accuracy included in systematic reviews. BMC Medical Research Methodology 2003;3(25). Whiting P, Rutjes AWS, Dinnes J, Reitsma JB, Bossuyt PMM, Kleijnen J. Development and validation of methods for assessing the quality of diagnostic accuracy studies. Health Technology Assessment 2004;8(25).

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Original article

The relationship of cervical joint position error to balance and eye movement disturbances in persistent whiplash Julia Treleaven, Gwendolen Jull, Nancy LowChoy Division of Physiotherapy, School of Health and Rehabilitation Sciences, The University of Queensland, Australia Received 25 October 2004; received in revised form 7 March 2005; accepted 7 April 2005

Abstract Cervical joint position error (JPE) has been used as a measure of cervical afferent input to detect disturbances in sensori-motor control as a possible contributor to a neck pain syndrome. This study aimed to investigate the relationship between cervical JPE, balance and eye movement control. It was of particular interest whether assessment of cervical JPE alone was sufficient to signal the presence of disturbances in the two other tests. One hundred subjects with persistent whiplash-associated disorders (WADs) and 40 healthy controls subjects were assessed on measures of cervical JPE, standing balance and the smooth pursuit neck torsion test (SPNT). The results indicated that over all subjects, significant but weak-to-moderate correlations existed between all comfortable stance balance tests and both the SPNT and rotation cervical JPE tests. A weak correlation was found between the SPNT and right rotation cervical JPE. An abnormal rotation cervical JPE score had a high positive prediction value (88%) but low sensitivity (60%) and specificity (54%) to determine abnormality in balance and or SPNT test. The results suggest that in patients with persistent WAD, it is not sufficient to measure JPE alone. All three measures are required to identify disturbances in the postural control system. r 2005 Elsevier Ltd. All rights reserved. Keywords: Balance; Whiplash; Postural control; Proprioception; Dizziness; Eye movement

1. Introduction Evidence is emerging to suggest that patients with persistent whiplash-associated disorders (WADs) have impairments in the postural control system. These include altered kinaesthetic sense with increased cervical joint position error (JPE) (Heikkila and Astrom, 1996; Treleaven et al., 2003), altered eye movement control, detected in the smooth pursuit neck torsion test (SPNT) (Tjell and Rosenhall, 1998; Tjell et al., 2003; Treleaven et al., 2004a) and altered standing balance (Kogler et al., 2000; Michaelson et al., 2003; Sjostrom et al., 2003; Treleaven et al., 2003, 2004b). These impairments are more pronounced when the whiplash patient reports dizziness and or unsteadiness in association with their Corresponding author. Tel./fax: +61 7 3365 2275.

E-mail address: [email protected] (J. Treleaven). 1356-689X/$ - see front matter r 2005 Elsevier Ltd. All rights reserved. doi:10.1016/j.math.2005.04.003

neck pain (Tjell and Rosenhall, 1998; Treleaven et al., 2003, 2004a, b). The impairments have also been shown to be independent of the patient’s anxiety level, medication use and compensation status suggesting that the symptom of dizziness is related to disturbances in the postural control system (Treleaven et al., 2003, 2004a, b). It is probable that these impairments reflect abnormal cervical afferent input to the postural control system especially in cases where there is no evidence of a concurrent head injury or primary injury to the vestibular apparatus associated with the whiplash injury (Hildingsson et al., 1993; Rubin et al., 1995; Gimse et al., 1997; Tjell and Rosenhall, 1998; Wenngren et al., 2002). The measure of cervical JPE is considered to primarily reflect afferent input from the neck joint and muscle receptors (Taylor and McCloskey, 1991; Mergner et al., 1998). It is used regularly as an objective measure of

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cervical afferent input in both cross-sectional and intervention studies (Revel et al., 1991; Heikkila and Astrom, 1996; Heikkila and Wenngren, 1998; Treleaven et al., 2003). In appraising the intervention studies, there seems to be a presumption that JPE is the pivotal test for cervical afferent disturbance and abnormalities in JPE reflect other impairments such as disturbances to eye movement control and even balance. For example, JPE has been the representative quantitative outcome measure for programmes which have addressed either eye/head co-ordination, gaze stability as well as cervical joint repositioning practice (Revel et al., 1994), exercises for eye, head and arm co-ordination (Humphreys and Irgens, 2002), body awareness retraining (Heikkila and Astrom, 1996) or neck manipulation and acupuncture (Heikkila et al., 2000). In defense of the use of JPE as the representative measure, Heikkila and Wenngren (1998) did find that whiplash subjects with oculomotor disturbances were less accurate in head repositioning than subjects with normal oculomotor tests, suggesting a possible relationship between these measures. Such a suggestion may oversimplify the complex reflex and central interactions between the cervical afferents and other areas important for postural control, particularly the vestibular and visual systems (Chan et al., 1987; Dutia, 1991; Fischer et al., 1995; Bolton, 1998). There was a need to further investigate whether there were any relationships between the suite of measures (i.e. measures of cervical (JPE), balance and SPNT), contributing to disturbance of postural control in patients following a whiplash injury. Thus, the aim of this study was to determine whether any relationships existed between cervical JPE, SPNT and balance, and in particular, whether the tests were highly correlated which would support the notion that assessment of cervical JPE alone is sufficient to detect postural control disturbances following a whiplash injury. A secondary aim was to determine the incidence of postural control abnormalities (based on normative data) in both subjects with whiplash complaining and not complaining of these symptoms as well as the usefulness of an abnormal score in cervical (JPE) in indicating abnormalities in the other tests. Knowledge of such relationships is important for future direction in assessment and management of postural control disturbances in whiplash patients.

2. Materials and methods 2.1. Subjects One hundred and forty subjects were included in this case control study. They comprised 100 subjects with WAD classifiable as WAD 11 (Spitzer et al., 1995) with persistent pain and disability (longer than 3 months

since injury) and 40 healthy control subjects. To ensure a spread of measures, half (n ¼ 50) of the subjects with whiplash reported symptoms of dizziness and unsteadiness (Group WAD D) while the other 50 subjects did not report these symptoms (Group WAD ND). Subjects were recruited from eligible patients attending the Whiplash Research Unit in the Division of Physiotherapy at The University of Queensland and from local advertising. Subjects were not considered if they reported either a period of unconsciousness or concurrent head injury associated with their injury or a previous history of dizziness prior to the injury, which could introduce other causes of dizziness or unsteadiness. Potential participants were also not considered if they did not have at least 30 1 of cervical rotation to either side, as this would preclude their ability to undertake the SPNT test. Subjects were asked to refrain from taking any medication at least 24 h prior to the study. There were 38 female subjects in each WAD group. The mean age of the WAD D group was 35.5 years (range 19–46 years) and the WAD ND group 35.0 years (range 18–46 years). The mean time since injury was 1.4 years (range .35–3 years) WAD D and 1.6 years (range .3–3 years) WAD ND. A control group was included in the study to derive normative values to identify subjects with whiplash with postural control abnormalities for the secondary analysis. They were drawn from healthy volunteers who responded to advertising in the local media. To be included in the study, healthy controls were required to have had no current or past history of whiplash, neck pain, headaches or dizziness. Twenty-three subjects in the control group were females. The mean age of this group was 29.6 years (range 19–45 years). All participants provided their informed consent. Ethical clearance for this study was granted from the Human Medical Ethics Committee of The University of Queensland. 2.2. Instrumentation and measurement 2.2.1. Cervical joint position error (JPE) The subject’s accuracy in relocating the natural head posture (cervical JPE) was tested following active cervical movements into left and right rotation and extension, using methodology previously described (Treleaven et al., 2003). The Fastrak (Polhemus, Navagation Science Division, Kaiser Aerospace Vermont) was used to measure the difference in degrees between the starting (zero) and the return position for each of the three movements tested. One sensor was placed on the spinous process of C7 and the other was attached to a lightweight helmet adjacent to the subject’s forehead. The error in the primary plane of movement was used as the measure for JPE as this had previously been shown to depict differences between healthy controls and WAD subjects (Treleaven et al., 2003).

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2.2.2. Smooth pursuit neck torsion test (SPNT) Electro-oculography (EOG) was used to measure and record eye movement while a moving target was followed when the subject’s head and trunk was set in a neutral (forward facing position), and with head in neutral while the trunk was rotated (torsioned) 45 1 to the left and then to the right. The procedure has been described in detail elsewhere (Treleaven et al., 2004a) and is similar to that described by Tjell and Rosenhall (1998). The moving target was a laser light driven by a motor to move through a visual angle of 40 1 to the left and right on 10 consecutive occasions. Pairs of Ag/AgCl surface electrodes (Cleartrace ConMed USA) were placed on the subject’s skin just lateral to the eyes to record changes in the corneo-retinal potential during eye movement. A ground electrode was placed on the forehead. The signals were passed through a 70 Hz low-pass filter and stored on an IBM compatible PC. The data were then graphed using a Labview Programme. Data collection and analysis were performed by the same examiner (JT), however the subject data were deidentified prior to analysis by an independent member of the research team to ensure the examiner was blinded to the subject group during data management. For each test, the data were graphed using a labview programme. The average velocity of the eye movements as they followed the target, was calculated by subtracting the corrective movements from the total excursion of the gaze (Tjell and Rosenhall, 1998). A software programme (Labview) was written to calculate the total excursion of each gaze and to allow manual identification and subtraction of the corrective saccades. The

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programme then formulated the corrected gain for each cycle. The top and bottom directional changes of the trace, the square waves as defined by Schalen (1980) and blinks (judged from recorded examples of an actual blink from each subject) were disregarded from the analysis. The mean gain (i.e. the ratio between the eye movements and of target) from the sixth to the ninth cycles was the measure used to define SP movements. This method of analysis was adopted from Tjell and Rosenhall (1998). Choosing the appropriate elements of the signal to assure that ‘‘true pursuit’’ is calculated is thought to be vital for correct calculation of the velocity gain (Wieser et al., 2004). The SP gain was calculated with the neck in a neutral position, and also with the neck in a torsioned position. The average gain was calculated for neutral (SP neutral) and torsion to the left (SP left) and right (SP right). The difference between the gain in neutral and the average values in torsion equalled the SPNT difference. An example of an eye trace sixth to ninth cycle, depicting corrective saccades and square waves is depicted in Fig. 1. 2.2.3. Computerised posturography (CDP) A computerised, stable force platform (40 cm 60 cm) measured force changes over time in both the medial– lateral (ML) and anterior–posterior (AP) directions for each of the 6 test conditions of the Clinical Test for Sensory Interaction in Balance (CTSIB) (Shumwaycook and Horak, 1986) while the subjects were in a standardised comfortable stance position. The six conditions were eyes open, eyes closed and visual conflict on a firm surface and then eyes open, eyes closed and visual conflict on a soft surface. The soft

1100.0 1000.0 900.0 800.0 Amplitude

700.0 Corrective saccade

600.0 500.0

Square wave

400.0 300.0 200.0 100.0 0.0 0

500 1000 1500 2000 2500 3000 3500 4000 4500 5000 5500 6000 6500 7000 7500 8000

Time Fig. 1. Example of an eye trace from the sixth to the ninth cycle. The top and bottom of the directional changes of the graph are disregarded, as is the square wave. Examples of some of the corrective saccades are highlighted between the horizontal lines. The corrective saccades were subtracted from the total excursion to formulate the velocity gain.



surface was a piece of high-density (10 cm thick) foam rubber placed on the platform. Visual conflict was provided by placing a light-weight paper dome over the subject’s head. This methodology is described in detail elsewhere (Treleaven et al., 2004b,c). As directed by our previous research (Treleaven et al., 2004c), wavelet analysis was the method of analysis chosen to measure and summarise the sway trace for each test condition. 2.3. Procedure Each subject undertook each of the three postural control tests in a randomised order. For the SPNT, the subject was seated, the skin was prepared and the electrodes applied. The subjects were instructed to follow the moving laser light as closely as possible, trying not to blink, while keeping their head still. The examiner gently held the head still during each testing procedure (Tjell and Rosenhall, 1998; Treleaven et al., 2004a). This protocol was performed for the three test positions: with the neck in a neutral position, the head in neutral with the torso turned to an angle of approximately 45 1 to the left and then to the right. For those rare subjects where this position caused pain, the angle was decreased to a minimum of 30 1. For tests of standing balance, subjects stood on the force platform. The standardised procedure of the six conditions of the CTSIB was performed with the subjects in comfortable stance. One 30-s trial was performed for each condition (Treleaven et al., 2004b, c). The starting position for the JPE 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 to the starting position and this was marked electronically. The examiner, guided by real-time display, manually repositioned the subject’s head back to the original starting position before each trial. Three trials were performed for each of left and right neck rotation, and extension. The subject was able to visually re-centre their starting position prior to each new movement direction (Treleaven et al., 2003).

analysis and this summary of the sway trace was selected as it has previously been useful in determining differences between control subjects and subjects with whiplash with and without the symptom of dizziness (Treleaven et al., 2004b, c). JPEs were calculated by using the mean of the absolute errors for the three trials of each movement for the primary planes of extension, rotation to the left and rotation to the right (Treleaven et al., 2003). The values of SP gain in neutral, and the average SP gain for the left and right torsioned position (Av SP) were used to calculate the SPNT value i.e. the difference between neutral and torsioned positions. A correlation analysis, using Pearsons r calculations, was performed to determine any association between the 6 conditions of the balance test, the SPNT difference, and cervical JPE scores for rotation to the left, rotation to the right and extension. This analysis was performed for all subjects (whiplash and controls), then separately for control subjects, the total whiplash group, and then subjects with whiplash complaining of dizziness (WAD D) and subjects not complaining of dizziness (WAD ND), to determine whether relationships were influenced by subjects’ symptomatic complaints. To determine the frequency of postural control abnormalities in the whiplash group and the usefulness of the cervical (JPE) scores in indicating abnormalities in the other tests, the upper 95% confidence interval for control subjects was used to determine whether an individual whiplash subject’s score for each of SPNT, rotation cervical JPE and a global balance score was either normal or abnormal. A decision on how to condense the JPE and balance data were made post hoc after analysis of the relationships between the tests was reviewed. For joint position error an abnormal score for either or both of the rotation errors (left or right) was considered abnormal. For balance, an abnormal score was given if at least 2 of the 6 tests were considered abnormal based on the 95% confidence interval of the control group. The sensitivity, specificity and positive predictive value of an abnormal cervical rotation JPE score in indicating the status of the other postural control tests was calculated. The statistical programmes R and SPSS were used for all calculations.

2.4. Data analysis For the balance tests, the sway trace was analysed by a Wavelet analysis using Daubechies filter 6. This was performed for both AP and ML traces for each test condition. The variance of the wavelet coefficients is a measure of the amount of information coming from the different frequencies and is termed ‘‘energy’’. In this study, the total of energies combined from the AP and ML traces at the first four frequencies to summarise the information contained in the trace was used. Wavelet

3. Results The correlation co-efficients (Pearsons) between the six balance tests, JPE for rotation to the left and right and extension and the SPNT scores for 140 whiplash and control subjects, and each groups separately (the total whiplash group, the 50 (WAD D) and 50 (WAD ND) subjects and the 40 control subjects) are depicted in Table 1. For all subjects, weak-to-moderate correlations


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Table 1 Correlation co-efficients (Pearsons r) between the six balance tests, cervical joint position error for extension, rotation to the left and right and the smooth pursuit neck torsion score, for all subjects, the total whiplash group (WAD), subjects with whiplash complaining of dizziness (WAD D), subjects with whiplash not complaining of dizziness (WAD ND) and control subjects Cervical joint position error Ext All subjects n ¼ 140 Ext 1 Rot L .24 Rot R .28 SPNT .08 WAD n ¼ 100 Ext 1 Rot L .25 Rot R .25 SPNT .01 WAD D n ¼ 50 Ext 1 Rot L .18 Rot R .13 SPNT .11 WAD ND n ¼ 50 Ext 1 Rot L .28 Rot R .39 SPNT .05 Controls n ¼ 40 Ext 1 Rot L .00 Rot R .29 SPNT .11

Balance EOF

SPNT

Rot L

Rot R

ECF

VCF

EOS

ECS

VCS

SPNT

.24 1 .5 .15

.28 .5 1 .23

.10 .36 .61 .31

.14 .34 .42 .28

.02 .23 .31 .29

.02 .24 .33 .31

.06 .35 .32 .31

.09 .42 .61 .32

.08 .15 .23 1

.25 1 .5 .06

.25 .5 1 .16

.10 .36 .64 .28

.13 .33 .42 .22

.06 .20 .30 .22

.00 .20 .32 .25

.04 .32 .31 .25

.09 .41 .65 .28

.01 .06 .16 1

.18 1 .60 .03

.13 .60 1 .09

.08 .43 .72 .25

.10 .39 .45 .15

.17 .25 .32 .16

.03 .24 .45 .21

.01 .39 .33 .24

.04 .51 .75 .24

.11 .03 .09 1

.28 1 .28 .01

.39 .29 1 .11

.07 .11 .09 .22

.13 .10 .01 .21

.04 .03 .05 .14

.02 .09 .04 .21

.00 .11 .01 .01

.28 .10 .01 .07

.05 .01 .11 1

.00 1 .20 .20

.29 .20 1 .15

.14 .05 .08 .04

.15 .14 .17 .05

.02 .01 .18 .09

.29 .49 .10 .12

.01 .33 .13 .10

.13 .16 .18 .33

.11 .20 .15 1

Rot L ¼ Rotation left. Rot R ¼ Rotation right. Ext ¼ Extension. EOF ¼ Eyes open firm. ECF ¼ Eyes closed firm. VCF ¼ Visual conflict firm. EOS ¼ Eyes open soft. ECS ¼ Eyes closed soft. VCS ¼ Visual conflict soft. SPNT ¼ Smooth pursuit neck torsion test. Significance at Po.05.

were observed between all six of the comfortable balance scores and cervical JPE for rotation to the left and right. There was only a weak correlation between the SPNT score and the right rotation cervical JPE score. For subjects with WAD complaining of dizziness, the correlation between cervical JPE for rotation to the left and right and the majority of the balance scores was stronger but no correlation was seen between the other measures. For subjects with WAD not complaining of dizziness no correlations were evident. In control subjects, a moderate correlation was observed between left rotation cervical (JPE) and the eyes open on a firm surface balance test. Fig. 2 and Table 2 present the frequency of abnormal and normal scores for SPNT, global balance and global rotation cervical JPE for the whiplash subjects. Thirty-

four of the 50 WAD subjects with dizziness had an abnormal global rotation JPE score. Of these, 18 also had abnormal scores on both the other tests of SPNT and global balance. Only two subjects had an abnormal JPE score and normal scores for balance and SPNT. In contrast, four of the 16 subjects with a normal JPE score had an abnormal score on both of the other tests, and 11 had an abnormal score on one of the other tests. Twenty-five of the 50 WAD subjects without dizziness had an abnormal JPE score, and five of these subjects had an abnormal score for all three tests. Five subjects had an abnormal score for JPE but normal scores for the other tests. Of the 25 subjects with a normal JPE score, five had an abnormal score for both other tests and 15 had an abnormal score on one or both of the other tests (Table 2).


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Table 3 presents the sensitivity and specificity of an abnormal global JPE score to determine abnormalities in the other postural control tests. The presence of an abnormal global JPE score had a 60% sensitivity to predict an abnormality in one or both of the other postural control tests when all whiplash subjects were considered. The specificity was 54%. The positive predictive value of an abnormal global JPE score

Abnormal Normal

Abnormal Normal

WAD D

WAD ND

50

50

40

40

30

30

20

20

10

10

0

0 JPE

Balance

SPNT

JPE Balance

SPNT

Fig. 2. Number of whiplash subjects complaining of dizziness (WAD D) and not complaining of dizziness (WAD ND) with abnormal and normal scores for each postural control test: cervical rotation joint position error (JPE), balance and smooth pursuit neck torsion.

indicating abnormal scores in one or both of the other postural control tests was 88% (Table 3).

4. Discussion The results of the study have implications for assessment and management of postural control disturbances in WAD. Both cervical JPE and SPNT are thought to reflect abnormal cervical afferent input and both of these tests correlated to all balance tests, suggesting that balance is also likely to be disturbed due to abnormal cervical afferent function. However, this premise was only found for cervical (JPEs) in rotation but not extension. An unexpected finding was the comparatively strong correlation between right rotation JPE and the balance tests of eyes open on a firm surface (.72) and visual conflict on a soft surface (.75) for whiplash subjects with dizziness. In our previous research these tests have not been as sensitive in discriminating whiplash subjects from controls, with the tests of balance with the eyes closed being more discriminative (Treleaven et al., 2004b, c). This finding may support the notion that those with greater disturbances to the postural control system will demonstrate the most marked differences even on the simplest balance test. In addition, it may indicate that cervical

Table 2 Number of subjects from each whiplash group, dizzy (WAD D) or non-dizzy (WAD ND) with abnormal or normal scores (based on the upper 95% confidence interval of the control subjects) for each of the postural control tests JPE score

SPNT score

Balance score

WAD D n ¼ 50

WAD ND n ¼ 50

Total WAD N ¼ 100

Normal Normal Normal Normal Abnormal Abnormal Abnormal Abnormal

Normal Normal Abnormal Abnormal Abnormal Normal Abnormal Normal

Normal Abnormal Normal Abnormal Abnormal Normal Normal Abnormal

1 1 10 4 18 2 13 1

5 0 15 5 5 5 14 1

6 1 25 9 23 7 27 2

Table 3 Sensitivity, specificity and predictability of the average global cervical joint position (JPE) score in determining outcome of the other postural control tests in subjects with whiplash-associated disorders (WAD)

JPE abnormal JPE normal Sensitivity JPE Specificity JPE Positive prediction value Negative predication value SPNT ¼ Smooth pursuit neck torsion.

WAD subjects with abnormal balance or SPNT scores

WAD subjects with normal balance and SPNT scores

Total

n ¼ 52 n ¼ 35 Total ¼ 87 52/87 ¼ 59.7%

n¼7 n¼6 Total ¼ 13

n ¼ 59 n ¼ 41 n ¼ 100

7/13 ¼ 53.8% 52/59 ¼ 88.1% 7/41 ¼ 17.1%


(JPE) in rotation reflects a general disturbance to postural control rather than a unique expression of altered cervical afferent input. There was only a weak correlation between right rotation cervical JPE and the SPNT test when all subjects were considered and no other correlations were observed between the results of cervical JPE in rotation left and extension and SPNT. This has implications for future assessment and management of these disturbances. To date studies have implied a direct relationship between these two measures by including both eye movement and cervical joint position training in interventions but only re-evaluating JPE (Revel et al., 1991, Heikkila and Wenngren, 1998). The results from this study would suggest that cervical JPE and SPNT should be examined, managed and re-evaluated independently. These tests may be measuring independent features of cervical afferent disturbances on postural control. SPNT may predominantly demonstrate cervical afferent influences on the visual system (Tjell and Rosenhall, 1998), whereas cervical JPE may reflect cervical afferent input with respect to the vestibular system (Mergner et al., 1998; Schweigart et al., 2002). It has been argued that adaptive vestibular dysfunction is possible following a whiplash injury as a result of limited neck/head movement, or triggered by the abnormal input from neck afferents (Hinoki, 1975; Fischer et al., 1995). Further research is required to better understand the precise mechanisms of each test, particularly the cervical (JPE) tests. It is of particular importance to determine in future studies whether cervical JPE tests are able to specifically differentiate between cervical and vestibular contributions to tests of postural control. The results also demonstrated that postural control disturbances are frequent in subjects with whiplash particularly those who complain of dizziness (Fig. 2, Table 2). In this group, 72% of the subjects presented with abnormalities in two or more of the postural control measures and 36% had abnormalities in all three of the tests. Even in those without dizziness, 50% had deficits in two or more of the tests. Thus, it is recommended that a routine examination of postural control be included in all patients with persistent whiplash disorders. The use of cervical (JPE) testing as a screening test for other postural control deficits cannot be recommended. Sensitivity of an abnormal global JPE test was moderate (60%), such that a normal JPE score was often seen (40%) in those with abnormalities in one or both of the other tests. Nevertheless, selection of subjects for intervention studies based on cervical JPE may be useful, as a high positive prediction value was seen. Eighty-eight percent of subjects who had an abnormal score in global cervical rotation joint position error also had other postural control deficits.

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While the SPNT measure may be highly specific and sensitive for identifying patients with WAD, particularly in those with dizziness (Tjell et al., 2003), the use of the SPNT test may not be as useful in identifying other postural control abnormalities. Eighty–four percent of subjects with WAD had an abnormal SPNT score but of these, 29% had no other abnormalities (Table 2). Thus assessment of all three measures of postural control seems necessary to identify the specific disturbance and to direct the relevant interventions to improve postural control. Further research is needed to assess the effect of different interventions on each of the three measures of postural control. The results of the high positive prediction of cervical (JPE) in this study would imply that past studies that have selected subjects with abnormalities in cervical JPE (Revel et al., 1994; Heikkila et al., 2000; Humphreys and Irgens, 2002) were also likely to have had deficits in SPNT or balance or both. Treatment directed towards eye head control and cervical joint position relocation may have fortuitously addressed the majority of the problem areas, but more specific evidence is required. Treatment should be based on the impairments demonstrated in the physical examination. The results of this study indicate that whiplash patients, especially those complaining of dizziness or unsteadiness, require management aimed at normalising cervical afferent input. Some of the causes of the abnormal cervical mechanoreceptor input may be addressed by decreasing pain and inflammation locally within the cervical spine and improving cervical muscle function. However, conflict between cervical, vestibular and visual input, could cause adaptations within the brain stem mechanisms receiving and managing input from these sources creating secondary disturbances to the postural control system. In this instance, it is possible that the addition of the specific exercise strategies for the disturbances seen in postural control may better address these resultant secondary effects of abnormal cervical input. This might include tailored exercises to improve any identified deficits in cervical (JPE), eye head co-ordination, gaze stability or balance (Revel et al., 1991; Heikkila et al., 2000). It is also likely that balance retraining will need to include both surface and visual challenges to ensure optimal management of clients with whiplash.

5. Conclusion The study demonstrated that postural control deficits are evident in subjects with persistent WAD and while some relationships exist between SPNT and balance, and balance and the cervical JPE, assessment of cervical JPE alone is not sufficient to detect all possible postural control disturbances in those with WAD. It is recommended that all three measures are assessed and



managed according to an individual’s specific impairments. Future research is needed to determine the precise mechanisms behind each test, the usefulness of each test in identifying primary cervical dysfunction as well as the most efficacious management strategies.

Acknowledgements This research was supported by grants received from the Physiotherapy Research Foundation and The Centre of National Research on Disability and Rehabilitation Medicine (CONROD). We would also wish to acknowledge statistical assistance from Dr. Robert Murison for establishing the protocol for the wavelet analysis. References Bolton P. The somatosensory system of the neck and its effects on the central nervous system. Journal of Manipulative and Physiological Theraputics 1998;21:553–63. Chan YS, Kasper J, Wilson VJ. Dynamics and directional sensitivity of neck muscle-spindle responses to head rotation. Journal of Neurophysiology 1987;57:1716–29. Dutia MB. The muscles and joints of the neck: their specialisation and role in head movement. Progress in Neurobiology 1991;37:165–78. Fischer A, Huygen PLM, Folgering HT, Verhagen WIM, Theunissen E. Vestibular hyperreactivity and hyperventilation after whiplash injury. Journal of the Neurological Sciences 1995;132:35–43. Gimse R, Bjorgen IA, Tjell C, Tyssedal JS, Bo K. Reduced cognitive functions in a group of whiplash patients with demonstrated disturbances in the posture control system. Journal of Clinical Experiments in Neuropsychology 1997;19:838–49. Heikkila H, Astrom PG. Cervicocephalic kinesthetic sensibility in patients with whiplash injury. Scandinavian Journal of Rehabilitation Medicine 1996;28:133–8. 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;5:151–7. 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;79:1089–94. Hildingsson C, Wenngren BI, Toolanen G. Eye motility dysfunction after soft-tissue injury of the cervical-spine—a controlled, prospective-study of 38 patients. Acta Orthopaedica Scandinavica 1993;64:129–32. Hinoki M. Vertigo due to whiplash injury: a neuro-otological approach. Acta Otolaryngol (Stockh) 1975;419:9–29. Humphreys B, Irgens P. The effect of a rehabilitation exercise program on head repositioning accuracy and reported levels of pain in chronic neck pain subjects. Journal of Whiplash and Related Disorders 2002;1:99–112. Kogler A, Lindfors J, Odkvist L, Ledin T. Postural stability using different neck positions in normal subjects and patients with neck trauma. Acta Orthopaedica Scandinavica 2000;120:151–5.

