NZ JOURNAL OF SPORTS MEDICINEInstructions to Authors

GENERALThe New Zealand Journal of Sports Medicine is the official journal of Sports Medicine New Zealand, publishing material relevantto sports medicine and related disciplines. The New Zealand Journal of Sports Medicine welcomes submissions of originalmanuscripts from both members and non-members of Sports Medicine New Zealand in the following areas: sports medicine,sports physiotherapy, clinically relevant sports science, rehabilitation, coaching issues as they relate to sports medicine, exerciseprescription and training, sports chiropractic, sports podiatry, and sports psychology.

Manuscripts must not have been published elsewhere except in abstract form. Manuscripts will be reviewed by the editorial boardand/or experts in the field of interest. Submissions are in the following categories:

a Original Research b Case Reports c Review Articles d Editorialse Letters to the Editor f Sports Medicine Pearls g Policy Statements

SUBMISSION DETAILSManuscripts are to be sent to The Editor, New Zealand Journal of Sports Medicine, Sports Medicine New Zealand, PO Box 6398,Dunedin, New Zealand. Telephone +64 3 477 7887, facsimile +64 3 477 7882, email smnznat@xtra.co.nz. The manuscript textshould be submitted in MS Word format (if using Vista please save the file as Office 2003 compatible, ie, .doc. Please do not usestyles for headings, etc, ensure your manuscript is in the style ‘Normal’. (For submission of graphics, please see Tables, Illustrations,Figures, Photos below). The manuscript may be sent via email however one hard copy must also be submitted, including anytables, figures, and photographs. Manuscripts should be double-spaced with wide margins. Each page should be numbered. Themanuscript should include the following: title page; structured abstract (followed by five key words); introduction; methods;results; discussions; conclusion; acknowledgements; references; tables; figures.

Case reports are to have no more than two figures and are not to include an abstract. There should be no more than 12 referencesfor a case report. The structure of a case report is as follows: introduction; case report; discussion.

Structured abstracts are to be no longer than 300 words and should use the following subheadings: aim; study design; setting;participants/subjects; interventions; outcome measures; results; conclusions.

Abstracts for review articles should use the following headings: aim; data sources; study selection; data extraction; datasymphysis; conclusions.

The title page should include the title of the article and a running title not exceeding 45 letters and spaces, authors’ names (firstname, middle initials, last name), degrees, affiliations with institutes, contact details for the corresponding author (to include name,address, telephone, fax, and email).

The standard for spelling is to be in accordance with the Oxford Dictionary.

TABLES, ILLUSTRATIONS, FIGURES, PHOTOSOne hard copy of tables, illustrations, figures, photos, etc, must be submitted. Tables should be included on a separate sheet ratherthan in the body of the text. Identify all illustrations with the manuscript title, name of author, figure number, and. if necessary,identification of the top of the image, on the back of the illustration in pencil. All markings should be removed from x-rays beforephotographing. Please do not produce graphics in Microsoft Word. Graphics should be supplied in TIF, EPS or PDF format,preferably at a resolution of no less than 300 dpi.

STYLEDrug names: generic only are to be used. Abbreviations: the American Medical Association Manual of Style (9th edition 1998)(published by the American Medical Association, 535 North Dearborn St, Chicago, IL 60610, USA) is to be used for abbreviationstyle. The List of Journals Indexed in Index Medicus (Superintendent of Documents, US Government Printing Office, Washington,DC 20402, USA, DHEW Publication No. (NIH) 83-267;ISSN0093-3821) is to be used for abbreviations for journal titles.

REFERENCESReferences are to be numbered in alphabetical order. Names of journals should be abbreviated according to the format approved byIndex Medicus. All references listed must be sited in the text. Journal titles that are single words only should be spelt out in full.All authors must be listed. Pagination should be inclusive. Examples of the appropriate formatting of references are given below:

Journal Article: Speedy D B, Kelly M, O’Brien M. The effect of pre-exercise feeding on endurance exercise performance.NZ J Sports Med 1998; 26:34-37.

Book: McRae R. Practical fracture treatment. Edinburgh; Churchill Livingstone, 1989.Chapter in Book: Figoni S F. Spinal cord injury. In, Wikgren S (ed.): ACSM’s exercise management for persons with chronic

diseases and disabilities. Champaign: Human Kinetics, 1997; 175:179.COPYRIGHTThe New Zealand Journal of Sports Medicine is copyrighted by Sports Medicine New Zealand Inc. No portion(s) of the work(s)may be reproduced without written consent from the publisher. Permission to reproduce copies of articles for non-commercial usemay be obtained from Sports Medicine New Zealand Inc, PO Box 6398, Dunedin, New Zealand, phone +64-3-477-7887, fax +64-3-477-7882, email smnznat@xtra.co.nz.

The opinions expressed throughout thisjournal are the contributors’ own and donot necessarily relfect the view or policyof Sports Medicine New Zealand (SMNZ).Members and readers are advised thatSMNZ cannot be held responsible for theaccuracy of statements made inadvertisements nor the quality of the goodsor services advertised. All materialscopyright. On acceptance of an article forpublication, copyright passes to thepublisher. No portion(s) of the work(s)may be reproduced without written consentfrom the publisher.

PUBLISHERSPORTS MEDICINE NEW ZEALANDPO Box 6398, DunedinNEW ZEALANDTel: +64-3-477-7887Fax: +64-3-477-7882Email: smnznat@xtra.co.nzWeb: www.sportsmedicine.co.nz

EDITORDr Bruce Hamilton

ASSISTANT EDITORMr Chris Whatman

ContentsEditorialsBruce Hamilton ___________________________________________ 38

Chris Whatman ___________________________________________ 39

Interview withDAVID GERRARD _______________________________________ 40Bruce Hamilton

Best of British _____________________________________________ 44Chris Milne

Invited CommentaryTHE CENTRAL GOVERNOR OF EXERCISE ________________ 47PERFORMANCE: FACT OR FICTION?Simeon Cairns

Cardiology ConundrumsT-WAVE INVERSION IN ATHLETES _______________________ 51Mathew Wilson, Bruce Hamilton, François Carré, Hakim Chalabi

Case ReportACUTE CERVICAL MYELOPATHY IN A PATIENT __________ 53PRESENTING WITH KNEE INSTABILITYJoel Winders

Book Review‘BLAST FROM THE PAST’ _______________________________ 56Chris Milne

Conference ReviewACSM ANNUAL CONFERENCE DENVER 2011 ______________ 58

Postgraduate PonderingsNOT ALL WRIST LUMPS ARE GANGLIA ___________________ 61Daniel Pettigrew, Hamish Osborne

New Zealand Journal of

SPORTS MEDICINE

NZJSM Vol 38 No 2, 2011

SPORTS MEDICINENEW ZEALAND

EDITORIAL

38 NZJSM

When Chris Milne took the Editorial role in 2009, he paid tribute to the Editors before him, comprisingthe surprisingly short list of Noel Roydhouse, Dale Speedy and Peter Milburn. I would like to add mytributes, but add recognition of the huge influence that Chris has had on the journal, extending well

beyond his recent stint as Editor. It doesn’t take much looking through back issues of the NZJSM to see that Chrishas been a constant source of information, inspiration and intellect. Chris has provided vast amounts of materialfor the journal, and I would like to voice my appreciation for his efforts over many years. I look forward to hisongoing insight and involvement as the journal moves forward.

On taking on the role of Editor of the NZJSM, I recognise that one of the major differences between myself and mypredecessors in this role is that most Sports Medicine NZ members probably have no idea who I am. This mayreflect my working career, which to date has predominantly been offshore; what started as a windsurfing sojournto Perth, Western Australia after completing physical education and medicine at Otago University and never wantingto open a book again, turned into an extended adventure through sports medicine in Australia, the United Kingdomand now Qatar. I hope that I can add value to the journal over the next phase of its development.

The developmental direction of the journal has clearly been a longstanding and hot topic. Previous editorial titlesincluding “Whither the Journal” (Chris Milne 1999), “The Way Forward” (Dale Speedy 2002) and “A Call toArms” (Peter Milburn 2006) all addressed this issue. At its outset, the journal had clinical sports medicine as itscore (Milburn 2006), with the goal of providing SMNZ members with a high quality, useful and relevant resource.These goals remain unchanged, but with the passage of time the number of challenges that the journal has faced inmeeting those goals has increased. Information availability via electronic resources was recognised as a threat byChris Milne as long ago as 1999 (“Whither the Journal” – and addressed by Dr Iain Bell “Sports Medicine and theInternet 2000”) and this remains a challenge for the NZJSM, to which we must continue to adapt. In 2002, aneditorial debate presented, essentially as diametrically opposing alternatives, the development of a high qualitymedline listed academic journal (“The Way Forward” 2002 Dale Speedy) and the maintenance of a clinicallyuseful journal for the membership (“Medline Listing” 2002 Peter Sperryn). This debate was rejuvenated in 2007(“Who do we Serve?” Peter Milburn 2007). My tendency is to side with Gregory Kolt (Summer 2002) when hesuggests that a medline listed journal can still have relevance for the membership, but I recognise that the keydeterminant of both of these objectives is the consistent inclusion of quality content in the journal. Hence our goalfor the journal is to encourage quality content, and that will, as always, depend on you the membership. We havea number of initiatives that we would like to establish, re-establish and re-create, in order to facilitate a regularflow of high quality manuscripts. I hope that you will see the evolution of this over the next few editions.

In this edition, you will see the continuation of the “Best of British” series, which first appeared in 2005. We havealso consolidated student and post-graduate student manuscripts into a “Post-grad Ponderings” reflecting theimportance of encouraging early publishing careers. I hope that as we move forward you will take time from yourclinical practices to both read the journal and consider submitting a manuscript.

Evidence Based MedicineIn this journal’s “Best of British”, Chris Milne chose the article by Paul McCrory1 and colleagues as his pick ofarticles. This BJSM editorial, entitled “Sports and exercise medicine – specialists or snake oil salesmen?” takes abig swing with a long handled bat at sports medicine practitioners who reportedly utilise non-evidence basedtechniques in their practice. I entirely agree with Chris that this article is worth reading, pondering, and ponderingsome more. Being one of the co-authors on the manuscript that this article criticises2, this choice by Chris hasgiven me a great opportunity for further rebuttal3 at the size of the swing that was taken.

Evidence based medicine is frequently associated with level one or two studies, providing “definitive” evidence orotherwise for a treatment, technique or intervention. However, it is important to remember that while the leastsubstantiated form of evidence, expert opinion forms a recognised part of the clinical evidence base. For proponentsof evidence based medicine (of which I am one), it is easy to fall back on the lack of evidence from high quality,double blind randomised controlled trials, and exclude a treatment option on this basis. This appears to have beenthe approach that McCrory and colleagues have taken, claiming the scientific and moral high ground on this issue.However, in 2004, even Chris Milne himself decried the increasing reliance on evidence based medicine andhighlighted the need to “keep honing your critical faculties and have faith in your own gut instincts based onexperience”.

I agree with McCrory and colleagues that sports medicine practitioners whom suggest that the onus is on scienceto disprove any practice (which experts may suggest work), rather than the burden of proof being on those who useit to substantiate its use, are working outside the acceptable norm. However, I moderate this by recognising thatwithout practitioners who are prepared to think outside the square, go back to basic principles and explore noveltreatment options (within the legal limitations we have) based on those principles, it is unlikely that we would ever

EDITORIAL

Vol 38 No 2, 2011; 39

move forward in any field of medicine. Remarkably, as you all know, most of what we do in sports medicine lacksa substantial evidence base and the onus is on us all to constantly be challenging this status quo.

I believe that to ignore the evidence of experienced practitioners and years of accumulated experience wouldpotentially be to our (and our patients’) great cost. That experience should be harvested, evaluated and scientificallychallenged by those with the skills and abilities to do so. That is the benefit of enquiry, interdisciplinary sharedapproaches and supportive communication; this is what we should be promoting within sports medicine.

1 Franklyn-Milller A, Etherington J, McCrory P. Sports and exercise medicine—specialists or snake oil salesmen? BritishJournal of Sports Medicine 2009; 45(2):83-84.

2 Orchard J, Best TM, Mueller-Wohlfart H-W, et al. The early management of muscle strains in the elite athlete: best practice ina world with a limited evidence basis. British Journal of Sports Medicine 2008; 42:158-159.

3 Orchard J, Best T, Hunter G, Hamilton B. Response to McCrory et al. “Sports and exercise medicine - new specialists or snakeoill salesmen?” British Journal of Sports Medicine 2009;bjsm.2009.068999Published Online First: 29 November 2009doi:10.1136/bjsm.2009.068999.

