Musculoskeletal Medicine · ISSN 1324-5627 Australasian Musculoskeletal Medicine Vol. 9 No. 1 May...

ISSN 1324-5627

AustralasianMusculoskeletal

Medicine

Vol. 9 No. 1 May 2004

!!!!! Managaement of chronic low back pain!!!!! Pain and chronic low back pain: a new model!!!!! Chronic neck pain: risk factors and prevention!!!!! Cervical arthroplasy for the treatment of cervical spine disease!!!!! Efficacy of 300 mW, 830 nm laser in the treatment of chronic

neck pain!!!!! Prolotherapy for peripheral joints! Management of shoulder pain in general practice!!!!! The orphan organ!!!!! Individual medication effectiveness test comparing celecoxib

with extended release paracetamol for osteoarthritis

2 Australasian Musculoskeletal Medicine

ContentsEditorial ........................................... 3

From AAMM President ... ................ 5

From NZAMM President .. ............... 6

Letter to the editor ........................... 7

Management of chronic lowback pain ........................................ 8

Pain and Chronic Low BackPain: A New Model? Part 1 ........... 14

Pain and Chronic Low BackPain.Part 2 .................................... 20

Chronic neck pain: risk factorsand prevention ............................... 26

Cervical arthroplasy for thetreatment of cervical spine disease28

Efficacy of 300 mW, 830 nm laserin the treatment of chronic neckpain ............................................... 32

Prolotherapy for peripheral joints ... 38

Management of shoulder pain ingeneral practice ............................. 42

The orphan organ .......................... 45

Individual medicationeffectiveness test comparingcelecoxib with extended releaseparacetamol for osteoarthritis ........ 49

Book reviews ................................. 50

Journal abstracts .......................... 51

Education committee report .......... 58

Secretary-general AGMaddress, 2003 ............................... 60

Vale Dr John Martin Bosler ........... 62

Conference reports ........................ 63

Red Flag clinical indicators ........... 66

Educational Activities .................... 67

Australasian Musculoskeletal Medicine ispublished by the Australian Association ofMusculoskeletal Medicine for medical prac-titioners interested in the aetiology andmanagement of musculoskeletal disorders.Opinions expressed are those of the au-thors and not necessarily those of the editoror the Association. Editorial comment mayreflect the opinions of the editor alone.

Contributions on any relevant topic arewelcome for submission to the editor, DrDavid Roselt26 Crofton St, Bundaberg 4670Phone +61 7 4152 2888Fax +61 7 4153 3245Email [email protected]

AAMM website: www.musmed.comNZAMSM website: www.musculoskeletal.co.nzAFMM website: www.biziworks.com.au/afmm/FIMM website: www.fimm-online.org

Australian Association ofMusculoskeletal MedicineOffice Bearers 2003-2004

New Zealand Association ofMusculoskeletal MedicineOffice Bearers 2003-2004

PresidentDr Scott Masters MBBS, Dip Musc Med,FRACGP, FAFMMCaloundra Spinal & Sports Medicine Centre39 Minchington St, Caloundra, Qld 4551Ph: +61 7 5491 1144Fax: +61 7 5491 1253

Vice-PresidentDr Michael Yelland MBBS, Dip Musc Med,FRACGP, FAFMM64 Wirraway Pde, Inala, Qld 4077Ph: +61 7 3275 5444Fax: +61 7 3278 9987

Honorary SecretaryDr Brian Lovell MBBS, Dip Phys Med, MMed Phys MedMetropolitan Spinal Clinic, 302 Malvern Rd,Prahran, Vic 3181Ph: +61 3 9529 1988Fax: +61 9529 1844

Honorary TreasurerDr Esther Langenegger MBBS, Dip MuscMed, FAFMM482 Macauley St, Albury, NSW 2640Ph: +61 2 6041 4494Fax: +61 2 6021 6373

Committee MembersDr Steve Jensen MBBS, Dip Musc Med,FAFMM; Immediate Past President5 Stanlake St, Footscray Vic 3011Ph: +61 3 93185233Fax: +61 3 93186630

Dr Derek Davey MBBS, Dip Obs, Dip OccHealth, Dip Musc Med, FAFMM29 Craigie Rd, Newtown Vic 3220

Dr Geoffrey Harding MBBS, Dip MuscMed, FAFMM1st Flr, 67 Brighton Rd, Sandgate, Qld 4017Ph: +61 7 32695522Fax: +61 7 3269 6407

Dr Michael Oei MBBS, Dip Phys Med, MMed Phys Med, Cert Man Med213 Darlinghurst, NSW 2010Ph: +61 2 8302 1180, +61 2 9969 2198Fax: +61 2 8302 1195

Dr David Roselt MBBS, Dip Musc Med,FRACGP, FAFMM26 Crofton St, Bundaberg 4670Phone +61 7 4152 2888Fax +61 7 4153 3245

Dr Margaret Taylor BSc, MBBS, FACNEM,FIBCTPO Box 570, Fullarton SA 5063Ph/fax: +61 8 8338 3778

WebmasterDr Victor Wilk MBBS, M Med Pain Med, DipMusc Med, FAFMM441 Bay St, Brighton, Vic 3186Ph: +61 3 9596 7211Fax: +61 3 9596 7871

PresidentDr Steve Bentley MBChB, Dip Obst, DipMusc Med, Dip Sports Med, FAFMM72 Newington Ave, DunedinPh: +64 3 4672046Fax: +64 3 4672042

Vice-PresidentDr John Robinson BSc, MBChB, M MedPain Med, Dip Musc Med, Dip Occ Med,FAFMM, Cert Spinal Inj256 Papanui Rd, ChristchurchPh: +64 3 3550342Fax: + 64 3 3100516

Honorary SecretaryDr Gary Collinson MBChB, Dip Musc Med,FAFMM4 Kinross St, Blockhouse Bay, AucklandPh: +64 9 6271024Fax: +64 9 6271181

Honorary TreasurerDr Clemens Franzmayr Specialist for Con-servative Orthopoedics 197515 Frank St, ChristchurchPh: +64 3 3527761Fax: +64 3 3527762

Committee MembersDr Charlie NG MBChB, Dip Musc Med, DipSports Med, FAFMM, Cert Spinal Inj8 Archibald Rd, Kelston, AucklandPh: +64 9 8185208Fax: +64 9 8185208

Dr Peter McKenzie BSc, MBChB, Dip Obs,Dip Musc Med, FRNZCGP, FAFMM217 Bridge St, NelsonPh: +64 3 5483455

Dr James Watt MBChB, Dip Mus Med,FAFMM, Cert Spinal Inj308 Lake Rd, Takapuna, AucklandPh: + 64 9 4895059Fax: + 64 9 4894937

Dr Grant Thomson MBChB, Dip Mus Med,MLCOMBush Rd Medical Centre, Kamo, WhangareiPh: +64 9 4350692Fax: +64 9 4352634

Dr Mark Johnston MBChB, M Med PainMed, Dip Mus Med, FAFMM, Cert Spinal Inj394 Hibiscus Coast Highway, OrewaPh: +64 9 4261260Fax: +64 9 4261136

Dr Jim Borowczyk BSc, MBChB, Dip MuscMed, MRCP, FAFMM256 Papanui Rd, Merivale, ChristchurchPh: + 64 3 3550342Fax: +64 3 3557071

May 2004 3

Editorial

It is a great honour indeed toaccept the editorial baton for Aust-ralasian Musculoskeletal Medi-

cine (AMM) from Dr Scott Masters.Scott has been a driving force for theAustralian Association of Musculoskel-etal Medicine (AAMM) these past fewyears. A plethora of articles from hisword processor have graced the pagesof this journal, Medical Observer maga-zine, and other learned tomes. Scotthas been elected to the AAMM presi-dency. Congratulations Scott.

I become the latest in the editorialline, following in the footsteps of DrsMasters, Yelland, Palmer, King, andothers before them. I wish to thankthese hard-working, enthusiastic col-leagues for their previous efforts forthe Association. I will do my best touphold their fine tradition.

The editor is, among other things, aconduit to help crystallize into print thethoughts and words, the sentimentsand feelings of members and othercolleagues, to record them for thepurpose of education, enlightenment,and for posterity.

I wish to thank all contributors fortheir fine efforts in this edition, and toencourage more journal articles, morediscussion and feedback, and morecontributions via the letters pages.

The 33rd AAMM Annual ScientificMeeting (ASM) in Sydney on Novem-ber 27-30,2003, was a big hit. It fo-cused on neck pain, and some speak-ers have kindly provided or contributedto articles in this edition of the journal.The conference dinner, a cruise aboardthe MV John Cadman II, was memora-ble, especially for the views of SydneyHarbour at sunset. The meeting isreviewed by Immediate Past PresidentDr Steve Jensen in this edition of theJournal.

The Evidence-Based Managementof Acute Musculoskeletal Pain wasreleased with NHMRC approval in No-vember 2003.1 This was based heavilyon work from Professor Nikolai Bogduk,Professor of Pain Medicine at New-castle University, and other colleaguesin the Australasian Faculty of Muscu-loskeletal Medicine (AFMM), as part ofthe National Musculoskeletal MedicineInitiative.

Dr Michael Yelland, new AAMM vice-

president, had his randomized con-trolled trial on prolotherapy publishedin Spine on January 1, 2004, to wel-come the New Year. It has been praisedfor the quality of its conception, execu-tion, and methodology.2 Congratula-tions to Michael.

Professor Nikolai Bogduk had hisarticle “Management of Chronic LowBack Pain” published in the MedicalJournal of Australia on January 19. Itlooks at the evidence base, and high-lights the reductionist approach, withprecision diagnosis and treatment ofchronic somatic lumbar spinal pain fea-tured.3 This very important paper is re-printed here with the kind permission ofthe MJA.

The first randomized controlled trialon IDET has been published in SpineJournal this year. 4 It showed signifi-cantly greater improvement in pain,disability, and depression in the IDETgroup compared to placebo, for treat-ment of discogenic low back pain. Thiswas with six months’ follow up, whichhas been shown in another study to bepredictive of outcomes at 12 and 24months.5 It has been shown in control-led studies using precision diagnosisthat internal disc disruption, which hasmore stringent diagnostic criteria thandiscogenic pain, is responsible for40% of chronic low back pain.6

The Australian Pain Society ASM inCanberra on March 7-10 was also anotable event on the musculoskeletalpain medicine calendar, where theAssociation and Faculty were well rep-resented in terms of lectures in theplenary sessions and topical concur-rent sessions. The convenor, DrGeoffrey Speldewinde, and his organ-izing committee did a fabulous job, wellsupported by DC Conferences PtyLtd. I hope you enjoy my report in thisedition.

The 26th Annual Scientific Meetingof the Australian Pain Society will beheld in Sydney in August 2005. It willbe held in conjunction with the Interna-tional Association for the Study ofPain (IASP) 11th World Congress onPain, August 21-26, 2005, and shouldbe well worth attending, so mark it inyour diaries, and keep the time free.Details at http://www.iasp-pain.org/05Cong.html.

Dr Breck McKay has produced twopapers on “Pain and Chronic LowBack Pain: A New Model” to follow hisarticle in the last edition of AMM. Breckhas followed on the work of StefanBlomberg, our invited overseas speakerat the 2002 AAMM ASMheld in Mel-bourne, and has a large case series ofsome 550 patients which certainlypoints to this approach being effica-cious.

Dr Geoffrey Speldewinde has pro-duced a paper on risk factors andprevention for chronic neck pain.

Dr Jonathon Parkinson and Associ-ate Professor Lali Sekhon have co-authored a paper on cervical arthro-plasty, used primarily for cervicalmyelopathy and radiculopathy.

There is an interesting retrospectivestudy on laser treatment for chronicneck pain in primary care by Dr RobertaChow as part of her PhD thesis intolaser therapy for pain. This PhD isbeing supervised by Associate Pro-fessor Les Barnsley.

Dr Margaret Taylor has produced aprovocative article on prolotherapy forperipheral joints. It too looks very inter-esting, with studies to support a usefulrole in treating musculoskeletal painand dysfunction in the appendicularskeleton and soft tissues.