Mergner T, Schweigart G, Botti F, Lehmann A. Eye movements evoked by proprioceptive stimulation along the body axis in humans. Experimental Brain Research 1998;120:450–60. Michaelson P, Michaelson M, Jaric S, Latash ML, Sjolander P, Djupsjobacka M. Vertical posture and head stability in patients with chronic neck. Journal of Rehabilitation Medicine 2003;35: 229–35. Revel M, Andre-Deshays C, Minguet M. Cervicocephalic kinesthetic sensibility in patients with cervical pain. Archives of Physical Medicine and Rehabilitation 1991;72:288–91. Revel M, Minguet M, Gergory P, Vaillant J, Manuel JL. 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;75:895–9. Rubin AM, Woolley SM, Dailey VM, Goebel JA. Postural stability following mild head or whiplash injuries. American Journal of Otology 1995;16:216–21. Schalen L. Quantification of tracking eye movements in normal subjects. Acta Otolaryngol 1980;90:404–13. Schweigart G, Chien RD, Mergner T. Neck proprioception compensates for age-related deterioration of vestibular self-motion perception. Experimental Brain Research 2002;147:89–97. Shumwaycook A, Horak FB. Assessing the influence of sensory interaction on balance—suggestion from the field. Physical Therapy 1986;66:1548–50. Sjostrom H, Jh JA, Carpenter MG, Adkin AL, Honegger F, Ettlin T. Trunk sway measures of postural stability during clinical balance tests in patients with chronic whiplash injury symptoms. Spine 2003;28:1725–34. Spitzer W, et al. Scientific monograph of quebec task force on whiplash associated disorders: redefining ‘‘Whiplash’’ and its management. Spine 1995;20:1–73. Taylor JL, McCloskey DI. Illusions of head and visual target displacement induced by vibration of neck muscles. Brain 1991; 114:755–9. Tjell C, Rosenhall U. Smooth pursuit neck torsion test: a specific test for cervical dizziness. American Journal of Otology 1998;19: 76–81. Tjell C, Tenenbaum A, Sandstro¨m S. Smooth pursuit neck torsion test—a specific test for whiplash associated disorders? Journal of Whiplash and Associated Disorders 2003;1:9–24. Treleaven J, Jull G, Low Choy N. Smooth pursuit neck torsion test in whiplash associated disorders—relationship to self reports of neck pain and disability, dizziness and anxiety. Journal of Rehabilitation Medicine 2004a In press. Treleaven J, Jull G, Low Choy N. Standing balance in persistent WAD—comparison between subjects with and without dizziness. Journal of Rehabilitation Medicine 2004b In Press. Treleaven J, Jull G, Murison RM, LowChoy N, Brauer S. Is the method of signal analysis and test selection important for measuring standing balance in chronic whiplash? Gait and Posture 2004c In press. 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;35:36–43. Wenngren B, Pettersson K, Lowenhielm G, Hildingsson C. Eye motiliy and auditory brainstem response dysfunction after whiplash injury. Acta Orthopaedica Scandinavica 2002;122:276–83. Wieser T, Wolff R, Hoffmann KP, Schulte-Mattler W, Zierz S. Persistent ocular motor disturbances in migraine without aura. Neurological Sciences 2004;25:8–12.

ARTICLE IN PRESS


Original article

Effects of a manual therapy technique in experimental lateral epicondylalgia Helen Slatera,b,, Lars Arendt-Nielsena, Anthony Wrightb, Thomas Graven-Nielsena a

Laboratory for Experimental Pain Research, Center for Sensory-Motor Interaction, Aalborg University, Aalborg, Denmark b School of Physiotherapy, Curtin University of Technology, GPO Box U1987, Perth 6845, Western Australia, Australia Received 9 September 2004; received in revised form 3 March 2005; accepted 7 April 2005

Abstract In patients with lateral epicondylalgia, mobilization-with-movement (MWM) is used as an intervention aimed at achieving analgesia and enhancing grip force, although the mechanisms underlying these effects are unclear. The present study investigated the acute sensory and motor effects of an MWM intervention in healthy controls with experimentally induced lateral epicondylalgia. Twenty-four subjects were randomly allocated to either a MWM or a placebo group (n ¼ 12). In both groups, to generate the model of lateral epicondylalgia, delayed onset muscle soreness (DOMS) was provoked in one arm 24 h prior (Day 0) to hypertonic salineinduced pain in the extensor carpi radialis brevis muscle (Day 1). Either a MWM or placebo intervention was applied during the saline-induced pain period. Saline-induced pain intensity (visual analogue scale: VAS), pain distribution and pain quality were assessed quantitatively. Pressure pain thresholds (PPTs) were recorded at the common extensor origin and the extensor carpi radialis brevis muscle. Maximal measures of grip and wrist extension force were recorded. In both groups (pooled data), DOMS was efficiently induced as demonstrated by a significant decrease in pre-exercise to pre-injection PPT at the common extensor origin (45719%) and at the extensor carpi radialis brevis (61723%; Po0:05), and a significant decrease in maximal grip force (2576%) and maximal wrist extension force (40712%; Po0:001). Moreover, both groups experienced a significant increase in muscle soreness (3.970.2; Po0:0001) at Day 1 compared to pre-exercise. During saline-induced pain and in response to intervention, there were no significant between-group differences in VAS profiles, pain distributions, induced deep tissue hyperalgesia or force attenuation. These data suggest that the lateral glide-MWM does not activate mechanisms associated with analgesia or force augmentation in subjects with experimentally induced features simulating lateral epicondylalgia. r 2005 Elsevier Ltd. All rights reserved. Keywords: Manipulation; Mobilization; Lateral epicondylalgia; Tennis elbow; Experimental muscle pain; Movement

1. Introduction Mobilization-with-movement (MWM) is a manual therapy intervention commonly used in the management of patients with lateral epicondylalgia. A specific form of MWM—a lateral glide at the elbow—has been reported to exert rapid pain-relieving effects and to enhance grip strength in patients with clinical lateral epicondylalgia (Vicenzino and Wright, 1995; Mulligan, 1999; Abbott Corresponding author. Tel.: +61 89 266 3099; fax: +61 89 266 3699. E-mail address: [email protected] (H. Slater).

1356-689X/$ - see front matter r 2005 Elsevier Ltd. All rights reserved. doi:10.1016/j.math.2005.04.005

et al., 2001; Vicenzino et al., 2001; Paungmali et al., 2003a). Vicenzino et al. (2001) investigated the effects of the lateral glide-MWM in a group of 24 patients with clinical unilateral lateral epicondylalgia using a randomized, double-blind, placebo-controlled design. In the affected arm, the lateral glide-MWM produced significant and substantial increases in pain-free grip force immediately post-application compared with pre-application (58%), and a modest but significant increase (10%) in pressure pain threshold (PPT) (Vicenzino et al., 2001). Abbott et al. (2001) demonstrated similar effects showing a significant increase in maximal grip strength (magnitude of change: 5%) and pain-free grip


H. Slater et al. / Manual Therapy 11 (2006) 107–117

strength (magnitude of change of 17%) following a lateral glide-MWM in 23 patients with lateral epicondylalgia. While specific physiological effects of the lateral glideMWM have been documented, the mechanisms underlying the effects of this physical intervention have yet to be elucidated. What has been demonstrated experimentally is that the analgesic effect in response to the lateral glide-MWM in patients with clinical lateral epicondylalgia appears to be rapid in nature, is associated with sympathoexcitation (Vicenzino et al., 1998; Vicenzino et al., 2000) and does not demonstrate decay over repeated administrations (Paungmali et al., 2003b). Wright (1995) proposed that the apparent concurrency of hypoalgesic and autonomic responses might suggest activation of descending inhibitory pathways in the central nervous system. It is unclear if the treatment effects of the lateral glideMWM that have been demonstrated in a clinical lateral epicondylalgia patient population can be replicated in subjects with experimentally induced features simulating lateral epicondylalgia. Slater et al. (2003) have previously demonstrated that the pain-inducing effects of injecting hypertonic saline into the extensor carpi radialis brevis muscle, combined with known deep tissue sensitizing effects of delayed onset muscle soreness (DOMS), generated similar sensori-motor characteristics to those seen in patients with clinical lateral epicondylalgia; that is, pain and mechanical hyperalgesia extending along the myotendinous unit from the common extensor origin to the extensor carpi radialis brevis muscle (Slater et al., 2005); pain radiating into the dorsal forearm (Leffler et al., 2000) and attenuation of grip force (Haker, 1993; Stratford et al., 1993; Vicenzino et al., 1996; Vicenzino et al., 1998; Pienimaki et al., 2002a, b). One advantage of using an in vivo model simulating lateral epicondylalgia is that the origin of myotendinous pain and hyperalgesia and the cause of associated motor attenuation are known, and the associated sensory manifestations and motor effects are quantifiable. In contrast, clinical studies are unlikely to provide such insights as the diagnosis of lateral epicondylalgia is still sign and symptom based, and a cause–effect relationship is not clear. While clinical studies of interventions in patients with lateral epicondylalgia have provided important insights into the effects of physical treatments, the mechanisms underlying these effects have not yet been proven. Furthermore, the experimental model simulating lateral epicondylalgia provides a potential vehicle for better insight into the pain mechanisms that may mediate the clinical effects associated with the lateral glide-MWM. The aim of this experimental study was to assess the treatment effects of the lateral glide-MWM in healthy subjects with induced sensory changes and motor effects that simulate lateral epicondylalgia (via provoked

DOMS and saline-induced pain). The specific hypothesis to be tested was that in healthy subjects with experimentally induced features of lateral epicondylalgia, the lateral glide-MWM would activate mechanisms associated with analgesia and force augmentation in contrast to a placebo intervention.

2. Materials and methods 2.1. Subjects Two groups each of 12 subjects participated in the study. There were seven males and five females in the MWM group (mean age 23.0 years, range 19–31 years), and six males and six females (mean age 23.1 years, range 19–31 years) in the placebo group. All subjects were right hand dominant with the exception of two, both of whom were in the placebo group. Subjects had no history of upper limb pain, fractures or neurological disorders, were not taking any medications, had not previously received manual therapy for the upper quarter, and nor had they had previous experience of eccentric wrist extensor training. A physical examination was performed to ensure that all subjects had full pain-free range of elbow and wrist motion, and no abnormal tenderness to palpation of the soft tissues in the extensor muscles of the forearm and wrist (Travell and Simons, 1983), or abnormal muscle length. Clinical tests of wrist stability were performed (Taleisnik, 1988) as a precaution against excessive intercarpal motion during the eccentric exercise period. Written informed consent was obtained prior to inclusion in the study. The study was performed in accordance with the National Health and Medical Research Council guidelines and with the Helsinki Declaration. The Human Research Ethics Committee at Curtin University of Technology had approved the study. 2.2. Study design The study used a randomized, placebo-controlled design. For all subjects, a set of quantitative tests (PPT, muscle soreness, maximal grip force and maximal wrist extension force) was performed, and repeated at each time period (Fig. 1). The effect of combined DOMS and saline-induced pain on deep tissue sensitivity and force inhibition was assessed in the non-dominant arm. Subjects participated in three sessions (Day 0, Day 1 and Day 7). Exercise to induce DOMS was performed at Day 0. There were 23–25 h between Day 0 and Day 1 sessions. For both groups on Day 1, hypertonic saline was injected to evoke pain in the extensor carpi radialis brevis muscle of the DOMS arms. During the salineinduced pain period, either MWM or placebo intervention was administered. The intervention was therefore

ARTICLE IN PRESS H. Slater et al. / Manual Therapy 11 (2006) 107–117

Day 0

Day 1 Injection hypertonic saline

Eccentric exercise (non-dominant arm only)

Quantitative tests performed for both groups in non-dominant arm:

~ 50 minutes

109

Day 7 MWM or placebo intervention

Pain duration ~10 minutes

• Pressure pain thresholds • Muscle soreness • Maximal grip force • Maximal wrist extension force

Pre-exercise measures

Pre-injection Pre-intervention Post-intervention measures measures measures

Day 7 repeat measures

Fig. 1. All subjects performed the eccentric exercise protocol on Day 0. The day following (Day 1), subjects were injected with hypertonic saline into the extensor carpi radialis brevis muscle. During saline-induced pain, subjects received one of two test conditions: a mobilization-with-movement (MWM) or a placebo intervention. A series of quantitative tests were repeated pre exercise Day 0, and at each time point Day 1 and at Day 7.

aimed at alleviating pain associated with the combined effects of DOMS and hypertonic saline. The Day 7 session involved a repeat of pre-exercise measures for all subjects. 2.3. Saline-induced deep pain Hypertonic saline was infused using a computercontrolled pump (IVAC, model 770, USA), with a 10 ml plastic syringe (Graven-Nielsen et al., 1997a). A tube (IVAC G30303, extension set with polyethylene inner line) was connected from the syringe to the disposable needle (27G, 20 mm). A bolus injection of 1.0 ml of sterile hypertonic (5.8%) saline was injected over 40 s. The needle was removed at the completion of the injection. The site of injection in the extensor carpi radialis brevis muscle belly was identified using a technique described by Riek et al. (2000) and previously used in this model (Slater et al., 2003). Prior to injection, the posterior interosseus nerve was identified by palpation to avoid any direct contact with the nerve. The needle was inserted approximately 10 mm into the muscle belly. Saline-induced pain intensity was scored continuously on a 10 cm electronic visual analogue scale (VAS) where 0 cm indicated ‘no pain’ and 10 cm ‘most pain imaginable’. The VAS rating was sampled every 5 s by the computer. The saline-induced pain period was divided into two epochs: (1) pre-intervention and; (2) intervention. The duration of the pre-intervention period was approximately 5 min. The intervention epoch incorporated the VAS recorded whilst administering the intervention (approximately 3 min) and the period

between completion of the intervention and the termination of the pain period (approximately 2 min). The area under the VAS–time curve (VAS area), time of pain onset and duration of pain were determined from the VAS recordings. Post-intervention, subjects described the pain for the total pain period (that is, both VAS epochs) using the McGill Pain Questionnaire (MPQ) (Melzack, 1975). Words from the MPQ chosen by at least 30% of the subjects were used in data analysis. The saline-induced pain distribution as experienced by each subject was also mapped on a body chart. The circumference was later digitized (ACECAD D9000 Digitiser, Taiwan) and the area calculated in arbitrary units (Sigma-Scan, Jandel Scientific, Canada). Pain areas were also classified from the body charts as local and/or referred. Local pain was defined as a continuous area of pain that may or may not be associated with spread or radiation. Referred pain was defined as a discrete area of pain outside the local pain area (GravenNielsen et al., 1997a). 2.4. Delayed onset muscle soreness Repeated eccentric wrist extension contractions were used to provoke DOMS in the non-dominant arm. The eccentric-exercise protocol used the isokinetic mode of the Kin-Com dynamometer (Chattecx Corp. Hixson, TN). The total exercise period was 25 min, with five bouts each of 5 min duration (60 repetitions per bout), each bout separated by a minute rest interval (Slater et al., 2003). The protocol in this study is identical to that used previously and has been described elsewhere (Slater et al., 2005).



2.5. Assessment of deep tissue sensitivity PPTs were recorded using an electronic algometer (Somedic AB, Sweden) with a stimulation area of 1.0 cm2. PPT was calculated as the mean of three trials with a 30 s interval between repetitions. The pressure was increased at a rate of 30 kPa/s until the subject detected the pain threshold. Two sites were assessed: the attachment of the common extensor origin at the lateral epicondyle and the muscle belly of the extensor carpi radialis brevis muscle. 2.6. Assessment of grip force and wrist extension force Grip force was assessed using an electronic digital dynanometer (MIE Medical Research Ltd., Leeds, UK). The subject’s upper limb was positioned in pronation and elbow extension. Peak values determined the maximal grip force, and were found as the mean of three trials. Wrist extension force was recorded via a specifically designed padded hand attachment connected to a force transducer (AFG, range 0–500 N, Mecmesin Ltd., England). The transducer was mounted on a flat platform and placed on a table to the side of the plinth. The height of the hand attachment and force transducer was adjustable to allow for variations in hand sizes. The wrist was positioned in pronation and wrist extension (201) with the third knuckle abutting the centre of the hand attachment. Subjects were instructed to maximally extend the wrist by pushing the dorsal surface of the hand onto the padded surface of the hand attachment. The height of the device was noted for each subject to ensure reliable measures. Peak values determined the

maximal extension force, and were found as the mean of three trials. Subjects were requested to perform maximal contractions for each motor task. 2.7. Mobilization-with-movement intervention The lateral glide-MWM technique involved the application of a sustained force (glide) produced across the elbow joint with the force being directed against the ulna from medial to lateral, and the humerus being stabilized lateral and proximal to the elbow joint (Fig. 2). This technique is adopted from the description outlined by Mulligan (1999) and previously investigated in clinical studies (Vicenzino and Wright, 1995; Abbott et al., 2001; Vicenzino et al., 2001; Paungmali et al., 2003a). Clinical indications for use of this technique include movement-related pain or stiffness (Mulligan, 1999), features experimentally induced in the current model of lateral epicondylalgia (Slater et al., 2003). The subject lay supine with the upper limb supported on a treatment plinth. The upper limb was positioned in 201 shoulder abduction with elbow extension and forearm pronation. The lateral glide technique was coupled with an isometric gripping action performed actively by the subject. The glide was sustained throughout the 30 s bout of repeated isometric grip. This allowed six repetitions of grip within a 30 s period. The MWM was repeated on three occasions (total 90 s of MWM) with a 30 s rest between the three bouts (Fig. 2A); therefore the total intervention duration was 2.5 min. The placebo technique was the application of a constant, firm manual contact around the medial and lateral aspects of the subject’s elbow for an analogous

Fig. 2. During saline-induced pain, subjects received either a mobilization-with-movement (A), or a placebo (B) intervention. The white arrows in photograph A indicate the lateral glide force applied to the proximal ulna (1), and the stabilizing counter-force on the lateral aspect of the distal humerus (2). The technique was sustained while the subject maintained an isometric gripping action (3). The placebo condition (B), involved the application of light manual contact to the medial and lateral aspects of the subject’s elbow joint while the subject maintained a relaxed grip. For both conditions the contact was sustained for 30 s, with a 30 s interval of rest. Three bouts of each intervention were applied.


time and number of bouts as the MWM intervention (Fig. 2B). Subjects maintained a relaxed grip position throughout the placebo technique. An experienced manipulative physiotherapist performed the interventions. 2.8. Statistical analysis Based on the results of previous studies on the effects of the lateral glide-MWM in clinical lateral epicondylalgia patients (Abbott et al., 2001; Vicenzino et al., 2001; Paungmali et al., 2003a), a difference of 15% for PPT and motor force parameters was set as a conservative level to detect a significant intervention effect. Between-group differences in means and standard deviations were drawn from a previous study of clinical lateral epicondylalgia patients and matched controls using this experimental pain model (Slater et al., 2005). To achieve power of 0.80 with alpha at 0.05 required a sample size of 12 per group. Mean and standard error (SE) values are given in the text, tables and figures. A majority of measurements associated with the VAS data failed to meet the requirements of a normal distribution as determined by the Shapiro–Wilk normality test. Consequently, the non-parametric Mann–Whitney-U Test was used to compare VAS data between groups. Post-intervention VAS data (pain area and pain peak) was normalized to pre-intervention. PPT, maximal grip force and maximal wrist extension force data were normalized (100%) to pre-injection values. For analysis of PPT, maximal grip force and maximal wrist extension force, two-way repeated measures ANOVA were used, with factors ‘time’ (repeated, with two levels for pre-exercise and pre-injection; and five levels for pre-exercise-Day 7 times) and ‘group’ (between group with two levels: ‘mobilization-with-movement’ and ‘placebo’). When significant this was followed by the post hoc Student– Newman–Keuls (SNK) test. Significance was accepted at Po0:05.

111

Table 1 Effects of an acute bout of eccentric exercise on mean (SE, n ¼ 12) pressure pain thresholds, muscle soreness, maximal grip force and maximal wrist extension force for the mobilization-with-movement and placebo groups

Deep tissue soreness PPT-CEO (kPa) MWM group Placebo group PPT-ECRB (kPa) MWM group Placebo group Muscle soreness (AU) MWM group Placebo group Maximal grip force (N) MWM group Placebo group Maximal wrist extension force (N) MWM group Placebo group

Day 0 Pre-exercise

Day 1 Pre-injection

332 (52) 362 (45)

277 (54)* 251 (34)*

236 (41) 283 (33)

206 (56)* 191 (30)*

0.00 (0.00) 0.00 (0.00)

4.00 (0.17)* 3.92 (0.18)*

313 (17) 316 (23)

267 (12)* 256 (18)*

128 (12) 145 (15)

105 (11)* 110 (13)*

PPT: pressure pain threshold; CEO: Common extensor origin; ECRB: Extensor carpi radialis brevis; RH: Radial head; AU: arbitrary units. *Po0:05 (SNK) significantly different compared with pre-exercise.

(Table 1; ANOVA: F1,22 ¼ 927.8, Po0:0001). Post hoc tests revealed an increase in muscle soreness in the exercised arm at pre-injection (Day 1) compared with pre-exercise (Day 0; SNK: Po0:0001). No subjects reported pain at rest. 3.1.2. Effect of exercise on maximal grip force and maximal wrist extension force Following exercise, maximal grip force and maximal wrist extension force changed in both groups (Table 1; ANOVA: F1,22 ¼ 35.8, Po0:0001) with significant decreases at pre-injection compared with pre-exercise (SNK: Po0:001). 3.2. Effect of intervention on saline-induced deep tissue pain in DOMS arms

3. Results 3.1. Effects of eccentric exercise in mobilization-withmovement and placebo groups 3.1.1. Effects of exercise on deep tissue sensitivity PPT at the common extensor origin and the extensor carpi radialis brevis changed in both groups following eccentric exercise (Table 1; ANOVA: F1,22 ¼ 5.1, Po0:03). Post hoc tests demonstrated hyperalgesia to pressure at the common extensor origin and extensor carpi radialis brevis for both groups at pre-injection compared with pre-exercise (Day 0; SNK: Po0:03). Muscle soreness changed pre-injection in both groups

The injection of hypertonic saline into the extensor carpi radialis brevis muscle of the DOMS arms on Day 1 induced similar pain intensity and temporal characteristics between groups (Table 2 and 3; Fig. 3). In response to hypertonic saline subjects reported a localized pain response around the muscle belly with radiation of pain into the dorsolateral forearm (MWM, n ¼ 12; placebo, n ¼ 10). Pain was reported to spread proximally into the distal upper arm but only in the MWM group (n ¼ 2). Subjects reported pain referral to the distal forearm and hand (n ¼ 5 each for MWM and placebo groups; Fig. 3). The pain descriptors most commonly used were ‘‘intense’’, ‘‘aching’’ and ‘‘pressing’’. There was no


112

Table 2 Mean (SE, n ¼ 12) pre-intervention and intervention (% pre-intervention) pain intensity and peak pain following saline-induced pain in the extensor carpi radialis brevis muscle of the mobilization-with-movement and placebo groups Pre-intervention (0–300 s)

Intervention (% of pre-intervention)

VAS data

MWM group

Placebo group

MWM group

Placebo group

VASarea (cm s) VASpeak (cm)

1352.7 (166.0) 5.8 (0.6)

1427.2 (142.9) 6.1 (0.5)

41.5 (6.9) 66.7 (5.2)

40.7 (9.1) 72.4 (5.8)

AUC: area under curve; MWM: mobilization-with-movement.

Table 3 Mean (SE, n ¼ 12) VAS parameters and pain areas in response to saline-induced pain in the extensor carpi radialis brevis muscle and following intervention for the mobilization-with-movement group and placebo group VAS parameters

MWM group

Placebo group

VASonset (s) VASduration of preintervention (s) VASduration of postintervention (s) Pain area (AU) Pain descriptors (% of subjects) Intense Aching Radiating Boring Pressing

25.8 (3.1) 274.2 (3.1) 251.7 (38.0) 5.5 (1.1)

21.3 (2.8) 278.8 (2.8) 242.9 (43.3) 7.6 (2.0)

58 50 50 — 33

50 33 — 50 33

MWM: mobilization-with-movement. AU: arbitrary unit.

3.4. Effect of intervention on maximal grip force and maximal wrist extension force There was no significant force augmentation following intervention in either group. For both groups maximal grip force changed Day 1 (Fig. 6; ANOVA: F 4;88 ¼ 28:6, Po0:0001), with a significant decrease at all Day 1 times compared with Day 0 (pre-exercise) and Day 7 (SNK: Po0:001). Maximal wrist extension force demonstrated a similar change in both groups Day 1 (ANOVA: F 4;88 ¼ 30:6; Po0:0001) with a significant decrease at all Day 1 times compared with Day 0 (preexercise) and Day 7 (SNK: Po0:001). Both groups experienced a further attenuation of maximal wrist extension force on Day 1 at pre-intervention (during saline-induced pain) and at post-intervention compared with pre-injection (SNK: Po0:05). 3.5. Post hoc power analysis

apparent analgesic effect from the intervention as the spread of pain and referred pain areas were similar between groups (Table 3). 3.3. Effect of intervention on deep tissue sensitivity Intervention did not influence deep tissue sensitivity in either group. Both groups demonstrated a significant main effect for time on PPT at the common extensor origin (Fig. 4; ANOVA: F4,88 ¼ 8.9, Po0:0001), consistent with a pressure hyperalgesia at all Day 1 times compared with Day 0 (pre-exercise) and Day 7 (SNK: Po0:05). Additionally, in response to saline-induced pain (but at pre-intervention) there was a significant hypoalgesic effect at the common extensor origin in both groups compared with pre-injection values (SNK: Po0:02). The PPT at the extensor carpi radialis brevis demonstrated a main effect for time (ANOVA: F4,88 ¼ 14.4, Po0:0001), revealing pressure hyperalgesia at all Day 1 times compared with Day 0 (pre-exercise) and Day 7 (SNK: Po0:002). Muscle soreness changed at Day 1 in both groups (Fig. 5; ANOVA: F4,88 ¼ 611.9, Po0:0001), with a significant increase in muscle soreness at all times Day 1 compared with Day 0 (preexercise) and Day 7 (SNK: Po0:0001).

A post hoc power analysis of this study showed that a change of 15% would have been detected with the following probabilities: 89% for PPT; 100% for muscle soreness; for the majority of VAS parameters 483%; 97% for force parameters.

4. Discussion In the current study, the application of a lateral glideMWM intervention in healthy subjects with experimentally induced features of lateral epicondylalgia failed to elicit significant analgesia or to augment force. This is in contrast to the beneficial effects of the MWM that have been reported in patients with clinical lateral epicondylalgia. The MWM intervention may activate mechanisms that influence central sensitization as suggested to occur in clinical lateral epicondylalgia. 4.1. Sensory manifestations The current study demonstrated no significant shortterm analgesic effects in response to the lateral glideMWM intervention in subjects with experimentally


113

7 6 *

VAS (cm)

5

Injection site

4 3 2 MWM

Placebo

Pain areas

1 0 0

300

Time (sec)

600

Pre-intervention pain period Injection Intervention

900

1200

Post-intervention pain period

Pressure pain thresholds (% pre-injection)

Fig. 3. Mean (n ¼ 12) VAS profiles for two pain epochs (pre-intervention and intervention) and the associated mapped areas of pain in response to saline-induced pain in the extensor carpi radialis brevis muscle for mobilization-with-movement (black line) and placebo (grey line) groups. MWM: mobilization-with-movement intervention.