Dr Bruce HamiltonEditor

A colleague recently suggested that all research is important. In the discussion that followed I proposedthere was increasing amounts of research that may have little clinical relevance, to which he replied thatwithout each grain of sand you would not have a beach! A nice analogy which undoubtedly has merit, but

I still get the impression there are large parts of the beach that many clinicians involved in sports medicine wouldnever bother visiting. Perhaps the beach has just got too big, built up by forces other than those ensuring highquality, clinically relevant development.

A common theme in all the discussions I’ve heard about this journal over the years has been the wish to keep itrelevant to the clinicians – especially local clinicians. Having been a musculoskeletal/sports physiotherapist forover 10 years I offered to assist with the journal in the hope of helping to continue that theme – easy to say, harderto do. As a full time academic I now have an obligation to undertake research - or should I say publish! Hopefullymy time as a clinician and ongoing contact with clinically active colleagues will help maintain the clinical relevanceof this research. It’s always frustrating to attend conferences where the discussion between the researchers andclinicians is all too often a confused conversation. Clinicians want the take home message for clients on Monday– often they don’t get it. This process could be assisted by more collaboration between clinicians and researchersand/or contributions to the journal from clinicians (such as case studies). You may all feel that you are too busy butif you have an idea or you want help to get something done then feel free to let me know. For most there is theadded bonus of professional development points to be gained.

Research in sports medicine is important, especially as the call for evidence based practice continues to grow in allrelated disciplines. However in these times of access to limitless sources off online information the poor oldclinician may struggle to find the ‘golden sand’. To my way of thinking there is a major onus on the researchers,reviewers and editors to publish quality findings in a way that means something to clinicians. Clinicians should beable to read information in well established journals expecting a high quality of methodology and results thattranslate into practical applications.

At the risk of getting a little technical one example where researchers could assist is by avoiding reliance on p <0.05 when deciding if outcomes are useful or not. Many have suggested it is better to consider the size of the effect(and its confidence interval) relative to a justified smallest clinically important effect.1 This allows inferences tobe made as to the likelihood the outcome of a study is clinically/practically useful. Recently we made the followingstatement in a review on the effect of kinesio tape on pain – “the effect of kinesio tape is trivial when compared toestablished thresholds for meaningful change”,2 this has meaning to a clinician. Greater use of this style of reportingresults would help clinicians to find the sunny patch on the beach – or at least give then confidence they areswimming between the flags!

1 Hopkins W G, Marshall S W, Batterham A M, & Hanin J. Progressive statistics for studies in sports medicine and exercisescience. Medicine and Science in Sports Exercise, 2009; 41(1), 3-13.

2 William S, Whatman, C, Hume P A, & Sheerin K. Kinesio taping in treatment and prevention of sports injuries: A meta-analysis of the evidence for its effectiveness. Sports Medicine, 2011, In Review.

Chris WhatmanAssistant Editor

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INTERVIEW

Since 1999 when WADA took over responsibility for anti-doping policy and implementation we have seenmany changes; how do you feel that WADA has done over this time?

In 1999, WADA set itself the task of bringing consistency to the world of anti-doping. To be truthful I believethey have made huge strides and although the war is still being waged, several critical battles have been won.

Notable successes include consistency in laboratory accreditation, the prohibited list, application of an informedTUE process and the enforcement of harmonised sanctions across International Federations. These areas areunder consistent review and with a few notable exceptions, IFs, NOCs and Governments are all fully compliantwith the WADA Code and the UNESCO Convention against the misuse of drugs in sport.

Over and above catching athletes who may be deliberately cheating, do you believe that WADA, sportsmedicine, sport science and the legal field have been able impact on the desire of athletes to cheat in order towin?

I sense that these organisations and professional disciplines have been successful in engendering a commonethical approach to the misuse of drugs in sport. This is evident when athletes provide feedback on howcheating should be dealt with and how regulations such as the “whereabouts” requirements should beimplemented. It is right and proper for peer review and opinion to be sought on all issues of anti-dopingreform. The athletes themselves deliver a consistent, strong message condemning all forms of cheating -sadly this is offset by a small minority of underachieving competitors who are seduced by financial return ormalpractising health professionals or coaches.

Where do you believe the future challenges lie for WADA – is gene doping the future threat to sport?

Clearly gene doping represents unchartered waters. However I am informed that the potential exploitation ofthis technology is not only possible in humans but is, in fact, already demonstrated in the laboratory animalmodel. Using viral vectors, genes expressing traits desirable for elite athleticism have already been introducedand shown to benefit their recipients. Bigger muscles, enhanced EPO production and vascular proliferationare among the advantages endowed by gene transfer technology.

WADA has recognised this potential and has enlisted the advice of some of the world’s most celebratedgenetic researchers, to anticipate how this form of performance enhancement may present, and just as important,how it may be detected.

Even post the 1998 Tour de France, Cycling as a sport has been rocked by numerous drug “scandals”. Doyou believe that international cycling has finally cleaned up its act?

Associate Professor David GerrardOBE CNZM MBChB(Otago) FACSP

David Gerrard, academic, Olympian and Commonwealth swimming gold medallist, is an AssociateProfessor at the University of Otago where he is Director of Development and Alumni Relations inthe Office of the Vice Chancellor.

David is Chair Emeritus of Drug Free Sport New Zealand, the New Zealand Drowning PreventionCouncil, and an immediate past Member of the Medical Committee of the World Anti-DopingAgency (WADA) where he chaired the WADA Expert Group on Therapeutic Use Exemption.

His publications and areas of medical research include paediatric sports medicine, injury prevention,bioethics and anti-doping strategies in sport.

He was an Olympic Team Physician in 1984 and 1988, Chef de Mission of the New Zealand Olympic Team to Atlanta(1996) and Medical Commissioner in Sydney (2000), Athens (2004) and Beijing (2008).

David remains an avid surfer, fancier of Central Otago wines, student of calligraphy, reader of historic novels and devotee ofthe Highlanders Rugby Team.

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INTERVIEW

The reputation of cycling has definitely taken a hammering over the past couple of decades with numerousexamples of drug misuse. To be fair, I believe they did themselves no good by engaging in a number ofattempts at “cover-up”. In the top professional ranks, Landis, Cantador and of course Armstrong have eitherreceived sanctions or are linked with doping scandals. There has been clear evidence that the drugs issue incycling has involved a sophisticated network of collaboration implicating support staff, medical advisors andcoaches. However there are signs that the tide is changing and the ICU is now sitting at the WADA table andmaking every attempt to improve the reputation of their sport. The imminent US Federal case against LanceArmstrong will unfortunately air some dirty laundry, but the public deserves to know the truth in thislongstanding debate. So watch this space.

There have been repeated changes to the WADA prohibited list when it comes to the prohibition of asthmamedications. Currently, all B2-Agonists except for salbutamol require a full TUE. Is this just based on a lackof evidence for the other generic B-agnoists, or is there something specifically different about salbutamol thatwarrants this specific treatment?

The whole debate over the place of beta-2 agonists on the prohibited list has consumed a disproportinateamount of time and energy. There are many who contend that the ergogenic effect of these agents is highlyquestionable when taken in appropriate therapeutic doses. Clenbuterol used systemically is an obviousexception. However the nub of the matter to my mind relates to two issues. First the recognised high prevalenceof clinically proven, exercise-induced bronchospasm in athletes and second, the fact that we appear to befocussing on the wrong group of “potential” sports drug misusers. Does this group represent the real drug“cheats”? I suggest we should be investing our energy in monitoring the misuse of peptide hormones andother heavy duty agents with far greater potential for ergogenesis.

However, I qualify these comments by saying that there is a significant duty of care and professionalresponsibility to be borne by all physicians treating athletes with asthma in any one of its variant forms. Anaccurate diagnosis based on history, clinical findings and confirmatory laboratory investigations must at alltimes underpin the diagnosis. Critical to the successful management of asthma is patient education and athletesare no different to any other patients in this regard.

Cardiac screening of athletes is gaining increasing profile and academic attention around the world, withgreat debate surrounding the use of ECG and Echocardiography. Part of this argument becomes a cost –benefit argument, which is particularly relevant in a small country like New Zealand. In Italy, all participantsin sport are required to have a cardiac clearance. Do you feel in New Zealand that we are doing enough toprotect our elite and non-elite athletes from potential underlying cardiac anomalies? What would you like tosee us doing?

Compulsory pre-participation screening of athletes remains a contentious and highly expensive exercise,cost-prohibitive in the New Zealand setting. I personally favour the system whereby athletes who are identifiedin our elite “carded” pool become the clinical responsibility of the Medical Director for that sport. At thatpoint it ought to be decided on the basis of history and clinical examination whether “cardiac screening” is anappropriate or necessary option. To undertake extensive screening prior to all or any sports participation isbeyond our resources and is of dubious benefit in terms of detecting any undeclared cardiac pathology. I amaware of the Italian mortality data that relate to the implementation of pre-participation screening and find thecost-benefit argument unconvincing.

Platelet Rich Plasma (PRP) appears to be increasing in popularity, despite limited clinical evidence to supportits use. Over the years sports medicine has had many “fads”; do you think this is another, or do you think thatthis may eventually turn out to be a useful tool for the musculoskeletal specialist?

It would appear that the jury is still out on the real therapeutic benefits of PRP. The WADA List Committeewas of the mind to withdraw this intervention from the list of prohibited practises and I supported this move.There was no convincing scientific evidence that PRP met any of the criteria for inclusion on the ProhibitedList and at the end of the day it continues to be applied by many physicians in the management of a range ofmusculoskeletal disorders with varying rates of success.

Many years ago, in this journal (I think it was a letter to the editor!) you wrote about the use of non-steroidalanti-inflammatory drugs in sports medicine. Over the last 10 years there has been increasing evidence as to

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INTERVIEW

the impact that NSAIDs may have on athletes bodies. What is your feeling about the use of NSAIDs in eliteand recreational athletes and your impression of the current utilization patterns of clinicians?

Yes I did comment on the cavalier use of NSAIDs, and still contend that the potential of these agents is notwell understood by many clinicians. And when I hear anecdotal reports of team physiotherapists and othersupport staff handing out NSAIDs to athletes on scant evidence I am particularly concerned. NSAIDs have apotent anti-prostaglandin effect that has the potential, amongst other things to reduce renal vascular perfusionand the rate of glomerular filtration. In a stressed, dehydrated athlete already imposing insult upon his kidneys,the added effect of NSAID administration is a potential for life-threatening consequences. There have beenseveral documented cases of acute renal failure in athletes mediated through the diminished vasodilatoryeffect of prostaglandins. This potential also exists with the use of selective COX-2 inhibitors and over-the-counter agents heralded as “safe” alternatives. The bottom line is that while NSAIDs have a place in the acutemanagement of musculoskeletal injury, they should be considered along with primary anti-inflammatorymeasures and physical therapy. Their use ought to be under the direction of a physician and avoided wherethere may be added renal stress accentuated by physical insult through sport.

Sports medicine has many elements (elite athlete care, public health, research, recreational athlete,musculoskeletal, medial elements), as well as being truly multi-disciplinary, which is what attracts manypractitioners to the field. You have witnessed a massive development of sports medicine over the last 20years, but where do you think we will be in 20 years’ time?

I have often reminded students that sports medicine should not be linked only with the popular image ofdoctors tending the needs of elite, highly-paid professional athletes whose demands are often inconsistentwith “normal” clinical practice. Sports medicine is a team game that applies equally to issues of public healthand generic exercise prescription for the wider population. Sport and exercise medicine is an appropriatereflection of the scope of our work that has developed over the last 20 years. What the future holds is anyone’sguess but I would favour a stronger relationship with public health as it specifically relates to children andpre-adolescence. We need to establish early patterns of physical activity and healthy eating and address publichealth issues such as smoking and alcohol misuse in children. Obviously the clinical implications of physicalactivity for an aging population is becoming another issue of increasing economic significance. I am sure thatthese will be important challenges for the sport and exercise physicians of the future.

Achieving success on the international stage has always been difficult, but seems to be increasingly challengingwith vast resources being mobilised behind athletes in some countries. What do you see as the challenges toNZ’s success internationally in the future, and how can sports medicine contribute?

It is an overused expression that Kiwi athletes “punch well above their weight” on the international scene.However hackneyed, I hold with this statement and consider New Zealand – a tiny country with a populationof less than that of the state of NSW to continue to produce some of the World’s most outstanding athletes.