We have another article on manage-ment of shoulder pain in general prac-tice especially with respect to imagingby Associate Professor NormBroadhurst.

It confirms the lack of utility of ultra-sound scanning for diagnosing thecause of shoulder pain.

There is a short paper documentinga case series highlighting the value ofsteroids for treating frozen shoulderfrom Brisbane rheumatologist Dr BillDouglas, presented in Letters to theEditor.

Dr Peter Jackson brings us the latestthoughts on myofascial pain after thevery successful New Zealand meetingin Queenstown in September. Thatmeeting involved Drs David Simons,Nik Bogduk, and Sigfried Mense asinvited international guest speakers.

Dr Michael Yelland espouses thevalue of individual medication effec-tiveness tests (IMETs), currently look-ing at Celebrex versus Panadol Extend


for osteoarthritis, and available free ofcharge though the IMET Service atUniversity of Queensland.

The importance of the Red FlagChecklist is emphasized for assessingboth acute and chronic low back pain,where it can help minimize unneces-sary investigations, and reassure bothdoctors and their patients.

We say farewell to past president ofthe AAMM Dr John Martin Bosler, whopassed away on December 24, 2003,and will be sadly missed.

We also have abstracts of some ofthe latest journal articles, with commen-tary by members of the association.

The Australasian Faculty of Muscu-loskeletal Medicine has reapplied tothe AMC for recognition as a specialty.The outcome is awaited with greatinterest.

Certainly there are good argumentsfor this. There is a need for recognitionof the role for specialist musculoskel-etal pain medicine physicians to offerconsultant assistance to general prac-titioners in the community to managesubacute and chronic musculoskeletalpain. This is rampant in the communityand often managed suboptimally. Thereare a growing number of reliable andvalid diagnostic procedures in painmedicine that can assist with accurate,precision diagnosis. This offers theoption of precision treatment, and willreduce morbidity from incorrect diag-nosis, and incorrect subsequent treat-ment.

So there is much happening in themusculoskeletal world of late and muchat stake as we pursue the Holy Grail ofMusculoskeletal Truth.

The life of Dr Brian Lovell, our newsecretary, and our other new commit-tee members, Dr Esther Langenegger,our new treasurer, and Dr MargaretTaylor, has changed, for the better ofcourse – thanks to them. I have beenco-opted onto the committee as well.

Thanks also to the rest of the commit-tee who are staying on: ImmediatePast President Jensen, Past Treas-urer Dr Derek Davey, Drs GeoffHarding and Michael Oei, andWebmaster Dr Victor Wilk. Manythanks to the hard-working outgoingcommittee members, Drs RobertGassin, Des Shimeld, and PhilipWatson.

Remember to always look on thebright side of life.

David Roselt

1. http://www.nhmrc.gov.au/publications/synopses/cp94syn.htm

2. Yelland M, Glasziou P, Bogduk N, et al.Prolotherapy Injections, Saline Injections,and Exercises for Chronic Low Back Pain:A Randomized Trial. Spine 2004; 29: 9-16.

3. Bogduk N. Management of Chronic LowBack Pain. Med J Aust 2004; 180 (2): 79-83.

4. Pauza KJ, Howell S, Dreyfuss P, et al. Arandomized, placebo-controlled trial ofintradiscal electrothermal therapy for thetreatment of discogenic low back pain.Spine J 4 (2004) 27-35.

5. Bogduk N, Karasek M. Two-year follow-up of a controlled trial of intradiscalelectrothermal anuloplasty for chronic lowback pain resulting from internal disc dis-ruption. Spine J 2002; 2: 343-50.

6. Schwarzer AC, Aprill CN, Derby R,et al.The prevalence and clinical features ofinternal disc disruption in patients withchronic low back pain. Spine 1995; 20:1878-83.

Editorial

May 2004 5

From the AAMM President

One of my first jobs as pres-ident of the AAMM has beento award life membership to

three doyens of the musculoskeletal(MS) field, namely John Murtagh, NormBroadhurst, and Nikolai Bogduk. In the1980s Professor Murtagh was largelyresponsible for bringing MS medicineinto the view of GPs around Australiavia regular articles in Australian Fam-ily Physician (AFP). Together withClive Kenna, he toured extensivelyaround Australia running workshopson managing spinal pain. These work-shops were based on their book Backpain and spinal manipulation and wereespecially useful to rural GPs.

At a similar time, ProfessorBroadhurst was agitating for MS rep-resentation at a university level. He wassuccessful in organising the first Aus-tralian-run postgraduate diplomacourse for musculoskeletal medicine,through Flinders University. Simulta-neously, he was educating GPs insimple strategies to assist manage-ment of the common MS presentationsto primary practice; for example, ver-tebral dysfunction, piriformis syn-drome, slipping rib syndrome, tarsaltunnel syndrome, iliolumbar ligamentsprain, and ischial bursitis. Summaryarticles on these and other topics gavehandy office tips to GPs via the AFPjournal.

Without the two professors the voidin MS education for primary practition-ers would have been terminal. Theirenthusiasm and dedication helpedspark an interest in the optimal man-agement of MS pain and encourageda critical analysis of the acceptedwisdom. Thus the Bogduk juggernautwas born. Initially, Professor Bogdukwas drawn into the fold by claims fromDr Rees that back pain could be curedby percutaneous rhizolysis of thenerves supplying the zygapophysialjoints. Bogduk and others subsequentlyshowed that the nerves were not beingaffected by Rees’s treatment, and thenwent on to elucidate the role of medialbranch blocks and radiofrequencyablation in the management of lowback pain. Professor Bogduk’s role inestablishing a research base for mus-culoskeletal medicine, largely throughthe Australasian Faculty of Muscu-

loskeletal Medicine, has been enor-mous. His combinations of Herculeanoutput with precision quality are unsur-passed in the world literature on MSpain.

On a sadder note, I received thenews that one of our past presidentspassed away this year. Dr John MartinBosler from Tamworth was a memberof the AAMM from the 1970s and rana predominantly MS practice based onthe Cyriax model. He will be sorelymissed by family, community, andcolleagues.

This year’s annual conference willbe held in Adelaide starting on October29. South Australia is lovely this time ofyear and it is a perfect opportunity tomix some recreation with education.There will be a mixture of workshopsand presentations to suit all tastes. In2005 we will run our conference inQueensland towards the beginning ofthe year. The theme will be muscu-loskeletal problems in the elderly. Theannual conferences are a great oppor-tunity to expand your MS network, findout the latest research findings, andextend your practical skills.

The follow-up to the evidence-basedguidelines first produced by the Na-tional Musculoskeletal Medicine Initia-tive is now available online. Theseguidelines were put together by theAustralian Acute Musculoskeletal PainGuidelines Group coordinated by Pro-fessor Peter Brooks, Dean of the Fac-ulty of Health Sciences at the Univer-sity of Queensland. The other three onthe executive committee were Profes-sor Nikolai Bogduk, Associate Profes-sor Lyn March, and Professor NickBellamy. The five areas covered wereacute low back pain, acute thoracicspinal pain, acute neck pain, acuteshoulder pain, and anterior knee pain.The musculoskeletal fraternity werewell represented amongst the reviewgroups with Professor Bogduk, Pro-fessor John Murtagh, Dr Yelland, DrGiles, Associate Professor Barnsley,Dr King, Dr Vivian, and me all contrib-uting to the final document. You can visitthe guidelines at www.nhmrc.gov.au/publications/synopses/cp94syn.htm.

Finally, I have a personal request ofall members. I have recently receivedfunding to perform an observational

study on acute shoulder pain in pri-mary practice. If any members areinterested in being involved, could theyplease contact me.

Scott Masters


From the NZAMM President

Over the last six months, theNZAMSM executive com-mittee has directed its at-

tention to setting in place a training andeducation structure for members withdiffering needs and on upgrading theNZAMSM website.

The upgraded website includes apublic section where general informa-tion on musculoskeletal medicine isavailable to the public, including thehistory of our organization, a publicdirectory of musculoskeletal physiciansand practitioners in NZ and a confer-ence page. There are links to AAMM,AFMM, and FIMM. The “members only”section requires a member’s pass-word to gain access and I am graduallygetting through our list of memberssetting this in place.

Within the “members only” sectionthere is a full members directory, de-tails on training and education, includ-ing a list of regional and national co-ordinators who will be responsible formeetings with GPs (CME meetings)and peer review or specific trainingmeetings for local NZAMSM mem-bers.

The full registrar training manual forAFMM is available to download fromthe website.

There is a Journal Review page cov-ering Pain, Spine, AJSM, ManualTherapy. The latest editions of thesejournals will be reviewed and articles ofparticular relevance and importancediscussed.

There is also a Discussion Page thatis now operational. Here specific prob-lems can be presented; for example, aparticular case presentation for mem-bers to comment on and contributeideas on management or to learn from.The problem or case can be emailed tome (website administrator) and thenmembers can directly enter comments,following a thread. It is anticipated thiswill be very beneficial to members whoare isolated in their practice, but will bean important medium to discuss vari-ous problems, such as, “What is ourposition with regard to the meaningand use of the term disc degenera-tion?”, which is used commonly byACC, radiologists, and other medicalspecialists in NZ. We need a unifiedunderstanding and position on such

matters.The NZAMSM is shortly to have a

new logo. Feedback on this, which willbe displayed on the website, or anyother inspirational logo ideas are mostwelcome.

In the first week of March 2004,Professor Johannes Fossgreen, rheu-matologist from Denmark, conducteda three-day course on myofascial re-lease, followed by a three-day courseon functional indirect technique (FIT) inChristchurch. FIT is a soft, safe osteo-pathic technique which can be appliedto treat any painful restricted joint. Thiswas Johannes’s fifth teaching visit toNZ.

Thirty years ago Dr Barrie Tait, him-self a rheumatologist with a stronginterest in musculoskeletal medicine,met Johannes in Japan at a rheumatol-ogy conference. Barrie invited Johannesand Torbin Pripp out to NZ to a manualtherapy course that was duly held inAuckland in 1975. This was the firstcourse of its kind and heralded thebeginnings of musculoskeletal medi-cine in NZ, with the formation of ourAssociation a few years later.

In an historic moment duringJohannes’s recent course onmyofascial release, at which Barriewas a participant, Johannes presentedBarrie with original photos of their firstmanual therapy course in Auckland 30years ago.

The NZAMSM owes a great deal tothese two men for its existence anddevelopment over 30 years. The recenttwo courses were full, very well re-ceived and provided participants withvery useful soft and safe techniques.

There are now three musculoskel-etal physicians in Christchurch andseven in Auckland who have com-pleted spinal injection training at New-castle with Professor Nik Bogduk. Boththe Auckland and Christchurch grouphave contracts with ACC to performspinal injection diagnostic proceduressuch as medial branch blocks forzygapophysial joint pain, third occipi-tal nerve blocks, transforaminal corti-costeroid injections and sacroiliac jointinjections.

In addition these two groups havejust recently been granted exclusivecontracts with ACC to perform percu-

taneous radio frequency neurotomy.Dr John MacVicar, musculoskeletalphysician in Christchurch, is chair-man of the Pain Intervention Commit-tee set up by ACC to advise on suchmatters and procedures.

It is essential for our organizations,as we gain greater status and recogni-tion in medicine, that we maintain andcontinually improve our professionalstandards and reporting, conduct propertrials and research on our manage-ment, particularly with regard to out-comes in whatever area of muscu-loskeletal medicine we are practicing.There is a strong need for outcomes-based, quality research on the varioustreatments we as musculoskeletalphysicians are using in our daily prac-tices.

Steve Bentley

May 2004 7

Treatment of Idiopathic FrozenShoulder with Oral and Intra-articu-lar Corticosteroids

Oral corticosteroids were first usedin the treatment of frozen shoulder in1951.1 Its use remains controversial.Since 1951, reported trials of corti-sone or prednisolone in the treatmentof frozen shoulder with or without theuse of intra-articular corticosteroidsuspensions have produced conflict-ing and generally disappointing re-sults.2 Reported studies have includedpatients with well-established adhesivecapsulitis, one with a mean duration atpresentation of 5.5 months before oralcorticosteroids were trialled.3 Includedin these studies were patients withserious underlying shoulder disordersand insulin dependent diabetics.