260

CEO

MWM Placebo

220 180

#

140

*

*

*

100

Pressure pain thresholds (% pre-injection)

60

260

ECRB

220 180 140 100

*

*

*

Preinjection

Preintervention

60

Preexercise Day 0

PostDay intervention 7

Day 1

Assessment time

Fig. 4. Mean (7SE, n ¼ 12) normalized pressure pain thresholds Day 0 (pre-exercise), Day 1 (pre-injection, pre-intervention, post-intervention) and at Day 7, are shown. At Day 1, hypertonic saline was injected into the extensor carpi radialis brevis muscle in both groups, and subjects received either mobilization-with-movement (MWM) or a placebo intervention during the saline-induced pain period. Pressure pain thresholds were assessed at two sites: the common extensor origin at the lateral epicondyle (CEO) and the extensor carpi radialis brevis muscle belly (ECRB). *A significant decrease in PPT for both groups at Day 1 compared with Day 0 and Day 7 times values (SNK: Po0.05); #A significant increase in PPT in both groups compared with pre-injection Day 1.

induced acute lateral epicondylalgia. Following intervention, there were no significant between-group differences in saline-induced pain intensity parameters (VAS area, peak, onset, offset and pain area). Pain profiles and the mapped areas of pain were similar to those previously demonstrated using this experimental pain model (Slater et al., 2003; Slater et al., 2005). For both groups, the decreased PPT in the myotendinous unit (comprising the extensor carpi radialis brevis and common extensor tendon origin) at pre-injection (Day 1), was consistent with an exercise-induced deep tissue hyperalgesia to pressure as previously demonstrated for this model (Slater et al., 2003). In both groups the persistence of hyperalgesia in the myotendinous unit at post-intervention, and the unchanged muscle soreness levels, indicated that the intervention had no significant analgesic effect on combined DOMS/ saline-induced pain. These findings are in contrast with those of Vicenzino et al. (2001) who demonstrated a modest but significant increase in PPT at the common extensor origin in patients with clinical lateral epicondylalgia following application of the lateral glide-MWM at the elbow. If descending pain inhibitory systems are activated by the MWM lateral glide, a generalized analgesic effect may be anticipated; however, Vicenzino et al. (2001) have demonstrated a selective and specific anti-hyperalgesic effect at the affected site (common extensor origin). This difference in effect of the lateral glide-MWM in patients with


114

MWM

Muscle soreness (AU)

6

Placebo

*

5

*

*

Preinjection

Preintervention

4 3 2 1 0 Preexercise Day 0

Postintervention

Day 7

Fig. 5. Mean (7SE, n ¼ 12) muscle soreness for all groups in response to eccentric exercise and intervention during saline-induced pain. Muscle soreness was assessed at Day 1, (pre-injection, pre-intervention and at post-intervention), and at Day 7. *A significant increase in muscle soreness compared with Day 0 (pre-exercise) and Day 7 (SNK: Po0:05), is shown for both groups. MWM: mobilization-with movement.

MWM Placebo

Maximal grip force (% of pre-injection)

140

120

*

*

*

*

#

Preinjection

PrePostDay intervention intervention 7 Day 1

Maximal wrist extension force (% of pre-injection)

80

160 140 120 100

*

#

*

80 60

Preexercise Day 0

4.2. Motor effects

Day 1

Assessment time

100

disorders (Mulligan, 1999), may be more efficacious in chronic conditions as opposed to acute pain. Alternately, in this study the effect size of the intervention may have been insufficient to effectively modulate the induced deep tissue pain, or an analgesic response may have been slow acting and therefore not demonstrated given the brief post-intervention period.

Assessment time Fig. 6. Mean (7SE; n ¼ 12) normalized maximal grip force and maximal wrist extension force at Day 0 (pre-exercise), Day 1 (preinjection, pre-intervention, post-intervention) and Day 7. *A significant decrease in maximal force, unchanged by intervention, compared with Day 0 (pre-exercise) and Day 7 is shown for both groups (SNK: Po0:05). #A significant decrease in maximal force following salineinduced pain compared with pre-injection values (SNK: Po0:05), is also demonstrated for both groups. MWM: mobilization-withmovement.

clinical lateral epicondylalgia as opposed to subjects with experimentally induced features of lateral epicondylalgia may indicate that different neural mechanisms are operating to modulate pain associated with prolonged central sensitization, as suggested to occur in patients with clinical lateral epicondylalgia (Slater et al., 2005). The lateral glide-MWM while indicated for use in movement-related pain or stiffness in musculoskeletal

For both groups, the substantial decrease in maximal grip force and maximal wrist extension force following DOMS and saline-induced pain was unaltered by the lateral glide-MWM. The absence of force-augmentation may be interpreted as a limited effect for the lateral glide-MWM in musculoskeletal pain conditions associated with partial myotendinous disruption. Given the efficient induction of DOMS in this study, it is reasonable to assume a substantial degree of ultra-structural muscle damage, and given the induced sensitization of the proximal bone–tendon junction, the possibility of additional tissue injury to the common extensor tendon. Furthermore, provoked muscle damage (DOMS) combined with additional force inhibition via saline-induced acute muscle pain will substantially compromise the contractile ability of the extensor carpi radialis brevis muscle. Attenuation of maximal force is consistent with current experimental models of muscle pain demonstrating that muscle pain can reduce maximal voluntary force (Graven-Nielsen et al., 1997b; Svensson et al., 1998; Wang et al., 2000; Slater et al., 2003; Arima et al., 2000). The fact that saline-induced pain in the extensor carpi radialis brevis further decreased the maximal wrist extension force illustrates the parallel effects of compromised peripheral contractile apparatus due to DOMS and the central inhibitory action of salineinduced pain. An intervention operating via mechanisms thought to facilitate the muscle contractile apparatus would conceivably be less effective where there is compromise of contractile elements as in the current study. 4.3. Mechanisms associated with mobilization-withmovement In this study, failure of the MWM intervention to promote analgesia and improve force capability suggests that: (1) different pain and tissue mechanisms may be involved in experimentally induced and clinical lateral epicondylalgia; (2) the lateral glide-MWM may exert different effects in the patients with clinical lateral epicondylalgia compared with the effects in subjects with experimentally induced lateral epicondylalgia; (3) the effect size of the lateral glide-MWM may be too small to be demonstrated in the experimental model of lateral epicondylalgia used in this study; (4) the post-


intervention time period was too short to measure any potential benefit of the lateral glide-MWM technique. Effective modulation of DOMS-associated pain is relevant when discussing the lack of efficacy of the lateral glide-MWM intervention in the current study. Very few interventions have demonstrated efficacy in modulating DOMS-associated pain, probably because the mechanisms underlying DOMS-associated pain are still poorly understood. In a placebo-controlled, double-blind study, high or low-intensity transcutaneous electrical nerve stimulation (TENS) demonstrated no convincing evidence of reducing DOMS-associated pain or improving function (Craig et al., 1996b). Additionally, other clinical trials have indicated that post-exercise muscle strength recovery or soreness is not affected by ultrasound treatment (Craig et al., 1999b; Plaskett et al., 1999), by acupuncture (Barlas et al., 2000b) or by combined phototherapy/low-intensity laser therapy at low pulse repetition rates (Craig et al., 1996a; Craig et al., 1999a). A lack of efficacy of selected oral systemic analgesics (aspirin, codeine, paracetamol) compared with placebo has also been demonstrated in experimentally induced muscle soreness (Barlas et al., 2000a). However, application of transdermal ketoprofen appears to be effective in reducing self-reported DOMS after repetitive muscle contraction, particularly after 48 h (Cannavino et al., 2003). Topical application of ibuprofen compared with systemic ibuprofen and placebo, has been shown to increase PPT but not pressure pain tolerance or maximal voluntary force of the masseter muscle with DOMS (Svensson et al., 1997). Similarly, the non-steroidal medications, flurbiprofen (Howell et al., 1998a) and ibuprofen (Howell et al., 1998b), were shown to be ineffective in relieving DOMSassociated pain and stiffness in trained cyclists. Modulation of deep tissue hyperalgesia and the concurrent excitation of the motor and sympathetic nervous system previously demonstrated in response to the lateral glide-MWM in patients with clinical lateral epicondylalgia has been suggested to involve descending pain inhibitory systems (Vicenzino et al., 1998; Vicenzino et al., 2001; Paungmali et al., 2003b). Additionally, in patients with clinical lateral epicondylalgia, the lateral glide-MWM has been shown to induce rapid onset analgesia that does not decay over repeated applications (Paungmali et al., 2003b), possibly indicating facilitation of non-opioid endogenous pain inhibitory systems. Animal studies have also examined the effects of manipulation-induced antihyperalgesia in an attempt to better understand the involved pain mechanisms. Skyba et al. (2003) using behavioural pharmacology techniques in an animal model of experimental pain found that following injection of capsacin into the ankle joint, rats demonstrated an increase in threshold of the mechanical withdrawal reflex for 45 min post-manipulation of the ipsilateral knee joint. Blockade of various

115

spinal receptors suggested that manipulation-induced antihyperalgesia appeared to involve descending inhibitory mechanisms that utilize both serotonin and noradrenaline as neurotransmitters. In contrast, in the same study spinal blockade of opioid or g-aminobutyric acid (GABAA) receptors had no effect on manipulationinduced antihyperalgesia. Sluka and Wright (2001) have also shown that in response to knee joint manipulation capsaicin-induced secondary mechanical hyperalgesia in rat paw is reduced. However, despite the findings of these human and animal studies, the specific mechanisms underlying the effects associated with the manual physiotherapy techniques, including the lateral glideMWM, remain largely putative. We propose that beneficial effects associated with the lateral glide-MWM in clinical studies of clinical lateral epicondylalgia are likely to be related to multiple and potentially interacting mechanisms. For example, in regard to motor mechanisms, the phenomenon of postexercise facilitation may be relevant to the improved grip force associated with the lateral glide-MWM. Muscle facilitation is achieved via a voluntary contraction of a target muscle (in the case of the lateral glideMWM there is synergistic activity of wrist flexors and wrist extensors associated with the active task of sustained gripping). Facilitation has been shown to increase the response rate, shorten latency and enhance the amplitude of motor evoked potentials post-contraction (Nørgaard et al., 2000). Post-exercise facilitation has been demonstrated to be associated with greater potentiation for sustained contraction (Lentz and Nielsen, 2002) and the facilitation persisted beyond the cessation of the contraction (Brasil-Neto et al., 1993). This post-exercise facilitation may imply that for a few seconds following muscular contraction, the excitability of the motor pathways innervating the muscle is increased, thereby facilitating repetitive movements (Nørgaard et al., 2000). In this way, the lateral glideMWM that involves a sustained gripping action may help to facilitate improved grip function. However, in the present experimental model such an effect is not likely due to the inefficient contractile elements as discussed above. Furthermore, activation of proprioceptive mechanisms via the lateral glide-MWM may contribute beneficially to joint position sense, to the sensation of force or effort of a required workload, or possibly to the perceived timing of muscle contraction. These are all important aspects of proprioception, a key sensory mechanism for motor control (Gandevia et al., 1992; Gandevia, 1994). To date, there is a lack of research investigating proprioceptive function in patients with lateral epicondylalgia and the implication of alteration of proprioceptive function on motor control strategies. Such a mechanism would be consistent with the lack of response in the current study where DOMS was



generated in the wrist extensors, and the wrist flexor group passively exercised. Altered proprioceptive input from the wrist flexor muscles would be less likely in this situation. Factors such as the role of expectation and selective attention in motor learning also need to be considered. Expectant patients (as opposed to experimentally induced pain in healthy controls) may tend to concentrate their attention on a therapeutic stimulus such as the lateral glide-MWM, thereby potentially suppressing nociceptive input and favouring a different pattern of proprioceptive input (Zusman, 2004).

5. Conclusion Based on the findings of this study, the mechanisms evoked by DOMS and saline-induced pain and the mechanisms underlying the effects of the lateral glideMWM do not match. There was no evidence of modulation of combined DOMS and saline-induced myotendinous pain in response to the lateral glideMWM intervention. It is possible that the effects of the MWM intervention are too weak to be detected or the technique is ineffective or inappropriate in this experimental pain model. Alternately, central sensitization as suggested to occur in clinical lateral epicondylalgia, may be affected by this technique and therefore explain the beneficial responses previously demonstrated. Further investigation is required in order to improve the understanding of pain and tissue mechanisms associated with lateral epicondylalgia and the mechanisms underlying the effects of specific physical therapy interventions in this musculoskeletal condition. This will allow better ‘‘matching’’ of interventions to patients with the potential for better clinical outcomes.

Acknowledgements The authors would like to acknowledge the support of the Danish National Research Foundation. References Abbott JH, Patla CE, Jensen RH. The initial effects of an elbow mobilization with movement technique on grip strength in subjects with lateral epicondylalgia. Manual Therapy 2001;6:163–9. Arima T, Svensson P, Arendt-Nielsen L. Capsaicin-induced muscle hyperalgesia in the exercised and non-exercised human masseter muscle. Journal of Orofacial Pain 2000;14:213–23. Barlas P, Craig JA, Robinson J, Walsh DM, Baxter GD, Allen JM. Managing delayed-onset muscle soreness: lack of effect of selected oral systemic analgesics. Archives of Physical Medicine and Rehabilitation 2000a;81:966–72. Barlas P, Robinson J, Allen J, Baxter GD. Lack of effect of acupuncture upon signs and symptoms of delayed onset muscle soreness. Clinical Physiology 2000b;20:449–56.

Brasil-Neto JP, Pascaul-Leone A, Valls-Sole´ J, Cammarota A, Cohen LG, Hallett M. Postexercise depression of motor evoked potentials: a measure of central nervous system fatigue. Experimental Brain Research 1993;93:181–4. Cannavino CR, Abrams J, Palinkas LA, Saglimbeni A, Bracker MD. Efficacy of transdermal ketoprofen for delayed onset muscle soreness. Clinical Journal of Sport Medicine 2003;13:200–8. Craig JA, Barlas P, Baxter GD, Walsh DM, Allen JM. Delayed-onset muscle soreness: lack of effect of combined phototherapy/lowintensity laser therapy at low pulse repetition rates. Journal of Clinical Laser Medicine and Surgery 1996a;14:375–80. Craig JA, Cunningham MB, Walsh DM, Baxter GD, Allen JM. Lack of effect of transcutaneous nerve stimulation upon experimentally induced delayed onset muscle soreness. Pain 1996b;67:285–9. Craig JA, Barron J, Walsh DM, Baxter GD. Lack of effect of combined low intensity laser therapy/phototherapy (CLILT) on delayed onset muscle soreness in humans. Lasers in Surgery and Medicine 1999a;24:223–30. Craig JA, Bradley J, Walsh DM, Baxter GD, Allen JM. Delayed onset muscle soreness: lack of effect of therapeutic ultrasound in humans. Archives of Physical Medicine and Rehabilitation 1999b;80:318–23. Gandevia SC. The sensation of effort co-varies with reflex effects on the motoneurone pool: evidence and implications. International Journal of Industrial Ergonomics 1994;13:41–9. Gandevia SC, McCloskey DI, Burke D. Kinaesthetic signals and muscle contraction. Trends in Neurosciences 1992;15:62–5. 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; 69:111–7. Graven-Nielsen T, Svensson P, Arendt-Nielsen L. Effects of experimental pain on muscle activity and coordination during static and dynamic motor function. Electroencephalography and Clinical Neurophysiology 1997b;105:154–64. Haker E. Lateral epicondylalgia: diagnosis, treatment and evaluation. Critical Reviews in Physical Medicine 1993;5:129–54. Howell JN, Conatser R, Chleboun G, Karapondo DL, Chila AG. The effects of nonsteroidal anti-inflammatory drugs on recovery from exercise-induced muscle injury 1. Flurbiprofen. Journal of Musculoskeletal Pain 1998a;6:59–68. Howell JN, Conatser R, Chleboun G, Karapondo DL, Chila AG. The effect of nonsteroidal anti-inflammatory drugs on recovery from exercise-induced muscle injury 2. Ibuprofen. Journal of Musculoskeletal Pain 1998b;6:69–83. Leffler AS, Kosek E, Hansson P. The influence of pain intensity on somatosensory perception in patients suffering from subacute/ chronic lateral epicondylalgia. European Journal of Pain 2000;4:57–71. Lentz M, Nielsen JF. Post-exercise facilitation and depression of Mwave and motor evoked potentials in healthy subjects. Clinical Neurophysiology 2002;113:1092–8. Melzack R. The McGill Pain Questionnaire: major properties and scoring methods. Pain 1975;1:277–99. Mulligan B. Manual therapy––‘NAGS’, ‘SNAGS’, ‘MWMS’, etc. Wellington, NZ: Plane View Services; 1999. Nørgaard P, Nielsen JF, Andersen H. Post-exercise facilitation of compound muscle action potentials evoked by transcranial magnetic stimulation in healthy subjects. Experimental Brain Research 2000;132:517–22. Paungmali A, O’Leary S, Souvlis T, Vicenzino B. Hypoalgesic and sympathoexcitatory effects of mobilization with movement for lateral epicondylalgia. Physical Therapy 2003a;83:374–83. Paungmali A, Vicenzino B, Smith M. Hypoalgesia induced by elbow manipulation in lateral epicondylalgia does not exhibit tolerance. Journal of Pain 2003b;4:448–54.

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ARTICLE IN PRESS


Original article

Clinical tests of musculoskeletal dysfunction in the diagnosis of cervicogenic headache G. Zitoa,, G. Jullb, I. Storyc a

School of Physiotherapy, The University of Melbourne, Vic. 3010, Australia b Division of Physiotherapy, The University of Queensland, Australia c Faculty of Health and Behavioural Sciences, Deakin University, Australia

Received 20 January 2003; received in revised form 22 March 2005; accepted 27 April 2005

Abstract Persistent intermittent headache is a common disorder and is often accompanied by neck aching or stiffness, which could infer a cervical contribution to headache. However, the incidence of cervicogenic headache is estimated to be 14–18% of all chronic headaches, highlighting the need for clear criterion of cervical musculoskeletal impairment to identify cervicogenic headache sufferers who may benefit from treatments such as manual therapy. This study examined the presence of cervical musculoskeletal impairment in 77 subjects, 27 with cervicogenic headache, 25 with migraine with aura and 25 control subjects. Assessments included a photographic measure of posture, range of movement, cervical manual examination, pressure pain thresholds, muscle length, performance in the cranio-cervical flexion test and cervical kinaesthetic sense. The results indicated that when compared to the migraine with aura and control groups who scored similarly in the tests, the cervicogenic headache group had less range of cervical flexion/extension (P ¼ 0:048) and significantly higher incidences of painful upper cervical joint dysfunction assessed by manual examination (all Po0:05) and muscle tightness (Po0:05). Sternocleidomastoid normalized EMG values were higher in the latter three stages of the cranio-cervical flexion test although they failed to reach significance. There were no between group differences for other measures. A discriminant analysis revealed that manual examination could discriminate the cervicogenic headache group from the other subjects (migraine with aura and control subjects combined) with an 80% sensitivity. r 2005 Elsevier Ltd. All rights reserved. Keywords: Cervicogenic headache; Migraine; Cervical movement; Muscle function

1. Introduction Headache is a common disorder with an estimated lifetime prevalence of 96% and a point prevalence of 16% (Rasmussen et al., 1991). Henry et al. (1987) determined that approximately 70% of persons with frequent intermittent headache report neck symptoms associated with their headache, which may encourage delivery of treatment to the cervical region. Whilst it is proposed that the cervical spine may contribute to Corresponding author. Tel.: +613 8344 4171; fax: +613 8344 4188.

E-mail address: [email protected] (G. Zito). 1356-689X/$ - see front matter r 2005 Elsevier Ltd. All rights reserved. doi:10.1016/j.math.2005.04.007

different types of headache such as migraine and tension type headache (Watson, 1995), studies estimate that only 14–18% of chronic headaches are cervicogenic, that is, headaches which actually result from musculoskeletal dysfunction in the cervical spine (Pfaffenrath and Kaube, 1990; Nilsson, 1995). There is the potential for many headache patients to receive ongoing physical treatments even when there is a high possibility that such treatments are likely to be unsuccessful (Parker et al., 1978; Tuchin et al., 2000; Astin and Ernst, 2002). The call for substantiation of efficacy of manual therapy emphasizes the need for accurate diagnosis to distinguish cervicogenic headache from other causes of

ARTICLE IN PRESS G. Zito et al. / Manual Therapy 11 (2006) 118–129

chronic headache so that the appropriate patients receive manual therapy treatment. Comparatively little research has been conducted on characterizing the physical impairments which might confirm a cervical cause. The International Headache Society (IHS) has published criteria for the classification of headache (IHS, 2004) although Sjaastad et al. (1998) has provided more detailed criteria for cervicogenic headache. Such criteria are based mainly on the history, temporal pattern and aggravating features of headache. However, there is considerable overlap in symptoms of headache of various origins. Furthermore, the musculoskeletal criteria to identify a cervical cause of headache are general in nature. More specific descriptions might assist differential diagnosis. Research has begun to identify impairments in the musculoskeletal system, which could assist in diagnosing cervicogenic headache. Studies have investigated features of the articular, muscle and neural systems. For example, Zwart (1997) using Cybex dynamometry (albeit without reported reliability), showed that cervical flexion, extension and rotation ranges were significantly less in subjects with cervicogenic headache in comparison to those with migraine and tension headache. Additionally, a number of studies have consistently linked cervicogenic headache to painful dysfunction in the upper three cervical segments (C0–3) (Trevor-Jones, 1964; Bogduk and Marsland, 1986; Bovim et al., 1992; Dreyfuss et al., 1994; Lord and Bogduk, 1996). Tenderness is also a feature. Bovim (1992) measured pressure pain thresholds (PPTs) at 10 points on the head and suboccipital region in subjects with cervicogenic, tension and migraine headaches and found that when all PPT values were summed, the score was significantly lower in the cervicogenic headache group than for the tension and migraine headache and control groups. A relationship has been proposed between a forward head posture and cervicogenic headache although the evidence is not definitive (Watson and Trott, 1993; Treleaven et al., 1994; Haughie et al., 1995). In relation to muscle function, several studies using different tests of the cervical flexor muscles have identified dysfunction in this muscle group in neck pain and headache subjects (Watson and Trott 1993; Treleaven et al., 1994; Jull et al., 1999). Two studies have noted a higher prevalence of cervico-brachial muscle tightness, assessed clinically, in cervicogenic headache subjects as compared to control subjects (Treleaven et al., 1994 Jull et al., 1999). Deficits in cervical kinaesthesia have been identified in various neck syndromes (Revel et al., 1991; Loudon et al., 1997; Heikkila¨ and Wenngren, 1998) but no studies to date have investigated cervical kinaesthesia in cervicogenic headache. There is little knowledge of the prevalence of mechanosensitive neural tissue, although its occurrence has been described (Rumore 1989) and its involvement alluded to in a

119

small pilot study, which suggested altered mechanosensitivity in patients with cervicogenic headache (Rankin, 1993). Previous studies have examined one or two features of the cervical musculoskeletal system in cervicogenic headache patients. The aim of this study therefore was to investigate the sensitivity of these tests as a group to determine if there was a pattern of musculoskeletal dysfunction, which might better characterize cervicogenic headache for differential diagnosis. Three groups of subjects were compared, cervicogenic headache, migraine with aura and a non-headache control group. Migraine with aura was chosen as there is no evidence that cervical musculoskeletal dysfunction has a role in its pathogenesis.

2. Methods 2.1. Subjects Seventy-seven female volunteers aged between 18 and 34 years were invited to join the study. The crosssectional study was conducted under single blind conditions in that the principal investigator, an experienced musculoskeletal physiotherapist, was blind to the diagnostic category of the subjects. The subjects were recruited from neurologists, general medical practitioners and musculoskeletal physiotherapists or by advertisement (control subjects). They entered one of three groups, a control group (n ¼ 25, mean age 22.973.5 years), a cervicogenic headache group (n ¼ 27, mean age 25.373.9 years) or a migraine with aura group (n ¼ 25, mean age 22.973.5 years) and comparisons between the three groups were made. Headache subjects entered their respective groups according to established diagnostic criteria for migraine with aura (IHS, 2004) and cervicogenic headache (Sjaastad et al., 1998). Anaesthetic blockades were not used as a criterion for cervicogenic headache as the procedure was considered too invasive and costly for this study and is not readily accessible to most clinicians. The total length of the history of the headache ranged from 9 months to more than 10 years (Table 1). Young subjects were selected as it is the period of life when vascular symptoms are more frequently encountered (Lance and Goadsby, 1998), and when the effects of age or disease in the musculoskeletal system are still Table 1 Total length of history of headaches

CEH Migraine

9 months–5 years

5–10 years

410 years

18 (67%) 6 (24%)

6 (22%) 10 (40%)

3 (11%) 9 (36%)


120

relatively negligible. The inclusion criteria for control subjects were no history of headache, cervical pain or injury for which they had sought treatment. Headache subjects were deemed ineligible if they had a history of combined forms of headache, were involved in compensation or, in the case of migraine with aura subjects, if they had a history of a neck injury or condition. Ethical clearance for the study was granted by the Human Research Ethics Committee of The University of Melbourne and all participants gave their informed consent. 2.2. Measurements Questionnaires: Headache subjects completed a questionnaire about the history and nature of headache to ensure they fulfilled the diagnostic criteria of their headache group (Appendix A) as well as the McGill Pain Questionnaire (Melzack, 1975). Physical examination: The sequence and content of the physical examination is summarized in Table 2. Postural measurement: A photographic measurement of posture was taken according to the method of Refshauge et al. (1994). Subjects were photographed looking straight-ahead in their natural stance using a Kodak DC50 digital camera and postural angles were calculated using NIH Image software (National Institutes of Health, USA). The cranio-vertebral angle (CV), reflecting the forward head posture position, was the acute angle created between the horizontal plane and the line from the tip of the C7 spinous process to the tragion. Head posture was measured as the acute angle

between the horizontal plane and the line from the corner of the eye to the tragion (ETH). Pressure pain thresholds (PPTs): PPTs were measured with a pressure algometer (PD&T—Italy) applied at a constant rate of approximately 1 kg/cm2/s until the subjects reported a change of sensation from pressure to pain. A familiarization session was first performed on the wrist. The following sites were identified and tested with the subject in prone lying: the areas over the C2 nerve root, the greater occipital nerve, the transverse process of C4 (Fredriksen et al., 1987; Pfaffenrath et al., 1988; Sjaastad et al., 1998) and the C2/3 zygapophyseal joint (Lord et al., 1994). Five readings were taken over each site and averaged for analysis. Range of cervical movement: A cervical range of movement device CROM (Performance Attainment Associates, St. Paul, MN, USA) was used to measure the mobility of the cervical spine (Youdas et al., 1991) using the standard protocol for upper cervical flexion/ extension, cervical flexion/extension, lateral flexion and rotation. In this study, rotation of the head was also measured in a position of full flexion of the neck as an estimate of upper cervical spine rotation (Dvorak et al., 1984). For this measure, the research assistant held the magnetic yoke of the CROM in a plane parallel to the compass on the subject’s head so that the compass meter could be seen in between the two magnetic rods. All movements were performed twice and averaged for analysis. Cervicocephalic kinaesthetic sense: The protocol of Revel et al. (1991) was used to measure the subject’s ability (while blindfolded) to relocate the natural head

Table 2 Domains of assessment Assessment

Domains

Clinical utility

Postural measurement

Eye-tragion angle (ETH) Craniovertebral angle (CV)

Head on neck posture Forward head posture position

Pressure pain threshold

Pressure points associated with CEH

Cervical range of movement

Flexion, extension, rotation lateral flexion Upper cervical rotation, lateral flexion

Cervicocephalic kinaesthetic sense Manual assessment Muscle extensibility Mechanosensitivity of neural tissues Craniocervical flexion test

C4 transverse process C2/3 z-joint C2 nerve root Greater occipital nerve

Flexion, extension, rotation O/C1, C1/2, C2/3 and C3/4 Upper trapezius, Scalenes, Levator Scapulae, Short Cx Extensors, Pec major & minor Pre-tensioning dura with upper Cx flexion whilst adding brachial plexus provocation test and SLR Progressively inner range craniocervical flexion positions head nodding tests aiming to reach and hold steadily targeted pressure (22, 24, 26, 28, 30 mm Hg) for 5 s

Decreased mobility associated with CEH Assessing repositioning error associated with cervical dysfunction hypomobility and pain associated with cervical z-joints dysfunction Muscle tightness associated with cervical dysfunction Increased sensitivity of neural tissues associated with cervical dysfunction To detect excessive synergistic activity of long neck flexors


posture (NHP) following the movements of left and right rotation, flexion and extension. The relocation error (joint position error, JPE) was the difference between the starting position and the NHP after movement. Five trials were undertaken for each movement and the average JPE was calculated for analysis. The value was the absolute error, that is, the positive and negative values (undershoot or overshoot of the target) were not considered. Manual examination of the upper cervical joints: A manual examination of the upper four cervical spine segments was conducted by the principal researcher as per the normal clinical procedure (Maitland et al., 2001). Joint motion was rated on a conventional 7-point scale (hypermobility (grades 1–3) normal (4) hypomobility (grades 5–7) as proposed by Jull et al. (1994). The subject rated verbally any pain provoked by the examination (local or referred) at any joint on an 11point scale (verbal analogue scale: VAS). To emphasize the essential differences between the groups, the joint motion rating was collapsed to a 3-point scale prior to analysis: normal (ratings 3, 4, 5), hypermobile (ratings 1, 2) and hypomobile (ratings 6, 7). Muscle extensibility: Extensibility of selected cervical and axio-scapular muscles was assessed using standard clinical tests of muscle length (Evjenth and Hamberg, 1984; Janda, 1994). Extensibility was initially rated on a 4-point scale as used by Treleaven et al. (1994), normal, slightly, moderately and very tight which, for analysis, was collapsed into a 2-point scale: normal (normal and slightly) and tight (moderate and very). Mechanosensitivity of neural tissues: Neural tissue mechanosensitivity was assessed by holding an upper cervical flexion position and then tensioning neural tissues by placing the upper and lower limbs in the brachial plexus provocation test and the straight leg raise test positions respectively (Jull, 1997). A positive test was a perceived change in tissue resistance with provocation of neck pain or headache with the added movements. The cranio-cervical flexion test: The cranio-cervical flexion test as described by Jull (2000) was used to assess the cervical flexor synergy. In a supine position, the subject performed cranio-cervical flexion (head nod) in 5 progressive stages of increasing range. They were guided by feedback from a pressure sensor positioned behind the neck (Stabilizer, Chattanooga, USA) and targeted 2 mm Hg increases in pressure from a baseline of 20 to 30 mm Hg. Each stage was held for 5 s, with a 10 s rest between stages. Myoelectric signals (EMG) were measured from the sternocleidomastoid muscles (SCM), but no direct measure of the deep neck flexors was made in this clinical study. Nevertheless, it has been shown that there are higher signal amplitudes in these muscles in neck pain patients as compared with control subjects in this test (Jull, 2000; Jull et al., 2004). The indication that

121

this is a compensatory strategy was confirmed by Falla et al. (2004) who demonstrated that this higher activity was associated with lesser measured activity in the deep neck flexors in neck pain patients. In this study, pairs of standard EMG Red-Dot Bipolar Ag–AgCl electrodes were positioned along the muscle bellies of the SCM, following skin preparation. Signals were amplified (Associated Measurements Pty Ltd., Australia, Amlab), passed through a 20–500 Hz bandwidth filter and sampled at 1000 Hz. Data were analysed with a third party software program (Igor Pro V3). The maximum root mean squared (RMS) value for signal amplitude was identified for each trace using a 1 s sliding window, incremented in 100 m s steps. RMS values were normalized for each subject to the RMS of the resting level for that subject. Subjects first practised the cranio-cervical flexion test and then performed the test formally for measurement. Repeatability tests: Prior to the commencement of the main study, the principal investigator undertook repeatability studies for each measure. The ranges of the ICC and Kappa scores for the tests are summarized in Table 3. The results indicated that there was acceptable intra-examiner repeatability for the measures used in this study. 2.3. Procedure All potential subjects completed the questionnaire to confirm that they met the inclusion criteria for their relevant group and that they were asymptomatic at the time of testing. The principal investigator performed the measurements in the same sequence for all subjects and was blinded to the subject’s group status. 2.4. Statistical methods w2-tests were used to analyse the data obtained from manual examination and tests of muscle extensibility. The data for neural tissue mechanosensitivity were analysed descriptively. One-way analysis of variance (ANOVA) was used for all other data. The level of Table 3 Summary of the ranges of ICC and Kappa scores for the reliability studies Test

ICC value range

Postural angles Pressure pain thresholds Cervico-cephalic kinesthetic sense Range of movement Manual examinatiom (Jull et al., 1997) Muscle extensibility

0.96–0.99 0.82–0.98 0.51–0.62

Kappa score range

0.86–0.97 0.78–1.0 0.4–1.0


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significance was set at Pp0:05. A discriminant function analysis was conducted to determine if any physical measures discriminated cervicogenic headache from the migraine with aura and control subjects.