I am confident that this trend will continue, with the proviso that we aren’t seduced into spreading ourselvestoo thinly. At the risk of offending supporters of certain sporting codes, we are unlikely to ever produce anOlympic gold medallist in gymnastics or platform diving or a World Championship team in ice hockey orhandball. But we continue to excell in rowing, equestrian, cycling, athletics and yachting and team sportssuch as rugby, netball and possibly cricket.

I strongly advocate the focussed use of our limited financial and human resources to the events and sports inwhich we traditionally excel. Our teams to Olympic and Commonwealth Games should be restricted to thosewith a proven track record and not as the opportunity to provide “experience” for a future star or simply tomake up the numbers. Potential may be tested at regional events, World Cups and other international eventsthat have become so common-place in almost every sport. As a fledgling swimmer in the 1960s I competed inone Commonwealth Games before heading to the Olympics two years later without any intervening overseasexperience. It was only at my final Commonwealth Games that I felt remotely familiar with the internationalcompetitive arena. Today, swimmers have a schedule of international events placed before them each yearand ample opportunity to gain experience and to demonstrate their capabilities.

Finally we must recognise that sport is part of our social fabric in this country and we are obligated to providetalented youngsters with the opportunity to develop as people as well as athletes. We have been blessed witha recent crop of outstanding sports ambassadors in this country – athletes of the ilk of Sarah Ulmer, Hamish

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INTERVIEW

Carter, Georgina and Caroline Evers-Swindells, Valerie Adams, Daniel Carter and Richie McCaw. Add thoseto outstanding names of the past like Sir Brian Lochore, Sir Murray Halberg and Yvette Williams and wequickly realise that the best athletes are also amongst the best people.

Undergraduate training in sports medicine used to be non-existent. Has this changed now, and what wouldyou like to see in the future?Undergraduate sports medicine training still remains essentially non-existant. Medical school curricula givelittle lip service to the topic as such but ironically use elements of sport and exercise medicine to teachsubjects such as orthopaedics, musculoskeletal medicine, epidemiology and public health issues includingasthma, diabetes, coronary heart disease and obesity. I would like to see more sport and exercise-related casesbeing introduced to undergraduate students in medicine to reflect the broad implications of our specialistdiscipline.

In New Zealand, post-graduate education in sports medicine was pioneered in Auckland and Otago Universitiesthrough diploma studies that continue to provide general medical practitioners with the basis for their interestin the subject and a qualification required by almost every sport seeking to appoint a medical director.Specialisation in sport and exercise medicine and vocational registration in New Zealand is obtained throughFellowship of the Australasian College, still regarded enviously by many other countries.

Increasing numbers of physiotherapists are completing PhD’s in clinical research, adding greatly to theevidence base in sports medicine practice. Unfortunately, limited numbers of physicians are involved inresearch on a regular basis, which is required if we are to move the profession forward. Do you have anyobservations or thoughts on how to increase our physician involvement in research?

There is a College requirement for research necessary to obtain Fellowship and this is consistent with othermedical colleges. However very few clinicians find time to continue their research interests. There is a wealthof research opportunity and physicians so inclined are encouraged to collaborate with groups existing atrecognised tertiary institutions.

Dunedin is a great place to train in medicine and sports medicine (Editor’s parochialism!) - what are some ofthe new developments going on down there to keep it that way?!

Naturally I am about to declare a marked bias for the University of Otago and this will come as little surpriseto those who know me.

Otago still boasts a unique collaboration of kindred academic schools and departments that provide the scopeof teaching in sport and exercise medicine. These include schools of medicine, physiotherapy, physical educationand pharmacy as well as departments of human nutrition and clinical psychology and an injury preventionresearch unit. The University is complemented by sports facilities including the Moana Pool complex, theCaledonian athletics track, field hockey turf and the new Dunedin Stadium all located within 10 minutes ofthe main campus. The Dunedin Stadium, to be opened for Rugby World Cup, boasts the only fully covered,natural grass stadium in the world.

Many thanks.

Dr Bruce HamiltonEditor

Vol 38 No 2, 2011; 43

BEST OF BRITISH

Welcome back to thisregular column.Although I have passed

on the editorship of the Journal tomy colleague Bruce Hamilton, Iwill continue to contribute thiscolumn. It seems to have capturedthe interest of readers and I believeit is a worthwhile service to ourmembers, so here goes.

FebruaryThe February issue of BJSMcontained a number of usefularticles. One of the editorialsrelated to revalidation of sport andexercise medicine from a UKperspective. This is worthconsulting for those of us who haveconcerns regarding audit andreaccreditation to get an externalperspective on the issue.

The second editorial was entitled‘High performance sportsmedicine: an ancient but evolvingfield’. Two of the leading UK-based protagonists, Cathy Speedand Rod Jaques, explain that highperformance sports medicinestarted in the era of Hippocrates,who described the use of a medicalapproach is to optimise the effectsof and recovery from training, butthen lay dormant until the 19th

Century, re-emerging when a newera of formal competitive sportbegan. They define highperformance sports medicine as theprovision of an integrated model ofmedical care of the highperformance athlete. It focuses onthe maintenance and optimisationof health, wellbeing andcompetition sporting performanceunder circumstances of highphysiological and psychologicalstress. They champion theinterdisciplinary model and this islabelled the Integrative Medicineand Science Support Team(IMAST). They describe the roleof the physician as one of medicalguardianship and go on to explainthat the working environments canvary from the conventional clinicalsetting to the side of a pitch ortraining venue, a hotel room, orindeed by distances through

telemedicine approaches. As wellas caring for the athletes, thepractitioner will have to providecare for the support staff; this leadsto an occupational health role.They recommend further researchto document responses to trainingprogrammes that accuratelyreplicate the demands of highperformance sport so that these canbe integrated into routine clinicalpractice. This article should becompulsory reading for all of ourpractitioners who have significantcontact with elite athletes,especially those allied to the NewZealand Academy of Sport.

My most recommended article inthis issue is entitled ‘Sports andexercise medicine – specialists orsnake oil salesmen?’ Written byleading practitioners including PaulMcCrory, the article concentrateson the promotion of Actovegin, adeproteinised hemodialysatemanufactured from calf blood pluslocal anaesthetic, and Traumeel, acompound containing 12 botanicalsubstances. Comments from UK-based physicians suggest that theyare under pressure by the athlete touse Traumeel S and that the onuswas on “science” to disprove thistherapy rather than the burden ofproof being on those who seek touse it. As the authors point out, thisis wholly at odds with the practiceof medicine and other medicalspecialties. They go on to say thatwe must resist any pressures whichmay compromise our standing asrational, safe evidence-basedclinicians worthy of specialiststatus. To do any less compromisesour standing as a specialty. To allthis I would say “hear hear”. Thereare far too many substances beingconsumed by suggestible athleteswith little or no evidence base fortheir use and potentially harmfulside effects. It is our role asresponsible clinicians to be trueguardians of and advocates forathlete health and wellbeing and wesurrender this role at our peril.

The third article worthy ofcomment is entitled ‘Contribution

of free play towards physicalactivity guidelines for New Zealandprimary school children aged 7-9years’. The authors found that nochildren met the recommended 60minutes of moderate to vigorousphysical activity each day. Notsurprisingly, they found childrenwere more active during schoolplaytime compared to after schooland weekends. These arecharacteristics of the screengeneration, be it PlayStation,television, Facebook or a mobilephone. Even the most coordinatedof us would find it difficult to runat four minute kilometre pace whiletexting or looking at a screenwithout colliding with others.

Another article of New Zealandauthorship in the same issue wasentitled ‘Spreading the word onsports concussion: citation analysisof summary and agreement,position and consensus statementson sports concussion’. Arguablyone of the major achievements ofsports medicine in the last 20 yearshas been the publication ofinternational consensus guidelinesfollowing the meetings held inVienna in 2000, Prague in 2005 andZurich in 2008. These plus otherconsensus guidelines from ACSMpublished in 2005 have been widelydistributed, with co-publications inmany journals. This has led toincreasing penetration of theircontents throughout the academicand clinical community asevidenced by the rising number ofcitations. Sridhar Alla, JohnSullivan et al from the Universityof Otago School of Physiotherapywere responsible for collating thispaper.

Finally in the February issue, therewas an excellent pictorial essay onthe spectrum of knee extensormechanism injuries. This wascollated by Bruce Forster andcolleagues from the Department ofRadiology in the University ofBritish Columbia, Vancouver. Theauthors beautifully outline thespectrum of knee extensormechanism injuries with well

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labelled diagrams to emphasise keypoints. They use x-ray and MRIimaging extensively and this articleis highly commended for allclinicians who deal with kneeinjuries, which is most of us.MarchThe March issue contained a usefuleditorial on physical activity asmedicine, with the second half ofthe title being ‘Time to translateevidence into clinical practice’.The article uses New Zealand’sgreen prescription as one of theexemplars of this process. This isbasically a call to arms by seniorSwedish researchers from theworld-renowned KarolinskaInstitute to incorporate exercise intoour daily routine of prescribing.The definitive reference work is‘Physical activity in the preventionand treatment of disease’ and wasoriginally published in Swedish.However, a recently translatedEnglish version is now availableand is the most comprehensiveguide published to date. It consistsof 47 chapters including 33 onspecific aspects of different organsystem disease and how treatmentcan be helped with the aid ofphysical activity.

Later in the same issue is an articleon atrial fibrillation in endurancetrained athletes. This is written byPaul Thompson, one of the worldexperts in the area, plus co-authors,and summarises the best availablecurrent knowledge. In essence,management of atrial fibrillation inathletes follows similar principlesto those used to manage atrialfibrillation in the generalpopulation. The authorsrecommend determining thefrequency of symptomatic AFepisodes via an event recorder.Their first-line treatment wouldinclude pharmacologicalsuppression with Flecainide 50mgtwice or three times daily. Withpersistent atrial fibrillationanticoagulation may be required.They mention radiofrequencyablation as an additional attractivetreatment approach and ourexperience with this intervention is

growing all the time; I suspect thatwithin a few years it will assume asignificantly greater place inmanagement. The main thing to beaware of with highly competitiveathletes is that, if at all possible,they should be maintained in sinusrhythm. The mere presence of atrialfibrillation causes a drop off inmaximal cardiac output and this isclearly unacceptable to athletes insports which require a high level ofaerobic fitness.

Later in the same issue there is acontinuation of the excellent serieson supplements. This particulararticle discusses glutathione,glutamate and glutamine. Itsauthors include the renowned EricNewsholme of Merton College,Oxford, UK, who sadly diedrecently. He worked with HansKrebs in his early days and wasamong the first to suggest thatglutamine deficiency may be alimiting factor in the ability to trainhard. Glutamine supplementationhas been studied by several authorswith mixed results. Some havefound an ergogenic effect but mosthave found no benefit. The currentconsensus would suggest thatglutamine is effective in decreasingthe self-reported incidence of upperrespiratory tract illness but nospecific evidence of an effect onany particular aspect of the immunesystem has been proven thus far.

April SupplementThe April supplement was entitled‘Tackling osteoarthritis in sport’.Timed to coincide with the IOCWorld Conference on Prevention ofInjury and Illness in Sport held inMonaco recently, the issue providesan excellent update on the currentstate of play with regard toosteoarthritis and sport. MarcPhilippon in Vail, Colorado,reported on innovations in hiparthroscopy and surmised that ifFAI and the associatedchondrolabral lesions can beidentified early and treatedappropriately, athletes could getback to their same level of activitywith good outcomes. They make a

strong case for active interventionto resolve bony impingement in aneffort to halt the progression ofosteoarthritis.

Later in the same issue there wasan article entitled ‘Contact sportand osteoarthritis’. As the greatcoach Vince Lombardi pointed out,dancing is a contact sport whereasfootball is a collision sport. Bearingthis in mind, it is no surprise thatcollision sports are associated withincreased development ofdegenerative arthritis in later life.Some of these cases result fromtraumatic injury to the ACL or otherstructures, whereas others havemore of a genetic basis. Theauthors conclude that injuryresulting in joint damage is thegreatest single risk factor for laterarthritis. This is best termedposttraumatic arthritis rather thanosteoarthritis.

Meniscal tears have long beenimplicated in the development oflater degenerative change and anarticle by Ian McDermott entitled‘Meniscal tears, repairs andreplacement: their relevance toosteoarthritis of the knee’ exploresthe issue in depth. Mostexperienced surgeons will tell youthat the previously recommendedtreatment of completemeniscectomy led to dramaticdegenerative change in the ensuingcouple of decades. More recenttreatment via arthroscopic partialmeniscectomy has lessened thatrisk but not eliminated it entirely.Current research focus is onmeniscal repair and the use ofmeniscal scaffolds or thereplacement of the entire meniscusby meniscal allografttransplantation. Results of theseinterventions are under intensescrutiny and the jury is still out –watch this space.