MRI studies in frozen shoulder con-firm the clinical impression that theacute painful or fibrinous phase ispresent during the first few months ofthe disease.4 By five months the frozenshoulder has passed through the firstphase of the condition and has enteredthe second or frozen phase whencapsular adhesions and contractureoccurs. Thus one could expect thatearly intervention with powerful anti-inflammatory preparations before fourmonths have elapsed is likely to beeffective. By five months, recoveryfrom frozen shoulder is largely in thehands of Mother Nature and occasion-ally orthopaedic intervention.

Since 1993, I have treated 30 pa-tients suffering from idiopathic frozenshoulder (16 males and 14 females)with a mean age of 55. All patientsfulfilled the criteria for idiopathic fro-zen shoulder.5 The mean duration ofthe initial phase with severe night painand stiffness was 9.5 weeks beforespecialist referral. Plain x-rays androutine blood studies were performedfor all patients. Sophisticated imagingstudies were not usually indicated,although ultrasound of the shoulderwas performed in five patients.

Therapy consisted of 1-2 intra-ar-ticular injections of one ampoule ofCelestone Chronodose with 2 ml of 2%Xylocaine followed by oral prednisone.The prednisone dose was 15-25 mgper day (mean 15 mg) for two weeks.Oral steroids were then reduced and in

all cases phased out by eight weeks.No physiotherapy was given, althoughsimple daily exercises and a homepulley for passive stretching of theshoulder capsule was advised. Allpatients in this group regained fullrange of movement of the affectedshoulder with freedom from pain andwithout relapse. Average time to recov-ery from initiation of treatment was 4.5weeks.

Insulin dependent diabetics were notincluded in this series. I believe bilat-eral frozen shoulders to which thesepatients are predisposed is a form ofcherioarthropathy and thus has a dif-ferent pathogenesis and prognosis toidiopathic frozen shoulder.

It is my experience with this series ofpatients with frozen shoulder that earlyintervention with local and oralcorticosteroids is beneficial and war-rants a formal trial.

References1. Coventry MB, Problem of painful shoul-der. JAMA 1953; 155: 177-85.

2. Blockey NJ, Wright JK, Kellgren JH. OralCortisone Therapy in Periarthritis of theShoulder. BMJ 1954; 1: 1455-57.

3. Binder A, Hazelman BL, Parr G, RobertsS, A Controlled Study of Oral Prednisolonein Frozen Shoulder. Br J Rheumatol 1986;25: 288-92.

4. Noël E, Thomas T, Schaeverbeke T, etal, Frozen Shoulder. Joint Bone Spine 2000;67: 393-400.

5. Harryman II DT, Lazarus MD,Rozencwaig R, In Rockwood CA andMatsen III FA, eds. The Shoulder, 2nd ed.Philadelphia: WB Saunders. 1998; 1064-1112.

Dr William A Douglas FRACPFRCP(London)Physician Rheumatologist201 Wickham TerraceBrisbane Qld 4000

Letter to Editor


Abstract

Treatment for chronic low backpain (pain persisting for overthree months) falls into three

broad categories: monotherapies,multidisciplinary therapy, andreductionism.

Most monotherapies either do notwork or have limited efficacy (for ex-ample, analgesics, non-steroidal anti-inflammatory drugs, muscle relaxants,antidepressants, physiotherapy, ma-nipulative therapy and surgery).

Multidisciplinary therapy based onintensive exercises improves physicalfunction and has modest effects onpain.

The reductionist approach (pursuitof a pathoanatomical diagnosis withthe view to target-specific treatment)should be implemented when a spe-cific diagnosis is needed.

While conventional investigations donot reveal the cause of pain, jointblocks and discography can identifyzygapophysial joint pain (in 15%-40%),sacroiliac joint pain (in about 20%) andinternal disc disruption (in over 40%).

Zygapophysial joint pain can be re-lieved by radiofrequency neurotomy;techniques are emerging for treatingsacroiliac joint pain and internal discdisruption.

IntroductionMultiple, evidence-based guidelines

worldwide have indicated how acutelow back pain should be managed.1

These are soon to be complementedby Australian guidelines, one set de-veloped by the Royal Australian Col-lege of General Practitioners and an-other by the Acute MusculoskeletalGuidelines Group. These guidelinesemphasise effective communicationwith the patient to provide explanationand assurance, allay fears, promoteactivity and avoid passive therapies.Followed conscientiously, these guide-lines are safe, effective, and cost-effective. Over 70% of patients canexpect to become pain-free, with arecurrence rate of less than 25%.2

For chronic low back pain, the situ-ation is entirely different. By definition,

this is pain that has persisted for longerthan three months.3 In addition to thepain, patients typically suffer physicaldisabilities and psychological distress.They may be unable to work and de-pressed. No organisation has devel-oped evidence-based guidelines forchronic low back pain. Yet evidence isnot lacking. This article cites evidencedistilled in two monographs,3,4 supple-mented by later systematic reviews(Box 1).

The prevailing approaches to chroniclow back pain fall into three categories:monotherapies, multidisciplinarytherapy, and reductionism.3

MonotherapiesMonotherapies are interventions of a

single, particular kind that a medicalpractitioner might prescribe as sole

treatment. Some might be used simul-taneously, but there is no evidence thatsuch combinations are more effectivethan monotherapies used alone.

Paracetamol and non-steroidal anti-inflammatory drugs (NSAIDs) may beof short-term benefit, but no publisheddata vindicate their long-term use forchronic low back pain.3,5,6 Intriguingly,willow bark has been shown to besuperior to placebo and as effective asNSAIDs for treating relapses of recur-rent low back pain.24,25

Opioids are more effective thannaproxen or placebo for relievingchronic low back pain,26 but the aver-age effect is little more than a 10-pointreduction on a 100-point scale.7,26 Nordo they improve the psychological orfunctional status of patients treated.7

Antidepressants are slightly more

Management of Chronic Low Back Pain*Professor Nikolai Bogduk, Director, Newcastle Bone and Joint Institute, Royal Newcastle Hospital

* Bogduk N. Management of chronic low back pain. MJA 2004; 180: 79-83. © Copyright 2004. The Medical Journalof Australia - reproduced with permission.

Box 1. Evidence-based practice points*

• There is no evidence of long-term efficacy for drug therapy with analgesics,non-steroidal anti-inflammatory drugs, muscle relaxants or antidepres-sants for treatment of chronic low back pain (E1); 5-7 opioids are onlypartially effective and do not improve function (E2).8,9

• Orthoses, transcutaneous electrical nerve stimulation, electromyographicbiofeedback, traction, acupuncture, magnet therapy, injections into triggerpoints, and hydrotherapy are no more effective than sham therapy (E1);3,5 manipulative therapy is barely more effective than sham therapy (E1).10

• While exercise therapy is more effective than other interventions, it has alsonot been shown to be better than sham therapy (E1).11

• Surgery is more effective than physiotherapy, but outcomes are modest(E2).12

• Multidisciplinary therapy based on intensive exercises improves physicalfunction but has modest effects on pain (E1).13

• Conventional investigations do not reveal the cause of pain (E1),3 butdiagnostic joint blocks and discography can provide a diagnosis in manycases (E2).14-17

• Between 15% and 40% of patients have zygapophysial joint pain (E2); 3,15,16

about 20% have sacroiliac joint pain (E2),3,14 and over 40% have internaldisc disruption (E2).17

• Zygapophysial joint pain can be relieved by radiofrequency neurotomy(E2, E3),18,19 and techniques are emerging for treating sacroiliac joint painand internal disc disruption (E2, E3, E4).20-22

* Grading of evidence is based on the system of the National Health and MedicalResearch Council:23 E1 Evidence obtained from a systematic review of all relevantrandomised controlled trials; E2 Evidence obtained from at least one properly designedrandomised controlled trial; E3 Evidence obtained from pseudorandomised controlledtrials or comparative studies; and E4 Evidence obtained from case series, either post-test or pre-test and post-test.

May 2004 9

effective than placebo for relief ofchronic low back pain, but have notbeen tested for longer than eightweeks.8 They provide only partial re-lief, and their utility is limited by sideeffects. Some muscle relaxants (forexample, cyclobenzaprine) are effec-tive for short-term relief, but are notavailable in Australia.9

Orthoses, transcutaneous electri-cal nerve stimulation (TENS), andelectromyographic biofeedback showno evidence of efficacy.3,5

Traction, acupuncture, magnettherapy, injections into trigger points,and hydrotherapy are no more effec-tive than sham treatment, placebo, orbeing put on a waiting list.3,5,27,28

Manipulative therapy was found inthe latest meta-analysis to be slightlymore effective than sham therapy (by4 points on a 100-point scale), but notmore effective than other forms ofcare, including care by a general prac-titioner, physiotherapy or exercises,“back school”, or therapies known tobe ineffective.10 A contemporary re-view echoed these findings.27

Massage is a relative newcomer asa scientifically tested treatment forchronic low back pain. Three control-led trials show that it is more effectivethan sham therapy, self-care educa-tional materials, acupuncture, musclerelaxation and remedial exercises.27

Botulinum toxin is more effectivethan placebo at eight weeks, but nolong-term studies have been con-ducted.29

Prolotherapy (the injection ofsclerosing agents into tender ligaments)has given mixed results in the past,3 butwas found in a recent study to be nomore effective than placebo.30 How-ever, even the placebo treatment (in-jecting normal saline into tender points)achieved complete relief of pain thatwas sustained at 12 months in 20% ofpatients, and more than 50% relief ofpain in just under half of all patients.

Behavioural therapy is better thanno therapy and better than placebo,but it is not better than exercise therapy,and provides no additional benefit whenadded to other interventions.3,31 Al-though some systematic reviews haveconcluded that back school is effec-tive, this has been in the context ofmultidisciplinary treatment.3,5

Exercise therapy is more effectivethan usual care by a GP,32 and betterthan back school; but the evidence isconflicting on whether exercise is moreeffective than an inactive, sham treat-ment.3,5,11 There is strong evidencethat strengthening exercises are notmore effective than other types ofexercises.11

Surgery for back pain lacks compel-ling evidence of efficacy.3,33 The onecontrolled study showed it to be moreeffective than physical therapy, withmore than 60% of patients feeling“much better” or “better” after surgery,compared with 30% of patients treatedwith physical therapy.12 However, sur-gery was not curative; mean pain scores(on a 100-point scale) fell from 64 atbaseline to 30 at six months, but re-verted to 43 by two years.12 Mean painscores for patients treated with physi-cal therapy did not differ from baselineat any time.

Spinal cord stimulation and intraspi-nal opioids are sometimes used totreat patients whose back pain has notresponded to surgery. Their use issustained only by consensus viewsbased on descriptive studies.34 Simi-larly, no data vindicate epidural lysis ofadhesions.35

Multidisciplinary therapyThere is no universal definition of

multidisciplinary therapy. In the litera-ture and in practice, it comprises vari-ous combinations of exercises, edu-cation, and behavioural therapy. Whenwork-hardening is emphasised, it hasbeen called functional restoration.3 Adistinguishing characteristic of all pro-grams is that they address physicaldisabilities and patients’ beliefs abouttheir pain and resulting behaviour. Painrelief is not an overt objective. Nor area diagnosis and specific anatomicaltreatment pursued.