All subjects fulfilled the inclusion criteria for their diagnostic classification and the groups were deemed to be representative of cervicogenic headache, migraine with aura and asymptomatic control populations. The data for the postural, PPT and JPE are presented in Table 4. The results of the analyses of variance showed no significant between group differences in postural angles and no relationship between CV angle and ETH angle was evident. There were no between group differences in PPTs with the exception of the area over the transverse process of C4 where both the headache groups had significantly lower PPTs than did the control group (Po0:05). There were no significant between group differences in JPEs in any movement. The data for the measurement of cervical range of movement are presented in Fig. 1. The cervicogenic headache group demonstrated consistently less movement than the migraine and control groups, although this was statistically significant only for cervical flexion/ extension (P ¼ 0:048). The frequency of findings of painful and stiff joints in the manual examination for the three groups is presented in Table 5. As can be observed, the cervicogenic headache group had a high incidence of pain associated with joint hypomobility

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Subject groups Measurements

Controls (n ¼ 25)

Cervicogenic (n ¼ 27)

Migraine (n ¼ 25)

Posture (deg)

CV angle ETH

50.3 (4.6) 13.0 (5.7)

51.1 (5.8) 15.2 (5.0)

53.3 (3.9) 15.9 (4.9)

PPTs (kg/cm2)

C2 GON C2-3 C4 TP

3.2 4.9 3.6 4.5

3.3 4.3 3.4 3.9

3.0 4.5 3.3 3.8

JPE

Flexion Extension (L) rotation (R) rotation

4.1 (1.9) 5.2 (2.1) 6.1 (2.1)

4.3 (2.0) 5.4 (2.7) 5.6 (2.6)

4.3 (1.7) 5.3 (2.7) 5.5 (2.7)

6.2 (2.8)

5.3 (2.5)

4.7 (2.6)

(1.0) (1.6) (1.1) (1.2)

(1.1) (1.4) (1.0) (1.1)*

GON greater occipital nerve; TP transverse process. po0:05.

(1.1) (2.0) (1.2) (1.2)*

120 100 80 60 40 20 0 UppCx Flex/Ext

Flex/Ext

Lat Flex

Rotation

UpperCx Rot

Direction of movement Fig. 1. The mean ranges of movement (degrees).

Table 5 The frequency of hypomobile and painful segments and pain score in each subject group Level

Groupa

Stiff and painful segments

Average VAS score

O/C1

Control Cervicogenic Migraine Control Cervicogenic Migraine Control Cervicogenic Migraine Control Cervicogenic Migraine

12 38 14 10 39 14 4 26 10 2 11 8

2 5 2 2 5 2 1 3 2 1 2 1

C1/2

C2/3

C3/4 Table 4 The means (SD) for the postural angles, pressure pain thresholds (PPTs) and joint position errors (JPE) in the tests of kinaesthetic sensibility for the three subject groups

Controls Cervicogenic Migraine

140

Mean range (degrees)

3. Results

180

Subjects could be assessed to have hypomobility at one or more segments. Note two joints (left and right sides) were assessed for each segment. a Control (n ¼ 50), cervicogenic (n ¼ 54), migraine (50).

while in contrast the incidence in both the control and migraine groups was relatively low. The majority of joints in these latter two groups were rated as normal motion (88% control group and 84% migraine with aura group). The analyses (w2) confirmed the observed differences for the cervicogenic headache group for all segments when compared to the migraine and control groups (all Po0:05). Similarly pain was provoked more frequently and to a greater extent in the manual joint examination in the cervicogenic headache group (all Po0:005) with the exception of the C3–4 segment, the segment with least perceived dysfunction in any group (Table 5). It should be noted that whilst all hypomobile joints were not necessarily painful, all painful joints were hypomobile.


The frequency of muscle tightness in each group is presented in Fig. 2. The findings of bilateral muscles have been summed and results expressed as a percentage for that muscle. There was a statistically significant difference (w2) between the incidence of tightness in the cervicogenic headache group compared to the migraine and control groups for the upper trapezius (P ¼ 0:003), levator scapulae (P ¼ 0:001), scalenes (P ¼ 0:001) and the suboccipital extensors (P ¼ 0:035) but not for the pectoral muscles. The finding of mechanosensitivity of neural tissue was rare. Positive findings (increased resistance with provocation of pain) were only determined in two of the 27 cervicogenic headache subjects (7.4%) and in no subjects in the migraine or control groups. One cervicogenic headache subject complained of reproduction of the headache with the addition of the straight leg raise test and the other complained of reproduction of the headache, neck and arm symptoms with the addition of the upper limb tension test. Fig. 3 presents the change in normalized EMG activity in each stage of the cranio-cervical flexion test for the three subject groups. The cervicogenic headache group displayed higher normalized RMS values for signal amplitude in the SCM than the migraine or control groups at the 26, 28 and 30 mm Hg test targets, but the differences did not reach statistical significance possibly reflecting the between subject variance. For the discriminant analysis, the averages of the left and right measurements for each test were used along with other predictors to identify which test would classify cervicogenic headache subjects from migraine with aura subjects and asymptomatic volunteers. The eigenvalue for the discriminant function was 0.462 and the only variable selected for weighting was the palpatory finding at the C1/2 level. Classifications using this discriminant function gave poor results with only 25

Controls Cervicogenic Migraine

Frequency of occurrence

20

15

10

5

0 U Trap

Lev Scap

Scalenes

Sub-occ ext

Pec Maj

Pec Min

Muscles Fig. 2. Frequency (percentage) of muscle tightness in the three subject groups.

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half of the cases correctly classified as compared to one third expected by chance. This level of classification could reflect the fact that 56% of the cases from the migraine with aura group were classified with the control group. The discriminant analysis was therefore repeated combining the control and migraine with aura subjects into one group. With this regrouping, the classification rate was improved with 80% of cases correctly identified on the basis of the manual palpatory finding at C1/2 level and the muscle length of pectoralis minor.

4. Discussion Clinical signs of impairment in the articular and muscle systems identified the cervicogenic headache subjects in this study from the migraine and control subjects. However, no differences were evident between the groups with respect to static posture, PPTs mechanosensitivity of neural tissues, and measures of cervical kinaesthetic sense. The results of this study determined that range of cervical movement was reduced in the cervicogenic headache subjects, albeit significant for flexion and extension only. This finding of reduced movement supports the current criteria for cervicogenic headache (Sjaastad et al., 1998; IHS, 2004). Furthermore, our results reflect those of Zwart (1997) who likewise identified reduced neck motion in cervicogenic headache subjects but found similar motion in migraine and nonheadache control groups. The presence of painful segmental dysfunction in the upper three cervical joints as detected with manual examination most clearly identified the cervicogenic headache subjects in this study. The upper cervical segments in both the control and migraine groups were rated as normal and non-painful for the vast majority of joints assessed. Gijsberts et al. (1999) also found that manual examination successfully identified the 38 cervicogenic headache subjects within a cohort of 105 headache subjects on the basis of painful joint dysfunction. Upper cervical joint arthropathy is regarded as a common cause of cervicogenic headache (Trevor-Jones, 1964; Bogduk and Marsland, 1986; Bovim et al., 1992; Dreyfuss et al., 1994; Lord and Bogduk, 1996) but there is no evidence of its role in the pathogenesis of migraine with aura. This is supported in this study by the lack of finding of painful segmental dysfunction in the migraine subjects, who were no different from control subjects. There were no group differences in measures of PPTs over sites in the cervical region, except for those over the C4 transverse process where both the migraine with aura and cervicogenic headache groups had lower PPTs than the control groups. This was a curious finding given the higher pain scores in the cervicogenic headache group


124

EMG amplitude (percent of value at 20 mm Hg)

300 Pressure 20.00 22.00 24.00 26.00 28.00 30.00

250

Standard deviations Control Cervico Migraine 59.52 76.28 56.13 50.42 105.10 78.30 96.03 193.61 93.46 115.20 269.64 87.93 142.80 268.94 80.94 180.10 296.90 115.37

200

150

Control Cervico Migraine 100 20

22

24

26 Pressure (mm Hg)

28

30

32

Fig. 3. Normalized EMG activity for sternocleidomastoid in each stage of the cranio-cervical flexion test for the three subject groups.

on manual examination and the findings of reduced PPTs in other studies of cervicogenic headache and migraine (Bovim, 1992). In relation to the muscle system, the incidence of muscle tightness was significantly higher in the cervicogenic headache group (34.9% of all muscle length tests) than the migraine with aura or controls groups, where the incidence was low (16.7% and 16.3%, respectively). No one cervico-brachial muscle predominated and tightness in the pectoral muscles was not common in the cohort of this study. These findings concur with those of Treleaven et al. (1994) and Jull et al. (1999). The cervicogenic headache group also demonstrated poorer performance in the cranio-cervical flexion test, as indicated by the higher RMS values for signal amplitude for the SCM, which were evident in the latter three stages of the test. However, these differences failed to reach significance and this possibly reflects the large variance and the patient sample size in this study. The higher RMS values for signal amplitude of the SCM indicate an altered pattern within the neck flexor

synergy which infers a poorer contractile capacity of the deep neck flexors in patients with cervical disorders (Jull et al., 1999; Jull, 2000; Falla, 2004; Falla et al., 2004; Jull et al., 2004). The dura mater of the upper spinal cord and posterior cranial fossa are supplied by the upper cervical nerves and thus are capable of contributing to a cervicogenic headache syndrome. However, the occurrence of positive tests for mechanosensitivity of neural structures was rare and occurred in only two subjects in the cervicogenic headache group (7.4%) in this study. No positive tests were determined in the migraine with aura or control subjects. A low incidence of mechanosensitivity of neural structures (10%) was also determined by Jull (2001) in a study of 200 cervicogenic subjects. No between group differences were found in the static postural measurements of forward head posture (CV angle) and head inclination (ETH). This is in contrast to other studies (Watson and Trott, 1993) but parallels the findings of Treleaven et al. (1994). In common, this current study and that of Treleaven et al. (1994) tested


younger subjects, and it is possible that postural factors may only be involved in an older subject cohort, as it is known that the FHP is age related (Dalton and Coutts 1994). No between group differences were found in cervical kinaesthetic sense (JPE). This could also be a factor of the age group studied, or could possibly relate to the extent of the cervical pathology. For example, Sterling et al. (2004) found that only whiplash subjects with higher levels of pain and disability indicative of more severe injuries demonstrated kinaesthetic deficits whereas those with lesser scores of pain and disability did not. A discriminant function analysis was used to determine if there were physical measures, which most discriminated cervicogenic headache from the migraine and control subjects. Not unexpectedly, when considering the overall results of this study, the analysis confirmed that the factors of upper cervical joint dysfunction, principally at the C1/2 segment and pectoralis minor muscle length, were able to discriminate the cervicogenic headache group from the migraine and control subjects (as a whole) with a sensitivity of 80%. A current criterion for diagnosis of cervicogenic headache is the elimination of headache by anaesthetic blocks nerve or joint blocks (Sjaastad et al., 1998). Manual examination could be considered as a simple, conservative and inexpensive clinical alternative to anaesthetic blocks for the large population of headache sufferers to diagnose the presence of painful joint dysfunction through pain provocation. In this respect, this study adds to the evidence of other studies of the

sensitivity of manual examination for this purpose (Jull et al., 1988, 1997; Gijsberts et al., 1999).

5. Conclusion This study determined that the presence of upper cervical joint dysfunction most clearly differentiated the cervicogenic headache sufferers from those with migraine with aura and control subjects. The cervicogenic headache group also presented with restriction in cervical motion, a higher frequency of muscle tightness and a poorer (albeit non significant) performance at the higher levels of the cranio-cervical flexion. Such musculoskeletal dysfunction was not apparent in the group with migraine with aura who did not differ from the control group. These musculoskeletal criteria are in accordance with, but better define those listed by the IHS (2004). Identification of these physical impairments in the musculoskeletal system linked to clinical features will contribute to the justification and selection of treatment for cervicogenic headache. Further work is necessary to address issues of generalizability and reliability of these results.

Acknowledgements The authors would like to acknowledge the invaluable contributions of Mrs. Robin Zito and Dr Ross Darnell (statistician) to this study.

Appendix A. Subjective questionnaire for headache subjects

Reference number: Name: Diagnostic group: Date of birth: Date of examination:

(1) Cx/Ha / /

125

(2) Migraine / /

1. PLEASE SHADE IN WHERE YOU FEEL YOUR HEAD/NECK SYMPTOMS


126

2. Do you suffer any of the following symptoms with your headache? NEVER a)

Neck pain

b)

Pins and needles or numbness

c)

Dizziness

d)

Ringing in ears

e)

Sight disturbances (blurring/double vision)

f)

Associated vomiting

g)

Associated nausea

h)

Other, please specify

OCCASIONALLY

ALWAYS

Comments:

3(i)

DO YOU HAVE ANY WARNING SIGNS THAT YOU ARE ABOUT HAVE A HEADACHE EPISODE ?

3(ii)

HOW LONG DO THE WARNING SIGNS LAST?

YES

NO

Hours ............... Mins.. ..............

3(iii) IF YOU HAVE WARNING SIGNS PLEASE DESCRIBE THEM

3(iv) IF YOU HAVE WARNING SIGNS, DO YOUR HEADACHES COMMENCE IMMEDIATELY AFTER THE WARNING SIGNS SETTLE ?

YES

NO

4. ARE YOUR HEADACHES/NECK PAINS MADE WORSE BY ANY OF THE FOLLOWING: a)

Turning your head?

...............................................................................................

b)

Reading or watching TV? ......................................................................................

c)

Looking up? ............................................................................................................

d)

Driving? ...................................................................................................................

e)

Stress / tension? .......................................................................................................

f)

Tying back your hair? ............................................................................................

g)

Menstruation ? .........................................................................................................

h)

Certain types of food / drink?

i)

...............................................................................

Other triggers? ....................................................................................................... Please specify

5.

HOW LONG DO YOUR HEADACHES LAST? a)

1 - 3 hours ................................................................................................................

b)

3 - 6 hours ...............................................................................................................

c)

6 - 12 hours .............................................................................................................

d)

12 - 24 hours ...........................................................................................................

e)

Other ........................................................................................................................


6(i)

127

ARE YOU ABLE TO DO SOMETHING TO RELIEVE YOUR SYMPTOMS?

6(ii)

a)

Yes ..........................................................................................................................

b)

No ...........................................................................................................................

IF YES, WHAT DO YOU DO? a)

7.

Find an easing position

........................................................................................

b)

Put on a collar, or other support.........................................................................

c)

Take medication ...................................................................................................

d)

None of the above.................................................................................................

HOW DO YOU CONSIDER YOUR GENERAL STATE OF HEALTH? a)

8(i)

Good .......................................................................................................................

b)

Moderate ................................................................................................................

c)

Poor ........................................................................................................................

ARE YOU TAKING ANY MEDICATION FOR YOUR SYMPTOMS?

8(ii)

a)

Yes ..........................................................................................................................

b)

No ...........................................................................................................................

ARE YOU/HAVE YOU BEEN TAKING ANY OTHER MEDICATION ? a)

No ...........................................................................................................................

b)

Yes .......................................................................................................................... Please specify: ______________________________________________________ ___________________________________________________________________

9(i)

HAVE YOU HAD ANY X-RAYS OF YOUR HEAD OR NECK TAKEN?

9(ii)

a)

Yes ..........................................................................................................................

b)

No ...........................................................................................................................

IF YES, WHERE? _________________________________________________________________________

9(iii) WHAT WAS THE RESULT GIVEN TO YOU _________________________________________________________________________ _________________________________________________________________________

10.

CAN YOU RELATE YOUR HEADACHES/NECK PAINS TO HAVE STARTED WITH: Yes a)

An accident (eg, motor car, sporting, fall) .................................................

b)

Following illness...........................................................................................

c)

Following stress............................................................................................

d)

Prolonged sessions at the computer .........................................................

e)

Following adverse events, please specify .................................................

f)

Other ..............................................................................................................

g)

Cannot relate to anything ............................................................................

No


128

11.

12.

13.

14.

DID YOUR PROBLEM START: a)

Suddenly? ..............................................................................................................

b)

Gradually?.............................................................................................................

FOR HOW LONG HAVE YOU SUFFERED FROM HEADACHES? a)

6 months or less....................................................................................................

b)

6 months to one year ............................................................................................

c)

1 year to 5 years....................................................................................................

d)

5 years to 10 years .................................................................................................

e)

Longer (Specify) ....................................................................................................

HAVE YOU HAD ANY PREVIOUS TREATMENT FOR YOUR HEADACHES/ NECK PAINS? a)

Yes ..........................................................................................................................

b)

No ...........................................................................................................................

WHAT WAS THE NATURE OF THE TREATMENT? a)

15.

16.

b)

Medicines/tablets .................................................................................................

c)

Heat/ice and exercise ..........................................................................................

d)

Mobilization/manipulation ................................................................................

e)

Other, please specify ............................................................................................

WHAT WAS THE OUTCOME OF PREVIOUS TREATMENT YOU RECEIVED? a)

Improvement (state %)........................................................................................

b)

No difference.........................................................................................................

c)

Aggravation (state %) ..........................................................................................

OVERALL, IS YOUR CONDITION: a)

17.

Advice....................................................................................................................

Getting better?.......................................................................................................

b)

Getting worse?......................................................................................................

c)

Not changing.........................................................................................................

ARE YOU REGULARLY INVOLVED IN SPORT? a) b)

No ........................................................................................................................... Yes .......................................................................................................................... Please specify: ______________________________________________________ ___________________________________________________________________

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ARTICLE IN PRESS


Original article

Mulligan bent leg raise technique—a preliminary randomized trial of immediate effects after a single intervention Toby Hall, Sonja Hardt, Axel Scha¨fer, Lena Wallin School of Physiotherapy, Curtin University of Technology, Bentley, Western Australia Received 20 May 2004; received in revised form 1 April 2005; accepted 27 April 2005

Abstract The aim of this study was to investigate the effects over 24 h, on range of motion and pain, of a single intervention of Mulligan’s bent leg raise (BLR) technique in subjects with limited straight leg raise (SLR) and low back pain (LBP). Mulligan techniques are frequently used in practice but their effectiveness has not been adequately researched. Ninety-four subjects were contacted by telephone and 46 volunteered for assessment. Of these, 24 fulfilled inclusion criteria of unilateral SLR limitation and LBP. All subjects were naı¨ ve to physiotherapy, blinded, and randomly allocated to either a BLR (n ¼ 12) or placebo group (n ¼ 12). Range of SLR was measured by an assessor blind to group allocation, prior to, immediately following, and 24 h after the intervention. Similarly pain was assessed prior to, and 24 h after the intervention. After adjusting for differences in baseline values of SLR range, there was no difference between the two groups immediately after the intervention. However, 24 h later, there was a significant increase in the range by 71 in the BLR group, which may be clinically important. In addition there was a one-point reduction in pain, but no difference between groups. This preliminary study provides limited support for the use of the BLR technique; however, further research is required. r 2005 Elsevier Ltd. All rights reserved. Keywords: Low back pain; Manual therapy; Straight leg raise; Mulligan

1. Introduction Mulligan (1999) manual therapy treatment techniques are frequently used in clinical practice. Konstantinou et al. (2002), reported that in Britain, according to a postal survey, 41% of physiotherapists treated low back pain (LBP) using Mulligan techniques. In spite of its popularity, the efficacy of the Mulligan Concept has not been adequately established by clinical trials. The Mulligan bent leg raise (BLR) technique has been described as a means of improving range of straight leg raise (SLR) in subjects with LBP and/or referred thigh pain (Mulligan, 1999). The intention of this technique is to restore normal mobility and reduce LBP and physical Corresponding author. 81 Northwood Street, West Leederville, Perth, Western Australia 6007. Tel.: +61 8 93811863. E-mail address: [email protected] (T. Hall).


impairment. Impairment is defined as abnormalities of structure or function, as indicated by signs or symptoms (American Physical Therapy Association, 2001). Several authors have stated that in general terms the link between pain and impairment is weak (Strong, 2002; Waddell, 1998). In contrast, the SLR test is one impairment which has been linked to LBP (Deville et al., 2000; Deyo et al., 1992; Grieve, 1970; Meszaros et al., 2000). However, according to others, this test has poor correlation with respect to disability (Hazard et al., 1994; Nattrass et al., 1999). It has been suggested that improving SLR mobility reduces the degree of impairment in LBP (Blunt et al., 1997; Hall et al., 2001; Hanten and Chandler, 1994). Unfortunately, there is no research evidence to support these conjectures. In addition, it has become increasingly recognized, that although mobilization has a place to play in the management of LBP (Bronfort et al.,

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2004), there is disagreement as to how it should be used (Koes et al., 2001). Hence physiotherapists use a range of different approaches to manage LBP (Gracey et al., 2002). Physiotherapists routinely reassess patients immediately post-treatment. This information guides treatment selection and predicts possible longer-term outcomes (Hahne et al., 2004). The SLR test is a useful measure, in this regard, because immediate effects of treatment can be determined. In contrast, other forms of assessment, such as functional disability questionnaires, are difficult to be used in this context. The SLR test has biomechanical effects on pelvis movement, on lumbosacral neural structures (Breig and Troup, 1979; Butler, 1991) and hamstring muscles (Burns and Mierau, 1997). Hence, it is important when investigating SLR to evaluate the component movements that include hip flexion and posterior pelvic rotation (Hall et al., 2001). The aim of this study was to investigate the immediate effect of a single intervention of the Mulligan BLR technique on pain and range of movement in subjects with LBP.

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Assessed for eligibility Via telephone (N=94) Excluded - Not meeting inclusion criteria or unsuitable (n=48) Physical assessment (n=46) Excluded - Not meeting inclusion criteria or unsuitable (n=22) Randomized (N=24)

Allocation Intervention (N=12) 7 female, 5 male

Allocation Placebo (N=12) 8 female, 4 male

Post-test (N=12)

Post-test (N=12)

Fig. 1. Flow diagram demonstrating progress of participants through the study.

2.2. Variables 2. Methods This small-scale prospective, explanatory, doubleblind, randomized placebo-controlled trial compared the immediate effects of the BLR technique to a placebo. Curtin University Human Research Ethics Committee gave ethical approval for the study. All data collection was carried out at this facility. Hypotheses were that the BLR technique would improve range of SLR and reduce pain, greater than a placebo and that any change in range would be maintained 24 h later.

Independent variables were treatment (BLR, placebo) and time (pre, post, follow-up). Dependent variables were range of SLR, pelvic rotation and hip flexion at the onset of pain as well as average pain intensity over 24 h. Range of SLR and pelvic rotation were measured by two bubble inclinometers (Chattanooga Group Baseline, Hixson, TN 37343, USA), with an accuracy of 11. Range of hip flexion was calculated by subtracting pelvic rotation from SLR. Pain was measured using a 10 cm visual analogue scale (VAS) (Scott and Huskisson, 1979). 2.3. Procedures and randomization

2.1. Subjects Ninety-four participants volunteered for the study, following local community advertising. In effect this group were self-selected. Fig. 1 demonstrates the flow chart for subject entry and subsequent passage through the study. All subjects were contacted by telephone and those with LBP and/or thigh pain (Mulligan, 1999) were invited to be physically assessed for inclusion in the study. Subsequently participants were included if they had a unilateral limitation of SLR more than 151. Exclusion criteria were the presence of clinical features of lower quarter neurological compromise (Hall and Elvey, 2004). Twenty-four subjects were identified as fitting the entry criteria and provided informed consent.

Subjects were randomly assigned to either BLR or placebo group, by lottery ticket picked at random from a concealed container. Two examiners, blinded to group allocation, performed all measurements. The participants were asked to lie with one leg on each side of a vertical board. A modified ankle foot orthosis (AFO) was used to maintain the ankle in neutral plantargrade, while a rigid knee extension brace was used to maintain the knee in full extension (Fig. 2). Range of SLR and pelvic-rotation were recorded, before, immediately after and 24 h following the treatment. The subject was asked to indicate their average level of pain 24 h prior to and 24 h following the intervention.


T. Hall et al. / Manual Therapy 11 (2006) 130–135

2.4. Statistical analysis

Fig. 2. Measuremant apparatus.