Imaging studies are not alwaysperfectly correlated with clinicalsymptoms and David Felson writesin the same issue regarding imagingabnormalities that correlate withjoint pain. Writing from the North

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American perspective, where MRIis used routinely, he concludes thatjoint pain often originates in thebone or synovium so, logically,these are the places we should lookfor abnormalities.

David Hunter from theRheumatology Department ofRoyal North Shore Hospital inSydney believes that we need aparadigm shift in our managementof lower extremity osteoarthritis inan excellent article in the Aprilissue. He believes we need to focuson people at high risk of developingor with early stage disease in whichstructural changes may bepreventable or reversible.Currently the major focus is on latestage disease. He believes weshould focus on the modifiable riskfactors, e.g. altered alignment,obesity and muscle weakness, andtarget each of these specifically.

Finally in the same issue, there is aposition statement from theInternational ParalympicCommittee on the scientificprinciples of classification inparalympic sport. This should berequired reading for all clinicianswho have a significant involvementin paralympic sport.

AprilThe routine April issue of BJSMconcentrated on tendinopathy. Itincluded leading articles from suchluminaries as Hakan Alfredson,who wrote an excellent one pageeditorial entitled ‘Where to nowwith achilles tendon treatment?’‘Where to’ includes mini surgicalscraping for patellar tendinopathy.

Later in the same issue there is acomparative study betweensclerosing Polidocanol injections orarthroscopic shaving; 52 patientswere studied and both techniquesshowed good clinical results butpatients treated with arthroscopicshaving had less pain and returnedto sport more rapidly. This is aprocedure which may gain morewidespread acceptance as a resultof these findings.

The technique of Doppler guidedmini surgery to treat midportionachilles tendinosis is described byAlfredson in the same issue, and hereported good short term results in103 patients with midportionachilles tendinosis. The mean scoreon a visual analogue scaledecreased from 77 pre-operativelyto 2 post-operatively.

Topical glyceryl trinitrate has beenused for a variety of tendonproblems; George Murrell andcolleagues report on the effects oftopical GTN for treatment of lateralepicondylosis at the elbow. Theyhad previously reported short termbenefits for up to six months, buton analysing later data at five yearsthere did not seem to be significantclinical benefits compared with astandard tendon rehabilitationprogramme alone. By contrast,patients with achilles tendinopathywere found to derive sustainedbenefit from use of topical GTN.

So what do we take out of all ofthis? Probably the best summationis by Jill Cook in her editorialentitled ‘Tendinopathy: no longera one size fits all diagnosis’. Inother words, like many other areasin medicine, once we know moreabout the issues we can tailortreatment to individual patientrequirements.

My pick for most value article inthis series of journals surveyedwould be that by Paul McCrory andcolleagues in the February issueentitled ‘Sports and exercisemedicine: specialists or snake oilsalesmen?’ It gets to the heart ofthe issues confronting modern-dayclinicians. We must remain true toour scientific principles whateverperipheral issues are going on. Itis only by doing this that we willretain the professional credibilitythat has been so long in coming toour specialty

Dr Chris MilneSports PhysicianHamilton

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The central governor of exerciseperformance: Fact or fiction?Simeon P CairnsAssociate ProfessorSchool of Sport and Recreation and Health and Rehabilitation Research UnitFaculty of Health & Environmental SciencesAUT UniversityAuckland

CorrespondenceSchool of Sport and RecreationFaculty of Health & Environmental SciencesAUT UniversityPrivate Bag 92 006Auckland 1020New ZealandTel +64-9-921 9999 Ext 7125Fax +64-3-9-921-9960

For many years, scientists,coaches and clinicians havebeen interested in establishing

just what limits performance duringvarious types of exercise. Now, in theearly new millennium, a group ofSouth African exercise scientists ledby Professor Tim Noakes believethey have solved this issue with apostulate they call the CentralGovernor. This model, which theythink includes the critical regulatorof exercise performance, hasprovoked considerable thought andhas led to several emotionallycharged articles with fiery exchangeswithin the recent scientific literature.For example, articles have appearedentitled “Is it time to retire the“central governor”?,21 “Theimprobable central governor ofmaximal endurance performance”6

and “Do we really need a centralgovernor to explain brain regulationof exercise performance?”.10 In afeisty rebuttal, Noakes respondedwith a publication called “Is it timeto retire the A.V. Hill model?”14 - anexercise model that apparentlyopposes his ideas. Never-the-lessNoakes is not alone as other scientistshave given support to the centralgovernor hypothesis.12,13 The presentcommentary is not meant to be anextensive evaluation of the centralgovernor model, but rather it is myattempt to clarify some of the ideasunderpinning the model and to

provide a more balanced view onsome of the recent spiriteddiscussions, especially in relation toits role in fatigue of sportperformance.

What is the central governor andwhat does it do?The model was initiated by Ulmerbut first laid out in detail over severalpapers in 2004-2005, when it wasproposed that the central governor isa specific subconscious centre in thecentral nervous system (CNS) thatacts in an anticipatory (feed-forward)manner to regulate exerciseperformance through de-recruitmentof skeletal muscle/motor units.9,17,18,24

It was argued from evolutionaryperspectives that such a governorwould control motor drive to workingskeletal muscles in order to conservehomeostasis and ultimately preventcatastrophe, ie, damage to the heart,skeletal muscles, lungs, or brainitself. Several features of this modelare still undergoing development.First, although it includes asubconscious brain centre there isnow mounting importance placed onthe rating of perceived exertion(RPE) which is a conscious aspect ofthe sensation of fatigue.9,15,22 Second,teleoanticipation, a central feed-forward mechanism, is regarded as akey feature but there is alsoacceptance that feedback from theperiphery interacts with the central

governor to help set the intensity ofexercise.7,9,15,25 Third, Noakes andassociates argue that the centralgovernor is a regulator of exercisebehavior, rather than being anenforcer to limit exerciseperformance. However, thisdistinction is speculative and cannotbe made with certainty simply bymeasuring the fatigue symptoms.Many studies on the central governorfocus on exercise termination duringeither prolonged or incrementalmaximal exercise.4,9,17,18,24 However,several other impairments toperformance appear as fatiguesymptoms prior to this extremepoint.8 The South African group hasalso investigated pacing (ie,regulation of exercise intensity)which they regard to be anotherfeature of the central governor,23

rather than it being just an exercisestopper. Finally, Noakes andcoworkers propose that the centralgovernor indirectly controlsmaximum cardiac output and peakoxygen consumption16 but that willnot be considered further here.

What is fatigue?There is ongoing debate as to whatis the best measure of fatigue.Traditionally, fatigue is defined asany exercise-induced reduction in thecapacity of muscles to generate forceor power.1,8 However, we recently

○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○ ○

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emphasised that fatigue during sportcompetition can manifest as any oneof a number of symptoms relating toimpaired performance.8 Thisincludes a drop-off of pace, loss ofmaximum speed during a sprint,fewer high-intensity exercise bursts,changes of technique leading toreduced skill outcomes, subjectivesensations of fatigue, or impaireddecision-making, but their specificoccurrence depends very much on thesporting event or task of interest. Inmost cases the complete cessation ofexercise is termed exhaustion.5,8

When fatigue is quantified as adecline in maximal muscle forceproduction it is usually subdividedinto peripheral and centralcomponents.

What is peripheral fatigue?This component involves a directreduction in the ability of musclefibres to generate force, and occursgradually by mechanisms which arenot just an on and off switch mediatedvia the CNS. In consequence, someexercise scientists including myselfhave taken a reductionist approach tostudy fatigue induced by electricalstimulation of isolated musclepreparations.1,3,8 Indeed, the longstanding AV Hill model for exerciseperformance, which is stronglychallenged by Noakes,14 postulatesthat factors changing in musclereduce its function and ultimatelyimpair whole-body exerciseperformance. Hill was one of the earlyresearchers to drive the notion thatlactic acid is the culprit which impairsmuscle function.14,17 Despite thishypothesis now losing favor,1,2 thereare still several other peripheralfatigue factors that can impair musclefunction such at muscle phosphagenchanges, glycogen depletion,electrolyte changes and production ofreactive oxygen species.1,3 Incontrast, Noakes appears to totallyrefute the occurrence of peripheralfatigue15 despite what many regard asconvincing evidence that itoccurs.1,3,5,8 Moreover, we haveshown emphatically with subjectswho underwent prolonged cycling toexhaustion that peripheral fatiguecontributes about two thirds of the30% decline of maximal isometricvoluntary contractile (MVC) force.20

What is central fatigue?This component (ie, the inability ofthe CNS to maximally activatemuscle during fatiguing voluntarycontractions) is usually tested withelectrical stimulation superimposedon an isometric MVC.5,19,20 Thismethod indeed tests for any declineof maximal motor drive (ie, de-recruitment or severely loweredmotor neuronal firing frequency) dueto the preceding exercise, but it doesnot confirm that impaired motordrive has functional consequencesduring the sub-maximal dynamiccontractions which normally occurduring exercise.8,17 We show thatcentral fatigue assessed in thismanner accounts for about one thirdof the decline of peak MVC forcewith prolonged cycling.20 Sucheffects could, in principle, involvealtered command by a centralgovernor. This could occur eithercentrally or via feedback from theperiphery, and possibly includessignals originating from workingmuscles.5,8,9,15,18-20,25 Such peripheralsignals include hypoglycaemia,hypoxia, acidosis, elevated reactiveoxygen species and potentially raisedplasma potassium.5,8,9,19,25

Interestingly, a long held hypothesisfor exhaustion during prolongedexercise, that of muscle glycogendepletion, may involve release of thecytokine, interleukin-6, fromfatigued muscles to exert detrimentaleffects via the CNS.5,8

What is the sensation of fatigue?This subjective aspect involves theconscious sensation associated withincreasing effort during sub-maximalwork (ie, RPE), together with muscleweakness and other sensations thatremain after exercise.8,22 As a resultthere has been much interest inRPE,4,8-11,18-20 which is now postulatedto be the conscious interpretationmade by the homeostatic centralgovernor.9,15 Its importance becomesapparent since maximal levels ofRPE (ie, 18-20 on the Borg scale) arecommonly observed at exhaustionwhen exercise becomesunbearable.4,7,8,19,20 Moreover, thetime-to-exhaustion is intimatelyrelated to the rate of rise of RPE earlyin exercise.4,20 Clearly RPE is afeature of the CNS but just how it islinked to central fatigue, the loss of

muscle force/power and other fatiguesymptoms, and the central governor,remains unclear.

It is also recognised that RPE islinked to increasing central motordrive through both central andperipheral factors (eg,hypoglycaemia, hypoxia, acidosis,serotonin, hyperthermia,dehydration), some of which alsocontribute to central fatigue.8 In awell designed study, Marcora andassociates show that a cognitivechallenge leading to mental fatiguealso causes a higher RPE insubsequent exercise and a shortertime-to-exhaustion.11 Clearly, suchinfluences occur through the CNS, asshown with other interventions suchas hypnosis.26 Certainly, moreresearch is needed to understand thefactors which underpin andmanipulate RPE, and presumablywith it an altered exerciseperformance.

Does the brain regulate exerciseperformance?It is established that the braincontains cardiac, vasomotor,respiratory, thermoregulatory, andvarious other control centres whichare able to influence body functionsduring exercise, in part via feedbackloops.14 So the idea of centralregulation is not new. Moreover,higher cortical centres can provideinput to these control centres toenhance pre-exercise function in ananticipatory manner as observed withelevated pre-race heart rates. Weshould also be aware of beneficialmotor control adjustments whichallow compensatory effects asmuscle fibres/motor units graduallyfatigue.1,5,8 A slightly lowered motorneuron firing frequency can conveybenefits known as muscle wisdom,1

a rotation of motor unit recruitmentmay let fatigued motor units undergorest and recovery,5 and motor drivecan alternate between muscle groupsto permit a sharing of the work loadat a more gross level.8 Motivationand other psychological constructsthat act via the CNS can also modifymotor output andperformance.5,7,8,10,16,17,19 Yet anotherCNS feature which can influenceperformance is that of decision-making, and this aspect often

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improves with exercise.8 However,it appears that it is only withconditions such as severehypoglycaemia, hyperthermia, ordehydration that decision-makingcan worsen.8

Is there evidence supporting thecentral governor model?The initial reasoning involvedevolutionary ideas and a need toavoid catastrophe,9,17,18,24 but furtherarguments appear to involve moreobjective evidence. First, a decline ofelectromyographic activity inworking muscles is interpreted as thecentral governor switching off somemotor units.24 However, thisinterpretation is not exclusive to areduced motor drive as it may alsorelate to electrolyte effects whichdiminish muscle excitability.1,3

Second, there is a need to localise thespecific central governor area withinthe cerebral hemispheres, and areasin the frontal lobe and thalamus havebeen implicated especially in relationto RPE and the perception offatigue14,22,26 However, this work isin its infancy. An ultimate experimenthere would be the selective ablationof identified central governorneurons and then test for changes toexercise performance but suchexperiments clearly cannot be doneon humans. Third, the presence of anend-spurt, ie, the increased poweroutput at the end of a race,14,18 isargued that it cannot be explained byanything other than a centralcontroller.14,15,23 However, thisshould be addressed correctly bycomparing the peak power output atthe end of a race with that achievedwhen the subjects are fresh at thestart, since this truly accounts for acontribution from peripheral fatigue.Fourth, the muscles of exhaustedindividuals usually show less than30% decline of peak MVC force,5,8,14-

17,20 suggesting a peripheral reservewith motor units still being availableto contract.14,15 In contrast,electrically stimulated isolatedmuscles, which bypass CNSregulation, sometimes involves amuch greater loss of force.1,8 Thus,arguments have been put forward insupport of the central governorhypothesis although none areabsolutely conclusive.