While proponents of multidisciplinarytherapy have published favourablereviews of its efficacy for chronic painin general,36 a review focusing onchronic low back pain was less en-couraging.13 There is strong evidencethat intensive multidisciplinarybiopsychosocial rehabilitation withfunctional restoration improves func-tion, and moderate evidence that itreduces pain, when compared with

outpatient non-multidisciplinary reha-bilitation or usual care. The evidence iscontradictory on its effect on return towork. However, these conclusionsapply to intensive rehabilitation, whichmeans intensive exercises. The avail-able trials of less intensive multi-disciplinary rehabilitation did not showimprovements in pain, function, orvocational outcomes when comparedwith non-multidisciplinary outpatientrehabilitation or usual care.13

Although intensive rehabilitation ismore effective than some other inter-ventions, outcomes are variable andlimited.3 One study found that this typeof rehabilitation reduced disabilityscores from 15.5 (on a 30-point scale)to 8.5 at four months; yet another studyfrom the same institution found that itimproved disability scores from 16.9(also on a 30-point scale) to only 12.1.In these studies, pain scores werereduced from 5.3 (on a 10-point scale)to 2.7, and from 6.1 to 5.7, respec-tively. Another study found that painscores were reduced by only 17 pointson a 100-point scale. In these terms,multidisciplinary therapy cannot beregarded as curative. For some pa-tients, it offers the possibility of betterpain control and improved function,but overall it amounts only to palliativetherapy.3

ReductionismReductionism describes the pursuit

of a pathoanatomical diagnosis forchronic low back pain with the view toimplementing a target-specific treat-ment.3 In this regard it differs frommonotherapies and multidisciplinarytherapy, neither of which requires aclassical diagnosis to be established.Pursuing a cure has been criticised onthe grounds that it ignores the psycho-social aspects of chronic pain. Never-theless, proponents of reductionismhave persisted, as monotherapies andmultidisciplinary therapy have not pro-vided a satisfying solution to chroniclow back pain.

Pursuing a diagnosisIn most cases, causes for chronic

low back pain cannot be found usingconventional investigations, such asradiography and magnetic resonanceimaging (MRI), with fewer than 10% of

Management of Chronic Low Back Pain


cases diagnosed by these means.3

Degenerative changes and conditionssuch as spondylolysis and spondy-lolisthesis are not valid diagnoses ofthe cause of pain, as they are no morecommon in patients with pain than inasymptomatic individuals.3

However, sources and causes ofchronic low back pain can be estab-lished if less conventional investiga-tions are used (Box 2):• Joint blocks can be used to pinpoint

pain from the sacroiliac joint or thelumbar zygapophysial joints.3

• Provocation and computed tomog-raphy (CT) discography can beused to diagnose discogenic painand internal disc disruption.3 Thelatter differs from disc herniation. Itis characterised by radial and cir-cumferential fissures in the anulusfibrosus of the affected disc, inassociation with a degraded nu-clear matrix; externally the disc isintact.3 This condition is not relatedto degeneration or age changes,37

but appears to be caused by fatiguefailure of the vertebral endplate af-ter repeated loading.38

When diagnostic joint blocks areused, the source of pain can be tracedto the sacroiliac joint in about 20% ofpatients,14 while lumbar zygapophysialjoint pain is found in about 15% ofinjured workers,15 and as many as40% of people with chronic back painin older populations.16 CT discographyreveals internal disc disruption in atleast 40% of patients.17 These figuresbelie the assertion that 80% of patientswith chronic low back pain cannot bediagnosed. This is true if investigationsare limited to CT or MRI, but a diagno-sis becomes possible if diagnosticblocks and discography are used.

These investigations are not indi-cated for every patient with chronic lowback pain. They are indicated if thereis a desire or need to know. They havediagnostic utility in that they bringabout closure. They prevent the futilepursuit of a diagnosis by other non-valid means. They may have a benefi-cial psychological effect; patients maybe relieved to have an explanation fortheir pain. For medicolegal purposes,establishing a diagnosis under con-trolled conditions protects patients from


Box 2. Diagnostic and treatment methods for chronic low back pain

Joint blocksJoints thought to be the source of pain can be anaesthetised by injecting localanaesthetic into the joint (Fig. A) or by blocking the nerves that supply the joint(Fig. B).

A: Oblique anteroposterior radiograph of a sacroiliac arthrogram. A needle has beeninserted into the cavity of the sacroiliac joint and contrast medium (arrows) injected toconfirm intra-articular placement, before injection of local anaesthetic (image kindlyprovided by Dr Paul Dreyfuss, Seattle, Washington).

B: Anteroposterior radiograph showing a needle in place for a left L5 medial branchblock.

Provocation discography (Fig. C)To test if a particular intervertebral disc is painful, contrast medium is injectedinto the disc to distend it. The disc is deemed to be the source of pain if thepatient’s accustomed pain is reproduced at low pressure of injection, providedthat stimulation of adjacent discs does not reproduce pain.

Computed tomography discography (Fig. D)After a discogram has been performed, the internal architecture of the disccan be demonstrated by computed tomography (CT). Radial fissurescorrelate strongly with the disc being painful.

C: Lateral radiograph of an L4–L5 discogram, showing needles placed in the L4–L5 andL5–S1 intervertebral discs and contrast medium injected into the L4–L5 disc.

D: Post-discography CT scan of (a painful) L4–L5 intervertebral disc. Contrast mediumoutlines (a) a radial and (b) a circumferential fissure (arrows), diagnostic of internal discdisruption.

A B

CD

May 2004 11

accusations of malingering or imagin-ing their pain.

Target-specific treatmentThe ultimate measure of a diagnostic

test is its therapeutic utility. In the past,pursuing a pathoanatomical diagnosisof low back pain could be criticised onthe grounds that the diagnosis did notalter treatment. This is no longer thecase.

Zygapophysial joint pain can betreated with radiofrequency medialbranch neurotomy.3,18,19 A controlledtrial has shown that this treatment is nota placebo,18 and an observational studyhas shown that, provided patients arecarefully selected using controlled di-agnostic blocks, and provided a cor-rect surgical technique is used, some60% of patients can expect at least80% relief of their pain at 12 months,and 80% of patients can expect at least60% relief.19

For sacroiliac joint pain, there is noestablished, proven treatment, buttherapies involving denervation of thejoint are emerging.20

For internal disc disruption, themainstay of treatment has been arthro-desis. However, the hazards of thismajor surgery, and its questionableefficacy, have prompted the explora-tion of minimally invasive alternatives.One of these has been intradiscalelectrothermal therapy (IDET), in whichthe fissures of the painful disc arecoagulated percutaneously with flex-ible electrodes introduced into the disc.Launched on the basis of observa-tional studies, this treatment becamecontroversial for lack of controlled tri-als. One study has now shown thatIDET is more effective than physicalrehabilitation;21 and a forthcoming studyfound it to be significantly more effec-tive than placebo for relieving pain andimproving function.22 However, IDETis not a panacea for chronic low backpain. It is indicated only for patientswith proven internal disc disruption,but even then fails to provide anybenefit in 50% of cases. Nevertheless,some 20% of patients can obtain com-plete relief of pain, sustained at twoyears, and a further 30% obtain greaterthan 50% relief, associated with returnto work.33

Failed back surgerysyndrome

Patients with chroniclow back pain who failto benefit from surgerycan be difficult to treat.These patients havegenerally been treatedwith multidisciplinarytherapy, spinal cordstimulation or intraspi-nal opioids. Althoughsome patients can ben-efit from each of theseapproaches, they havenot been universallysuccessful.

The prevailing atti-tude to patients withfailed back surgerysyndrome has beenthat it is futile to pur-sue a pathoanat-omical diagnosis. Re-cent studies are re-versing that attitude. Ifcarefully investigated,a treatable lesion canbe found in substan-tial proportions ofthese patients.39 Inthose who have pre-dominantly leg pain,unrecognised lateralstenosis is the mostcommon cause. In those who havepredominantly back pain, the mostcommon cause is unrecognised inter-nal disc disruption. Such findings aregrounds for optimism that, in the fu-ture, patients with failed back surgeryneed not be relegated to symptomatictreatment only.

Suggested approachThe evidence on treatment of chronic

low back pain leaves GPs with fewoptions. Established treatments eitherdo not work or have limited efficacy.Emerging treatments may still be re-garded as controversial, or are notwidely available.

The evidence indicates that prescrib-ing analgesics, tricyclic antidepres-sants and muscle relaxants is not theanswer; nor is sending the patient formore physiotherapy or manipulativetherapy. Nevertheless, some guidancecan be formulated (Box 3). Information

for patients is summarised in Box 4.For exacerbations of chronic low

back pain, the evidence supports theuse of willow bark. Massage is emerg-ing as an innocuous but effective inter-vention that is commonly available.Injections into tender attachment sitesfor ligaments are a simple treatmentthat GPs can perform. The agent usedis immaterial; even normal saline worksif the injection is given with confidence.They can achieve complete relief ofpain in 20% of patients and signifi-cantly reduce pain in 40%.30 Thesefigures are no worse than those for thebest alternatives, and better than most.

If a diagnosis is required, diagnosticblocks and discography can be under-taken. This should be in consultationwith a practitioner experienced in thetechnique and interpretation of results.If treatment is to follow, it should be inthe hands of an experienced practi-tioner of the technique.


Box 3. Algorithm for general practice management ofchronic low back pain


If a diagnosis is not required or is notpossible, the current mainstay of man-agement is multidisciplinary therapy.The evidence requires that this be aprogram based on intensive exercises,as less intensive programs are noteffective. Even so, neither GPs norpatients should be under the misap-prehension that multidisciplinarytherapy will be curative. While somepatients may have outstanding re-sponses, most will benefit only partiallywith respect to function and pain.

Opioids may be needed for patientswith persistent severe pain, but shouldbe used carefully. Patients must un-derstand that they will not be cured oftheir pain; relief will be only partial.Opioid therapy is best undertaken underthe aegis of a pain clinic, or according

to published guidelines if a pain clinicis not available.40,41

Although not proven in controlledtrials, spinal cord stimulation or intrath-ecal opioids constitute a final option forpatients with intractable back pain,particularly after failed surgery. Theyare costly but provide appreciable re-lief for up to 50% of those treated.

References1. Koes BW, can Tulder M, Ostelo R, et al.Clinical guidelines for the management oflow back pain in primary care: an interna-tional comparison. Spine 2001; 26: 2504-13.

2. McGuirk B, King W, Govind J, et al. Thesafety, efficacy, and cost-effectiveness ofevidence-based guidelines for the man-agement of acute low back pain in primarycare. Spine 2001; 26: 2615-22.

3. Bogduk N, McGuirk B. Medical manage-ment of acute and chronic low back pain:an evidence-based approach. Amsterdam:Elsevier, 2002.

4. Nachemson A, Jonsson E, eds. Neckand back pain: the scientific evidence ofcauses, diagnosis, and treatment. Phila-delphia: Lippincott, Williams and Wilkins,2000.

5. van Tulder MV, Goossens M, Waddell G,Nachemson A. Conservative treatment ofchronic low back pain. In: Nachemson A,Jonsson E, eds. Neck and back pain: thescientific evidence of causes, diagnosis,and treatment. Philadelphia: Lippincott,Williams and Wilkins, 2000: 271-304.

6. van Tulder MW, Scholten RJPM, KoesBW, Deyo RA. Nonsteroidal anti-inflam-matory drugs for low back pain. A system-atic review within the framework of theCochrane Collaboration Back ReviewGroup. Spine 2000; 25: 2501-13.

7. Moulin DE, Iezzi A, Amireh R, et al.Randomised trial of oral morphine forchronic non-cancer pain. Lancet 1996; 347:143-47.

8. Salerno S, Browning R, Jackson SL. Theeffect of antidepressant treatment ofchronic back pain. A meta-analysis. ArchIntern Med 2002; 162: 19-24.

9. van Tulder MW, Touray T, Furlan AD, etal. Muscle relaxants for nonspecific lowback pain: a systematic review within theframework of the Cochrane Collaboration.Spine 2003; 28: 1978-92.

10. Assendelft WJJ, Morton SC, Yu EI, et al.Spinal manipulative therapy for low backpain. A meta-analysis of effectiveness rela-tive to other therapies. Ann Intern Med2003; 138: 871-81.

11. van Tulder M, Malmivaara A, Esmail R,Koes B. Exercise therapy for low backpain. A systematic review within the frame-work of the Cochrane Collaboration BackReview Group. Spine 2000; 21: 2784-96.