All statistical testing was carried out using the Statistical Package for Social Science version 11.0 software. Differences were considered statistically significant at po0:05. An analysis of variance was used to determine the effect of treatment on pain and range of SLR immediately after the intervention and after 24 h follow-up, after adjusting for unbalanced baseline values. To ensure that the assumptions of the analysis of variance were satisfied, the residuals from each analysis were assessed for normality using the Kolmogorov–Smirnov and the Shapiro–Wilk tests. In addition, homogeneity of variances’ were tested using Levene’s test. An intra-tester reliability assessment was performed on the first 10 participants. Measurement of SLR and pelvic rotation were recorded, all equipment removed, re-applied, and further measures taken. Intraclass Correlation Coefficients (ICC) for SLR was 0.99 (SD 1.2, SEM .12, 95% confidence interval 0.96–0.99) and for pelvic rotation was 0.98 (SD 8.9, SEM 1.3, 95% confidence interval 0.92–0.99).

3. Results

Fig. 3. Mulligan BLR technique.

After measuring ROM, the two investigators left the room and a third investigator carried out the randomization process. This investigator, trained in the use of Mulligan techniques by an accredited Mulligan Concept teacher, carried out the assigned intervention before the first two investigators returned for subsequent remeasurement. The BLR technique (Mulligan, 1999) consisted of three repetitions of pain-free, 5 s, isometric contraction of the hamstrings, performed in five progressively greater positions of hip flexion (Fig. 3). The placebo consisted of soft tissue manipulation of the foot, with the knee flexed to 201. At the completion of the investigation subjects were asked if they thought they were in the BLR or placebo group, in order to assess the efficacy of the blinding. Six of 12 participants in the placebo group and seven of 12 in the BLR group believed to have had received the ‘‘real’’ treatment. Therefore, we concluded that the blinding of the participants was successful.

The BLR group contained 12 subjects (mean age 41716 years, VAS score 3/1072) and the placebo group 12 subjects (mean age 48713 years, VAS score 3/ 1072). Although the mean ages were statistically different, the small difference was not deemed clinically relevant. The descriptive statistics for raw measurements of SLR, pelvic rotation and hip flexion are shown in Table 1. Table 1 shows that there was a large difference, between the groups, at baseline assessment, for mean range of SLR and subsequently hip flexion and pelvic rotation. When accounting for this baseline difference, the results indicate, that the BLR technique did not have a significant effect on range of SLR (p ¼ 0:24), immediately after treatment. The adjusted means are shown in Table 2. The difference between these adjusted means was only 31. A power calculation was carried out to determine the sample size required to detect a significant difference between the two groups at this point (a ¼ :05, power ¼ 0:8). A minimum of 20 subjects in each group is recommended. In contrast, again after adjustment, the results 24 h after intervention indicate that the BLR technique had a significant effect on range of SLR (f value ¼ 5.87; p ¼ 0:025). The adjusted means are shown in Table 2. The adjusted mean difference between the two groups, at this point, was 71, the standard error of mean was 31

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Table 1 Descriptive statistics for unadjusted range of SLR, pelvic rotation and hip flexion Group

SLR1 (SEM)

BLR Placebo

Hip flexion1 (SEM)

Pelvic rotation1 (SEM)

Pre

Post

24 h

Pre

Post

24 h

Pre

Post

24 h

34(5) 49(4)

45(3) 54(4)

47(3) 54(4)

26(2) 38(1)

33(2) 42(2)

35(2) 41(2)

9(4) 11(3)

12(2) 12(4)

12(3) 12(3)

Key: SEM—standard error mean.

Table 2 Adjusted means for SLR immediately following the intervention Group

BLR Placebo

Mean SLR1 (SEM, 95% confidence interval) Immediately after intervention

24 h after intervention

51 (1.8, 48–55) 48 (1.8, 44–52)

54 (1.9, 50–58) 47 (1.9, 43–51)

Key: SEM—standard error mean.

and the 95% confidence interval for the difference was 1–131. The residuals from both the above analysis were normally distributed and the assumption of homogeneity of variance was satisfied. 3.1. Pain outcome In both groups the VAS pain scores significantly 1 reduced by 10 following the intervention (f value ¼ 7.71, po:01). However, the BLR technique was no more effective than the placebo (f value ¼ 0.205, po0:65). 3.2. Pelvic rotation and hip flexion We wanted to know the proportion of hip flexion and pelvis rotation influencing the SLR range in the BLR group. From the unadjusted data, we calculated the improvement of SLR is 70% due to hip flexion and 30% due to pelvic rotation.

4. Discussion Baseline values for range of SLR were different between the two groups. Presumably due to the small sample size and randomization. After adjusting for these differences, this study demonstrated a significant difference of 71 in range of SLR, 24 h following the intervention, between the BLR and placebo group. However, the difference was only 31 immediately after the intervention. Dixon and Keating (2000) suggest that improvement in range of SLR must be greater than 61 to

state that a real change in SLR range has occurred. Consequently, the change in range produced by the BLR group is of clinical relevance only 24 h after the intervention. Some caution is advised when interpreting these results, as the sample size was small and selfselected so the external validity is questionable. A number of studies have investigated techniques to improve range of SLR in asymptomatic samples (Clark et al., 1999; Hall et al., 2001; Sullivan et al., 1992; Worrell et al., 1994). The improvement in range determined in these studies ranged from 81 to 131. Only two other studies, known to us, have investigated the effect of treatment interventions on SLR range in subjects with LBP (Beyerlein et al., 2002; Meszaros et al., 2000). Improvement in SLR range was 111 (Beyerlein et al., 2002) and 81 (Meszaros et al., 2000). However, these studies did not incorporate a placebo or control group. It is uncertain why, in our study, improvement in range of SLR was effective 24 h after but not immediately after the intervention (after accounting for differences in baseline measures). No previous studies have investigated the BLR technique, but other Mulligan techniques designed to improve range of SLR show immediate improvements after the intervention (Beyerlein et al., 2002; Hall et al., 2001). Again, one explanation may be the small sample size and unequal range of SLR prior to the intervention. This study found that a placebo technique increased range of SLR. This gain is unlikely to be due to repeated application of SLR as previous studies have shown a limited conditioning effect of only 11 per trial with repeated measures of SLR (Taylor et al., 1990). As the placebo was not aimed at structures that could have a mechanical effect on SLR range, we assume that this improvement was a true placebo effect. The placebo response is known to be associated with conditioning and expectancy, involving activation of the limbic system and triggering analgesic centres (Wall, 1994). It is inevitable, like all manual therapy, that the BLR technique will also have a placebo response. However, 24 h after the intervention, there was a difference of 71 SLR, between the two groups. This indicates that the true effect of the BLR technique was 71, which is of clinically significant importance.


T. Hall et al. / Manual Therapy 11 (2006) 130–135

Both the BLR and the placebo significantly reduced pain after the intervention, but there was no difference between groups, and the improvement was only one on the VAS. Farrar, 2000 state that a pain reduction of 50% is considered to be a clinically significant outcome of a treatment programme, a reduction not achieved in the present study as only a single episode of treatment was given. In addition both groups had very low 3 baseline pain levels, with an average of 10 on the VAS. Clinically significant pain reduction is not to be expected when pain is at a relatively low level to begin with (Rowbotham, 2001). The small sample size probably also contributes to this result. A larger sample size, undergoing a complete treatment programme, would be required to determine any benefit the BLR technique might have on pain. Improvement of SLR range, by the BLR technique, might be due to mobilization of the painful, sensitized, nerve tissues, similar to the ‘‘slider’’ effects described by Butler (1991) and Elvey and Hall (1997). However, it is unlikely that this is the main treatment benefit; in a comparable LBP sample with SLR limitation, only onethird of the subjects had signs of sensitized neural tissue (Beyerlein et al., 2002). Another beneficial effect of the BLR technique might be a change in stretch tolerance of the hamstrings. Goeken and Hof (1994) demonstrated that the increased range of SLR, following stretching, is mediated via an increase in hip flexion and hamstring length, and not related to increased hamstring viscoelastic properties. This is consistent with the findings from the present study, where 70% of the improvement in range was due to a change in hip flexion. In addition, Harvey et al. (2003) found no increase in hamstring extensibility after 4 weeks of hamstring muscle stretching in patients with spinal cord injuries. It seems reasonable to extrapolate that increase in hamstring extensibility is closely connected to central neurophysiological processing, which is severely impaired in patients with spinal cord injuries. Thus it might be assumed that the BLR technique triggers neurophysiological responses influencing the muscle stretch tolerance. This is supported by the fact that in the present study there was a trend towards increased posterior pelvic rotation. An increase in hamstring extensibility might reduce stress on painful lumbar tissues and hence allow an increase in posterior pelvic rotation resulting in greater lumbar flexion. There are several limitations of this study including the small sample size, which may be the reason for the difference in mean range SLR prior to the intervention. In addition, the randomization process was not concealed from the therapist applying the intervention. Overall, these results indicate that the BLR technique provides limited benefit in the treatment of patients with LBP where there is limitation of SLR. We investigated the effect of only one single treatment session; the effect

size may be greater if the BLR technique is integrated in a whole treatment regimen, including exercise to maintain the treatment effect, as is current clinical practice.

5. Conclusion This study provided preliminary evidence that a single intervention of Mulligan’s BLR technique, resulted in improvement in range of SLR 24 h later but not immediately after the intervention. Pain also improved, but this technique was no better than a placebo. A larger study is required to verify these findings. References American Physical Therapy Association. Guide to Physical Therapy practice. 2nd ed. Physical Therapy 2001; 81(1): 746 Beyerlein C, Hall TM, Hansson U, Odemark M, Sainsbury D, Lim HT. Effektivita¨t der Mulligan-straight-leg-raise-Traktionstechnik auf die Beweglichkeit bei Patienten mit Ru¨ckenschmerzen. Manuelle Therapie 2002;6:61–8. Blunt KL, Rajwani MH, Guerriero RC. The effectiveness of chiropractic management of fibromyalgia patients: a pilot study. Journal of Manipulative and Physiological Therapeutics 1997;20(6):389–98. Breig A, Troup JDG. Biomechanical considerations in the straight-legraising test. Cadaveric and clinical studies of the effects of medial hip rotation. Spine 1979;4(3):242–50. Bronfort G, Haas M, Evans RL, Bouter LM. Efficacy of spinal manipulation and mobilization for low back pain and neck pain: a systematic review and best evidence synthesis. Spine 2004;4(3):335–56. Burns SH, Mierau DR. Chiropractic management of low back pain. In: Singer KP, editor. Clinical anatomy and management of low back pain. Oxford: Butterworth-Heinemann; 1997. p. 344–57. Butler DS. Clinical neurobiomechanics. In: Mobilisation of the nervous system. Melbourne: Churchill Livingstone; 1991. p. 35–54. Clark S, Christiansen A, Hellman DF, Hugunin JW, Hurst KM. Effects of ipsilateral anterior thigh soft tissue stretching on passive unilateral straight-leg raise. Journal of Orthopaedic and Sports Physical Therapy 1999;29(1):4–9. Deville WLJM, van der Windt DAWM, Dzaferagic A, Bezemer PD, Bouter LM. The test of Lasegue. Spine 2000;25(9):1140–7. Deyo RA, Rainville J, Kent DL. What can history and physical examination tell us about low back pain? The Journal of the American Medical Association 1992;268(6):760–70. Dixon JK, Keating JL. Variability in straight leg raise measurements: review. Physiotherapy 2000;86(7):361–70. Elvey RL, Hall TM. Neural tissue evaluation and treatment. In: Donatelli R, editor. Physical therapy of the shoulder 3rd. New York; PA: Churchill Livingstone; 1997. p. 131–52. Farrar JT. What is clinically meaningful: outcome measures in pain clinical trials. Clinical Journal of Pain 2000;16(2 Suppl):S106–112. Goeken LN, Hof AL. Instrumental straight-leg raising: results in patients. Archives of Physical Medicine and Rehabilitation 1994;75(4):470–7. Gracey JH, McDonough SM, Baxter GD. Physiotherapy management of low back pain: a survey of current practice in Northern Ireland. Spine 2002;27(4):406–11. Grieve GP. Sciatica and the straight-leg-raising test in manipulative treatment. Physiotherapy 1970;56:337–46.

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ARTICLE IN PRESS


Original article

Electromyographic assessment of the activity of the masticatory using the agonist contract–antagonist relax technique (AC) and contract–relax technique (CR) Susan Armijo Olivo, David J. Magee Department of Physical Therapy, Faculty of Rehabilitation Medicine, University of Alberta, 3-50 Corbett Hall, Canada T6G 2G4 Received 29 January 2005; received in revised form 5 May 2005; accepted 2 June 2005

Abstract Proprioceptive neuromuscular facilitation (PNF) techniques are a group of therapeutic procedures that may be used to cause relaxation of muscles. Studies have found controversial results when applying these techniques. The aim of the present study was to evaluate the effectiveness of masticatory muscle relaxation through the use of the contract–relax technique (CR) when compared with the agonist contract–antagonist relax technique (AC). A convenience sample of 30 students was recruited for this study. The CR and the AC techniques were applied to the subjects in order to cause relaxation of the masticatory muscles. Electromyography activity of all muscles was registered. Two way ANOVA with repeated measures analysis demonstrated that both the AC technique and the CR technique did not decrease the EMG activity of masticatory muscles (P40:05). Instead, both techniques caused an increase in electromyographic activity of the masticatory muscles. Based on the results obtained from this study, both the CR and the AC techniques were not effective in causing relaxation of the masticatory muscles. The purported physiological mechanisms of PNF techniques, which stated that they act through reciprocal inhibition and autogenic inhibition causing muscular relaxation, are not supported by this study. r 2005 Elsevier Ltd. All rights reserved. Keywords: Proprioceptive neuromuscular facilitation techniques (PNF); Electromyography (EMG); Masticatory muscles

1. Introduction Since 1900, when Sherrington defined the basic concepts of muscle facilitation and inhibition, these concepts have been the basis for proprioceptive neuromuscular facilitation (PNF) techniques. These concepts have been used as a reason for increased ROM and decreased resistance of the muscles through muscular relaxation. Although PNF stretching techniques are believed to reduce reflexive components that stimulate muscular contraction, few studies have provided neuro-

Corresponding author. Tel.: +1 780 492 5949; fax: +1 780-492 1626. E-mail address: [email protected] (S. Armijo Oliva).


physiologic evidence of the effectiveness of PNF stretching techniques in relaxing muscles. Previous investigations have shown that while PNF techniques achieve a gain in ROM, electromyographic (EMG) activity in the muscles being stretched is not necessarily reduced, and in some cases, is actually increased (Moore and Hutton, 1980; Osternig et al., 1990; Ferber et al., 2002). The contract–relax method (CR) of PNF, includes a static stretch performed by the clinician, followed by isometric contraction by the subject, of the muscle being stretched and finally, an additional static stretch performed by the clinician. The effectiveness of the CR technique is based on theories of autogenic inhibition. So that muscular relaxation follows a muscular contraction because of stimulation of the

ARTICLE IN PRESS S. Armijo Oliva, D.J. Magee / Manual Therapy 11 (2006) 136–145

Golgi tendon organ (GTO) and stimulation of the inhibitory neurons in the spinal cord (Stuart, 1996). The agonist contract–antagonist relax (AC) technique of PNF is characterized by contraction of the agonist muscle against a resistance provided by the clinician while simultaneously stretching and relaxing the antagonist muscle. This technique is based on the reciprocal inhibition principle, which produces muscular relaxation of the antagonist when the agonist muscle is contracted. This is thought to be due to afferent impulses from agonist muscle spindles stimulating an inhibitory neuron in the spinal cord, causing inhibition of the activity in the alpha motoneuron to the antagonist muscle (Stuart, 1996; Leonard, 1998). According to some authors (Etnyre and Abraham, 1986a, b; Guissard et al., 1988) PNF techniques, especially those involving reciprocal inhibition, such as the AC and the contract relax–antagonist contract (CRAC), do provide the greatest potential for muscle lengthening, due to increased suppression of the motor pool, which is manifest by early postcontraction latencies (Etnyre and Abraham, 1986b). These findings are in agreement with studies of reciprocal inhibition performed by Kasai and Komiyama (1991) and Leonard et al. (1999) in the lower extremities. Also, it has been found that passive stretching, preceded by a maximum voluntary isometric contraction of the stretched muscle (the CR method) or assisted by the contraction of its antagonist (the AC method), induced greater joint flexibility than static stretching (SS), and greater Hreflex inhibition after their application when compared to passive stretching technique alone (Guissard et al., 1988). These findings indicate that there was a decrease in the baseline activity of the muscles being exercised after the application of the AC and CR techniques. However, according to other authors (Osternig et al., 1987), these techniques (the AC, CR, and the CRAC) do not produce sufficient muscular relaxation but rather increased muscle vulnerability to soreness and strain if stretching is continued due to the increased level of muscle activity. Based on studies performed by Etnyre and Abraham (1986b) and Condon and Hutton (1987), comparing the AC, CR, and SS techniques, the H reflex in the AC technique showed a larger marked suppression when compared with the CR and the SS technique. This finding demonstrated that the AC technique was more effective in causing muscular inhibition or decreasing the motoneurons excitability than the CR technique. For this reason, it was thought that the AC technique would cause more relaxation in the masticatory muscles than the CR technique. As a result, the following hypothesis was tested in this study: the AC technique will lead to greater relaxation than the CR technique when exercising the masticatory muscles (the masseter and the anterior temporalis).

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The majority of studies analysed previously have focused on the evaluation of the hamstring and soleus muscles (Etnyre and Abraham, 1986a, b; Condon and Hutton, 1987; Osternig et al., 1987, 1990; Guissard et al., 1988, 2001; Handel et al., 1997; McHugh et al., 1998; Ferber et al., 2002; ), and as a result, information available on this topic is limited and comes primarily from work on the lower limbs. Therefore, the objective of this research was to evaluate the effectiveness of the AC and the CR technique when applied in masticatory muscles because their effectiveness in treating muscles of mastication has not been determined.

2. Methods 2.1. Subjects A convenience sample of 30 students who attend the University of Alberta was recruited for this study consisting of 17 females and 13 males (25.173.009 years, 1.6770.08 m, 65.11711.85 kg) (using a ¼ 0:05, b ¼ 0:20, power ¼ 99%, and size effect ¼ 0.25) (Cohen, 1977). Subjects were continually recruited until 30 subjects were found. To be included in this study, the subjects had to: be between 20 and 35 years of age; have four first molars; have normal occlusion and an appropriate quality of teeth as evaluated by a dentist. Subjects were excluded from this study if they had: any acute or chronic injury or systemic disease that could interfere with the outcome; chronic pain or clinical pathology or previous surgery related to the masticatory system or cervical spine or an abnormal cervical or thoracic spine sagittal alignment (Magee, 2002) or had complaint of symptoms of temporomandibular disorders before the test. Subjects were also excluded if they had been taking medication specifically designed to affect the musculoskeletal system such as anti-inflammatory or pain relief drugs, muscle relaxants or arthritic medications. Subjects signed an informed consent in accordance with the University of Alberta’s policies on research using human subjects. 2.2. Instrumentation and procedures 2.2.1. General considerations Demographic data were collected on all subjects who satisfied the inclusion criteria. These data included age, sex, weight, and height. Prior to the electrode application, the subjects’ skin was cleaned with alcohol and shaved when necessary to reduce its impedance and then the electrodes (EL 500 disposable electrodes, Biopac Systemss, Santa Barbara, Goleta, CA 93117) were held in place by an adhesive disposable patch during all experimental procedures


S. Armijo Oliva, D.J. Magee / Manual Therapy 11 (2006) 136–145

(see Fig. 1) on the masseter and anterior temporalis, bilaterally as described in the Ferrario et al.’s protocol (Ferrario et al., 2002) with a interelectrode distance of 2 cm for all muscles. A reference electrode was placed on the superior part of the sternum. Muscular activity was evaluated using an EMG 100C system, using a bipolar configuration (BIOPAC Systems Incs, Santa Barbara, Goleta, CA 93117) (CMRR: 110 dB min [50–60 Hz], Noise voltage: 0.2 mV rms— [10–500 Hz]). The data acquisition was sampled at 2000 Hz, and was amplified to 1000 (kilogain) (Ferrario et al., 2002). The EMG activity was analysed with specific software (AcqKnowledges from BIOPAC systemss, Inc. Santa Barbara, Goleta, CA 93117), which allowed filtering of the signals obtained and calculating the root mean square (RMS). Data obtained from masticatory muscles were band passed at 20–1000 Hz and band stop filtered at 50–60 Hz (Ferrario et al., 2002). RMS was automatically calculated through the AcqKnowledges software for all data and later used for the normalization procedure. 2.3. Testing procedure The testing session started with a warm-up procedure, consisting of active jaw movements. Then verification of the EMG signal quality was completed for each muscle by having the subjects perform isometric contractions in manual muscle test positions specific to each muscle of interest (Kendall and Kendall, 1983). As a normalization reference, EMG data were collected during maximal voluntary referential contraction (MVRC). This normalization process was necessary to compare measurements between subjects over time (De Luca, 1997; Burden and Bartlett, 1999). In order to normalize data from masticatory muscles, bite force was evaluated simultaneously with the EMG from

masticatory muscles. The masticatory muscles force was measured with a specific device (Figs. 2 and 3) that contained a miniature load cell (LCK-250, Omega, 976 Bergar, Laval-Quebec, H7L 5A1, Canada). To measure the bite force on one side (right or left side), the device was placed over the first molar region. The MVRC of the masticatory muscles was evaluated by asking each subject to close his/her mouth from the rest position, while pressing the load cell contained in the specific device for this purpose. The sensor located in the load cell measured the amount of force of the masticatory muscles. The time of contraction was 5 s with a rest period of 3 min between trials to avoid the effect of fatigue (Jensen and Westgaard, 1995). Each subject then performed 2 contractions in each region (left and right first molar). The force obtained from each register performed in the first molar and EMG activity was registered simultaneously. The average of the highest measurements was considered for the normalization procedure (McLean et al., 2003). The data of the amount of force and EMG activity produced (in Newtons and millivolts, respectively) was saved in a computer. The miniature load cell was calibrated with known weights obtaining a linear curve. The values of calibration were entered into the computer and used with AcqKnowledges software for doing the normalization procedure.

Fig. 2. Device which contains the load cell.

Fig. 1. Electrodes position of masticatory muscles (lateral view).

Fig. 3. Device and tubing used to measure bite force.


2.3.1. Application of the AC and the CR technique While in supine, subjects were asked to position their head in a normal position directing their eyes at a point in front of them (standardized position of the head) (Cook and Wei, 1988). The upper and lower extremities were relaxed in the resting position. Before performing the first evaluation, the subjects were asked to exert the maximum force during a mouth opening movement against resistance in midrange, to evaluate the maximum force of the suprahyoid muscles. This value was the 100% of the suprahyoid force and was registered by a hand held digital dynamometer (The Manual Muscle Test System. MicroFET 2, Hoggan Health, West Jordan , UT 84084, USA) (Mulroy et al., 1997; Ottenbacher et al., 2002), located on the chin of the patient. This value was a reference value when the AC procedure was performed since it was necessary to ask for a 25–30% of the MVRC of the suprahyoid muscles when this technique was applied in order to cause reciprocal inhibition (Leonard et al., 1999). The subject was trained in the procedure before starting the testing. The test was performed twice and the average value was used as a reference value (see Fig 4). The first EMG test evaluated the effectiveness of the AC and CR technique in the resting position of the jaw. In this position, the EMG activity of the selected muscles was measured (5 s). Then, a randomized selection was determined as to whether the subject would receive the AC technique or CR technique first to

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avoid sequencing bias. Each subject received both techniques, but the order of each was randomized. If the random selection decided that the AC technique was applied, the subject was asked to open his/her mouth pressing against the resistance given by the hand held dynamometer, maintaining 25% MVC in this position for at least 10 s in an attempt to cause reciprocal inhibition (Leonard et al., 1999). The subject was told when he/she reached the level required and was asked to hold this level for 10 s (Fig. 4). If the random selection decided that the CR technique was applied, the subjects were asked to generate the maximum force biting a rubber (disposable, specifically built to be used with food) in the anterior–intermediate teeth (CR technique) and to maintain this contraction for 10 s (Fig. 5). A second measurement was taken after the contraction of the suprahyoid muscles was completed (following the AC technique) or after masticatory muscles contraction was finished (CR technique) and lasted 10 s. In summary, the EMG activity was measured twice, before the application of each technique (baseline), and immediately after the application of the CR or the AC technique. After applying each technique there was a rest period. Before starting the next technique, the evaluator checked the EMG baseline activity in order to make sure that the EMG activity recovered its baseline values before starting the second technique. This sequence was repeated three times for every subject, with a 3 min rest period between each trial to

Fig. 4. Resistance provided by the therapist and registered with a dynamometer.


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avoid the possible confounding effect of fatigue (Jensen and Westgaard, 1995). All tests, for each subject were done on the same day. The testing was performed in the Biomechanics laboratory in the Faculty of Rehabilitation Medicine by a physiotherapist with 8 years of clinical experience who applied the procedure to all subjects.

3. Statistical analysis The data on the EMG activity of all muscles were analysed descriptively (e.g. mean, standard deviation). A

one way ANOVA with repeated measures was performed to see if there were any differences between right and left sides in each muscle pair (the masseter, the anterior temporalis). A two way ANOVA with repeated measures test (two independent variables: technique [AC technique and CR technique], and muscles [the masseter and the anterior temporalis]) to evaluate the EMG activity differences between both techniques in masticatory muscles was used. Paired comparisons using a ‘‘t’’ test were performed to determine if there were significant differences in EMG activity of the masseter and the anterior temporalis before and after application of each procedure. The level of significance was set at a ¼ 0:05. The statistical procedures were analysed by the researcher using the SPSS Statistical Program version 11.0 (Statistical Package for the Social Sciences).

4. Results 4.1. Subjects characteristics Forty-eight subjects were initially screened and 30 subjects were finally included in this study; 17 females and 13 males (Table 1). 18 subjects were not included in this study because: 14 did not meet the inclusion criteria, 3 subjects had poor quality EMG data, and the data obtained from 1 subject was not recognized by the format of the software program. The demographic descriptive statistics for all 30 subjects is listed below. 4.2. Compaction of variables

Fig. 5. Patient and rubber’s position for the CR technique.

A one way ANOVA with repeated measures and pair wise comparisons demonstrated no significant differences (Po0:05) between right and left side for the pairs of muscles for the AC and the CR technique. Because there were no significant differences, it was decided to condense all variables and concentrate right and left into one common variable containing the mean of right and left sides to make the statistical analysis easier.

Table 1 Descriptive statistics for study subjects height, weight and age Subjects

All subjects Males Females

Height (m)

Weight (kg)

Age

Mean

SD

Mean

SD

Mean

SD

1.667 1.755 1.600

70.089 70.040 70.045

65.107 72.725 59.288

711.889 77.825 711.281

25.1 26.461 24.058

73.009 72.933 72.703

Height was measured in meters, weight in kilograms, and age in years.


A two way ANOVA with repeated measures analysis (technique [the AC and the CR] and muscles [the masseter and the anterior temporalis]) demonstrated that there were no significant differences in the differences of normalized EMG activity (before–after) between the masticatory muscles for the AC and the CR techniques. There were no significant differences between each technique (AC and CR) and between muscles (the masseter and the anterior temporalis). Table 2 presents the F value and the significance value for all variables. Fig. 6 presents the combined mean (left and right) of the differences (before–after) of normalized EMG activity for masticatory muscles (the masseter and the anterior temporalis) for the CR and the AC technique. Analysis of Fig. 6 shows that the activity of the masticatory muscles (the masseter and the anterior temporalis) was increased after the application of each technique. The CR technique did increase the normalized EMG muscles activity in greater magnitude than the AC technique but the difference was not statistically significant. The paired comparisons demonstrated that both techniques increase the activity of the masseter muscle significantly, while the activity of the anterior temporalis was increased significantly only with the CR technique (for details see Table 3).