Personal viewpoint on the centralgovernor.The appearance of the centralgovernor model has been valuable toprovoke extensive discussion andmore critically appraise ourunderstanding of exerciseperformance. However, it is difficultto obtain good experimental evidenceto confirm a role for a centralgovernor, and hence it is difficult toeither prove or disprove the model.Never-the-less the model has severalappealing aspects and as such shouldnot be retired as suggested.21

Similarly, being adamant that thecentral governor is the universalexercise regulating mechanism ismost surely flawed. Notably, manyresearchers who question theimportance or need for a centralgovernor still give considerablesupport to a role of the brain in theregulation of exerciseperformance,10,21,25 and are notendorsers of a brainless model assuggested.15 To that end the brainworks in an integrated manner withmuscles, heart and lungs duringexercise. Although the brain mayhave the ability to restrictperformance all by itself, it is usuallyinfluenced by changes external to theCNS such as lowered glucose levels,hypoxia, hyperthermia, dehydration,raised potassium, acidosis etc. Socould the central governor really justbe the brain itself?

A notable restriction with the centralgovernor model is that it has beenapplied mainly to exercise cessationduring prolonged or incrementalmaximal exercise. Although pacinghas been introduced,14,15,23 otherimpairments occur before disasterthat also need to be considered for afuller evaluation of exerciseperformance. Moreover the centralgovernor model has not yet beenapplied to clinical exercise situations,such as occur with effort syndromes,and this needs development. A majorproblem arising from the ideas ofNoakes and colleagues, in my view,stems from rejection of anycontribution from peripheralfatigue.14,15 It appears that in mostforms of sport or exercise that thereare fatigue contributions from severalsources including peripheral andcentral fatigue along with fatigue

sensations,8 and the key questionreally involves establishing therelative contribution of the differentaspects. We also recently proposedthat with peripheral fatigue there areconsiderable safety margins so thatquite large perturbations ofhomeostasis can occur beforeimpairment of muscle function.3

Peripheral fatigue is clearly morecomplex than simply being a linearmodel.

The real issue is probably not aboutestablishing which model bestexplains exercise performance, asthey may all contribute to someextent, but instead sorting out justwhat are the main fatigue factors andwhat can be done about them. Anunderstanding of central andperipheral processes gives insight asto how best to intervene with the likesof diet, training and psychologicaltricks. Most importantly we haverecently indicated that several fatiguefactors can have a protective roleprior to being detrimental,8 althoughlarger changes interactivelycontribute to peripheral and centralfatigue, RPE and the sensation offatigue, impaired motor skills, andoccasionally to decision-making.8

Hence it may be possible tomanipulate some factors andinfluence performance via many siteswhich potentially includes actions viaa putative central governor.

SummaryIt is difficult to comment withcertainty about whether the centralgovernor hypothesis is right or wrongbut the following comments seem tobe acceptable.

1 There is indeed brain regulationof exercise performance. Thispotentially includes a centralgovernor area although such anentity may be the entire brain.

2 Many fatigue symptoms aremediated via the CNS and notjust exercise termination.

3 Central fatigue is involved inmost forms of exercise that lastfor some duration.

4 The occurrence of peripheralfatigue to various extents is a realphenomenon.

5 The conscious sensation offatigue plays a big part in

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exercise performance.6 Exceedingly high RPE

(intimately related to thesensation of fatigue) coincideswith impaired exerciseperformance. Manipulation ofthe factors which contribute toRPE (eg, lowered blood glucose,hypoxia, acidosis) can alter thetime-to-exhaustion and mostlikely influence several otherfatigue symptoms at the sametime.

Regardless of whether the centralgovernor model is ultimatelyconfirmed as fact or fiction it is anextremely valuable concept toinvestigate further and apply to allforms of sporting event along withclinical exercise situations.

References1 Allen D G, Lamb G D, Westerblad H.

Skeletal muscle fatigue: cellularmechanisms. Physiol Rev 2008;88:287-332.

2 Cairns S P. Lactic acid and exerciseperformance: culprit or friend? SportsMed 2006; 36(4):279-291.

3 Cairns S P, Lindinger M I. Domultiple ionic interactions contributeto skeletal muscle fatigue? J Physiol2008; 586(17):4039-4054.

4 Crewe H, Tucker R, Noakes T D. Therate of increase in rating of perceivedexertion predicts the duration ofexercise to fatigue at a fixed poweroutput in different environmentalconditions. Eur J Appl Physiol 2008;103:569-577.

5 Gandevia S C. Spinal and supraspinalfactors in human muscle fatigue.Physiol Rev 2001; 81:1725-1789.

6 Hopkins W G. The improbable centralgovernor of maximal enduranceperformance. Sportscience 2009;13;9-12.

7 Kayser B. Exercise starts and ends inthe brain. Eur J Appl Physiol 2003;90:411-419.

8 Knicker A J, Renshaw I, OldhamARH, Cairns S P. Interactiveprocesses link the multiple symptomsof fatigue in sport competition. SportsMed 2001; 41(4):307-328.

9 Lambert E V, St Clair Gibson A,Noakes T D. Complex systems modelof fatigue: integrative homeostaticcontrol of peripheral physiologicalsystems during exercise in humans.Br J Sports Med 2005; 39:52-62.

10 Marcora SM. Do we really need acentral governor to explain brain

regulation of exercise performance?Eur J Appl Physiol 2008; 104: 929-931.

11 Marcora S M, Staiano W, Manning V.Mental fatigue impairs physicalperformance in humans. J ApplPhysiol 2009; 106:857-864.

12 Marino F E. Is it time to retire the“Central Governor”? A philosophicaland evolutionary perspective. SportsMed 2010; 40(3): 265-270.

13 Micklewright D, Parry D. The centralgovernor model cannot be adequatelytested by observing its components inisolation. Sports Med 2010; 40(1):91-94.

14 Noakes T D. Is it time to retire theA.V. Hill Model? A rebuttal to thearticle by Professor Roy Shephard.Sports Med 2011; 41(4):263-277.

15 Noakes T D. Time to move beyond abrainless exercise physiology: theevidence for complex regulation ofhuman exercise performance. ApplPhysiol Nutr Metab 2011; 36:23-35.

16 Noakes T D, Calbert JAL, Boushel R,Søndergaard H, Rådegran G, WagnerP D, Saltin B. Central regulation ofskeletal muscle recruitment explainsthe reduced maximal cardiac outputduring exercise in hypoxia. Am JPhysiol Regul Integr Comp Physiol2004; 287:R996-R1002.

17 Noakes T D, St Clair Gibson A.Logical limitations to the‘catastrophe’ models of fatigue duringexercise in humans. Br J Sports Med2004; 38:648-649.

18 Noakes T D, St Clair Gibson A,Lambert E V. From catastrophe tocomplexity: a novel model ofintegrative central neural regulationof effort and fatigue during exercisein humans. Br J Sports Med 2004;38:511-514.

19 Nybo L, Secher N H. Cerebralperturbations provoked by prolongedexercise. Prog Neurobiol 2004;72:223-261.

20 Presland J D, Dowson M N, Cairns SP. Changes of motor drive, corticalarousal and perceived exertionfollowing prolonged cycling toexhaustion. Eur J Appl Physiol 2005;95:42-51.

21 Shepard R J. Is it time to retire the‘central governor’? Sports Med 2009;39(9):709-721.

22 St Clair Gibson A, Baden D A,Lambert M I, Lambert E V, HarleyYXR, Hampson D, Russell V A,Noakes T D. The consciousperception of the sensation of fatigue.Sports Med 2003; 33(3):167-176.

23 St Clair Gibson A, Lambert E V,Rauch LHG, Tucker R, Baden D A,

Foster C, Noakes T D. The role ofinformation processing between thebrain and peripheral physiologicalsystems in pacing and perception ofeffort. Sports Med 2006; 36(8):705-722.

24 St Clair Gibson A, Noakes T D.Evidence for complex systemintegration and dynamic neuralregulation of skeletal musclerecruitment during exercise inhumans. Br J Sports Med 2004;38:797-806.

25 Weir J P, Beck T W, Cramer J T,Housh T J. Is fatigue all in your head?A critical review of the centralgovernor model. Br J Sports Med2006; 40:573-586.

26 Williamson J W, McColl R, MathewsD, Mitchell J H, Raven P B, MorganW P. Hypnotic manipulation of effortsense during dynamic exercise:cardiovascular responses and brainactivation. J Appl Physiol 2001;90:1392-1399.

50 NZJSM

CARDIOLOGY CONUNDRUMS

Management Recommendations1) authorise full competitive activity;but offer the option of genetic testing,educate the athlete for personalsymptoms, and place under annualcardiac examination includinghistory physical examination, restingand stress ECG, echocardiogram andcMRI. 2) propose a systematiccardiac examination (non-invasiveexamination with ECG andEchocardiography) in first degree-relatives (>10 years old).

Current StatusThe player returned to fullcompetition, and at present (8 monthspost evaluation) has remainedasymptomatic (self reported) with noadverse cardiac events.

T-wave inversions in athletes:Electrocardiographic changes inhighly trained athletes are commonand usually reflect benign structuraland electrical remodelling of theheart as a consequence of regular andintensive physical activity. Thisremodeling is commonly known as‘athlete’s heart’. However,repolarisation abnormalities may bean expression of an inherited cardiacdisease, placing the athlete atsignificant risk of sudden cardiacdeath, either during or followingsport.

Deep T wave inversions in the lateralleads are a major concern forscreening physicians, as these ECGalterations are a recognisedmanifestation of HypertrophicCardiomyopathy andArrhythmogenic Right VentricularCardiomyopathy (ARVC).2 InvertedT-waves may represent the only signof an underlying inherited heartmuscle disease even in the absenceof any other features and beforestructural changes in the heart can bedetected.The clinical significance of deep Twave inversions in athletes is yet tobe fully understood, with thisplayer’s ECG currently classed asneither physiological norpathological. Recently, Pelliccia et al(2008) reported on 81 athletes (froma database of 12,550) with diffuselydistributed and deeply inverted Twaves, with no apparent cardiacdisease, who had undergone serial

clinical, ECG, and echocardiographicstudies for 9 ±7 yrs (range, 1 to 27yrs). From the 81 identified, five(6%) ultimately proved to havecardiomyopathies, including onewho died suddenly from undetectedARVC. The authors suggest thatthese abnormal ECG’s may representthe initial expression of anunderlying genetic cardiac diseasethat may not be phenotypicallyevident for many years. Pelliccia etal’s (2008) investigation underscoresthe importance of continued clinicalsurveillance and clinical follow-upfor this football player; with serialECG, echocardiographic and cMRIeven in the absence of cardiacsymptoms and/or clinicallydemonstrable heart disease.

cMRI and GeneticsThere has been considerable progressin recent years in the development ofimaging technologies capable ofcharacterising a much wider numberof cardiomyopathic processes.

In particular, the advent ofgadolinium enhanced cMRI hasdramatically changed the non-invasive work-up of athletes with asuspected cardiomyopathy. cMRIprovides a comprehensiveassessment of both ischemic and non-ischemic cardiomyopathiesproviding detailed information oncardiac anatomy, function, tissuecharacterisation, epicardial andmicrovascular perfusion, valvularflows, and coronary and peripheralangiography. The presence of LGEis indicative of abnormal myocardialinterstitium typically due to thepresence of myocardial fibrosis orinfarction.