12. Fritzell P, Hagg O, Wessberg P,Nordwall A, Swedish Lumbar Spine StudyGroup. 2001 Volvo award winner in clinicalstudies: lumbar fusion versus nonsurgicaltreatment for chronic low back pain. Amulticenter randomized controlled trial fromthe Swedish Lumbar Spine Study Group.Spine 2001; 26: 2521-34.

13. Guzman J, Esmail R, Karjalainen K, etal. Multidisciplinary rehabilitation for chronicback pain: systematic review. BMJ 2001;322: 1511-16.

14. Maigne JY, Aivaliklis A, Pfefer F. Re-sults of sacroiliac joint double block andvalue of sacroiliac pain provocation tests in54 patients with low-back pain. Spine 1996;21: 1889-92.

15. Schwarzer AC, Aprill CN, Derby R, etal. Clinical features of patients with painstemming from the lumbar zygapophysialjoints. Is the lumbar facet syndrome a clini-cal entity? Spine 1994; 19: 1132-37.

16. Schwarzer AC, Wang S, Bogduk N, etal. Prevalence and clinical features of lum-bar zygapophysial joint pain: a study in anAustralian population with chronic low backpain. Ann Rheum Dis 1995; 54: 100-106.

17. Schwarzer AC, Aprill CN, Derby R, etal. The prevalence and clinical features ofinternal disc disruption in patients withchronic low back pain. Spine 1995; 20:1878-83.

18. van Kleef M, Barendse GAM, KesselsA, et al. Randomized trial of radiofrequencylumbar facet denervation for chronic lowback pain. Spine 1999; 24: 1937-42.

19. Dreyfuss P, Halbrook B, Pauza K, et al.Efficacy and validity of radiofrequency neu-rotomy for chronic lumbar zygapophysialjoint pain. Spine 2000; 25: 1270-77.

20. Cohen SP, Salahadin A. Lateral branchblocks as a treatment for sacroiliac jointpain: a pilot study. Reg Anesth Pain Med2003; 28: 113-19.

21. Bogduk N, Karasek M. Two-year follow-


Box 4. Messages for patients withchronic low back pain

• Drug treatment does not cureback pain.

• Opioids only partially relieve thepain and must be used carefully.

• Willow bark is effective therapyfor exacerbations of pain.

• Massage can help relieve pain.• Manipulative therapy is barely

more effective than sham treat-ment, and other physical thera-pies and devices are no moreeffective than sham treatment.

• Exercises can be beneficial.• Multidisciplinary therapy can

help improve function, but will notcompletely cure pain.

• Surgery can help some patientsto various degrees, but nearlyhalf will not benefit.

• Spinal cord stimulators can helpsome patients who gain no relieffrom surgery.

• Tests are available to make adiagnosis when CT scans andMRI scans are said to be normal.

• Treatment is available forzygapophysial joint pain.

• New treatments are being devel-oped and tested for sacroiliacjoint pain and pain coming fromintervertebral discs.

CT = computed tomography. MRI =magnetic resonance imaging.

May 2004 13

up of a controlled trial of intradiscalelectrothermal anuloplasty for chronic lowback pain resulting from internal disc dis-ruption. Spine J 2002; 2: 343-50.

22. Pauza KJ, Howell S, Dreyfuss P, et al.A randomized, placebo-controlled trial ofintradiscal electrothermal therapy (IDET)for discogenic low back pain. Spine J 2004.In press.

23. National Health and Medical ResearchCouncil. A guide to the development, im-plementation and evaluation of clinical prac-tice guidelines. Canberra: NHMRC, 1999:56.

24. Chrubasik S, Eisenberg E, Balan E, etal. Treatment of low back pain exacerbationswith willow bark extract: a randomized dou-ble-blind study. Am J Med 2000; 109: 9-14.

25. Chrubasik S, Kunzel O, Model A, et al.Treatment of low back pain with a herbal orsynthetic anti-rheumatic: a randomisedcontrolled study. Willow bark extract forlow back pain. Rheumatology 2001; 40:1388-93.

26. Jamison RN, Raymond SA, SlawsbyEA, et al. Opioid therapy for chronicnoncancer back pain. A randomized pro-spective study. Spine 1998; 23: 2591-2600.

27. Cherkin DC, Sherman KJ, Deyo RA,Shekelle PG. A review of the evidence forthe effectiveness, safety, and cost of acu-puncture, massage therapy, and spinalmanipulation for back pain. Ann Intern Med2003; 138: 898-906.

28. McIlveen B, Robertson V. A randomizedcontrolled study of the outcome of hydro-therapy for subjects with low back or backand leg pain. Physiotherapy 1998; 84: 17-26.

29. Foster L, Clapp L, Erickson M, JabbariB. Botulinum toxin A and chronic low backpain. A randomized, double-blind study.Neurology 2001; 56: 1290-93.

30. Yelland M, Glasziou P, Bogduk N, et al.Prolotherapy injections, saline injections,and exercises for chronic low-back pain: arandomised trial. Spine 2004; 29: 9-16.

31. van Tulder MW, Ostelo R, VlaeyenJWS, et al. Behavioral treatment for chronicback pain. A systematic review within theframework of the Cochrane Back ReviewGroup. Spine 2000; 25: 2688-99.

32. O’Sullivan PB, Twomey LT, Allison GT.Evaluation of specific stabilizing exercisein the treatment of chronic low back pain

with radiologic diagnosis of spondylolysisor spondylolisthesis. Spine 1997; 22: 2959-67.

33. Waddell G, Gibson A, Grant I. Surgicaltreatment of lumbar disc prolapse and de-generative lumbar disc disease. In:Nachemson A, Jonsson E, eds. Neck andback pain: the scientific evidence of causes,diagnosis, and treatment. Philadelphia:Lippincott, Williams and Wilkins, 2000: 305-25.

34. Bennett G, Serafini M, Burchiel K, et al.Evidence-based review of the literature onintrathecal delivery of pain medication. JPain Symptom Manage 2000; 20: S12-S36.

35. Heavner JE, Racz GB, Raj P. Percuta-neous epidural neuroplasty: prospectiveevaluation of 0.9% NaCl versus 10% NaClwith or without hyaluronidase. Reg AnaesthPain Med 1999; 24: 202-207.

36. Flor H, Fydich T, Turk DC. Efficacy ofmultidisciplinary pain treatment centers: ameta-analytic review. Pain 1992; 49: 221-230.

37. Moneta GB, Videman T, Kaivanto K, etal. Reported pain during lumbar discogra-phy as a function of anular ruptures anddisc degeneration. A re-analysis of 833discograms. Spine 1994; 17: 1968-74.

38. Adams MA, McNally DS, Wagstaff J,Goodship AE. Abnormal stress concentra-tions in lumbar intervertebral discs follow-ing damage to the vertebral bodies: causeof disc failure? Eur Spine J 1993; 1: 214-21.

39. Waguespack A, Schofferman J, SlosarP, Reynolds J. Etiology of long-term fail-ures of lumbar spine surgery. Pain Med2002; 3: 18-22.

40. Graziotti PJ, Goucke CR. The use oforal opioids in patients with chronic non-cancer pain. Management strategies. MedJ Aust 1997; 167: 30-31.

41. Canadian Pain Society. Use of opioidanalgesia for the treatment of chronic non-cancer pain – a consensus statement andguidelines from the Canadian Pain Soci-ety. Pain Res Manage 1998; 3: 197-208.



Abstract

Pain and Chronic Low Backpain (CLBP) are subjectiveexperiences presenting fre-

quently, with wide economic, social,and community effects.

This new hypothesis compares thehuman body to a new computer, whichinitially “learns” and functions well,until finally the system “degenerates”and the hard disc “crashes”.

The human, from birth to death,follows a similar pathway, as it learnsby simple repetition, of single stagebehaviours, producing multiple Pavlo-vian conditioned reflexes, to surviveand function in the ever-changing en-vironment.

Parallel, but subservient conditionedreflexes, are the similar learnt behav-iours to nociceptive inputs that areexperienced as subjective “pain”. Asthe body ages or “degenerates”, thedamaged tissues increase the cer-ebral afferents, causing vestibulo-au-tonomic controlled, postural changesvia the balance between survival/func-tion and pain responses.

The new hypothesis and model havebeen developed from, and are sup-ported by, unexpected clinical resultsobtained by the author (reported inPart Two), while utilizing modifiedBlomberg spinal ligament injectionprotocols.

1. IntroductionChronic low back pain (CLBP) is a

major, but poorly understood and man-aged problem in every country of theworld. It has a very high economic,social, and personal cost to everysufferer, employer, and associatedfamily group.

To date, there have been very fewprograms that have provided eitherunderstanding or resolution to this dif-ficult problem. 1, 2 Dr Stefan Blomberg’s

Pain and Chronic Low Back Pain: A NewModel? Part 1. The Hypothesis andModelDr A Breck McKay, Family Physician, Brisbane, Queensland, [email protected]

“Discovery consists of seeing things that everybody sees, and thinking what nobody has thought” - (Albert vonSzert-Gyorgyi, Hungarian Biochemist, 1893-1986)

work in Sweden has shown positiveoutcomes in randomized trials,3 al-though the full mechanisms of action ofhis para-sacrococcygeal localanesthetic/steroid injections have notbeen fully elucidated.

McKay and Wall4 provided a newconcept for total human body function,both in health and following illness orinjury, and this has assisted in provid-ing a plausible reason for Blomberg’ssuccess.

By applying evolving modificationsof Blomberg protocols in over 550patients, the author has developed anhypothesis and model that may pro-vide an alternative explanation for boththe causation and continuation of CLBPand other pain conditions. It may alsoexplain the overall improvement of thequality of life measures observed bythe patients.

To produce the new model the authorhas utilized:1. The principles of learning observed

by Professor Ivan Pavlov in theformation of conditioned reflexes;5

2. Dr Edward de Bono’s neural pat-tern formation model,6, 7 and

3. A non-mathematical conceptualapplication of Chaos Theory to ex-plain the development of the learntparallel survival/function and painpathways from birth to death.

2. Hypothesis for Human Life: Sur-vival, Function, and The Role ofNociception and Pain.

From birth to death, the human bodyparallels a computer, operating as asingle functional human body, exposedto constantly changing internal andexternal environments.4

The total concurrent informationprocessing might be described as reso-nating and reverberating chaotic sys-tems with multiple constants, followingprior learnt neural patterns of condi-tioned reflexes. These have developedto conserve brain processing demandsat any point in time, while respondingto the chaos of external and internalinput stimuli.

2.1 The computer model (Fig. 1)Simplistically, when a new computer

is purchased, it consists of a fullyfunctional unit consisting simply of thebody, that is, case, CPU, I/O keyboardand components, floppy drives, CDROM drives, etc. (BODY), as well asthe basic operating software or back-ground functions (OS), and the emptyhard disk drive (HDD). The computercan “survive and function” to an ex-pected protocol over its “life”.

During the “life” of the computer, theoperator accepts the background, butessential functions of the OS, which

Computer Model

“Birth”Development Adult Ageing “Death”

Body OK Wear and Tear More damage+ + (Damage) + +OS I/O increase More I/O demand Still more I/O “Death” or+ + + + “HDD Crash”HDD HDD Capacity up HDD “full” HDD sector changes

Faulty/Isolated =“Degeneration”

Figure 1. “Birth to death” of a computer

! ! ! !

May 2004 15

keep the unit working. Via the variousinput/outputs (I/Os), gradually the HDDfills with data being used, stored,accessed, moved, and altered. As timegoes on, available HDD space gradu-ally fills up. This results in “wear andtear” (HDD “degeneration” in medicalterms), developing “bad sectors”, whichthe OS isolates and avoids, therebyreducing total useable space.

At times, inputs can trigger audio-like microphone/amplifier feedback

loops, which cause accelerating mal-functions. To stop such feedback loopsand malfunctions, the input must beblocked, volume decreased, or theamplifier turned off, just as in the audiofeedback loop.