5. Discussion 5.1. Effectiveness of both the AC and the CR techniques in relaxation of masticatory muscles The objective of this study was to compare the effectiveness of two PNF techniques in causing relaxation of two masticatory muscles. A two way ANOVA with repeated measures analysis demonstrated that there were no significant differences in normalized EMG

activity (before–after) between the masticatory muscles for either the AC or the CR techniques. However, when the mean differences of each technique were analysed, the AC technique caused a smaller increase in the activity of the masticatory muscles than the CR technique, but this difference was not statistically significant. Both techniques increased the activity of masticatory muscles, which means that both techniques did not cause relaxation of the masticatory muscles. However, the AC technique did not cause a statistically significant increase in the activity of the anterior temporalis muscle. In studies that analysed the effectiveness of the AC and the CR together using the EMG activity of muscles, the AC technique has always increased the activity of the muscles in a larger magnitude when comparing with the CR and the SS technique (Etnyre and Abraham, 1986a, b; Condon and Hutton, 1987; Osternig et al., 1987, 1990; Ferber et al., 2002). For example, Moore and Hutton (1980) when analysing the SS, the CR and the AC techniques found that the more common pattern was that the AC technique caused greater EMG activity in hamstring muscles than the SS or the CR technique. The CR and the Agonist Contract–Relax condition (ACR), a modified technique with similar principles to the AC technique produced median values of 300% and 710% more EMG hamstring activity, respectively, over

0 Combined Mean Differences EMG Activty ( % of MVRC)

4.3. Analysis of differences (before– after) of normalized EMG activity of masticatory muscles for the AC and the CR technique

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1

2

-0.1 -0.2 -0.3 -0.4 -0.5 -0.6 AC Technique CR Technique

-0.7 -0.8 Masseter

Anterior Temporalis

Fig. 6. Combined mean (left and right) of the differences (before– after) for the masticatory muscles (the masseter and the anterior temporalis) for the CR and the AC technique. Normalized EMG values are percentages of the maximum reference contraction.

Table 2 A two way ANOVA with repeated measures analysis of differences (before–after) of normalized EMG activity of Masticatory muscles for the AC and the CR technique Source

Type III sum of squares

df

Mean square

F

Sig.

Techniques (AC and CR) Error (Techniques) Muscles Error (Muscles) Techniques Muscles Error (Techniques Muscle)

1.201 24.334 0.006 18.513 0.512 5.971

1 29 1 29 1 29

1.201 0.839 0.006 0.638 0.512 0.206

1.431

0.241

0.010

0.921

2.485

0.126


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Table 3 ‘‘t’’ test comparisons between before and after for each muscle (the masseter and the anterior temporalis) for each technique Paired differences Mean

Masseter activities before and after the AC technique Temporalis activities before and after the AC technique Masseter activities before and after the CR technique Temporalis activities before and after the CR technique

Std. deviation

Std. error mean

t

df

Sig. (2-tailed)

95% confidence interval of the difference Lower

Upper

0.3257

0.5378

0.0981

0.5265

0.1249

3.317

29

0.002

0.1797

0.7720

0.1409

0.4679

0.1086

1.274

29

0.213

0.3935

0.6526

0.11916

0.6372

0.1497

3.302

29

0.003

0.5095

1.0015

0.1828

0.8835

0.1355

2.787

29

0.009

The mean difference is significant at the 0.05 level.

static stretch EMG levels. These findings were not supported by the results obtained in the present study. The increase in the EMG activity caused by the AC and the CR technique was not significantly different, thus both techniques caused an increase in the normalized EMG activity of masticatory muscles. Based on studies performed by Etnyre and Abraham (1986b); and Condon and Hutton (1987), the H-reflex in the AC technique showed a larger marked suppression as compared with the CR and the SS technique which showed that the AC technique was more effective in causing muscular inhibition or a decrease in motoneuron excitability than the CR technique. This greater suppression seen in the AC compared with the CR technique might be an explanation for the small difference in the results found by this study. Condon and Hutton (1987) also found that the AC technique was ineffective in minimizing EMG activity, although, the H reflex was smaller during the AC and the Hold–relax–agonist contraction (HR–AC) compared with the SS and the Hold relax (HR) techniques, which may reflect lower excitability of the motoneurons. These findings are in accord with those found by Etnyre and Abraham (1986b), who reported a marked suppression of the motor pool excitability through a decrease of the H reflex in soleus muscle during early postcontraction latencies of antagonist muscles during the AC technique, confirming the finding of Condon and Hutton (1987). Condon and Hutton (1987) stated that the reciprocal inhibition phenomenon may have occurred during the antagonist contraction but was masked by other neurogenic excitatory impulses to the antagonist motoneuron pool. They felt the final result was increased muscle tension and activity when muscles were stretched. In a study performed by Guissard et al. (1988), both the AC and the CR technique depressed the H reflex. This depression lasted at least 25 s during the stretching

procedure, showing no differences in effectiveness, which is in accord with the results obtained by this research. In the present study, both techniques caused the same effect in the masticatory muscles (an increased muscular activity). However, the results obtained in the current research are not in agreement with those of Guissard et al. (1988) as they caused an increase in the normalized EMG activity of the masticatory muscles instead of causing muscular relaxation. According to Moore and Hutton (1980), the increase of EMG activity in the CR technique could be explained by a static contraction promoting facilitation of the same muscle. In addition, Ib afferent activity has been shown to be momentarily depressed following tetanic contractions of muscle on stretch, contributing to an increase in the activity of the muscles following their contraction. The current study did not use tetanic contractions, so this explanation of increasing the EMG activity of the masticatory muscles may not contribute to the greater EMG activity during the CR technique. Etnyre et al. (1990) also studied the motor pool excitability, as measured by the Hoffmann reflex responses during the first few seconds after a maximum isometric contraction. They found that the most profound inhibitory influence was observed during the first 200 ms following the end of contraction. Nonetheless, the H reflex amplitudes for more than 200 ms following the end of contraction were not as greatly suppressed as those immediately following the end of the contraction. Therefore, after a maximum contraction, there is a suppression of the motoneurons that last no longer than 1800 ms. These results are in agreement with those obtained by Moore and Kukulka (1991) who found that H reflex depression began immediately (0.05 s) after contractile EMG activity declined. The duration of the phase of maximal reflex inhibition, however, was very brief. The period of maximal


inhibition obtained by these authors lasted from 0.1 to 1 s postcontraction, with recovery to 70% of control reflex amplitudes (baseline) within 5 s postcontraction, and 90% of control amplitudes at 10.05 s postcontraction. The H reflex was not investigated by this current research; therefore the conclusions obtained by those authors are not comparable with the results obtained by the present study. The immediate effect of postcontraction relaxation as stated by Etnyre et al. (1990) is a profound inhibition of the homonymous motor pool from the intrafusal fibers and other spinal influences. This immediate postcontraction inhibition may be attributed to the inhibitory influences of GTOs through Ib afferents or spindle secondaries through type II afferents. Tension from an isometric contraction has been shown to provide a very low stimulus threshold for the GTOs and to result in an inhibitory influence from the Ib afferents through interneurons on the motor pool of the homonymous muscle. The question is whether this short period of inhibition is clinically meaningful. Moreover, there is only limited evidence of the existence of GTOs in human or animal jaw muscles. According to Matthews (1975), tendon organs have been identified histologically in the masseter and temporalis of the cat. However, the study of these receptors in humans has not been performed. Also, the functional connections of these afferents in masticatory muscles are still unknown (Matthews, 1975; Turker, 2002). Thus, the role of these structures in causing autogenic inhibition in masticatory muscles is unidentified. Gollhofer et al. (1998) found that mechanical and electrical stimulation of the triceps surae muscles produced marked reductions in reflex excitability. However, the very fast recovery (o400 ms) of the excitability of the motoneurons after isometric precontraction contradicts the use for more efficient stretching of the musculotendinous system after the use of the CR technique. According to Carter et al. (2000), depending on the size of the muscle, it could be possible that larger muscles have more spindles per unit than small muscles. The more spindles they have, the more reciprocal inhibition, since more receptors can send a larger information through Ia afferents to the spinal cord and consequently cause a greater inhibition in the antagonist muscles. Studies in rats have demonstrated that jaw closing muscles contain muscles spindles (Matthews, 1975; Maier, 1979; Rokx et al., 1984; Scutter and Turker, 2001; Turker, 2002). Additionally studies in humans have established that temporalis muscle displayed approximately 342 spindles, the masseter muscle 114, the medial pterygoid 59, and the lateral pterygoid muscle contained six muscle spindles (Kubota and Masegi, 1977). However, the number of spindles of the jaw openers may vary. According to

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some studies in rats (Maier, 1979; Rokx et al., 1984), the number amount of spindles in suprahyoid muscles is not homogenously distributed. For example, the geniohyoid and mylohyoid muscles presented spindles, but anterior and posterior digastric and stylohyoid did not show any spindles. The infrahyoid muscles such as sternohyoid, omohyoid, and sternothyroid did show spindles (Rokx et al., 1984). These findings could explain the fact that perhaps the reciprocal inhibition was not evidenced in this current study since the few spindles located in the jaw openers did not stimulate the relaxation in masticatory muscles. Nevertheless, these conclusions are based mainly on animal studies with small samples of muscles. The study of muscular receptors in human masticatory muscles is still limited because the procedures are invasive. More research is necessary in this area in order to clarify their role in the control movement of the jaw. Other mechanisms that could influence muscular activity of the masticatory muscles might be the viscoelastic properties of the jaw muscles and surrounding tissues, which according to Peck et al. (2002), provide the major resistance to motion. Also, the stimulation of fluid dynamics by movement in the muscles (Lundvall et al., 1970, 1972), and the emotional aspects of each subject (Holstege, 2001) could influence muscular activity. However, these aspects were beyond of the objectives of this study.

6. Conclusions Based on the results of this study, the following conclusions can be stated: 1. The AC technique was not more effective than CR in decreasing the EMG activity of masticatory muscles in normal subjects in a very standardized setting. Both techniques were unable to cause muscular relaxation. Therefore, based on the results of this research, the use of these techniques as a method to cause muscular activity reduction is not supported. 2. The physiological mechanisms of PNF techniques, which state that they act through reciprocal inhibition and autogenic inhibition causing muscular relaxation, are not supported by this study. These mechanisms might have occurred, however, but could have been masked by complex neural interactions. The study of these interactions was beyond the methodology used by this research. More research looking for the possible mechanisms of PNF techniques and the positive responses obtained in flexibility and range of motion of the patients is necessary. The study of the effectiveness of these techniques on range of motion of the TMJ and also the H reflex responses could be a possible origin of future investigations.


S. Armijo Oliva, D.J. Magee / Manual Therapy 11 (2006) 136–145

Acknowledgments We would like to acknowledge Bernhard Seifried for designing and producing the bite force device, Dr. Darrel Boychuk for evaluating the dental condition of the subjects and Dr. Sandra Curwin for facilitating the use of the Biomechanics Laboratory. Susan Armijo Olivo is supported by a Full-time Studentship from the Government of Chile. References Burden A, Bartlett R. Normalisation of EMG amplitude: an evaluation and comparison of old and new methods. Medical Engineering & Physics 1999;21(4):247–57. Carter A, Kinsey S, Chitwood L, Cole J. Proprioceptive neuromuscular facilitation decreases muscle activity during the stretch reflex in selected posterior thigh muscles. Journal of Sports Rehabilitation 2000;9:269–78. Cohen, J. F test in means in the analysis of variance and covariance. In: Cohen J, editor. Statistical power analysis for the behavioral sciences. New York: Academic Press, Inc; 1977. p. 273–406. (Chapter 8). Condon SM, Hutton RS. Soleus muscle electromyographic activity and ankle dorsiflexion range of motion during four stretching procedures. Physical Therapy 1987;67(1):24–30. Cooke MS, Wei SH. The reproducibility of natural head posture: a methodological study. American Journal of Orthodontics and Dentofacial Orthopedics 1988;93(4):280–8. De Luca C. The use of surface EMG in biomechanics. Journal of Applied Biomechanics 1997;13(2):135–63. Etnyre BR, Abraham LD. Gains in range of ankle dorsiflexion using three popular stretching techniques. American Journal of Physical Medicine 1986a;65(4):189–96. Etnyre BR, Abraham LD. H-reflex changes during static stretching and two variations of proprioceptive neuromuscular facilitation techniques. Electroencephalography and Clinical Neurophysiology 1986b;63(2):174–9. Etnyre BR, Kinugasa T, Abraham LD. Post contraction variations in motor pool excitabiolity. Electromyography and Clinical Neurophysiology 1990;30:259–64. Ferber R, Osternig L, Gravelle D. Effect of PNF stretch techniques on knee flexor muscle EMG activity in older adults. Journal of Electromyography and Kinesiology: Official Journal of the International Society of Electrophysiological Kinesiology 2002;12(5):391–7. Ferrario VF, Sforza C, Tartaglia GM, Dellavia C. Immediate effect of a stabilization splint on masticatory muscle activity in temporomandibular disorder patients. Journal of Oral Rehabilitation 2002;29(9):810–5. Gollhoffer A, Schoop A, Rapp W, Stroinik V. Changes in reflex excitability following isometric contraction in humans. European Journal of Applied Physiology 1998;77:89–97. Guissard N, Duchateau J, Hainaut K. Muscle stretching and motoneuron excitability. European Journal of Applied Physiology and Occupational Physiology 1988;58(1–2):47–52. Guissard N, Duchateau J, Hainaut K. Mechanisms of decreased motoneurone excitation during passive muscle stretching. Experimental Brain Research. Experimentelle Hirnforschung. Experimentation Cerebrale 2001;137(2):163–9. Handel M, Horstmann T, Dickhuth HH, Gulich RW. Effects of contract–relax stretching training on muscle performance in athletes. European Journal of Applied Physiology and Occupational Physiology 1997;76(5):400–8.

Holstege G. Emotional motor system. Fourth interdisciplinary World Congress on low back pain and pelvic pain, Montreal, 2001. p. 160–77. Jensen C, Westgaard RH. Functional subdivision of the upper trapezius muscle during maximal isometric contractions. Journal of Electromyography and Kinesiology 1995;5(4):227–37. Kasai T, Komiyama T. Antagonist inhibition during rest and precontraction. Electroencephalography and Clinical Neurophysiology 1991;81(6):427–32. Kendall F, Kendall E. Muscles, testing, and function. Baltimore: Williams and Wilkins; 1983. Kubota K, Masegi T. Muscle spindle supply to the human jaw muscle. Journal of Dental Research 1977;56(8):901–9. Leonard CT. Principles of reflex action and motor control. In: The neuroscience of human movement. St Louis: Mosby; 1998. p. 70–99. Leonard CT, Sandholdt DY, McMillan JA. Long-latency contributions to reciprocal inhibition during various levels of muscle contraction. Brain Research 1999;817(1–2):1–12. Lundvall J, Mellander S, Westling H, White T. Dynamics of fluid transfer between the intra and extravascular compartments during exercise. Acta Physiologica Scandinavica 1970;80(4):31A–2A. Lundvall J, Mellander S, Westling H, White T. Fluid transfer between blood and tissues exercises. Acta Physiologica Scandinavica 1972;85:258–69. Magee D. Cervical spine. In: Orthopedic physical assessment. 4th ed. St Louis: Elsevier Sciences; 2002. p. 121–82. Maier A. Occurrence and distribution of muscle spindles in masticatory and suprahyoid muscles of the rat. The American Journal Of Anatomy 1979;155(4):483–505. Matthews B. Mastication. In: Lavelle C, editor. Applied physiology of the mouth. Bristol: John Wright and Sons Limited; 1975. p. 199–242. McHugh MP, Kremenic IJ, Fox MB, Gleim GW. The role of mechanical and neural restraints to joint range of motion during passive stretch. Medicine and Science in Sports and Exercise 1998;30(6):928–32. McLean L, Chislett M, Keith M, Murphy M, Walton P. The effect of head position, electrode site, movement and smoothing window in the determination of a reliable maximum voluntary activation of the upper trapezius muscle. Journal of Electromyography and Kinesiology 2003;13(2):169–80. Moore MA, Hutton RS. Electromyographic investigation of muscle stretching techniques. Medicine and Science in Sports and Exercise 1980;12(5):322–9. Moore MA, Kukulka CG. Depression of Hoffmann reflexes following voluntary contraction and implications for proprioceptive neuromuscular facilitation therapy. Physical Therapy 1991;71(4): 321–9. Mulroy SJ, Lassen KD, Chambers SH, Perry J. The ability of male and female clinicians to effectively test knee extension strength using manual muscle testing. The Journal of Orthopaedic and Sports Physical Therapy 1997;26(4):192–9. Osternig LR, Robertson R, Troxel R, Hansen P. Muscle activation during proprioceptive neuromuscular facilitation (PNF) stretching techniques. American Journal of Physical Medicine 1987;66(5): 298–307. Osternig LR, Robertson RN, Troxel RK, Hansen P. Differential responses to proprioceptive neuromuscular facilitation (PNF) stretch techniques. Medicine and Science in Sports and Exercise 1990;22(1):106–11. Peck CC, Sooch AS, Hannam AG. Forces resisting jaw displacement in relaxed humans: a predominantly viscous phenomenon. Journal of Oral Rehabilitation 2002;29:151–60. Ottenbacher KJ, Branch LG, Ray L, Gonzales VA, Peek MK, Hinman MR. The reliability of upper- and lower-extremity strength testing

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Original article

Reliability and validity of shoulder tightness measurement in patients with stiff shoulders Jiu-jenq Lina, Jing-Lan Yangb, a

School and Graduate Institute of Physical Therapy, College of Medicine, National Taiwan University, 7 Chun-Shan S Rd, Taipei, Taiwan b National Taiwan University Hospital, Department of Physical Medicine and Rehabilitation; 7 Chun-Shan S Rd, Taipei, Taiwan Received 17 September 2004; accepted 22 May 2005

Abstract The purposes of this study were (1) to examine intratester and intertester reliability of measurement of anterior and posterior shoulder tightness in patients with stiff shoulders (SS), and (2) to assess construct validity by determining the relations between shoulder tightness, shoulder range of motion (ROM), and self-report measures of functional limitation. Anterior and posterior shoulder tightness were measured by two testers in below-chest abduction and cross-chest adduction tests with an inclinometer, respectively, in 16 patients with SS. Both the intratester and intertester reliability for shoulder tightness measurements were good (intratester ICC ¼ 0.84 and 0.91; intertester ICC ¼ 0.82 and 0.89). The limit of intra-tester and inter-tester agreement (mean, 0.374.41) was acceptable as compared to the standard deviations of the measurements (range, 6.2–7.41). Significant relationships between internal rotation and posterior shoulder tightness (R2 ¼ 0:448, P ¼ 0:002), external rotation and anterior shoulder tightness (R2 ¼ 0:499, P ¼ 0:003), and functional disabilities and posterior shoulder tightness (R2 ¼ 0:432, P ¼ 0:006) were found. Significant correlations between shoulder internal rotation and cross-chest adduction, shoulder external rotation and below-chest abduction were observed, indicating that internal and external rotations might be related to posterior and anterior shoulder stiffness. The study also revealed significant relationship between functional disabilities and cross-chest adduction. Below-chest abduction and crosschest adduction were found to provide reliable data. The construct validity of the abduction and adduction tests is supported by the relationship among these measurements, shoulder ROM, and functional disabilities in patients with SS. r 2005 Elsevier Ltd. All rights reserved. Keywords: Reliability; Construct validity; Stiff shoulder; Shoulder tightness

1. Introduction Stiff shoulder (SS), which is characterized by a loss of shoulder motion, is one of the most common musculoskeletal disorders encountered in daily orthopaedic practice and remains challenging to treat (Codman, 1934; Neviaser and Neviaser, 1987; Vermeulen et al., 2000). Clinical syndromes include pain, a limited range of motion (ROM), and muscle weakness from disuse (Codman, 1934; Reeves, 1975). The manifestation of Corresponding author. Tel.: + 23 12 34 56X7564; fax: +23 83 28 34. E-mail addresses: [email protected] (J.-j. Lin), [email protected] (J.-L. Yang).


shoulder capsule tightness and muscle contractures in patients could be related to their syndromes (Warner et al., 1990; Vermeulen et al., 2000). Thus, much attention has been given to how capsule stretching exercises and mobilization might decrease shoulder capsule tightness and result in shoulder motion improvement (Vermeulen et al., 2000; Griggs et al., 2000). Clinically, however, a quantification of shoulder tightness in patients with SS has been inadequately researched. Cyriax proposed that tightness in a joint capsule would restrict motion in a predictable pattern, a capsular pattern (Cyriax, 1978). For the shoulder, a capsular pattern is one in which external rotation is more limited than abduction, which in turn is more limited than internal rotation. Researchers have

ARTICLE IN PRESS J.-j. Lin, J.-L. Yang / Manual Therapy 11 (2006) 146–152

documented, however, that no single capsular pattern emerges in patients with SS (Rundquist et al., 2003). Subsequently, tightness in the posterior capsule and anterior capsule has been hypothesized to restrict internal rotation and external rotation of the shoulder joint, respectively (Harryman et al., 1992; Johansen et al., 1995; Tyler et al., 1999, 2000). An investigation of the relationships between shoulder tightness and ROM loss, as well as those between shoulder tightness and functional disabilities, may help clinicians target only those aspects of shoulder tightness that are related to ROM loss and functional disabilities. An objective side-lying method for assessing posterior shoulder tightness has been developed and has demonstrated good reliability (intratester and intertester ICC40.80) and construct validity (r ¼ 0:61, between posterior shoulder tightness and internal rotation) in unimpaired subjects and baseball pitchers (Tyler et al., 1999). This assessment method, however, has some shortcomings. Posterior shoulder tightness comparisons between bilateral shoulders in patients with SS are not possible due to pain and discomfort that occur in the side-lying position. In addition, no method is specified for evaluating anterior shoulder tightness. The purpose of our study is to develop a clinically reliable method to evaluate anterior and posterior shoulder tightness in patients with SS. First, both the intratester and intertester reliability of the two methods were evaluated. Second, the methods’ construct validities were assessed by determining the relations between shoulder tightness and shoulder ROM as well as those between shoulder tightness and self-report measures of functional limitation and disability.

2. Methods 2.1. Participants Patients suffering from SS were recruited from National Taiwan University Hospital, Taiwan. All subjects were at least 18 years old. The inclusion criteria of patients with SS were: (1) a limited ROM of a shoulder joint (ROM losses of 25% or greater compared with the non-involved shoulder in at least two of the following shoulder motions: glenohumeral flexion, abduction, or internal/external rotation), (2) pain and stiffness in the shoulder region for at least 3 months, and (3) pain when sleeping on the affected side. Exclusion criteria were a history of (1) increased pain and/or stiffness in the past month, (2) surgery on the particular shoulder, (3) rheumatoid arthritis, (4) stroke with residual shoulder involvement, or (5) fracture of the shoulder complex. All subjects reviewed and signed the hospital-approved human subject informed consent document before participating. Then the subjects were

147

examined for ROM, resisted tests, and pain status of their affected shoulder. 2.2. Equipment A fluid type inclinometer (Isomed, Portland, Oregon) was used to assess cross-chest and below-chest shoulder ROM. The inclinometer resembles a flat goniometer with 3601 of graduation marked in single-degree increments on the circumference. We determined the angle by comparing the location of the arm on the inside of the inclinometer with the degree markings around the circumference. During the measurement, the inclinometer was held in a vertical position. Thus, the arm (gravity) remains in the downward position, indicating the change in limb position. In addition, a hand-held standard universal goniometer (Ever Prosperous Instruments, Inc., Taipei, Taiwan) was used to measure the range of the shoulder joint motion. This goniometer was a double-armed, full circle protractor made of transparent plastic. The arms of the goniometer were 20 cm long and marked off in 21 increments. 2.3. Measurement of posterior and anterior shoulder tightness For the assessment of posterior and anterior shoulder tightness, horizontal flexion ROM (cross-chest adduction) and horizontal extension ROM (below-chest abduction) were measured, respectively, in the supine position on a plinth with an inclinometer. To begin the test, the tester grasped the subject’s extremity distal to the epicondyles of the elbow. The humerus was passively moved into the starting position of 901 of flexion (if not possible, maximal flexion position) and 01 of adduction with neutral rotation for assessment of posterior shoulder tightness, and the other starting position of 901 of abduction (if not possible, maximal abduction position) with neutral rotation for assessment of anterior shoulder tightness. At this point, the scapula was palpated at the lateral border and stabilized with the hand. While the scapula was stabilized, the humerus was then passively moved into a cross-chest adduction or below-chest abduction with neutral rotation (Fig. 1). The test was aborted and restarted if the subject was unable to relax or if the scapula could not be stabilized effectively. The humerus was moved until the movement ceased (firm end-feel), indicating the end of shoulder tissue flexibility. At the end of the horizontal adduction ROM or horizontal abduction ROM, the angle measured by the inclinometer was recorded by a recorder. The recorder placed the inclinometer parallel to the humerus next to the medial epicondyle. The measured angles indicated the amount of flexibility of the posterior and anterior shoulder tissues. A greater angle indicated more flexibility of the shoulder tissue.


J.-j. Lin, J.-L. Yang / Manual Therapy 11 (2006) 146–152

(Cook et al., 2003). In this scale, respondents answer a single question that grossly classifies their level of function as low, medium, or high. They then respond to only the items that target their level of function. Scores were recorded from 1, with the most limited function, to 50, without any limited function in the subject. 2.6. Intratester reliability Intratester reliability of the measurement of shoulder tightness was assessed by one of the two testers. Both testers were physical therapists with a minimum of 5 years clinical experience. Measurements were taken twice with 3–5 days separation. The shoulder tightness measurement was taken as described in the previous section. 2.7. Intertester reliability Two testers were involved in assessing intertester reliability. One tester assessed the shoulder tightness as outlined in the methods section. The second tester then repeated the measure on the same shoulder within 20 min. Both testers were blinded to the results of the measurements. 2.8. Data analysis

Fig. 1. Illustration of the shoulder tightness measurement.

2.4. Measurement of shoulder ROM The tester also assessed passive ROM for the shoulder flexion, abduction, and internal and external rotation. The passive internal and external rotation of the shoulder was measured with the humerus at 901 of abduction (if not possible, maximal abduction) in the coronal plane. These passive ROM measurements were taken with the patient supine and the scapula stabilized by the tester’s hand. 2.5. Self-reported flexilevel scale of shoulder function (FLEX-SF)(Cook et al., 2003) Current literature has shown that various self-report scales for the assessment of functional limitation and disability of the shoulder are available (Michener and Leggin, 2001). The selection of the FLEX-SF scale to assess shoulder function and disability in this study is based on its entire continuum assessment of shoulder functions and appropriate psychometric properties of reliability, validity, and responsiveness to clinical change

The intraclass correlation coefficient [ICC(3,1)] was used to determine the intratester and intertester reliability of the shoulder tightness measurement. An ICC of greater than 0.75 is considered good reproducibility, and less than 0.75 indicates poor reproducibility (Portney and Watkins, 2000). Additionally, plots of the differences of the measurement values between the two trials (trial 1 vs. trial 2 by the first rater) as well as the two raters (rater 1 vs. rater 2) against the mean of the values generated by the two measurements, as initially described by Bland and Altman, were used (Bland and Altman, 1986, 1999) to examine intratester and intertester agreements, respectively. Pearson’s product moment correlation coefficient (g) was used to (1) determine if a significant relation existed between shoulder tightness and shoulder ROM, and (2) investigate the relationships between shoulder tightness and functional disabilities. The SPSS for Windows statistical analysis program [SPSS Inc., Chicago, USA] was used.

3. Results Sixteen patients with unilateral SS (six of them male) between the ages of 41 and 80 (mean ¼ 54.5, SD ¼ 9.2) years were recruited from an outpatient clinic at our hospital. The affected shoulders (11 dominant shoulders


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Table 1 Descriptive data for affected shoulders in patients with stiff-shoulder (N ¼ 16)

Passive ROM (mean7SD) Resisted testa Pain status Intensityb (mean7SD) Range (passive)

Flexion

Abduction

Medial rotation

Lateral rotation

0–1137231 a:1 b:2 c:3 d:10

0–937171 a:1 b:2 c:3 d:10

0–237171 a:1 b:2 c:1 d:12

0–367231 a:1 b:1 c:1 d:13

272 End range

372 End range

272 End range

371 End range

Duration of symptoms (mo) (mean7SD): 5.874.1 FLEX-SF scorec (mean7SD, range): 26.276.6, 16–40 a

Resisted test: a: strong and pain free, b: strong and painful, c: weak and pain free, d: weak and painful. Intensity: 0: no pain, 10: severe pain. c Self-reported FLEX-SF (Cook et al., 2003): scores were recorded from 1, with the most limited function, to 50, without any limited function in the subject. b

Table 2 Intratester reliability and intertester reliability

Cross-chest adduction Intratester reliability Tester 1 Intertester reliability Tester 1 Tester 2 Below-chest abduction Intratester reliability Tester 1 Intertester reliability Tester 1 Tester 2

N

Mean (1)

SD (1)

Min (1)

Max (1)

ICC (95% CI)

14

13.8

6.2

3

25

0.84 (0.72, 0.94)

16 16

13.7 14.6

6.5 7.4

4 2

24 30

0.82 (0.54, 0.94)

14

13.4

6.3

5

26

0.91 (0.78, 0.97)

15 15

13.5 13.8

6.3 6.5

5 5

26 28

0.89 (0.69, 0.96)

and 5 non-dominant shoulders) of the 16 patients were tested. Two patients did not return for the second examination within 5 days. One patient complained of pain and discomfort during the below-chest abduction test. Descriptive data of the subjects’ characteristics are summarized in Table 1.