A high proportion ofcardiomyopathies are of geneticorigin. There is probably a continuumbetween the initial stage of a fullyhealthy condition and the stage ofobvious cardiac expression with anintermediate stage of mild borderlineabnormalities. The earliest phase ofa cardiac expression may becharacterised by ECG abnormalitiessuch as T-wave inversion, precedingthe later development of otheridentifiable structural abnormalities.

Genetic testing was recentlydeveloped for routine clinical use in

order to improve both geneticcounselling and medicalmanagement of patients andrelatives.1 In a patient with an overtcardiomyopathy, the yield or rate ofmutation identification is variableaccording to the disease: 50-70% inHCM and around 40% in ARVD.3,5

Failure to identify recognisedmutation must not lead to the clinicalexclusion of a cardiomyopathy or ionchannelopathy for three importantreasons; 1) not all genetic regions areassessed, 2) current technology is notable to detect some forms ofmutation, and 3) a similar phenotypemay possibly develop without aspecific genetic constitution. In otherwords, only positive genetic testshave a diagnostic value, but negativetests do not exclude the disease.

References1 Charron P, Arad M, Arbustini E, et al.

“Genetic counselling and testing incardiomyopathies: a positionstatement of the European Society ofCardiology Working Group onMyocardial and PericardialDiseases.” Eur Heart J 2010; 31(22):2715-2726.

2 Corrado D, Pelliccia A, HeidbuchelH, et al. “Recommendations forinterpretation of 12-leadelectrocardiogram in the athlete.” EurHeart J 2010; 31(2): 243-259.

3 Fressart V, Duthoit G, Donal E, et al.“Desmosomal gene analysis inarrhythmogenic right ventriculardysplasia/cardiomyopathy: spectrumof mutations and clinical impact inpractice.” Europace 2010; 12(6):861-868.

4 Pelliccia A, Di Paolo F M, QuattriniF M, et al. (2008). “Outcomes inathletes with marked ECGrepolarisation abnormalities.” N EnglJ Med 2008; 358(2): 152-161.

5 Richard P, Charron P, Carrier L, et al.“Hypertrophic cardiomyopathy:distribution of disease genes,spectrum of mutations, andimplications for a molecular diagnosisstrategy.” Circulation 2003; 107(17):2227-2232.

52 NZJSM

CASE REPORT

Introduction

Obtaining a specific patho-anatomic source for neckand spinal pain can be

difficult for the vast majority ofcases.5 An alternate option is toclassify mechanical neck or spinalpain into groups, or syndromes,based on homogenous signs andsymptoms.3,7,8 The Canadian BackInstitute2 (CBI) has developed asyndrome based classificationsystem consisting of fourdistinctive categories or ‘patterns’of neck pain (see Table 1). PatternOne represents neck pain that isprimarily aggravated with cervicalflexion postures and movements.

Pattern Two is neck pain that is onlyaggravated with cervical extensionpositions. Pattern Three is arm painassociated with cervicalradiculopathy and Pattern Fourrepresents symptoms of neck orarm pain and upper motor neurondysfunction associated withcervical myelopathy. The CBImethodology offers clinicians acarefully structured assessment thatplaces particular emphasis on theimportance of a detailedsymptomatic history to determinethe location and constant orintermittent nature of the pain, andto identify the neck movement andpostures that aggravate and relieve

symptoms. Another essentialcomponent of the CBIclassification process is the routineassessment of upper and lowermotor neuron function for allpatients that present with neck pain.This standardised assessment andclassification approach was anessential factor in this case in whicha relatively inexperienced clinician(four month post graduatephysiotherapist) diagnosed an acutecervical myelopathy in a patientpresenting with symptoms of kneeinstability, and referred the patientappropriately to a specialist forfurther investigation.

Acute cervical myelopathy in apatient presenting with kneeinstability – a case reportJoel Winders BPhty (Otago)TBI HealthWellingtonNew Zealand

Correspondence to:Joel Winders31 Santley StreetLondon SW4 7QEUnited KingdomPhone +447501437549Email jd.winders@gmail.com

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Pattern of Neck Pain Location* Nature Aggravating and Relieving Posturesor Movements

One Neck dominant pain. Intermittent or constant pain. Cervical flexion increases pain.

Two Neck dominant pain. Intermittent pain. Cervical extension increases pain.

Three Arm dominant pain. Constant or previously Neck movement and postures affect armconstant pain. pain.

Four Neck or arm dominant Balance or gait disturbance Varied - but upper motor neuron signs suchpain. and/or loss of fine motor as hyperreflexia, spacticity, clonus and

skills. positive babinski may be present (clonusand babinski testing is standard with allneck pain patients).

TABLE 1: Diagnostic criteria for patterns of neck pain.*neck dominant indicates worst pain is proximal to the deltoid insertion and inferior angle of the scapula; arm dominantpain indicates worst pain is distal to the deltoid insertion.

CASE REPORT

54 NZJSM

Case ReportA 41 year old male recreationalfootball player attended a routinefollow up appointment threemonths following a right kneearthroscopic meniscectomy andsubsequent rehabilitation. Hecomplained of a one week historyof intermittent right knee instabilitythat was causing difficulty whenwalking downhill or descendingstairs. He also noticed someweakness in his left knee and wascomplaining that both lower limbsfelt cold and “jittery”, especially atnight and when cold. He reportedno other problems on level surfaceswith walking or running. He did notcomplain of knee pain and couldnot recall a recent injury to the knee.He intended to play football thefollowing day for his club team.

Because the patient was presentingwith new symptoms of bilateral legweakness and sensation changeswithout any history of a recent localinjury to the knee, the spine wasassessed as a possible cause of thesymptoms. On further questioning,the patient denied any low backdiscomfort but when asked aboutneck pain he recalled being hit frombehind in a mild traffic accident twoweeks earlier. He had beenexperiencing mild intermittent leftsided neck pain since the accidentbut these symptoms had beenslowly resolving. He had no historyof any previous significant neckpain, and at no stage did he everhave any arm pain or paraesthesiadistal to the acromion.

Physical examination revealed fullcervical range of motion with minorleft-sided neck discomfort in alldirections. There was grade 5strength bilaterally in both upperand lower limbs. Sensation testingwas normal in his lower limbs.Pulses were present equally in bothfeet. There was bilateralhyperreflexia in the tendons of hisbiceps and triceps brachii,brachioradialis, patella and Achillestendons. There was a positiveclonus test with at least four beats

FIGURE 1

FIGURE 2

CASE REPORT

Vol 38 No 2, 2011; 55

of clonus bilaterally. Babinskireponse was negative.

According to the CBI system, thesesymptoms of neck pain and uppermotor neuron disturbance mayindicate a cervical myelopathy(Pattern Four). An urgent x-ray wasarranged which showed a posteriorsubluxation of C3 on C4 facets(figure 1). The subsequent MRIscan showed a large disc bulge atC3/4 compromising the spinalcanal, where increased signalsuggested acute cord oedema(Figure 2).

The patient was referred urgentlyto the neurosurgical registrar at theWellington Hospital EmergencyDepartment. An anterior cervicaldiscectomy and fusion (ACDF) atC3/4 was performed two daysfollowing admission. When thepatient was reviewed several weeksfollowing surgery, he still had apositive clonus test but noticed thatthe episodes of knee instability haddecreased significantly. Onfollowing up this patient 3 yearsafter his surgery he states that henow only has occasional ‘jumping’sensations in his legs whendescending stairs. He describesthese symptoms are only present incold weather. He has no neck painand has resumed playing footballat his previous level. His symptomshave been slowly improving overthe last 3 years.

DiscussionBecause complaints of neck painand discomfort are so common, itis easy to become dismissive,especially when the pain is not thesignificant problem. In this case, apatient presenting with relativelyinnocuous symptoms of kneeinstability and mild neck pain hada very serious pathological causefor his symptoms.

In addition to the findings for thispatient, there are many other signsand symptoms that could suggestpresence of cervical myelopathy.Radiculopathy in the upper limb,bowel and bladder dysfunction and

lower limb stiffness or weaknesscan all commonly be associatedwith cervical myelopathy.1,4 Kim etal6 found the most commoncomplaints from patientsexperiencing myelopathy from softdisc herniation were gaitdisturbance and spasticity.One of the most interesting featuresof this case was the relative lack oflocal neck pain and discomfort insomeone who had such apotentially serious injury. Thisfinding is however not altogetheruncommon as Bednarik et al foundthat cervical myelopathy may oftenpresent without neck pain as spinalcord compression itself is notnecessarily symptomatic,especially in the early stages ofdevelopment.1

This patient’s positive upper motorneuron lesion signs could have beenbenign or from an unrelated, uppermotor lesion such as multiplesclerosis or a localised cerebrallesion but because the onset of bothneck pain and neurologicalsymptoms seemed to relate to aspecific recent event (motor vehicleaccident), it was necessary toinvestigate the cervical spineurgently. Since this patient’s ACDFsurgery he has noticed a slow butsteady improvement in both his leftand right knee strength andstability. This in itself supports thetheory that the neck pathology wasmost likely the cause of his lowerlimb symptoms, and that hissymptoms were not related to analternate upper motor neuronpathology or previous right kneemeniscetomy surgery.

This case reinforces the need toconsider cervical myelopathy in thepresence of symptoms associatedwith lower limb weakness or gaitdisturbance. It also emphasises theimportance of routine upper andlower motor function screening asan essential component of acervical spine assessment.

AcknowledgmentsChris GreggPhysiotherapist/General Manager,TBI Health, Wellington;

Derek YoungPhysiotherapist/ Clinic Manager,TBI Health - Newtown,Wellington;Mr Peter WelshOrthopaedic Spinal Surgeon/Director, TBI Health, Wellington;Mr Chris HoffmanOrthopaedic Spinal Surgeon/Director, TBI Health, Wellington.

References1 Bednarik J, Kadanka Z, Dusek L, et

al. Presymptomatic spondyloticcervical cord compression. Spine2004; 29:2260-69.

2 Hall H, McIntosh G, Melles T. Adifferent approach to back paindiagnosis: identifying a pattern ofpain. Can J CME 1994; Feb:31-42.

3 Hall H, Melles T, Wilson L, McIntoshG. Inter-tester reliability of a low backpain classification system. Spine1999; 24:248-54.

4 Harrop J S, Hanna A, Silva M T,Sharan A. Neurologicalmanifestations of cervicalspondylosis: an overview of signs,symptoms, and pathophysiology.Neurosurgery 2007; 60:S1-14 – S1-20.

5 Hazard R G. Low-back and neck paindiagnosis and treatment. Am J PhysMed Rehabil 2007; 86:S59-S68.

6 Kim Y J, Oh S H, Yi H J, et al.Myelopathy caused by soft cervicaldisc herniation: surgical results andprognostic factors. J KoreanNeurosurg Soc 2007; 42:441-5.

7 Loisel P, Vachon B, Lemaire J, et al.Discriminative and predictive validityassessment of the Quebec task forceclassification. Spine 2002; 27:851-7.

8 McKenzie R. Mechanical diagnosisand therapy for low back pain: towarda better understanding. In: TwomeyL, Taylor J, editors. Physical therapyof the low back. NewYork:ChurchillLivingstone, 1987:157–73.

BOOK REVIEW

Blast from the Past

Recently I had cause to goand look at DonO’Donoghue’s classic text

Treatment of Injuries to Athletes. Ihave the third edition published in1976. The first edition waspublished in 1962. For those of youwho are unaware, this is widelyregarded as the first true sportsmedicine textbook. DonO’Donoghue was Professor ofOrthopaedic Surgery at theUniversity of Oklahoma MedicalSchool and team physician to theUniversity of Oklahoma footballteam.

The book is a classic and reading itshows how far we’ve come in the35 years since this edition waspublished. He prefaces the bookwith the comment, “Everything Iknow I learnt at my mother’s kneeor some other joint.” In the firstedition he goes on to say, “I owe adebt of gratitude to the Americanathlete. That which began as aninteresting sideline to a life devotedlargely to paediatric orthopaedicshas burgeoned to become perhapsmy major interest.” By the time ofthe third edition he still obviouslyloves his work. He comments inthere, “I still greatly appreciate theAmerican athlete.”

The book starts off with a Bill ofRights for the School and CollegeAthlete which was drawn up by theAmerican Medical AssociationCommittee on the medical aspectsof sports. It emphasises goodcoaching, good officiating, goodequipment and facilities and goodhealth supervision. This is certainlya great place to begin.