As the functional capacity of theHDD is reduced with increasing in-puts, outputs, feedback, and storageaccessing, it becomes less reliableand finally there is a HDD “crash”. Adead computer! Luckily a computer is

Pain and Chronic Low Back Pain: A New Model? Part 1. The Hypothesis and Model

easier to resurrect than a human.

2.2 The human model (Figs. 2 and 3)A newborn baby is very similar to

such a computer. It is a unit that can“survive and function” to an expectedprotocol and consists of a body(BODY), an OS (consisting of all thetissues, central, peripheral, autonomicnervous systems, endocrine systems,and other input/output systems), andan “empty” hard disc drive (HDD) or

Human Body Model (A)

Birth Development Adult

Sensory Learnt by Simple Repetition of SurvivalA Motor I/O Single Stages +

Hormonal FunctionOther Following:

BodyBaby + Classic Pavlovian

OS Conditioned Reflexes +HDD (Brain)

ALL follow the Pain PerceptionMonitor EnvironmentMemory Check + Attention: injury, damage, or repair need

B Nociception Manage(3M Model: McKay and Wall 2003) Modified by: parents, peers, culture, edu

cation,military, sport, etc.

Both pathways form as de Bono “Neural Patterns”, to minimize required brain function.Total pathways produce multiple, but stable, Systems Resonating/Reverberating to Chaos Theory and constants

Age (years) 0 5 10 15 20 25 30

!

!

!

!

Figure 2. “Birth to adult” of human computer” system

Figure 3. Stage two: “Adult to death” of human “computer” system

Human Body Model (B)Adult Ageing Death

Survival Loss of Neurons in Brain+ Established Neural Pathways Faulty = Functional DecreaseFunction Decreased A beta inputs due to less activity

Survival Function Activation of “Flight/Fight”will over-rule Or “Fear/Freeze” autonomic pathwaysNociception / Pain Change in Total Posture and Disabled or

Total Body Status Death(LEARNT from parents, peers, to “flexed/semi-fetal” and protectiveculture, education sport, military, etc.)

Pain Perception Increased Tissue Damage: Increased Chemoceptors Inputs(Ignored causes feedback Increased “Degeneration”: Increased Mechanceptors Inputsloop, amplified at posterior horn) Increased Pain inputs: Increased Nociception Inputs= “Wind up” (Increased A delta and C fibres activity)

Massive information Input/Output is constantly balanced by Chaos Theory construct and Dr Edwardde Bono patterns causing simple staging “degeneration” of the human body.

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!



brain.4

The baby has the unique ability togrow its own brain/HDD in size andfunctions, maximally over the first fiveyears, then continuously, but at a re-ducing rate, to adult stage. By utilizinginherent neural plasticity, the brainand nervous system can manage tovary its functions, at all times respond-ing to massive volumes of concurrentdata, (its multiple I/Os), which mayappear to be chaotic, but are organ-ized and simplistic in action (Fig. 2).

Sometimes there are inputs that trig-ger positive feedback loops, similar tothe audio example of a microphonebeing moved too close to a speaker,with positive amplified feedback in-creasing sound. The resultant “feed-back” or “wind up” (as in nociceptiveinput effects at the posterior horn of thespinal cord10) can be stopped only bysuppression of the “input” at spinallevel or from higher centres, blockingthe “amplifier” effect. This is analo-gous, in the audio model, to adjustingthe volume control, turning off theamplifier, or removing the microphone/inputs.

Then ageing starts to affect manyparts of the body system (genericallyreferred to as “degeneration”), chang-ing and increasing the accepted inputs(mechano-receptors, nociceptors,chemoreceptors, etc.) to the HDD.The “damage”, due to fatigue failure,15

results in loss, malfunction, or inappro-priate functions of the HDD, whichattempts to compensate via neural plas-ticity. Finally there is a systems “crash”or death. Unfortunately, computer-likeresurrection is less simple with hu-mans (Fig. 3)! During this “birth todeath” of the human, the inputs/out-puts can be grouped into two maincategories: survival/function groupsand nociceptive groups.

Survival/Function groups: Theseenable the human to live and respondto the ever- changing external andinternal environments.

Nociceptive groups: These act aswarning signals to the human that in-jury or tissue damage may occur, hasoccurred, or continues to occur.

Each proceeds along simple, thenmore complex learning paths, follow-ing classical Pavlovian reflex condi-tioning, changing from the uncondi-

tioned reflexes present at birth. Eachnew sequence is gradually Learntby Repetition of Single Stages dur-ing the normal living experiencesfrom baby to adult to death, alwaysas a single, functioning whole hu-man body, as proposed in the modelby McKay and Wall.4

This might be seen as reductionism’sdifferent view of the functional partsof the whole human body, instead ofthe individual systems, organs, tis-sues, cells, and metabolic processesthat have been considered to date.

2.2.1. Survival/function groupThe learning of the survival/function

responses may be observed whilewatching any new baby, with its manyunconditioned reflexes,8 respondingto the environmental stimuli to gradu-ally develop, with actions such as smil-ing, rolling over, sitting up, standing,walking, running, catching a ball, read-ing, writing, playing sports, driving acar, up to a surgeon operating, me-chanic repairing a car, musician per-forming in a concert, etc.

They all have to be Learnt by SimpleRepetition of Single Stages, then viamultiple repetitions, memory storing,and modifying. There is created asingle vast database of three-dimen-sional (3D) self-images in any spaceor for any activity, with concurrent,learnt functions or activities needed tosurvive. The input information is de-rived from special sensory organs andgeneral sensory inputs relayed by A-beta, A-delta, and C fibers to the pos-terior horn of the spinal chord. Relayoccurs, via the anterior horn, to auto-nomic ganglia at the same level, butmostly by direct or cross-over path-ways ascending to the brain stem andhigher centres.

The human interacts with the exter-nal and internal environments by Moni-toring, orienting to any change,Memory checking the HDD, and Man-aging by applying learnt behaviours towhatever is confronted. This is the“3M” function from the McKay andWall Model, based on classical Pavlo-vian conditioned reflex formation andmodeling.4, 9

2.2.2. Nociceptive groupThe nociceptive management

protocols also have to be Learnt bySimple Repetition of Single Stages.Whenever the baby’s nociceptive in-puts are activated, that is, by noise,smell, noxious sensory input, etc., thereis triggered an unconditioned reflexresponse or “hurt”.8 This results inmovement, fear, crying, withdrawing,etc., which can be observed by theprotective adult or observers. The adultthen teaches the baby acceptance ormanagement protocols for each noci-ceptive experience. By reassurance,comforting, massaging, etc., the dif-ferent nociceptive inputs can be ac-cepted and responded to in manydifferent ways. The input pathways areagain via A-delta and C fibres whichpass to the posterior horn and can bemodulated by A-beta inputs, or the de-scending pathways from theperiaqueductal grey matter (PAG).10, 11

The learnt response is then ob-served as the baby’s “pain” and, andas the adult uses phrases such as “kissit better”, “rub it better”, “ignore it”,“you’re a big ... now!”; the babyLearns to suppress the “hurt” re-sponse to less important, and payattention to more important nocicep-tive inputs. As the child develops,friends, neighbours, school, sport,employment, etc., superimpose verydefinite culturally accepted behaviouralpatterns to the different nociceptiveinputs. As the human grows, so itcontinues to contextually learn manydifferent ways of accepting or reject-ing the nociceptive inputs of differenttypes and strengths. This is modifiedby adults, peers, community, culture,sport, military etc., and general com-munity expectation. These actions cre-ate the descending modulating path-ways that suppress the nociceptive A-delta and C fibres inputs arriving at theposterior horn.10, 11

The learnt responses constitute“Pain” and each individual learns tosuppress the different nociceptive in-puts in many different ways, formingthe individual pain perceptions andmanagements. This may be by in-creasing descending modulation oraccentuation of A-beta based inputs,that is, rubbing, squeezing, and usingrubefacients, or activity in the limbs.

Each person develops their own“pain” interpretation based on their

May 2004 17


personal, cultural, and past experi-ences.

By such learnt nociceptive inputsuppression, a person, when facedwith the ultimate survival/function asopposed to pain challenge, can forexample cut off their own hand toensure survival. This was seen re-cently in USA rock climbing and NSWmining accidents. Sporting personscan ignore injury until play has fin-ished, military personnel can suffersituations or injuries that others wouldnot tolerate, because they have learntto do it. In special circumstances manypeople can perform Herculean tasks,or achieve results that normally wouldnever be anticipated. A farmer with abroken leg, can overome severe painto crawl long distances for help. Vic-tims with severe injuries can get out ofa life-threatening situation, for exam-ple, or assist others in ways that cannotbe explained normally or by the sim-plistic adrenalin/noradrenalin effect.

Often these learnt pain modulationprotocols continue into later life andare not recognized as such, becausethey occur in different contexts, andmay be accepted as “normal” or “con-stant” by the individual, even thoughthe overall resultant effect may bedetrimental to the whole body function.The intensity needed for survival/func-tion to override other factors such aspain due to injury or illness, was de-scribed in 1916 by Pavlov in his lectureon the intensity of “The reflex of pur-pose”.12

2.3 Chaos Theory - “feedback” (elec-tronic) or “wind up” (nociceptive)

Chaos Theory describes the reso-nation and reverberation occurring insystems which can be modeled withdifferential mathematical equations,sensitive to even small changes to theirconstants. The Functional Whole Hu-man Body4 is such a resonating andreverberating complex system to the“chaos” of internal and external orient-ing stimuli. There are many constants,just as there are many variables insuch human systems. Both may varyin reference to time only.

Following the modeling of Dr Edwardde Bono,6, 7 as each new input experi-ence repeats, a neural pathway isformed and then followed, until all such

subsequent similar stimuli pass alongthe predetermined and establishedpathway. Considering one of Dr deBono’s own models, this is like rain-drops falling on dry dusty areas, wherethey initially form single wet spots. Asfurther drops fall they start to coalesceforming tiny rivulets, which becomelarger. All subsequent raindrops willfollow those preformed pathways. Hotwater drops on a jelly mould form morepermanent “memory” pathways.6, 7

So it is with the human brain.Each and every established condi-

tioned reflex follows the same previ-ously established neural pathway,thus conserving the number of op-tions that must be considered foreach impacting stimulus. The braincan therefore manage vast amountsof input information very economi-cally, utilizing the previously estab-lished pathways, and only respond-ing otherwise to new or novel stimuli,as described by Pavlov.13

Thus, once learnt, a particular con-ditioned reflex uses minimal neuralpathways, and the human conscious-ness is permitted to consider othermore novel stimuli or factors.

Examples are many, such as learn-ing to drive a car or play an instrument,the Aborigine learning to follow animaltracks, or a doctor learning a particularsurgical procedure. These initiallydemand a lot of conscious brain func-tion, but once learnt, become clearlydemonstrated subconscious reflexprocesses.

These follow the author’s conceptualmodel of Chaos Theory, which de-scribes altered resonation and/or re-verberation to small or large constantchanges. When a constant changes,the whole system changes, or restoresas the constant restores. These neuralsystems also emulate de Bono’s modelof neural pathway formation and func-tioning.

A simple example of such a ChaosSystem and changes might be ob-served in an adult person who, totallyblind from birth, lives and functions intheir own “known” unit. The furniture isarranged, and its position is known.Unknown to the owner, a helpful per-son cleans the unit and moves a pieceof furniture slightly, even though at-tempting to replace everything pre-

cisely. When the blind owner returnsand runs into the moved piece offurniture, they fall over knocking manyother items of furniture, and a newchaos system emerges. The constantshave changed. Until the blind personhas relocated every moved piece offurniture, the new chaos system re-mains. Once everything is replaced,the old chaos system restores with theold constants.

“Constants” in human body termscan be seen as the sensory or otherinputs from any part of the body thatoccur regularly and follow the prede-termined neural pathways of condi-tioned reflexes (de Bono patterns).