0.575.61 (mean difference72SD of the differences), respectively. For below-chest abduction, the limits of intra- and inter-tester agreement are 0.173.51 and 0.174.41(mean difference72SD of the differences), respectively. 3.2. Construct validity

3.1. Intratester reliability and intertester reliability A summary of the data is shown in Table 2 for the intratester and intertester comparison. The plots (Fig. 2) of the measurement within each tester and between the testers showed that the spread of scores (error) was evenly and randomly above and below the mean point (unbiased). These data indicate good reliability when the same tester measures anterior and posterior shoulder tightness in the same patient with SS on repeated trials within 5 days (intratester ICC ¼ 0.84 and 0.91). Additionally, two testers measuring anterior and posterior shoulder tightness in patients with SS can expect to find similar results (intertester ICC ¼ 0.82 and 0.89). For the cross-chest adduction method, the limits of intra- and inter-tester agreement are 0.474.01 and

Table 3 presents the relationships between shoulder tightness and shoulder ROM as well as shoulder tightness and functional disabilities. Significant relationships were found between internal rotation ROM and posterior shoulder tightness (R2 ¼ 0:448, P ¼ 0:002), external rotation ROM and anterior shoulder tightness (R2 ¼ 0:499, P ¼ 0:003), and posterior shoulder tightness and functional disabilities (R2 ¼ 0:432, P ¼ 0:006) in patients with SS (Figs. 3 and 4).

4. Discussion The reliability and validity of the measurement tools are important for pathology documentation and


150

cross-chest abduction 4

cross-chest abduction 6

+1.96 SD 3.5

3

+1.96 SD 5.1

4

1 0

Mean -0.4

-1

2

rater1 - rater2

trial1 - trial2

2

Mean -0.5

0 -2

-2 -4

-3 -4 -5

-1.96 SD -6.1

-6

-1.96 SD -4.4

-8 0

5

(A)

10 15 20 25 AVERAGE of trial1 and trial2

30

5

10 15 20 25 AVERAGE of rater1 and rater2

(B)

below-chest abduction 4

below-chest abduction 6

+1.96 SD 3.5

3

+1.96 SD 4.2

4 1 Mean -0.1

-1 -2 -3

rater1 - rater2

trial1 - trial2

2

0

-1.96 SD -3.6

-4

30

2 Mean -0.1

0 -2 -4

-5

-1.96 SD -4.5

-6 5

10

(C)

15 20 25 AVERAGE of trial1 and trial2

30

0 (D)

5

10 15 20 25 AVERAGE of rater1 and rater2

30

Fig. 2. Plots of difference between two trials as well as two raters against mean for the measurement of anterior and posterior shoulder tightness.

Table 3 Pearson’s product moment correlation coefficient between shoulder tightness and shoulder ROM as well as shoulder tightness and functional disabilities

Flexion Abduction Internal rotation External rotation FLEX-SF scorea

Cross-chest adduction

Below-chest abduction

0.31 0.27 0.69* 0.25 0.66*

0.29 0.29 0.34 0.70* 0.12

Po0:01. a Self-reported FLEX-SF (Cook et al., 2003).

outcome assessments in the clinic as well as in research. In patients with SS, soft tissue tightness has been postulated as a possible cause of ROM loss and functional disability (Harryman et al., 1992; Tyler et al., 1999). ROM can be measured objectively with a goniometer; however, valid and reliable measurements

of posterior and anterior shoulder tightness in patients with SS had yet to be established. In previous studies, the cross-chest adduction method was thought to be the gold standard for assessing posterior shoulder tightness, while no specific method was indicated for evaluating anterior shoulder tightness (Pappas et al., 1985; Warner et al., 1990; Tyler et al., 1999). Loss of posterior capsular flexibility has been implicated as one of etiologic factors in patients with shoulder pathology (Pappas et al., 1985; Warner et al., 1990; Tyler et al., 1999). With the cross-chest adduction method, although the reliability of the method was unmeasured previously, Warner et al. (1990) and Pappas et al. (1985) indicated posterior shoulder tightness in patients with instability/impingement shoulders and baseball pitchers, respectively. In our investigation, the cross-chest adduction method was demonstrated to have good intrarater and interrater reliability in patients with SS. Furthermore, we also presented a reliable measurement, the below-chest abduction method, for assessing

ARTICLE IN PRESS

R2 = 0.4483

25 20 15 10 5 0 0

10

Below-chest Abduction (Degrees)

(A)

(B)

20 30 40 50 60 Shoulder Internal Rotation (degrees)

70

R2 = 0.4988

25 20 15 10 5 0

10

20 30 40 50 60 70 80 90 100 Shoulder External Rotation (Degrees)

Fig. 3. Scatter diagram showing relationship between shoulder tightness and rotation range of shoulder motion in patients with stiff shoulders. The solid line represents the least-squares regression line.

anterior shoulder tightness. This finding is especially noteworthy because the limits of intratester and intertester agreement (average 0.374.41) were acceptable as compared to the standard deviations of the two measurements (range, 6.2–7.41, Table 2). These two measurements in our investigation provide objective and reliable methods for quantification of anterior and posterior shoulder tightness in patients with SS. The validity of our findings for decreased internal and external rotation of shoulder ROM as well as shoulder tightness was consistent with that of other research (Warner et al., 1990; Harryman et al., 1992; Ellenbecker et al., 1996; Tyler et al., 1999). Warner et al. (1990) demonstrated a significant limitation of both internal rotation ROM and cross-chest adduction in patients with shoulder impingement. Tyler et al. (1999) and Ellenbecker et al. (1996) found significant relationships between decreased internal rotation ROM and posterior shoulder tightness in elite pitchers. Specifically, Harryman et al. (1992) indicated that the coracohumeral ligament should limit external rotation of shoulder ROM, while the rotator interval and the superior glenohumeral ligament are potential factors limiting external rotation of shoulder ROM. Presumably, the anterior deltoid, pectoralis major, pectoralis minor, rotator interval, coracohumeral ligament, and superior glenohumeral ligament play a role in anterior shoulder tightness, while the posterior deltoid, infraspinatus, teres

(B)

151

30 25

R2 = 0.432

20 15 10 5 0 10

15

20 25 30 35 40 Self-reported score of Flexi level Scale of Shoulder Function

45

15

20 25 30 35 Self-reported score of Flexi level Scale of Shoulder Function

45

(A)

30

0

Cross-chest Adduction (degrees)

30

Below-chest abduction (degrees)

Cross-chest Adduction (Degrees)


30 25 20 15 10 5 0 10

40

Fig. 4. Scatter diagram showing relationship between shoulder tightness and self-reports of functional disabilities in patients with stiff shoulder. The solid line represents the least-squares regression line.

minor, teres major, and posterior band of the inferior glenohumeral ligament complex play a role in posterior shoulder tightness (Terry et al., 1991; Harryman et al., 1992). Subsequently, tightness in any or all of the structures may lead to the development of SS. Although our shoulder tightness measurements cannot identify which structures are responsible for limiting motion, it is likely that the primary structures that limit internal and external rotation of shoulder ROM are the posterior and anterior aspects of the shoulder, respectively. Functional disabilities and loss of motion in patients with shoulder pathology have been thought to be due to tightness in a joint capsule, and stretching/mobilization has been advocated. Based on our correlation analysis, a clinician using the cross-chest adduction measurement can expect that for every 41 of internal rotation ROM lost, posterior shoulder flexibility will decrease 11 in patients with SS. A clinician using the below-chest abduction measurement can also anticipate that for every 51 of external rotation ROM lost, anterior shoulder flexibility will decrease 11 in patients with SS. Additionally, a clinician using the cross-chest adduction measurement can expect that for every 4 points lost in functional disabilities measured by the FLEX-SF, posterior shoulder flexibility will decrease 21 in patients



with SS. Calculations were based on the judgment of what constitutes minimally clinically important difference and responsiveness (3.02 and 1.12 score on FLEXSF, respectively) from Cook’s investigation (2003) as well as the relationship between shoulder tightness and functional disabilities in our study. This suggestion is especially noteworthy because our shoulder tightness measurements are not only reflected in shoulder ROM loss but also decreased self-reported functional scores in patients with SS. The limitations of our study should be noted. Although our results demonstrated significant correlation between cross-chest adduction/below-chest abduction and internal/external rotations, the direct relationship between internal/external rotations and shoulder tightness cannot be assumed. Thus, no direct relationship between cross-chest adduction/below-chest abduction and shoulder stiffness can be established by our study. We believe, however, that loss of internal/external rotation ROM is an adaptive change related to posterior/anterior shoulder tightness, and stretching has been advocated (Johansen et al., 1995; Tyler et al., 1999, 2000). Another limitation of our study is the ability to palpate and manually stabilize the scapula. Because both testers in our study were physical therapists with a minimum of 5 years clinical experience in manual therapy and our results demonstrated good intratester and intertester reliability, the disadvantage of our manual method can be eliminated. The restricted subacute clinical condition of our subjects also limits generalizability outside of this subacute condition in patients with SS. Longitudinal investigations will be important to further validate the clinical use of this measurement. Perhaps our method of quantifying shoulder tightness will facilitate patient classification and improve the utility of stretching/mobilization, therapeutic modalities, and exercises. 5. Conclusion Below-chest abduction and cross-chest adduction tests are reliable for use in measurement of anterior and posterior shoulder tightness in patients with SS, respectively. Correlations between shoulder tightness and decreased rotation ROM as well as functional disabilities may guide clinicians in their implementation of proper stretching/mobilization and exercise programs. Acknowledgement The authors would like to thank physical therapist Wei-chun Yen for his help with recruiting subjects and all the subjects who participated in this study.

References Bland JM, Altman DG. Statistical method for assessment of agreement between two methods of clinical measurement. Lancet 1986;i:307–10. Bland JM, Altman DG. Measuring agreement in method comparison studies. Statistical Methods in Medical Research 1999;8:135–60. Codman EA. The shoulder. Rupture of the supraspinatus tendon and other lesions in or about the subacromial bursa. Boston: Thomas Todd; 1934. Cook KF, Roddey TS, Gartsman GM, Olson SL. Development and psychometric evaluation of the flexilevel scale of shoulder function. Medical Care 2003;41:823–35. Cyriax J. Textbook of orthopedic medicine. Diagnosis of soft tissue lesions, vol 1. New York: Macmillan Publishing; 1978. Ellenbecker TS, Roetert EP, Piorkowski PA, Schulz DA. Glenohumeral joint internal and external rotation range of motion in elite junior tennis players. Journal of Orthopaedic and Sports Physical Therapy 1996;24:336–41. Griggs SM, Ahn A, Green A. Idiopathic adhesive capsulitis: a prospective functional outcome study of nonoperative treatment. Journal of Bone and Joint Surgery 2000;82:1398–407. Harryman II DT, Sidles JA, Harris SL, Matsen III FA. The role of the rotator interval capsule in passive motion and stability of the shoulder. Journal of Bone and Joint Surgery: American 1992;74:53–66. Johansen RL, Callis M, Potts J, Shall LM. A modified internal rotation stretching technique for overhand and throwing athletes. Journal of Orthopaedic and Sports Physical Therapy 1995;21:216–9. Michener LA, Leggin BG. A review of self-report scales for the assessment of functional limitation and disability of the shoulder. Journal of Hand Therapy 2001;14:68–76. Neviaser RJ, Neviaser TJ. The frozen shoulder: diagnosis and management. Clinical Orthopaedics 1987;223:59–64. Pappas AM, Zawacki RM, McCarthy CF. Rehabilitation of the pitching shoulder. American Journal of Sports Medicine 1985;13:223–35. Portney LG, Watkins MP. Foundations of clinical research: applications to practice. East Norwalk: Conn: Appleton & Lange; 2000. Reeves B. The natural history of the frozen shoulder syndrome. Scandinavian Journal of Rheumatology 1975;4:193–6. Rundquist PJ, Anderson DD, Guanche CA, Ludewig PM. Shoulder kinematics in subjects with frozen shoulder. Archives of Physical Medicine and Rehabilitation 2003;84:1473–9. Terry DC, Hammon D, France P, Norwood LA. The stabilizing function of passive shoulder restraints. American Journal of Sports Medicine 1991;19:26–34. Tyler TF, Roy T, Nicholas SJ, Gleim GW. Reliability and validity of a new method of measuring posterior shoulder tightness. Journal of Orthopaedic and Sports Physical Therapy 1999;29:262–9. Tyler TF, Nicholas SJ, Roy T, Gleim GW. Quantification of posterior capsule tightness and motion loss in patients with shoulder impingement. American Journal of Sports Medicine 2000;28:668–73. Vermeulen HM, Obermann WR, Burger BJ, Kok GJ, Rozing PM, van Den Ende CH. End-range mobilization techniques in adhesive capsulitis of the shoulder joint: a multiple-subject case report. Physical Therapy 2000;80:1204–13. Warner JJ, Micheli LJ, Arslanian LE, Kennedy J, Kennedy R. Patterns of flexibility, laxity, and strength in normal shoulders and shoulders with instability and impingement. American Journal of Sports Medicine 1990;18:366–75.

ARTICLE IN PRESS


Short communication

Vertebral artery dominance and hand preference: Is there a correlation? Barbara Cagniea,, Mirko Petrovicb, Dirk Voetb, Erik Barbaixc, Dirk Cambiera a

Department of Rehabilitation Sciences and Physiotherapy, Ghent University Hospital, De Pintelaan 185, 6K3, B– 9000 Ghent, Belgium b Department of Sonography, Ghent University Hospital, Belgium c Department of Human Anatomy, Embryology, Histology and Medical Physics, Ghent University, Belgium Received 20 October 2004; received in revised form 2 June 2005; accepted 26 July 2005

Abstract The two vertebral arteries are usually unequal in size, the left one being generally larger than the right one. It is not clear why this asymmetry exists. One of the hypotheses is that this asymmetry is related to the vascular requirements of the brain. To support this statement, we investigated the correlation between a dominant left vertebral artery and right-handedness and vice versa. No correlation between differences in vertebral artery diameter and hand dominance was found. Hence, the hypothesis that a dominant left vertebral artery is associated with right-handedness and vice versa cannot be confirmed. r 2005 Elsevier Ltd. All rights reserved.

1. Introduction Handedness is the most obvious human behavioural asymmetry. Arguably 2–30% of any human population is left-handed or ambidextrous (Porac and Friesen, 2000). Most estimates hover around 10%, depending upon the criteria used to assess handedness. Reasons for differences in hand preferences are speculative, but may be correlated with asymmetry in cerebral blood flow (Risberg et al., 1975). Variations in normal anatomy in the extracranial vertebral artery are relatively frequent, ranging from asymmetry of both vertebral arteries to significant hypoplasia of one vertebral artery. According to postmortem, angiographic and sonographic studies, the average vertebral artery diameter is more often larger on the left side than on the right side (Scialfa et al., 1975; Argenson et al., 1979; Thiel, 1991; Bartels et al., 1992; Thiel et al., 1994; Yuan et al., 1994; Refshauge, 1994; Weintraub and Khoury, 1995; Abd-el Bary et al., 1995; Hedera, 1995; Rivett et al., 1998; Seidel et al., Corresponding author. Tel.: +32 9 240 52 65; fax: +32 9 240 38 11.

E-mail address: [email protected] (B. Cagnie). 1356-689X/$ - see front matter r 2005 Elsevier Ltd. All rights reserved. doi:10.1016/j.math.2005.07.005

1999; Haynes and Milne, 2001; Zaina et al., 2003; Jeng and Yip, 2004; Mitchell, 2004) It is not clear why this asymmetry exists. To the best of our knowledge, there are no studies available investigating the underlying mechanism of asymmetry in the vertebral arteries. In a recent article of Manual Therapy, Zaina et al. postulate that theories of embryological formation and vascular requirements of the brain have been put forward without evidence (Zaina et al., 2003). The latter theory has never been investigated but may be based on the assumption that, due to handedness, right-handed people may have dominant left vertebral arteries to satisfy the higher vascular demands of the left hemisphere. This statement can only be supported if the reverse, i.e. a dominant right vertebral artery in left-handed people, can be proven. Therefore, the purpose of this study is to investigate whether right-handed subjects have a dominant left vertebral artery and vice versa in left-handed subjects.

2. Materials and methods All the third- and fourth-year-students in Rehabilitation Medicine and Physiotherapy (n ¼ 137) were


B. Cagnie et al. / Manual Therapy 11 (2006) 153–156

requested to indicate on a list whether they were left or right handed. Of this list, 30 right- and 30 left-handed subjects were asked to participate. They were included if they had no pain from the cervical spine and were free of symptoms and risk factors associated with cardiovascular disease. They were asked to complete the Edinburgh handedness questionnaire to classify the subjects into right- and left-handers (Oldfield, 1971). Ten participants were excluded for further investigations, because they were ambidextrous. We finally examined 50 subjects (29 right handers, 21 left handers) with a mean age of 21.372.5years (ranging from 19 to 26 years). Written informed consent was obtained from all the volunteers after the nature of the procedure had been explained. An experienced ultrasonographer conducted an ultrasonographic investigation of the vertebral arteries with a duplex Doppler (HDI 5000, Philips Medical Systems, the Netherlands). All subjects were placed supine with the head in the neutral position. The diameter of both vertebral arteries was measured with a 7.5-MHz linear probe between the fifth and sixth cervical vertebrae on both sides. A series of three measurements at each side was taken and the mean diameter was used for further analysis. 2.1. Data analysis Differences in vertebral artery diameter between leftand right-handers were examined by an independent sample’s t-test. Left versus right as well as dominant versus non-dominant artery diameter were analysed by use of a paired-samples t-test. A vertebral artery was considered dominant when the side-to-side diameter difference was greater than the standard error of measurement (SEM). The probability threshold was set at Pp0:05.

Table 1 Mean (mm) and standard deviations (SD) of the left and right vertebral arteries

Left diameter Right diameter

Mean

SD

ICC

SEM

3.68 3.53

0.45 0.49

0.87 0.89

0.16 0.16

The corresponding values for intraclass correlation coefficient (ICC) and standard error of measurement (SEM) are presented. Table 2 Mean diameter (mm) (7SD) of the left and right vertebral arteries in right and left-handed subjects

Right-handed Left-handed Right handed versus left handed

Right artery

Left artery

Right versus left artery

3.58 (70.47) 3.46 (70.52) P ¼ 0:392

3.72 (70.44) 3.61 (70.46) P ¼ 0:391

P ¼ 0:286 P ¼ 0:387

The last column gives the probability of the paired-samples t-test between left and right sides. The bottom row gives the p-value defining the differences in vertebral artery diameter between right handed and left handed subjects. Table 3 Per cent dominance (side-to-side diameter difference 40.16 mm) of the vertebral artery in left- and right- handed subjects

Right-handed Left-handed Total

Left dominance (%)

Right dominance (%)

No dominance (%)

48.3 61.9 54.0

34.5 23.8 30.0

17.2 14.3 16.0

Table 4 Mean diameter (mm) (7SD) of the dominant and non-dominant arteries Dominant artery

Non-dominant artery

Dominant versus nondominant artery

3.88 (70.38)

3.32 (70.38)

Po0:001

3. Results Total group

The mean diameter of the left vertebral artery was 3.68 mm (70.45); the diameter of the right vertebral artery was 3.53 (70.49) with no significant difference between both diameters (P ¼ 0:165) (Table 1). There were no statistically significant differences between leftand right-handers regarding left (P ¼ 0:391) and right (P ¼ 0:392) vertebral artery diameter (Table 2). The SEM was 0.16 mm on both sides (Table 1). A vertebral artery was considered dominant when a sideto-side diameter difference 40.16 mm exists. In 54% of the cases the left diameter was dominant, whereas in 30% the right diameter was dominant. In 16% of the cases, the left arterial diameter was equal to the right (Table 3). The mean diameter of the dominant artery (3.92 mm70.39) was significantly greater than the mean

Comparison between dominant and non-dominant is determined by a paired-samples t-test.

diameter of the non-dominant artery (3.28 mm70.39) (Pp0:001) (Table 4). No differences in dominance of the vertebral artery between left- and right-handers were observed.

4. Discussion In this study we investigated whether right-handed people had a dominant left vertebral artery and vice versa in left-handed people.

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In right-handed, as well as in left-handed subjects, the left vertebral artery had a larger diameter than the right one, but the difference was not statistically significant. This is in accordance with the literature where the average vertebral artery diameter is larger on the left side (varying between 3.3 and 4.7 mm) than on the right side (varying between 3.0 and 4.3 mm), with no significant difference in vessel diameter between both sides (Scialfa et al., 1975; Argenson et al., 1979; Thiel, 1991; Bartels et al., 1992; Thiel et al., 1994; Yuan et al., 1994; Refshauge, 1994; Weintraub & Khoury, 1995; Abd-el Bary et al., 1995; Hedera, 1995; Rivett et al., 1998; Seidel et al., 1999; Haynes and Milne, 2001; Zaina et al., 2003; Jeng and Yip, 2004; Mitchell, 2004). The great variability in vertebral artery diameter between the different studies reported in the literature can be attributed to the variability of methods and protocols of examination. There are different methods of calculating dominance in the literature, although there is no wide agreement. Jeng et al. chose a side-to-side diameter difference of at least 0.3 mm as a criterion of vertebral artery asymmetry, based on ultrasound resolution limitation (Jeng and Yip, 2004). Smith and Bellon considered a dominant vertebral artery being one at least 30% greater in diameter (Smith and Bellon, 1995). In this study, the measurement of the SEM was regarded as more accurate to determine the dominance of the vertebral artery. In 54% of the cases the left diameter was greater than the right, whereas in 30% the right diameter was greater than the left. In 16% of the cases, the left arterial diameter was equal to the right. These percentages differ from the percentages found in the literature, where the left vertebral artery is dominant in 35.5–46.5% of individuals and the right in 22.4–35.7% of the cases. In 21.4–38.5% both vertebral arteries have a similar calibre (Adachi, 1928; Argenson et al., 1979; Abdel Bary et al., 1995; Cloud and Markus, 2003; Jeng and Yip, 2004). Different theories have been proposed to explain the asymmetry in vertebral artery diameters. The theory of vascular requirements of the brain has been postulated, but never investigated. Orlandini et al. found the arteries on the left side of the circle of Willis to be larger than those on the right, and related this to the usual dominance of the left cerebral hemisphere (Orlandini, 1985). There is a general consent that the left and right human hemispheres differ in anatomy and function: It is suggested that in the normal population, handedness and footedness are relevant factors in predicting cerebral dominance. Recent studies found in right-handed individuals strong left hemispheric dominance, while in lefthanders significant right hemispheric dominance was shown (Basic et al., 2004). Recent developments in functional transcranial Doppler sonography (fTCD) have made it possible to non-invasively and quantita-

155

tively measure lateralization and time course of brain activation. The technique of fTCD is based on the linkage of cerebral activation and perfusion (Knecht et al., 1998). Although it is tempting to associate the common left dominance of the vertebral arteries with this higher volume of blood flow needed to satisfy the increased vascular demands of the left hemisphere, there is little or no evidence for this link, which can explain our results. The second hypothesis is the theory of embryological formation. Although no references are found in the literature, we assume that this theory may be based on the different kind of embryological development of the left and right vertebral artery. The subclavian artery (which is normally the artery of origin of the vertebral artery) arises on the right side from the brachiocephalic trunk, on the left side directly from the aorta. In this case, the vertebral artery is the second branch on the left side, whereas it is only the third branch on the right side, which may explain the differences in size. The present results must be viewed within the limitations of the study. It could be argued that the study population of 50 young and healthy subjects does not adequately represent the population. To be conclusive, the current study should be replicated with a larger sample size. Secondly, although not obvious, it would be interesting to investigate other theories to explain the difference in vertebral artery diameter, such as the theory of embryological formation. Thirdly, cerebral blood flow is not only determined by the diameter of the vessel but also by the velocity of the blood flow. Therefore, a true understanding of vertebral artery dominance can only be achieved by measuring blood flow volume. In conclusion, no correlation between differences in vertebral artery diameter and hand dominance can be found. Hence, the hypothesis that a dominant left vertebral artery is associated with right-handedness and vice versa cannot be confirmed. Further research is required to investigate the underlying mechanism of asymmetry in the vertebral artery diameter.

References Abd-el Bary T, Dujnovny M, Ausman J. Microsurgical anatomy of the atlantal part of the vertebral artery. Surgical Neurology 1995;44(4):392–400. Adachi B. Das Arteriensystem der Japaner, vol. I. Kyoto: Maruzen; 1928. Argenson C, Francke J, Sylla S, Dintimille H, Papasian S, de Marino V. Les arte`res verte´brales. Anatomia Clinica 1979;2(1):29–41. Bartels E, Fuchs H, Flugel K. Duplex ultrasonography of vertebral arteries: examination, technique, normal values, and clinical applications. Angiology 1992;43:169–80. Basic S, Hajnsek S, Poljakovic Z, Basic M, Culic V, Zadro I. Determination of cortical language dominance using functional


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transcranial Doppler sonography in left-handers. Clinical Neurophysiology 2004;115:154–60. Cloud G, Markus H. Diagnosis and management of vertebral artery stenosis. Quarterly Journal of Medicine 2003;96:27–34. Haynes M, Milne N. Color duplex sonographic findings in human vertebral arteries during cervical rotation. Journal of Clinical Ultrasound 2001;29(1):14–24. Hedera P. Influence of extreme head rotations on brainstem auditory evoked potential. Clinical Neurology and Neurosurgery 1995; 97:290–5. Jeng J, Yip P. Evaluation of vertebral artery hypoplasia and asymmetry by color-coded duplex ultrasonography. Ultrasound in Medicine and Biology 2004;30(5):605–9. Knecht S, Deppe M, Ringelstein EB, Wirtz M, Lohmann H, Dra¨ger B, Huber T, Henningsen H. Reproducibility of functional transcranial doppler sonography in determining hemispheric language lateralization. Stroke 1998;29:1155–9. Mitchell J. Differences between left and right suboccipital and intracranial vertebral artery dimensions: an influence on blood flow to the hindbrain. Physiotherapy Research International 2004; 9(2):85–95. Oldfield R. The assessment and analysis of handedness: the Edinburgh inventory. Neuropsychologia 1971;9:97–113. Orlandini G, Ruggiero C, Orlandini S, Gulisano M. Blood vessel size of circulus arteriosus cerebri: a statistical research on 100 human subjects. Acta Anatomica 1985;123:72–6. Porac C, Friesen I. Hand preference side and its relation to hand preference switch history among old and oldest-old adults. Developmental Neuropsychology 2000;17:225–39. Refshauge K. Rotation: a valid premanipulative dizziness test? Does it predict safe manipulation? Journal of Manipulative and Physiological Therapeutics 1994;17(1):15–9.

Risberg J, Halsey JH, Wills EL, Wilson EM. Hemispheric specialization in normal man studied by bilateral measurements of the regional cerebral blood flow. A study with the 133-Xe inhalation technique. Brain 1975;98:511–24. Rivett DA, Milburn PD, Chapple C. Negative pre-manipulative vertebral artery testing despite complete occlusion: a case of false negativity? Manual Therapy 1998;3(2):102–7. Scialfa G, Ruggerio G, Salamon G, Mochotey P. Post mortem investigation of the vertebrobasilar system. Acta Radiologica (Suppl.) 1975;357:259–86. Seidel E, Eicke B, Tettenborn B, Krummenauer F. Reference values for vertebral artery flow volume by duplex sonography in young and elderly adults. Stroke 1999;30:2692–6. Smith A, Bellon J. Parallel and spiral flow patterns of vertebral artery contributions to the basilar artery. American Journal of Neuroradiology 1995;16(8):1587–91. Thiel H. Gross morphology and pathoanatomy of the vertebral arteries. Journal of Manipulative and Physiological Therapeutics 1991;14(2):133–42. Thiel AW, Wallace K, Donat J, Yong-Hing K. Effect of various head and neck positions on vertebral artery blood flow. Clinical Biomechanics 1994;9:105–10. Weintraub MI, Khoury A. Critical neck position as an independent risk factor for posterior circulation stroke. A magnetic resonance angiographic analysis. Journal of Neuroimaging 1995;5:16–22. Yuan R, Yip P, Liu H, Hwang B, Chen R. The value of duplex and continuous wave Doppler sonography for evaluation of the extracranial vertebral arteries: a prospective comparison with angiography. Zhonghua Yi Za Zhi (Taipei) 1994;53:42–8. Zaina C, Grant R, Johnson C, Dansie B, Taylor J, Spyropolous P. The effect of cervical rotation on blood flow in the contralateral vertebral artery. Manual Therapy 2003;8:103–9.