The book itself commences with achapter on prevention of injuriesand he states, “The physicalconditioning of a player should bea continuous thing.” So often thisis forgotten. He outlines a

recommended summer high schoolconditioning programme and it isfascinating to note under Item 11the comment “Temperate living”.This involves four aspects:

1 Sleep, which he defines as thegreat restorer and recommendsa minimum of nine hours.

2 No intoxicants - he goes on tosay it is not a food it is a poison.

3 No smoking.

4 No drugs.

This would make good reading fortoday’s athletes. He goes on todescribe the playing arena andathletic equipment plus protectivestrapping for the ankle.

Part 2 consists of general principlesof treatment. He lists five preceptsfor care of the athlete, which heterms the Five A’s:

1 Accept athletics.

2 Avoid expediency.

3 Adopt the best method.

4 Act promptly.

5 Achieve perfection.

He then goes on to champion therole of the physical examination.He comments that it may not bepossible to examine the player atonce but the goal should be toexamine him as soon as it can bedone properly. The book alsomentions x-ray examination andlaboratory testing, but waspublished before the explosion inmedical imaging which hasoccurred in the past few decades.Following that explosion the roleof physical examination has beendowngraded in some centres, to thedetriment of the player, in myopinion. Then follows a chapter onthe principles and the management

of specific injuries, both soft tissueand bony injuries.

The majority of the book is takenup with recommendations fordiagnosis and treatment of injuriesin specific areas. Starting from thehead down, it shows examples ofsubdural and extraduralhaematomas; Frank Netter’spictures are not for the squeamish.Interestingly, there are noconcussion guidelines listed, thisbook predating their development.Moving down the body to theshoulder, sternoclavicular disordersare well-covered. AC joint injuriesare discussed and he is clearly a fanof surgical fixation of third degreeAC joint injuries, as indeed aremost American authors. There isrelatively less information onglenohumeral joint problems orrotator cuff injuries, whichconsume a large part of our dailywork in this millennium.

The chapter on spinal injuries hasa good deal of information on thehyperextension injuries of the neckwhich are so common in Americanfootball. There is some mention oflow back problems but nothing likein the depth that one would expectgiven the frequency of theseconditions in most people’spractice.

The chapter on hip and groin rightlymentions the importance ofconditions such as slipped upperfemoral epiphysis. Our knowledgeof groin injuries is far fromcomplete but this book shows howfar we have come. It has nomention of entities such as sportshernia or labral injury, and onlyscant mention of osteitis pubis - inthe old days this was thought to bean infective condition.

Moving down to the knee, hedevotes a good deal of discussion

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BOOK REVIEW

to what was later termedO’Donoghue’s unhappy triad. Thisis a severe knee injury involving themedial collateral ligament, medialmeniscus and anterior cruciateligament. He was one of the firstto recognise the significance ofcruciate ligament injuries anddescribes repair of the ACL usingmattress sutures. He points out thatan avulsion injury involving a bonyplug provides a good opportunityfor early surgical intervention withgood results. Anterior knee painwas not well understood in the earlydays and, as befits a surgeon, thereis plenty of discussion ontechniques such as chondralshaving, trephine and drilling,facetectomy and even patellectomy.Fortunately, our knowledge of non-operative treatment has improvedexponentially and so the need forsurgery for anterior knee pain hasdramatically reduced in the last fewdecades.

Moving down the leg there isdiscussion of shin splints but, as hepoints out, there is “considerableand often raucous argument as towhat is actually meant by the term”.He goes on to say, “the title shinsplints is ‘a waste bucket’ includingmany different conditions.” Hecorrectly identifies that the tibialisposterior origin is most commonlyinvolved. There is even mentionof elevation of the heel by a halfinch felt pad and/or the insertion ofa cork and leather arch supportflexible enough to permit the footto flex. My how things havechanged - we now have a wholeindustry built around orthotics. InAmerica they tend to be overly inlove with rigid devices and onewonders how many athletes wouldbe better off using the flexiblematerials advocated byO’Donoghue.

Finishing off with the ankle andfoot, he emphasises early weight-bearing and active rehabilitationfollowing ankle injuries.The final chapter concernsrehabilitation following athletic

injuries and is written by FredAllman, one of the other earlygiants of our discipline fromGeorgia Tech in Atlanta. Onceagain the exercises include thesimple things such as neckstrengthening, which we have builton in subsequent decades. A lot ofthese have stood the test of time buta few have been discarded in thelight of subsequent evidence.All in all, it is salutary to pick up avolume such as this. In 1976 asingle author with a few fellowcontributors was able toencapsulate the entire field prettywell in just over 800 pages. Suchis not the case today and it is ameasure of how far we have come.However, those of us of a certainage will fondly remember beingtaught about O’Donoghue’sunhappy triad and it is interestingto read the description from theguru himself.

For anyone with an interest in howour discipline began, I would highlyrecommend this book.

Dr Chris MilneSports PhysicianHamilton

Vol 38 No 2, 2011; 57

CONFERENCE REVIEW

American College of Sports MedicineAnnual Conference, Denver 2011

The American College ofSports Medicine AnnualConference was held in

Denver Colorado over the week of31 May 31 – 4 June. This is a hugemeeting (everything is big in theUS), with over 6,000 participants(more than 1,200 international),and 3,200 presentations in multipleconcurrent streams. Typically thereis a heavy focus on physiology, andthis year was no exception. Frommy perspective this makes itinteresting, for as a clinician, itdrags you out of overtly clinicalpresentations, and enducesconsideration of a more ‘basic’scientific and multi-disciplinaryapproach to thinking.

This year there were a couple oftrends that were worth noting.Firstly, there were many clinicalultrasound (US) sessions. I havenot noticed this on the programmebefore, but illustrates that even inthe USA the use of US by sportsmedicine practitioners isexpanding. My own feeling is thatthis is an immensely usefulextension of the clinicalexamination, and in my experienceis a useful tool in the clinic (foreducation, monitoring, guidedinjections). Paradoxically, I firmlybelieve that if a diagnosis isrequired, and other differentialsneed exclusion, the opinion of askilled radiologist remainsparamount.

Secondly, there continues to be atrend to increasing study of geneticsin sports medicine. The impressionI received overall from the largenumber of posters andpresentations, was that the evidencefor most genetic influences onperformance remain contradictory,limited in study power and plaguedby limitations in study design. This

does however remain one of thereally interesting areas to watch inboth exercise performance andhealth.

Finally, if the number ofpresentations are anything to go by,there appeared to be very littleinterest in the clinical care of theelite athlete and the specificchallenges that this imposes.Rather, there was a predominanceof presentations considering thehealth of the population andexercise prescription for health.This is a very important element ofthe sports health industry, and mayreflect the direction sports medicineis heading.

ACSM is worthwhile attending, butchoosing which presentation toattend can be challenging andfrustrating – when you realise youare trapped in a lecture which isperhaps not what was expected, andthere may be two or three otherlectures you could be at. I met anumber of kiwis (not all workingin NZ!) and it was great to see thatindividual sports in NZ wererecognising the importance ofhaving their sports medicine staff(physiotherapists and nutritionists)attend this large internationalconference, and to support itfinancially. Denver is a beautifulplace, and well worth a visit! Thefollowing summarises a few of thetopics and lectures that I managedto get to and maintain an attentionspan in the face of dire jet lag andlecture fatigue. I hope that it mayencourage you to look at some ofthe work produced by the excellentpresenters, on really interesting andimportant topics – such that you cancheck the accuracy of myrecollections!

Exercise and HealthKarim Khan, a Fellow of theAustralasian College of SportsPhysicians but well known aroundthe world, gave a typicallycolloquial, entertaining and thoughtprovoking talk regarding theimportance of physical activity(PA) in health (“Supersize myExercise! Learning from MadMen, the Malboro Man andFreakonomics to Promote PhysicalActivity”). Highlighting theincreasing evidence that lack offitness results in more deaths thansmoking, diabetes and obesity(“smokadiabesity”) combined, aswell as the positive impact thatexercise can have on killers suchas cancer and cognitive function,Karim presented a strong case forthe prescription of exercise. Theparadox being that despite theincreased evidence for the benefitsof exercise in recent years, exerciselevels of populationsinternationally continue todecrease. Prescription of exerciseat an individual level needs to bepersonalised to optimise health,which may differ from the globalpopulation based recommendations– with evidence presented for ahyperbolic relationship betweenexercise volume and healthyoutcomes. Another interestingpoint for me, was the use of“exercise as the 5th vital sign” (seeSallis BJSM (45) 6; p 473 – 474),recording current exercise patternsas a marker of risk – an easy andeffective tool in clinical practice.Importantly, Karim highlighted theincreasingly recognised need forresearch on implementation ofpractices, rather than furtherevidence that exercise is a usefultool – that is, how can we best applywhat we now know, for betterclinical outcomes.

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Karim highlighted the movementaround the world for exercise asmedicine, but to my mind, the restof the world is just catching up withNZ’s Green Prescriptionprogramme.

Professor Juleen Zierath(“Promoting Effects of Exercise inDiabetes and Obesity; TranslatingBasic Science into PreventiveAction and Treatment”, Joseph BWolffe Memorial Lecture:Karolinska Institute Stockholm,Sweden) gave an insightful lectureinto the complex but progressiveunraveling of the mechanismsbehind the benefits of exercise intype II diabetes. We are all wellaware of this benefit, but thescience underlying this isfascinating. One point of note wasthe loss of “metabolic flexibility”in diabetes, whereby there is anincreased preference for fat storageover fat metabolism, and the effectthat muscle fibre type may have onthis. Exercise, amongst otherthings, will increase Glut 4 receptorexpression, thereby enhancingglucose uptake.

Advancing and SustainingEvidence-based practice inClinical SettingsFor a clinician, this lecture(Bernadette Melnyk, Exercise isMedicine Clinical Lecture) was abit of hard work, but a couple ofelements rang true with my way ofthinking. The first was thehighlighted point that evidencebased practice is not all about levelone, double blind randomisedcontrolled trials. By contrast, whileit does involve that assessment, italso incorporates consideration ofboth patient preferences and values,and the individual clinicianexpertise. As per my editorial inthis edition, I believe strongly thatthe opinion of experts andexperience needs to be consideredin any evidence based practice.Secondly, as with Karim in hislecture, Dr Melnyk highlighted theneed for translational approaches,to ensure that evidence is

adequately incorporated into ourclinical practice.

Sudden Cardiac Death (SCD) inthe Fitness SettingBoth speakers (Kyle McInnis /Barry Franklin) highlighted theunpredictability of SCD in the over35 population, and the fallibility ofexercise stress testing in this group.Clearly illustrated was thesurprising frequency of SCD ornear death in fitness centres, withunpublished data from the USAsuggesting up to 50% of fitnessfacilities may have experiencedthis. Rapid intervention andapplication of shock through theAutomated External Defibrillater(AED) remains the bestmanagement, but this requirestraining and confidence from thefitness centre staff. With thedemographics of fitness centreutilisation moving towards an older,middle-aged (not sure that I’mcomfortable with that term)population, there is an increasingneed for awareness of this issue infitness centres.

Nutritional Support for theInjured Athlete. A Focus onMuscle and Tendon InjuryThe most striking impression Ireceived from this session (KevinTipton (UK),Stuart Phillips(Canada), Bronwen Lundy (UK) –introduced by NZ’s own Jeni (I-really-do-speak-like-this) Pearcewas the lack of specific dataavailable to support this topic(bearing in mind I left before theend, so probably missed the bestpart!). This probably reflects thechallenges imposed by research inthis area, rather than either thescientific reality, or a lack ofinterest. Important inrehabilitation, particularly fromsurgery, is the maintenance of anadequate energy intake, and theavoidance of unnecessaryprolonged immobilisation.Immobilisation will result in disuseatrophy (affecting the muscle,tendons, ligaments and bones),predominantly as a result ofdecreased protein synthesis –

however and importantly, in shortdurations of immobilisation, aminoacid (AA) supplementation mayoffset that disuse atrophy (thenumbers discussed were: 16gessential AA, with 30 g CHO, 3 xdaily between meals). In the longterm immobilisation however, AAsupplementation has not beenshown to be useful. While proteinbreakdown is fairly stable duringthe day, protein synthesis fluctuatesconstantly with a reduction insynthesis between meals. Otherthan nutrition however, it isimportant to note that only a verylow number of isometriccontractions are required tomaintain muscle strength, andoffset disuse atrophy.Unfortunately, as most of us mayalready be aware, for some reason,the calf muscles are more difficultto preserve – they didn’t give mean answer to this perplexingquestion.