For example, the spinal muscles andassociated tissues producing the up-right posture, with their mechano-receptor inputs, learnt during develop-ment when sitting, standing, walking,etc., on reaching the brain, arechecked against the learnt “HDD” database. This is analogous to de Bonoraindrop pathways in dust. These indi-cate and maintain the body, whereverit is, functionally in a 3D virtual space,by learnt repetitive, conditioned reflexprotocols developed over time.

Now activated in parallel are thenociceptive inputs, which act as warn-ing signals of tissue injury or damage.These cause the human to orient to anyaffected area creating the input, andspecific management decisions aremade about whether to repair or cor-rect the effect.

Does the human accept and actionthe cause, or ignore, and continue tofunction as before?

This is where the above survival/function protocols can over-ride noci-ceptive inputs, for the benefit and con-tinuance of the whole human.

If the nociceptive input is ignored,and the threat of damage is great, thereis a “wind up” pathway followed, whichis similar to the audio feedback exam-ple given above.10, 11

However, if the need to survive isgreater, then those nociceptive “windups” can be fully suppressed by thelearnt prior management protocols,which work by activation of the de-scending modulation pathways.10

To stop the “wind up”, which is analo-gous to audio feedback, it is neces-sary to:



1. Stop the nociceptive activator input(move the microphone away);

2. Suppress the inputs by A beta ac-tivation or using chemicals (switchoff the amplifier);

3. Modulate or suppress the nocicep-tive pathway from higher neuralcenters (adjust the volume control).

2.4. Ageing or “degeneration”When tissue is damaged, due to

acute injury or fatigue failure,15 a“chemical soup” stimulates thechemo-, mechano-, and nociceptors.11

This causes activation of the nocicep-tive pathways, until the damaged areais repaired, or a new constant inputoccurs, which the brain then acceptsas a modification to the previous neuralpathway or conditioned reflex.10, 11

With ageing (or “degeneration”), themany repairs required may never fullyoccur, and a new set of input “con-stants” (nociceptive, mechanoceptive,chemoceptive, etc.) develop, causingvarious “wind-up” activations. In keep-ing with Chaos Theory, there has beena total system change, which may varyfrom minor and unobserved, gradualand slowly observed, to major andobvious, all occurring over varyingtime periods.

Such a change occurs in the readilyvisible postural system in erect hu-mans. The psoas muscles and associ-ated paraspinal tissues have changedthe spine to femur angle of 110 de-grees in four-legged animals, and in-creased it to 190 degrees in the erecthuman posture. The erector spinae,multifidus, and psoas muscles nowserve different postural purposes whencompared to quadripeds.14 The psoasand scalene muscles in the neck stillretain their direct involvement, how-ever, in the flight/fight or fear/freezeresponses, moderated via the vestibulo-autonomic brain stem pathways.15

When a threat occurs, they exertdifferent and more pronouncedbiomechanical effects on the body.The effects on the neural and muscu-loskeletal control systems with ageingor “degeneration” of the tissues in-crease the normal and nociceptiveinputs. Such increased inputs then re-balance the total system and the “mostcomfortable” position, with least acti-vation of nociceptors, is generated as

a new “postural constant” or position,moderated by the changes in the ves-tibular-autonomic regulation of thenervous system and posture.15

This is most often seen as the wholetrunk tilting forward. Fingers, fore-arms, and arms assume partly flexedpositions, as do the legs. The wholebody then assumes a more “protec-tive” or flexed stance, as in the boxer’sready or defensive position.

An alternative understanding of thismay be seen when a person is con-fronted by a major totally overwhelmingthreat, such as a gun in their face in aconfined space, an extremely loudthreatening noise, or chemically irri-tating, blinding smoke. The naturalprotective action is to assume a “fear/freeze”, or even “flight/fight” posture,with a resultant semi-fetal position oc-curring.

Pain (either severe acute, intermit-tent, or constant, or chronic) is asimilar, but internal threat to the wholefunctioning body system and the pro-tective semi-fetal position is assumedgradually or suddenly. Acute pain canmake a person “fold up” and becomefetal-like in posture.

When the altered receptors arechanged by physical or chemical in-put, including injections, or inactivatedin other ways, it may partially or fullyrestore the previous “constant” neuralinput, and by applying the concept ofChaos Theory, restoration of the “con-stants” leads to restoration of the pre-vious resonation and reverberation.The normal posture may be restored.

At the same time, the “wind up” oramplified inputs decrease, enhancingthe result, and more normal positionand function are restored. If activitylevels are increased, the increased A-beta sensory inputs may sustain therestored posture. If the A-beta inputsreduce, and the other nociceptive in-puts restore, then the change has onlya temporary effect, and the prior ab-normal condition can recur. This rein-forces the need for associated activityprograms after interventions.

With ageing, the HDD/brain is be-coming faulty, with sector damage anderrors both specific and functional.Concurrently the normal learnt inputsare still present, but the damage or“degeneration”, that is, fatigue fail-

ure15 to all the tissues has resulted inmore nociceptive and other inputs,and there is system overload and mal-function. This is similar to the computerHDD malfunctions prior to “HDD crash”(Fig. 3).

Age-related pain inputs also activatethe autonomic, endocrine, and im-mune systems, so there is usually avisible gradual return of the whole bodytowards the “protective” or flexed fetalposition. There is forward tilt of 10-35degrees, with strain applied to theinterspinous ligaments, due to the ac-tions primarily of the psoas and sca-lene muscles, with flexion of all limbjoints. This follows the normal activa-tion of the fight/ flight/ fear/ freezeprotocols and whole body function.4

Although commonly seen in older orinjured persons and especially in nurs-ing home patients, it can occur inyounger people with the same inputactivations.

The ageing process becomes moreobvious externally, as the whole bodyreturns to the fetal-like position. Thischallenges the current concept of os-teoporosis and disc shrinkage beingthe major component of age-relatedkyphosis. Once treated with the au-thor’s modified injections and gentlegeneral manipulation, many elderlypatients regain most of their uprightposture, and have significant pain re-duction and restored overall quality oflife!

3. DiscussionPain is experienced uniquely by each

person and has always been a verydifficult medical problem. Chronic lowback pain has been difficult for familyphysicians, who by default, have tomanage the problems long term. Pub-lished models or protocols have rarelyprovided comprehensive, whole-bodyfunctional explanations of causation,or provided useful long-term manage-ment benefits to date. Even using thecurrent evidence-based medicinemanagements, the overall outcomeshave usually been limited in their long-term benefits. 1, 2,16, 17

The above model considers an en-tirely different process, being frombirth to death, and considers the wholefunctional human body as a singleentity. A simple, rational, unifying ex-

May 2004 19


planation is possible for the involvedmechanisms.

There are two major learning path-ways involved, one permitting totalanimal survival and function, and theother identifying and restoring injuredor damaged tissues.

The model is based on the conceptof the whole functional human body4

using a single operating system (OS)and a single unit (or computer com-plex), responding to environmentalstimuli (internal and external) by theMonitor, Memory Check, and Man-age, or 3M protocol, in which theperson survives, functions, learns,repairs itself, and is able to reproduce,care for, and teach its young.

In the early 1900s, Professor IvanPavlov5 became one of the last experi-mental physiologists to examine thetotal functioning animal, and describeddevelopment of the conditioned re-flexes as learning protocols. Dr Edwardde Bono, in about 1969,6, 7 developedthe conceptual models of how neuralnetworks form in the human brain.Chaos Theory describes the rever-beration and resonation occurring withconcurrent multiple input/outputprocessing at any point in time.

A conceptual model and hypothesishas been developed to link these con-cepts into the described single learntmanagement model. This model formsfrom repetition of single stages pro-ducing classical conditioned reflexes,which follow the same neural path-ways, providing for economy of cen-tral neural function, while allowing at-tention to new or novel stimuli.

The most important concept isthat the human body responds toits complex environmental stimulias a single functional unit, and notmerely as the sum of its many de-tailed parts. The ultimate response tothe chaos of neural activity alwaysfollows the previously learnt behav-iours, originally described by Pavlovas conditioned reflexes and de Bonoas neural patterning.

The model and hypothesis devel-oped from the author’s clinical obser-vations, and these are reported in PartTwo. The model and hypothesis re-quires application and testing in clini-cal presentations to determine its valid-ity and usefulness in the management

of pain-related conditions.The human survives and functions,

concurrently with injury and repair byutilizing simple learnt protocols to man-age the chaos of input stimuli. Whenthe human systems start to fail due toage or fatigue failure, the observabletotal body changes follow similar sim-ple patterns of learnt behaviour.

4. AcknowledgmentsAnastasia (0-4yrs), Elliot (0-2yrs)

and Alexander (0-6/12 months), whoallowed me to observe their growingand learning processes, as they re-sponded to and learnt about the inter-nal and external stimuli in their worlds.They helped me to formulate the modeland hypothesis.

Sarah-Jane, Jean, and Donna,whose CRPS Type 1 responses forceda reconsideration of the basic patho-physiology involved in these persistentpain syndromes.

Phyllis G who challenged me in No-vember 2002, and proffered her backas my first case, which opened a wholenew world of management and con-cepts, from which this paper hasevolved.

Also the other patients, who providedthe observable changes, supportingthe model and hypothesis.

Professor Nikolai Bogduk, whosechallenges and assistance have beenvital in the production of the final con-cept.

Drs Daryl Wall, Scott Masters, DavidRoselt, Professor Ken Miles in the UK,and all the others who listened andhelped forge the model and hypoth-esis.

My wife and daughter, whose CRPSType 1 and CFS have now been par-tially explained, who have throughoutthe saga since 1995, been amazinglysupportive, appropriately critical, andyet demanding of simple common-sense explanations.

References1. van Tulder MW, Esmail R, Bombadier C,Koes BW. Back schools for non-specificlow back pain (Cochrane Review). TheCochrane Library. Chichester, UK: JohnWiley & Sons, Ltd, 2004.

2. Nelemans PJ, de Bie RA, de Vet HCW,Sturmans F. Injection therapy for subacuteand chronic low back pain (Cochrane Re-

view). The Cochrane Library. Chichester,UK: John Wiley and Sons, Ltd, 2004.

3. Blomberg S, Hallin G, Grann K, et al.Manual Therapy with steroid injection; anew approach to treatment of low backpain. A controlled multicenter trial with evalu-ation by orthopedic surgeons. Spine 1994;19(5): 569-77.

4. McKay AB, Wall D. The Orienting Re-sponse and the Functional Whole HumanBody. Aust Musculoskeletal Med 2003;8(2): 86-99.

5. Pavlov IP, Lectures on Conditioned Re-flexes. Vols 1 and 2. New York: Interna-tional Publishers, 1928. Reprinted 1991 byGryphon Editions.

6. de Bono E. The Mechanism of Mind.Simon and Shuster, 1969: 93-97 .

7. de Bono E. The Mechanism of Mind.Simon and Schuster, 1969: 111-16.

8. Pavlov IP. Unconditioned Reflexes. Lec-tures on Conditioned Reflexes. Vol. 1. NewYork: International Publishers, 1928: 51, 381.

9. Pavlov IP. The Function of ConditionedReflexes, etc. Lectures on ConditionedReflexes. Vol. 1. New York: InternationalPublishers, 1928: 131-43.

10. The Pathophysiology of Pain. North Ryde,NSW; Astra Pharmaceuticals Pty Ltd.

11. The Pain Series. Lancet 1999; 353: 8May - 26 June.

12. Pavlov IP. Reflex of Purpose. Lectureson Conditioned Reflexes. Vol. 1. New York:International Publishers, 1928: 275-81.

13. Pavlov IP. Orienting or FocusingResponse. Lectures on ConditionedReflexes. Vol. 1. New York: Interna-tional Publishers, 1928: 133-35.

14. Bogduk N. Clinical Anatomy of theLumbar Spine and Sacrum. 3rd ed. ChurchillLivingstone: 101-25.

15. Yates BJ, Millar AR. Vestibular Auto-nomic Regulation. CRC, 1999 (ISBN0-8493-7668-8).

16. Bogduk N. Management of Chronic BackPain. Med J Aust 2004; 180 (2): 79-83.

17. Bogduk N, McGuirk B. Medical man-agement of Acute and Chronic Low BackPain. Pain Research and Clinical Manage-ment. Vol. 13. Elsevier, 2002.