ARTICLE IN PRESS


Case report

Osteochondritis dessicans: A complex case of anterior knee pain John Davina,, James Selfeb a

Manchester United Football Club, Birch Road, Carrington, Manchester, M31 4BH, UK Reader in Physiotherapy, Allied Health Professions Unit, University of Central Lancashire, Preston, PR1 2HE, UK

b

Received 25 March 2004; received in revised form 4 February 2005; accepted 19 May 2005

1. Introduction This case highlights the difficulty in correctly identifying osteochondritis dessicans and alerts clinicians to the fact that although previously unreported as such, the condition may be prone to recurrence. Presenting symptoms and early positive responses to treatment may be misleading and indicative of dysfunction in structures that are not responsible for the complaint.

that his left leg felt considerably weaker than his right one and that this was more than the expected difference due to leg dominance. He had not sought help at the time of the initial pain as shortly thereafter he suffered from glandular fever and this had enforced a prolonged break from football. When the patient returned to the club for pre-season training, initially his knee felt normal. Four weeks into the season he recalled experiencing slight knee pain. This gradually worsened over a 2-week period until the pain became so intense that he could not complete the warmup.

2. The patient The patient was a 17-year-old male, right leg dominant, full-time professional football player. He appeared to be in good health and walked confidently into the treatment room. Movements of sitting to standing were completed effortlessly with no obvious visual cues as to the nature of the complaint. His past medical history consisted of a previous arthroscopy to the left knee when the patient was 14. This showed osteochondritis dessicans, with a large flap of articular cartilage on the medial femoral condyle. The medial femoral condyle was successfully repaired. In addition, the patient had an asymptomatic spondylolisthesis of L5/S1.

4. Subjective assessment

3. History of condition

The patient complained of a painful left knee as well as other symptoms (see Fig. 1). A Visual Analogue Scale (VAS) value of 7 was given by the patient for his knee pain. His primary complaint (P1) was described as a diffuse dull ache around the anterior aspect of the knee, sometimes spreading to the mid-thigh after 4–5 min of intense exercise including acceleration, deceleration and change of direction exercises. P2 was a general tightness around the knee, which came on after 20 min of sustained flexion. P3 was an occasional shooting pain along the lateral aspect of the calf from the knee to the Achilles tendon. He noted a link between P1 and P3 but stated that P1 could be felt at rest but not P3.

The patient recalled a 6-month history of left knee pain. Initially, it had not prevented him from training but he felt it had altered his running style. He reported

5. Objective examination

Corresponding author.

E-mail address: [email protected] (J. Davin). 1356-689X/$ - see front matter r 2005 Elsevier Ltd. All rights reserved. doi:10.1016/j.math.2005.05.003

The pain distribution suggested several possible structures as the source of symptoms. A previous


J. Davin, J. Selfe / Manual Therapy 11 (2006) 157–161

Fig. 1. Patient notes linkage between P1 and P3.

history of an L5/S1 spondylolisthesis is a red flag (Clinical Standards Advisory Group (CSAG), 1994). Although the previous history suggested that the spondylolisthesis was stable (concurrent X-rays taken at yearly intervals for 4 years) an objective assessment of the lumbar spine was undertaken. This was not only to rule out a possible source of symptoms but also to allay the patient’s fear in terms of diagnosis. The patient’s brother was also a professional footballer whose career had halted early due to a congenital active spondylolisthesis. The patient had expressed concern at this and any undue anxiety, as Main and Watson (1999) argue, may influence pain mechanisms. The only significant finding was related to posture. Postural assessment revealed a thoracic kyphosis, lumbar lordosis and anteriorly tilted pelvis. However, footballers often present with this altered posture due to

repeated activity of the hip flexor and knee extensor muscles combined with relative inactivity of the antagonistic muscle groups. Maitland (1991) notes that knee pain can be provoked from a painless hip. Although, pain referral patterns of the hip as described by Sims (1999) bore some relation to those experienced by the patient no significant hip abnormalities were found on objective examination. In this case long-standing symptoms around the knee combined with previous trauma, surgery and the subject’s occupation (four seasons of professional football since surgery) meant that the knee became the primary focus of the clinical assessment. Objective assessment of the tibiofemoral joint consisted of palpation, active and passive movements for flexion, extension, medial and lateral rotation and flexion extension quadrants with and without

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compression. All supporting ligaments were passively stressed and gave a strong end feel. There were no other comparable signs apart from a low-grade effusion. Spencer et al. (1984) reported that 20 ml of saline could inhibit the vastus medialis (VM) and 50 ml of saline could inhibit both rectus femoris and vastus lateralis. The presence of an extensor lag was noted which could implicate either the tibiofemoral joint or the patellofemoral joint (Maitland, 1991). The absence of any comparable signs in the lumbar spine, hip and tibiofemoral joint suggested that patellofemoral joint dysfunction might be the source of the symptoms. Objective assessment revealed a patella that was laterally shifted, laterally tilted and externally rotated, and tightness in the lateral retinaculum was also noted. Altered patella positioning may adversely affect patellofemoral biomechanics. However, it is acknowledged that the reliability of measurements of patella alignment abnormalities has been reported to be poor (Fitzgerald and McClure, 1995; Tomsich et al., 1996; Watson et al., 1999). Accessory movements of medial glide and medial rotation to the patella gave comparable signs. Neural screening showed a deficit in the L3 myotome. The lateral leg pain (P3) was further assessed in the slump position. Left leg dorsiflexion/inversion brought on P3 at 451 of knee flexion. Multidirectional functional running tests provoked P1 to a level of 8 out of 10 when running backwards and when cutting sideways from left to right. However, similar to the extensor lag noted previously, this finding does not discriminate between tibiofemoral or patellofemoral dysfunction. Corrective taping was applied to the patella and multidirectional running testing was repeated, and this time reported pain levels were 1 out of 10.

movement helps to ‘‘stir the inflammatory soup’’ (Butler, 2000, p. 53) increasing the fluid pH and decreasing acidity. This elevates the threshold at which nociceptors fire; a greater stimulus is therefore required to elicit a response (Butler, 2000). Severity, Irritability and Nature (SIN) factors (Maitland, 1991) allowed quick progression to grade IV to stretch tightened lateral structures. Patellar taping (see Figs. 2–4) in this case was used to maintain a stretch on the lateral tissues achieved in treatment. It was applied at the end of treatment two after it was established that medial glides (grade IV) were beneficial in reducing pain. Although effective in this case at significantly reducing pain, the decision to use patellar taping is controversial as it is unclear how the tape actually works (Harrison and Magee, 2001). Mini squats in the plie position were instructed to exercise the VM and complement the medial glide mobilisation, the aim being for the patient to gain active motor control around the patellofemoral joint. The function of the VM is to re-align the patella medially during extension of the knee. Any insufficiency of this muscle will increase the lateral drift of the patella, which may lead to patellofemoral pain (McConnell, 1986). A portable biofeedback machine was used in treatment sessions to ensure that the exercises were targeting the VM. The machine was then used for the home exercises, ensuring correct technique. A muscle-stretching regime was instructed as part of the home exercise programme to enhance the general condition of the knee joint. The influence of surrounding musculature is open to debate. Rouse (1996) questions the relevance of the iliotibial band (ITB) and its relationship with patellar problems. Mercer et al. (1999) state that the ITB is firmly attached to the linear aspera of the femur via the lateral inter-muscular septum. Therefore, clinical procedures for assessing/

6. Treatment Subjective questioning and objective assessment presented a strong case for patellofemoral joint dysfunction and the following treatment regime was instigated. It consisted of 6 treatment sessions which included 10 min of manual therapy and 20 min of active control work. The patient was also instructed in a home exercise programme. This consisted of rectus femoris and gastrocnemius stretching (15 s 4), 10 min of plie work using a biofeedback machine, and sliders 30 s 4 per night. Accessory movements to the patella gave comparable signs and so were used as the first treatment choice. Grade III medial glides (5 30 s) with a rest between sets were used. After treatment 2 this was progressed to Grade IV (5 30 s) with a rest between sets. These were performed to the patella to mobilize the joint through a more elastic phase and to increase joint nutrition. The

159

Fig. 2. Hypafix taping in a lateral–medial direction.


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patellofemoral problem the patient had been treated for was not the primary cause of his complaint. Shortly after his apparent recovery the symptoms returned and a decision was made to scan the joint. This showed a circular articular defect, 2.5 cm in diameter on the medial femoral condyle.

7. Discussion

Fig. 3. Hypafix re-enforced with strappal in identical lateral/medial direction.

Osteochondritis dessicans is a common disorder, affecting adolescents, Tatum (2000). According to Brier (1999), the medial femoral condyle, particularly the lateral portion, is the most common site for osteochondritis dessicans. It occurs more regularly in boys and patients who develop the condition tend to be very athletically active. The disease is characterized by a fragment of articular cartilage and subchondral bone that becomes separated from the underlying bone. Treatment of the condition is aimed at preservation of the articular cartilage. The patient’s age, sex and occupation clearly suggest that he could be a candidate for developing osteochondritis dessicans, yet, his patellofemoral joint became the primary focus for treatment. From a clinical-reasoning perspective combining the information gained from the patient’s past medical history, the objective assessment and the evidence available from the literature were very important; the key points were as follows:

successful reparative surgery at the age of 14; significant pain relief following patellar taping during the assessment; and a literature search failed to find any previous reports of osteochondritis dessicans recurrence.

Fig. 4. Strappal applied in a lateral supero-medial direction to rotate patella.

stretching the ITB should be re-examined. In this case no stretch was instructed for the ITB in the home exercises. However, exercises for rectus femoris and gastrocnemius were instructed due to their influence on the knee joint (McConnell, 1986). Home exercises were prescribed for the nervous system to maintain improvements achieved in treatment sessions. Sliders (a means of moving the nervous system without causing tension) were used to continue nourishment of the nervous system and induce mobilization in a non-sensitive way. Sliders were used in the slump position. As the ankle is dorsiflexed the cervical spine is simultaneously extended. This is then reversed so that as the ankle is plantar flexed the cervical spine is simultaneously flexed. This aids vascular dynamics and axonal transport along the nerve, Butler (2000). The treatment regime allowed the patient to return to football training. He successfully completed two consecutive training sessions pain free before being discharged. Unfortunately, it so happened that the

Following the decision to treat the patellofemoral joint, the treatment administered had a very positive effect on the symptoms and the patient successfully completed two consecutive training sessions pain free; this reinforced the consideration that the patellofemoral joint was the source of the symptoms. It is interesting to speculate as to whether there was any additional clinical testing that could have been performed to indicate that osteochondritis dessicans was a problem. Objective assessment of the tibiofemoral joint gave no comparable signs. Currently, using clinical testing it is not possible to differentiate between femoral condyle and meniscal dysfunction. Testing at the knee predominantly tests the meniscal structures. Even with compression or active loading it is difficult to attribute signs specifically to the femoral condyle. It is also interesting to consider why there was such an apparent improvement in symptoms to the level where the patient was able to complete football training, at a professional level, pain free when the problem was the

ARTICLE IN PRESS J. Davin, J. Selfe / Manual Therapy 11 (2006) 157–161

femoral condyle and yet the treatment was directed at the patellofemoral joint. It may be that altered mechanics at the tibiofemoral joint led to poor patellofemoral integrity, which in turn led to repeated micro trauma, which subsequently induced pain. One of the difficulties in trying to interpret this is that the treatment package consisted of a number of components any of which in isolation or combination could have had an effect. A recent report by Hinman et al. (2003) may shed some light on one of the components of the treatment package taping. These authors report the results of a blinded randomised-controlled trial of patellar taping in the management of osteoarthritic knees. In this report patellar taping was significantly more effective than placebo and no tape in a group of patients that included some patients who only had tibiofemoral joint disease. Although the report suggests that patellar taping can improve symptoms in patients who have only tibiofemoral problems, no explanation is provided as to how or why this occurs. It would seem that this patient’s condition provides another example of a femoral condition that initially responded to patellar taping. Further research is required to understand the mechanisms behind this pain-relieving effect.

8. Conclusion In sport the role of the first contact practitioner is already well established. In other, areas of musculoskeletal physiotherapy therapists are finding that they are becoming first contact/advanced practitioners with increasing levels of clinical autonomy, e.g. clinical specialists, extended scope practitioners and consultant therapists. It is vital that advanced practitioners wherever they are based, have the skills and knowledge to identify serious and/or unusual pathology when it presents. This case has highlighted the need for

161

clinicians to remain vigilant even when patients appear to be responding well to treatment. References Brier SR. Primary care orthopedics. USA: Mosby; 1999. p. 352. Butler DS. The sensitive nervous system, 1st ed. Australia: Noi Group Publications; 2000. Clinical Standards Advisory Group (CSAG). Back pain: report of a clinical standards advisory group on back pain, HMSO, 1994. Fitzgerald G, McClure P. Reliability of measurements obtained with four tests for patellofemoral alignment. Physical Therapy 1995;75(2):84–92. Harrison E, Magee D. Patellofemoral pain syndrome: the ongoing challenges in etiology diagnosis and management. Critical Reviews in Physical and Rehabilitation Medicine 2001;13(2&3):105–29. Hinman RS, Crossley KM, McConnell J, Bennell KL. Efficacy of knee tape in the management of osteoarthritis of the knee: blinded randomized controlled trial. British Medical Journal 2003;327: 135–41. Main CJ, Watson PJ. Psychological aspects of pain. Manual Therapy 1999;4(4):203–15. Maitland GD. Peripheral manipulation. 3rd ed. Oxford: Butterworth Heinemann; 1991. McConnell J. The management chondromalacia patellae: a long term solution. The Australian Journal of Physiotherapy 1986;32(4): 215–23. Mercer SJ, Rivett DA, Nelson RA. Stretching the iliotibial band: an anatomical perspective. New Zealand Journal of Physiotherapy 1999;August:5–7. Rouse SJ. The role of iliotibial tract in patellofemoral pain and iliotibial band friction syndromes. Physiotherapy 1996;82(3): 199–202. Sims K. Assessment and treatment of hip osteoarthritis. Manual Therapy 1999;4(3):136–44. Spencer J, Hayes K, Alexander I. Knee joint effusion and quadriceps inhibition in man. Archives of Physical Medicine 1984;65:171–7. Tatum R. Ostechondritis dessicans of the knee: a radiological case report. Journal of Manipulative and Physiological Therapeutics 2000;23(5):347–51. Tomsich DA, Nitz JA, Threlkeld AG, Shapiro R. Patellofemoral alignment reliability. Journal of Orthopaedic and Sports Physical Therapy 1996;23(3):200–8. Watson CW, Propps MM, Galt W, Dobbs D, Redding A. Reliability of the McConnell classification system of static patellar orientation. Journal of Sports Physical Therapy 1999;29(1):A-42.

ARTICLE IN PRESS


Book reviews Kathryn Oths, Servando Hinojosa, Healing by Hand: Manual Medicine and Bonesetting in Global Perspective, Altamira Press, ISBN 0759103933, 2004 (320pp., £ 32.95). This is an interesting and absorbing book, offering the reader an insight into the history, development and comparative contemporary practice of a number of manual medicine professions. The book’s anthropological perspective places present day practices in the context of traditional bonesetting, and also reviews the development of those practices in a number of societies around the globe. The 13 chapters each approach the subject from a different viewpoint, and high levels of scholarship are demonstrated. This reviewer was a little disappointed that two of the potentially most interesting and perhaps controversial chapters listed in the publisher’s release accompanying the book turned out not to have made it into the final version. One hopes they appear elsewhere.

As someone who has been engaged in teaching manual techniques for a number of years I found John O’Malley’s essay comparing chiropractic and ‘‘Hilot’’ models of treatment and skill acquisition particularly absorbing, with much of relevance to experienced teachers and practitioners as well as to perplexed students and novices. This is a well-written volume that deserves to be read. The book offers much to practitioners and teachers who have an interest in the origins of their work, or in how other practitioners approach their practice. It will also provide a fertile source of material for students who are engaged in Masters-level research. If nothing else, it serves to remind us that few, if any, of our professions are as special or as exclusive as they are sometimes believed or claimed to bey Clive Standen School of Health & Community Studies, Unitec, New Zealand

doi:10.1016/j.math.2005.08.004

Mario-Paul Cassar, Handbook of Clinical Massage. A Complete Guide for Students and Practitioners. 2nd ed., Churchill Livingstone, New York, ISBN 0443-07349-X, 2004 (price £32,99, 352pp.). The use of massage as a treatment modality is widespread amongst manual therapists. For this reason it is important that therapists are well informed about massage techniques and the clinical reasoning that surrounds its use. This book by Mario-Paul Cassar describes the application of massage as it relates to the various systems of the body and common pathologies that the therapist may encounter. In the early chapters he covers the fundamentals of the history and physical examination as it relates to the use of massage. This, however, seems to be covered at a fairly introductory level, which minimally emphasises the need for measurable objective and subjective signs to support the process of clinical reasoning. Palpation skills, however, are covered in quite a deal of depth and he considers well the various layers of

tissues and potential abnormalities which the therapist can feel. Chapter 3 of this book deals with the explanatory models of physiology behind massage. Although this section is quite comprehensive, there is a lack of consideration of well-controlled clinical trials in the use of massage. This leaves us with an explanatory handbook but minimal high-validity clinical evidence with which to base our practice. The rest of the book covers a wide range of conditions in which massage can be utilized ranging from systemic through musculoskeletal conditions. For each of these conditions the author sets out the indications, contraindications and the specific massage applications that could be considered. There is an emphasis on safety in practice throughout. In summary, this book could be considered to be a good hands-on text about massage, which provides a range of useful and practical management ideas for numerous conditions. The addition of sections on the need for measurable outcomes and the consideration of the

ARTICLE IN PRESS Book reviews / Manual Therapy 11 (2006) 162–163

growing body of clinical trials surrounding the use of massage would be welcome additions in future revisions.

163

Paul Andrew van den Dolder Justice Health, New South Wales, Australia

doi:10.1016/j.math.2005.08.003

M. Stanborough, Direct Release Myofascial Technique. An Illustrated Guide for Practitioners, Churchill Livingstone, ISBN 0443073902, 2004 (185pp., £ 24.99). I was pleased to be asked to review this text as I was looking for a helpful up-to-date manual for my own practice and as a reference for students. I found it very easy to read and as the author and forewords from Robert Schleip and Peter O’Reilly suggest it is a useful manual for the application of myofascial techniques. The initial chapters set out to provide an account of ‘‘the basics’’ including a chapter on developing a hypothetical model. There is a reasonable attempt at explaining the theories behind the myofascial/soft tissue dysfunction and the physiological effects of myofascial release. However supporting evidence is lacking, and when it is provided it is often dated. The author acknowledges the lack of good research; however I feel that if the reader is seeking a greater evidence base,

doi:10.1016/j.math.2005.08.002

especially in the current climate, then they should support this manual with their own search of the evidence which is now growing in this field. The second section of the book gives a regional account of different techniques to apply. There are particularly clear instructions on ‘‘how to’’ with headings to guide therapist and client positioning, the direction and type of technique. These descriptions are supported by photographic pictures which indicate the position but perhaps could have indicated the direction of the technique for the more novice practitioner. Overall this book may be criticised for lacking evidence however it could be a useful workbook or ‘aide memoire’ for clinicians and/or students in clinical practice.

John Hammond Faculty of Health and Social Care Sciences, St George’s University of London, Kingston University, UK

ARTICLE IN PRESS


Book reviews Kathryn Oths, Servando Hinojosa, Healing by Hand: Manual Medicine and Bonesetting in Global Perspective, Altamira Press, ISBN 0759103933, 2004 (320pp., £ 32.95). This is an interesting and absorbing book, offering the reader an insight into the history, development and comparative contemporary practice of a number of manual medicine professions. The book’s anthropological perspective places present day practices in the context of traditional bonesetting, and also reviews the development of those practices in a number of societies around the globe. The 13 chapters each approach the subject from a different viewpoint, and high levels of scholarship are demonstrated. This reviewer was a little disappointed that two of the potentially most interesting and perhaps controversial chapters listed in the publisher’s release accompanying the book turned out not to have made it into the final version. One hopes they appear elsewhere.

As someone who has been engaged in teaching manual techniques for a number of years I found John O’Malley’s essay comparing chiropractic and ‘‘Hilot’’ models of treatment and skill acquisition particularly absorbing, with much of relevance to experienced teachers and practitioners as well as to perplexed students and novices. This is a well-written volume that deserves to be read. The book offers much to practitioners and teachers who have an interest in the origins of their work, or in how other practitioners approach their practice. It will also provide a fertile source of material for students who are engaged in Masters-level research. If nothing else, it serves to remind us that few, if any, of our professions are as special or as exclusive as they are sometimes believed or claimed to bey Clive Standen School of Health & Community Studies, Unitec, New Zealand

doi:10.1016/j.math.2005.08.004

Mario-Paul Cassar, Handbook of Clinical Massage. A Complete Guide for Students and Practitioners. 2nd ed., Churchill Livingstone, New York, ISBN 0443-07349-X, 2004 (price £32,99, 352pp.). The use of massage as a treatment modality is widespread amongst manual therapists. For this reason it is important that therapists are well informed about massage techniques and the clinical reasoning that surrounds its use. This book by Mario-Paul Cassar describes the application of massage as it relates to the various systems of the body and common pathologies that the therapist may encounter. In the early chapters he covers the fundamentals of the history and physical examination as it relates to the use of massage. This, however, seems to be covered at a fairly introductory level, which minimally emphasises the need for measurable objective and subjective signs to support the process of clinical reasoning. Palpation skills, however, are covered in quite a deal of depth and he considers well the various layers of

tissues and potential abnormalities which the therapist can feel. Chapter 3 of this book deals with the explanatory models of physiology behind massage. Although this section is quite comprehensive, there is a lack of consideration of well-controlled clinical trials in the use of massage. This leaves us with an explanatory handbook but minimal high-validity clinical evidence with which to base our practice. The rest of the book covers a wide range of conditions in which massage can be utilized ranging from systemic through musculoskeletal conditions. For each of these conditions the author sets out the indications, contraindications and the specific massage applications that could be considered. There is an emphasis on safety in practice throughout. In summary, this book could be considered to be a good hands-on text about massage, which provides a range of useful and practical management ideas for numerous conditions. The addition of sections on the need for measurable outcomes and the consideration of the

ARTICLE IN PRESS Book reviews / Manual Therapy 11 (2006) 162–163

growing body of clinical trials surrounding the use of massage would be welcome additions in future revisions.

163

Paul Andrew van den Dolder Justice Health, New South Wales, Australia

doi:10.1016/j.math.2005.08.003

M. Stanborough, Direct Release Myofascial Technique. An Illustrated Guide for Practitioners, Churchill Livingstone, ISBN 0443073902, 2004 (185pp., £ 24.99). I was pleased to be asked to review this text as I was looking for a helpful up-to-date manual for my own practice and as a reference for students. I found it very easy to read and as the author and forewords from Robert Schleip and Peter O’Reilly suggest it is a useful manual for the application of myofascial techniques. The initial chapters set out to provide an account of ‘‘the basics’’ including a chapter on developing a hypothetical model. There is a reasonable attempt at explaining the theories behind the myofascial/soft tissue dysfunction and the physiological effects of myofascial release. However supporting evidence is lacking, and when it is provided it is often dated. The author acknowledges the lack of good research; however I feel that if the reader is seeking a greater evidence base,

doi:10.1016/j.math.2005.08.002

especially in the current climate, then they should support this manual with their own search of the evidence which is now growing in this field. The second section of the book gives a regional account of different techniques to apply. There are particularly clear instructions on ‘‘how to’’ with headings to guide therapist and client positioning, the direction and type of technique. These descriptions are supported by photographic pictures which indicate the position but perhaps could have indicated the direction of the technique for the more novice practitioner. Overall this book may be criticised for lacking evidence however it could be a useful workbook or ‘aide memoire’ for clinicians and/or students in clinical practice.

John Hammond Faculty of Health and Social Care Sciences, St George’s University of London, Kingston University, UK

ARTICLE IN PRESS

Manual Therapy 11 (2006) 164 www.elsevier.com/locate/math

Letter to the Editor I read with interest the paper by Cleland et al. on the immediate effects of thoracic manipulation in patients with neck pain (Manual Therapy 2005,10: 127–35), and wish to share some comments with your readers, in light of our practice. In 1998, the French Society of Manual Medicine (SOFMMOO) issued guidelines on cervical manipulation (Maigne, 1998; Vautravers and Maigne, 2000 and at www.sofmmoo.com, in English). One of them, the most important, advised against the use of maneuvers with rotational thrust in females under the age of 50 years. Instead of them, (non-thrust cervical techniques, and/or) thrust manipulations of the upper thoracic spine were recommended. Actually, it had been noticed empirically by the author that these latter could efficiently relieve some forms of common neck pain. The hypothetic mechanism was that they could act on


the cervicothoracic muscles (semispinalis, splenius) and relax them. I am pleased to see that, thanks to the study by Cleland et al., there are now serious scientific basis to this recommendation. References Maigne JY. les recommandations de la SOFMMOO. Rev Med Orthop 1998;52:16–7. Vautravers P, Maigne JY. Cervical spine manipulation and the precautionary principle. Jt Bone Spine 2000;67:272–6.

Jean-Yves Maigne President of the French Society of Manual Medicine E-mail address: [email protected]

Manual Therapy (2006) 11(2), 165

Diary of events

Janet G. Travell, MD Seminar Series, Bethesda, USA

The Belgian Scientific organisation of Manual Therapy (B.W.M.T.) presents ‘‘ECT 2006’’ ‘‘State of the art Managing Upper Limb Joint and Soft Tissue Disorders’’ A masterclass by Karim Kahn, Bill Vincenzino, Rachel Leary, JL Gielen, Ann Cools and Jean-Pierre Baeyens.

For information, contact: Myopain Seminars, 7830 Old Georgetown Road, Suite C-15, Bethesda, MD 20814-2432, USA. Tel.: +1 301 656 0220; Fax: +1 301 654 0333; website: www.painpoints.com/seminars.htm; E-mail: [email protected]

21, 22 & 23 September 2006 Venue: Provinciehuis, Antwerp, Belgium

Evidence-based manual therapy congress Further information: www.medicongress.com

Information & registration: www.bwmt.be or Tel./Fax: 0032 3 775 88 96

Intensive courses in Manual Therapy Further information: http://allserv.rug.ac.be/bvthillo If you wish to advertise a course/conference, please contact: Karen Beeton, Department of Physiotherapy, University of Hertfordshire, College Lane, Hatfield, Herts AL10 9AB, UK. There is no charge for this service.

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Manual Therapy Journal - Volume 11, Issue 2, Pages 91-166 (May 2006)

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

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

Manual Therapy Journal - Volume 11, Issue 4, Pages 241-358 (November 2006)

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

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 14, Issue 2, Pages 117-240 (April 2009)

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

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

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

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

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

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

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 13, Issue 1, Pages 1-90 (February 2008)

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

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

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

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

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

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

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

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 14, Issue 3, Pages 241-352 (June 2009)

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

Manual Therapy Journal - Volume 9, Issue 4, Pages 183-246 (November 2004)

Manual Therapy Journal - Volume 11, Issue 2, Pages 91-166 (May 2006)

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

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

Manual Therapy Journal - Volume 11, Issue 4, Pages 241-358 (November 2006)

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

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 14, Issue 2, Pages 117-240 (April 2009)

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

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

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

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

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

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

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 13, Issue 1, Pages 1-90 (February 2008)

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

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

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

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

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

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

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

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 14, Issue 3, Pages 241-352 (June 2009)

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

Manual Therapy Journal - Volume 9, Issue 4, Pages 183-246 (November 2004)

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