In a separate session, ProfessorMarco Narici (ManchesterMetropolitan University) discussed“Muscle and Tendon Remodellingin Use and Disuse” and presenteda really interesting story. Hereminded me that MyogenicRegulatory Factors (responsible foror reflecting muscle adaptation) areincreased within 12 hours ofstrength training – while measuredmuscle hypertrophy may notadequately reflect these earlychanges. Furthermore, more subtlearchitectural changes in muscle,including “pennate insertion angle”(the angle the fascicles insert intothe tendon/fascia) may be bettermeasures of muscle adaptation.Muscle bulk may increase byadding sarcomeres both in paralleland series, the latter obviouslyincreasing the length of thefascicles. Interestingly, it isproposed that concentric trainingmay result in increases in thepennate angle, while eccentrictraining will increase fasciclelength. Bed rest will both decreasethe muscle fascicle length and thepennate angle and result in a lossof muscle at a rate of 0.4% per day

Vol 38 No 2, 2011; 59

CONFERENCE REVIEW

(supposedly 2700 sarcomeres perday!) – but again, each muscle mayrespond differently to both trainingand bedrest. Similarly, tendonresponds to training with increasedtendon stiffness and increasedtendon cross sectional area, whilebed rest will reduce the stiffness ofthe tendon.

Rugby Injuries“Improving Safety in the RugbyTackle” seemed an unlikely topicfor ACSM (despite that fact that theUSA won the first Olympic Rugbymedal). Unfortunately, other thanan entertaining insight into therange of injuries sustained while ontour in New Zealand, this sessionfailed to deliver anything novel.It was always going to be toughconvincing a non-surgeon, who hasspent most of his career managingchronic overuse injuries, that ACLwas really an interesting injury (PerRenstrom “ACL – The MostIntriguing Injury in Sport”).However, Per Renstrom, bringinga generation of experience andperspective, gave a very interestingtalk on this, probably the mosttalked about sporting injury (at leastat orthopaedic oriented sportsmedicine conferences). Hehighlighted (despite the progressionin clinical surgical techniques) thelack of level one research in ACL(highlighting the recent and welldocumented randomised trial inNEJM showing no medium termdifferences between surgical andnon surgical management of youngnon professional athletes as anexception). He spent some timediscussing the importance ofanatomical reconstruction of theACL, but remained unconvinced asto the benefits of a double bundlereconstruction (as compared to awell performed single bundle),particularly when one considers thetechnical challenges, and the issueswith re-do of double bundle surgery(a challenge our clinic hasexperienced). His conclusion thatthe choice of surgeon was perhapsmore important than the choice oftechnique may well be widely

shared! The challenges of returnto play decisions remain, and againthe lack of evidence washighlighted, but his feeling was thatthe function and “movementquality” needs to be a keyconsideration. Finally, hehighlighted the risk of osteoarthritispost ACL reconstruction, which,given our failure to reduce the ratesof primary ACL injury, continuesto be a serious long termconsequence of sportsparticipation.

GeneticsFurther developing the concept ofthe genetic associations oftendinopathy, this group (MalcolmCollins / Martin Schwellnus, CapeTown, South Africa) have extendedtheir fascinating work intoperformance in endurance sport –using the high participation eventsin SA as their population (namelythe two Oceans Ultramarathon andthe SA Ironman). Continuing tofocus on the COL5A1 gene theypresented two posters suggestingthat a TT genotype may increasemRNA stability, leading toincreased Type V collagenproduction with subsequentincreased fibril assembly anddensity. This may then result inaltered mechanical properties of themusculo-tendinous unit with threeoutcomes:

1 Reduced flexibility,

2 Increased Achillestendinopathy risk, and

3 Increased running economyand secondary performance.

A nice concept!

By contrast, in a session entitled“Ethiopian and Kenya DistanceRunners: What makes them sogood?”, Prof Yannis Pitsilades fromGlasgow highlighted how despitealmost 10 years’ work on thepopulation genetics of theseathletes, they are really no closerto identifying any population based

60 NZJSM

differences in performance ability.They continue to pursue thistantalising question, butincreasingly recognise theimmensely importantenvironmental factors such associo-economic drive, diet, altitudeand lifestyle.

Dr Bruce HamiltonSports PhysicianQatar

POSTGRADUATE PONDERINGS

Not all wrist lumps are gangliaDaniel J Pettigrew MBChB, DCH, MRNZCGP1

Hamish R Osborne MBChB, MMedSci, FACSP 2

1 Division of Health Sciences, University of Otago2 Department of Medicine, Dunedin School of Medicine, University of Otago

Correspondence to:Dr Hamish OsborneDepartment of MedicinePO Box 913DunedinTel +64 3 474 7007 ext 8556Fax +64 3 474 7461hamish.osborne@otago.ac.nz

Introduction

Wrist lumps arec o m m o n l yencountered in both

general and sports medicinepractice. Whilst the vast majorityare benign and many are transient,there is a danger in viewing themall as insignificant, or quicklyjumping to pre-formed conclusionsabout their nature. Practitionersshould have a framework forevaluating these lesions such thatan atypical presentation of a wristlump will trigger appropriateinvestigations. This case illustratesa wrist lump initially misdiagnosedas a simple ganglion with importantimplications for the patient.

Case ReportA 37 year-old male universitylecturer presented with a lump overhis right wrist. Present for at leasttwo years, it had been slowlyenlarging over this time but was notpainful unless knocked. He deniedany altered sensation in his forearm,wrist and hand and had norestriction or pain with any hand orwrist movements. On examinationhe had a 3.5 cm x 2 cm masssituated over the dorsal ulnar borderof his right wrist at the level of theulnar styloid. It was relativelymobile and firm but not tethered,fluctuant or pulsatile. It was mildlytender on firm palpation butwithout radiation or paraesthesiaelicited by this pressure. Power and

sensation was normal in the handand wrist. A further lump, 1.5 cmby 1.5 cm with a similarconsistency to the first, was foundon the medial aspect of his leftupper arm 10 cm distal to the axillaand just medial to the body ofbiceps brachii, but he was lessconcerned about this one as it wasnot causing him any discomfort.

A diagnosis of ganglion was madefor the wrist lump whilst the leftarm lesion was suspected to be afibroma. Given the stability ofthese lesions it was decided tomonitor and to review if there wasany change in them.

The patient re-presented threemonths later. Whilst there had beenlittle or no change in the lesions,he was keen to proceed withdefinitive management as the wristlump was more frequently beingknocked and causing discomfort.The examination was unchanged.After discussing the procedure withhim, aspiration was attemptedunder local anaesthetic in sterileconditions but despite severalattempts no fluid of note wasaspirated. The texture of the lumpfelt through the needle was differentto what would be expected from asimple ganglion and in fact feltsolid right through. The diagnosiswas revised to unspecified softtissue tumour and a referral was

made to an orthopaedic surgeon forconsideration of excision.An MRI scan was subsequentlyperformed clearly showing that theright wrist mass arose from theulnar nerve and the left arm massarose from the median nerve. Theywere reported as likelyneurofibromas. The patientproceeded to uncomplicatedsurgical excision as a day case withhistological analysis of both lesionsbeing benign schwannoma.

Post-operatively, he had some mildtingling in the distribution of thedorsal branch of the ulnar nerve onthe right and in a median nervedistribution on the left butotherwise had no change in hisupper limb sensation or function.He was advised to monitor forfurther soft tissue masses as wellas any new neurological symptoms.

DiscussionWhilst ganglia are the mostcommon wrist lumps seen ingeneral practice making up 60% ofmasses found around the wrist andhand,9 there are certaincharacteristics that aid theirdiagnosis. Location is a primaryconsideration with 65% of gangliasituated in the dorsal wrist positionoverlying and arising from thescapholunate joint. A further 20-25% of ganglia are volar overlyingthe distal radius, with the other 10-

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POSTGRADUATE PONDERINGS

15% of ganglia arising from flexortendon sheaths at other locationsthroughout the wrist.7 An dorsalulnar border wrist ganglion wouldbe extremely rare other than if therewas involvement of the extensorcarpi ulnaris tendon sheath. Gangliaalso have a characteristic texturebeing filled with mucoid fluid andare thus “ballotable”, not a featurepresent in the case. A typicalganglion has a volume of around0.95ml,10 translating to a diameterof around 1.2 cm, and it is onlyrarely that they are larger than 2cm.8

The differential diagnoses for wristlumps is expansive, but each has acharacteristic history andexamination. Giant cell tumours ofthe tendon sheath are next mostcommon, being firm and alwaysarising in the vicinity of tendons,usually flexor.1 Aneurysms, moreoften pseudoaneurysms, areclassically pulsatile, arise fromarteries and are usually associatedwith trauma to the vessel. Thecommon neural tumours of theperipheries are neurofibromas andschwannomas, the formerincorporating many different typesof nerve sheath cells and structuralelements. Schwannomas are ahomogenous benign tumour ofSchwann cells, the myelin secretingcells of the nerve sheath.5

Schwannomas, being rare, arefrequently (as in this case)misdiagnosed, with up to 38%being misdiagnosed as ganglia.6

Other less common masses includesarcomas, haemangiomas andgranulomas.

Schwannomatosis is a recentlydescribed variant ofneurofibromatosis characterised byhaving only peripheralschwannomas. Diagnosis ofschwannomatosis requires two ormore histologically confirmed non-intradermal schwannomas in apatient over 30 yrs old.3 Multipleneurofibromas are the hallmark oftype 1 neurofibromatosis andbilateral acoustic neuromas aretypical of type 2 neurofibromatosis.4Schwannomatosis is thought to be

due to a mutation in SMARCB1, atumour suppressor gene, and is feltto be autosomal dominant. Familialcases are however relatively raredue to incomplete penetrance.2

Upon diagnosing schwannomatosisit is important that patients areaware that while they may formschwannomas anywhere in thecentral nervous system, peripheraltumours are more common. Thus,any unexplained neurologicalsymptoms should prompt earlyreferral for appropriateinvestigation.

In this case, a soft tissue tumourshould have been much higher onthe initial differential. The clue toan underlying neural tumour wasthe additional mass also arising inthe vicinity of a peripheral nerve.MRI is the diagnostic tool of choicefor differentiating these masses,11

particularly for the nerve sheathtumours. Ultrasound is a clinicallyreasonable convenient alternative.Attempted aspiration of non-pulsatile fluid filled lumps or fineneedle aspiration of more solidlumps has the added benefit ofpotentially yielding a histologicaldiagnosis.

This case illustrates the importanceof keeping an open mind to the fulldifferential diagnosis of lumpsabout the wrist. An appropriateevaluation may minimise thechance of misdiagnosingsomething rare, that we mayencounter only once in our medicalcareer.

References1 Collen J, Mount G, Pollock P, Shrout

J, Malafronte P, Vangeertruyden P,and Oglesby R. Giant cell tumor ofthe tendon sheath. J Clin Rheumatol2009; 15: 85-87.

2 Hanemann C O, and Evans D G.News on the genetics, epidemiology,medical care and translationalresearch of Schwannomas. J Neurol2006; 253: 1533-1541.

3 MacCollin M, Chiocca E A, Evans DG, Friedman J M, Horvitz R,Jaramillo D, Lev M, Mautner V F,Niimura M, Plotkin S R, Sang C N,Stemmer-Rachamimov A, and RoachE S. Diagnostic criteria for

schwannomatosis. Neurology 2005;64: 1838-1845.

4 McClatchey A I. Neurofibromatosis.Annu Rev Pathol 20007; 2: 191-216.

5 Mrugala M M, Batchelor T T, andPlotkin S R. Peripheral and cranialnerve sheath tumors. Curr OpinNeurol 2005; 18: 604-610.

6 Rockwell G M, Thoma A, and SalamaS. Schwannoma of the hand and wrist.Plast Reconstr Surg 2003; 111: 1227-1232.

7 Tallia A F, and Cardone D A.Diagnostic and therapeutic injectionof the wrist and hand region. Am FamPhysician 2003; 67: 745-750.

8. Teefey S A, Dahiya N, Middleton WD, Gelberman R H, and Boyer M I.Ganglia of the Hand and Wrist: ASonographic Analysis. Am JRoentgenol 2008; 191: 716-720.

9 Thornburg L E. Ganglions of the handand wrist. J Am Acad Orthop Surg1999; 7: 231-238.

10 Varley G W, Needoff M, Davis T R,and Clay N R. Conservativemanagement of wrist ganglia.Aspiration versus steroid infiltration.J Hand Surg Br 1997; 22: 636-637.

11 Wan J M, Magarelli N, Peh W C,Guglielmi G, and Shek T W. Imagingof giant cell tumour of the tendonsheath. Radiol Med 2010; 115: 141-151.

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