Pain and Chronic Low Back Pain. Part 2.Observations and Clinical MaterialDr A Breck McKay, Family Physician, Brisbane, Queensland, [email protected]

Abstract

Pain and Chronic Low BackPain are the clinical alb-atrosses of many medical

practitioners, who have to managerecurrent presentations with availableevidence-based programs that havehigh failure rates.

The author experimented with theBlomberg protocols and documentedthe changes occurring. This resultedin the formulation of a new hypothesisand model for pain and chronic lowback pain development, as detailed inPart 1.

To determine which component(s)of the injections was/were active, arandom group of 33 patients weretreated with “needling”, “needling” pluslocal anesthetic, and “needling” pluslocal anesthetic and depot steroid. Theresults were unexpected.

Clinical observation of patient re-sponses, especially the quality of lifechanges, suggest that such injectionsprotocols should be available in allmedical, pain, and back clinics, andoffered prior to any interventionalsurgery to the spine.

The findings suggest that replicationand multi-centre testing of the modeland hypothesis would be an appropri-ate future step.

A new challengeFollowing attendance at the October

2002 musculoskeletal medicine con-ference in Melbourne, the author wasencouraged by a determined patient totrial the Blomberg protocol.1 Most of theoutcomes were beneficial and unex-pected. Many other patients were of-fered similar treatments, with appropri-ate monitoring. Realizing that similarproblems were persisting, the authormodified the protocol to treat the triangu-lar areas from the PSIS to L5 bilaterally,and to the tip of the coccyx concurrently.The results are reported below.

Professor Nikolai Bogduk, profes-sor of pain medicine at NewcastleUniversity, questioned which of thethree injection components in theBlomberg protocol was causing theobserved effects. Was it the physicalinput by the needling of the ligaments,the local anesthetic, or the depot ster-oid, that was effective?

To address those issues, the authorchose to treat the next 33 proximatepatients to answer the question in Janu-ary 2004. They were randomly as-signed to the three possible treatments,with the expectation that there would bethree different groups of results.

However 32 of the results were verysimilar, though there was notable group-ing of some cases, and only one “fail-ure”. Follow-up local area re-injec-tions, and gentle general spinal ma-nipulation of identified musculoskel-etal dysfunctions, appeared to reducethe rate of relapse following the variousinjection protocols. Some patients re-quested total re-injection and multiplefollow-ups were required.

Increased activity levels or return toprevious activities also reduced therate of recurrence.

At the same time, a male paraplegicinjured in a motor vehicle accident 27years ago, with damage at T9 butpartial recovery to T12, volunteered tobe a human “guinea pig.” He wastreated with similar but more extensiveinjections, including interspinous liga-ment injections up to the T12 level.

The results of the experiments initi-ated by Professor Bogduk’s challengeare detailed below, and formed theclinical basis for constructing the newmodel and hypothesis. Further work isnow required to extend the testing andvalidate the model, to replicate thefindings of the author’s low back injec-tion protocol, modified from but basedon the original work of Stefan Blomberg.

The new model, hypothesis, and the

clinical protocols, have produced suchpositive care outcomes for the pa-tients, who now find they can rely moreon correctly skilled musculoskeletalphysicians, family physicians, andgeneral practitioners to diagnose andmanage their clinical problems withgreater confidence. There are eco-nomic benefits and improved total qual-ity of life outcomes for the whole com-munity at all age levels.

These management approaches arenow demonstrating long-term efficacyaugmented by activity programs, andusually only minor local area second-ary interventions are required after theinitial major procedure. Prospectivelong-term studies are now essentialand should be conducted in muscu-loskeletal medicine, general practice,and family medicine settings. This wouldbe in preference to back or pain clin-ics, apparently reluctant to changetheir “evidence-based models”, withfaulty application of the existing medi-cal scientific knowledge base. There isfailure to appreciate the importance ofthe whole functional human bodymodel,2 and a tendency to concentrateon isolated regions and systems.

1.1. Clinical material supportingthese models

All patients are taken through a simi-lar anatomical and physiological ex-planation, and shown multiple colourprints from Grant’s Atlas, the Astrabooklet on The Pathophysiology ofPain,3 the Autonomic Nervous Systemchart, and two other charts of thevestibulo-autonomic pathways, and theFrench musculoskeletal medicinenewsletter.4 Coupled with this, the con-cept of Chaos Theory explained, usingthe blind person analogy, and the neu-rological construct of altering the obvi-ous conditioned reflexes, was brieflymodeled for them.

The author has found that, despite

“Discovery consists of seeing things that everybody sees, and thinking what nobody has thought” - (Albert vonSzert-Gyorgyi, Hungarian Biochemist, 1893-1986)

May 2004 21

Pain and Chronic Low Back Pain. Part 2. Observations and Clinical Material

the complexity of the information base,patients can appreciate the principles,the interplay between Chaos Theoryand conditioned reflexes, and the ap-plication to the management of theirpain. This allows an equal sharing ofthe medical knowledge base, and theythen “own the solution” to their ownproblem, with help from the treatingdoctor. They are empowered by thisknowledge. The author’s main experi-ence base is in mutual aid and self-helpprotocols5, 6 and the above manage-ment fills these criteria. It allows thepatient to make their own decisionsabout which treatment or managementsolutions they wish to follow.

Such consultations usually involve30-60 minutes per patient.

Patients are advised that the treat-ment is experimental, and told that nopromises or guarantees are made or tobe expected. Side effects and compli-cations are also discussed. It is thenthe patient’s own choice whether toparticipate. Most injections are givenon a different day, except for patientstravelling significant distances, whenthe whole process is done in two sepa-rate sessions on the same day.

Injection methodThe injection protocol consists of the

patient being placed prone on a bedthat breaks in the middle. 2.5 ml of 2%Xylocaine local anaesthetic is injectedsubcutaneously at one injection siteper side, at the level of S2, 30 mm fromthe midline.

The triangulation injections use 5mlof 2% Xylocaine + 10ml saline + 2 mlDepo-Medrol, Celestone Chronodose,or Kenacort A-10, as the depot steroid.

Each injection region receives about4 ml of the solution gradually injected,as the multiple “sewing machine-like”needle actions are made into the liga-ments and tissues.

The two paraspinal ligament injec-tions are done using a 20 gauge 3.5inch spinal needle, from the level of S1to tip of the coccyx, via the one pen-etration site only on each side at thelevel of S2. It is done using multiplesewing machine-like needle actions tothe ligaments at their attachment to theedges of the coccyx and sacrum, withthe left index finger giving per rectumcontrol of needle location (Fig. 4).

Injections are then performed at thePSIS on each side, via the same entrypoint, with similar multiple needlingactions to the muscle, tendon, andligament attachments to the bone, lat-erally along the PSIS and medially tothe L5 spine on each side to the lengthof the needle.

2. ResultsThe following results were accumu-

lated since November 2002, withoutany attempt to prepare a specific sci-entific paper or trial. They are ad hocresults and are reported as such.

Previous treatments• 68 patients had previously been

treated with CT-controlled zyga-pophysial joint injections. One fe-male endured needle penetrationof her left L5 nerve root three timesduring the attempted injection andexperienced persistent post-injec-tion pain. She was referred to apain clinic without benefit, but hadfull resolution of all pain with theauthor’s modified protocol first donein December 2002, and repeated inFebruary 2004 after she reacti-vated the back pain lifting a child.

• Many patients (more than 110) hadexperienced previous lower backsurgery, that is, laminectomy, spi-nal fusion, discectomy, and coccy-gectomy.

• 37 patients had been treated withepidurals, which all described as

painful and of little benefit.• Five patients had been treated with

prolotherapy.• Three patients had been treated

with ultrasound-guided piriformismuscle injections.

To 31 March 2004, 549 patients weretreated, whose age ranged from 16 to95 years. Fifty-two required full repeatprotocols (at patient’s request). Onepatient required three extra treatments.Two patients required two extra treat-ments. Forty-nine patients requiredone extra treatment.

Total failures of whole procedurenumbered 24 (November 2002 to June2003).

Failures using the author-modifiedprotocol: six cases (July 2003 to March2004). One was a chiropractor mas-seur who had measured objective ben-efits, both immediately after the injec-tions, and three weeks later, followingcompetitive sailing in New Zealand, butsubjectively claimed no benefits.

Major side effectsOne patient was hospitalized for two

large hematomas (undeclared warfa-rin use with INR unexpectedly high)

Common side effects:• Local bruising• Sweating at the time of injection in

severe cases• Discomfort from the PR control of

injections initially,

Figure 4. Author’s multiple injection sites from four skin sites: 1 and 2: Injection edges ofsacrum and coccyx; 3 and 4: PSIS medial, lateral, and caudal. Original image copyrightFotosearch.com

1 2

34


• Vasovagal episodes post-injection

Overall responsesEighty-nine per cent were 50% or

better (some gave figures of 150-1000% improvement, after multipleother unsuccessful treatments), withreduced pain, restoration of mobility,increased quality of life, improvedsleep, and the ability to return to activi-ties previously ceased because of theirdisability.

The outstanding major benefit wasthe patients’ stated improvement intheir quality of life, and their ability toreturn to activities previously avoided!

Genuine radiculopathy with positiveslumps test was rarely encountered inthe 550 patients, but if present wasrevealed and more precisely definedfollowing these injections to settle thesomatic components of their pain.

Post-injection all patients were re-quested to maximally flex their spine bytouching their toes, extend, laterallyflex, and rotate at the thoracolumbarjunction. Then they were asked tosquat, kneel on each knee in turn, ariseon the opposite leg, and balance onone foot with the eyes shut. Then theywere asked to place one foot on the bedor chair and touch the toes with bothhands on alternate sides, and finally tobend over the bed or chair to test theback in this flexed position.11

Elderly and frail patients were sur-prised at how much improvement theyachieved immediately post-injection,with only some requiring assistancewith balance while completing the tasks.

Review• All patients are reviewed one week

later, and any persisting tenderpoints or dysfunctions are treatedby further injections or gentle spinalmanipulation as indicated. Inter-spinous ligaments are normally in-jected with local anesthetic alone,although steroid can be used aswell.

• This could not be done for patientsattending from interstate, but tel-ephone follow-up was performed.Some very severe cases had al-ready had steroids re-injected withincreasing benefit.

• Assessment of pain intensity, mo-bility, sleep changes, ability to sit or

stand, and restoration of normalfunctions are performed, and in-volves identification of persistingproblems in need of further treat-ment.

2.1.1. Special subgroup of 33 pa-tients (Bogduk Challenge January/February 2004)

These patients were selected from allpresenting who lived locally, allowingurgent review if required. Allocationwas performed by a receptionist blindlydrawing markers from a container.

Group A Full protocol Steroid, localanesthetic and needling

Group B Local anesthetic and nee-dling

Group C Needling only

Outcome descriptionsIt must be noted that all these patients

had experienced their problems formany years and have been offeredand tried almost every conceivabletreatment and even multiples of eachproffered treatment available, withoutcontinuing or acceptable benefit.

General treatment groupsThe most notable change was the

immediate restoration of more normalposture and functions as demonstratedby the post-injection range of move-ment activities.

The persistence of benefit has oc-curred in most treated patients, and themost common persisting problems andcauses for relapse were:1. Unequal functional leg length (meas-

ured with blocks 2, 4, 6, 12.5, 19,and 25 mm thick blocks, each 100x 250 mm in size).

2. Persisting single level tender spots(S1, S2, or S3 most commonly).

3. Other problems, for example, tro-chanteric tenderness, piriformissyndrome, shoulder pain syn-dromes, carpal tunnel syndrome,complex regional pain syndrometype 1 (CRPS Type 1), previouslycalled reflex sympathetic dystro-phy (RSD), etc.

4. Reactivation of PSIS sites.5. SIJ dysfunction, paraspinal joint

locking.6. Interspinous ligament tenderness

(located by palpation and flexion of

the spine).7. Tenderness at the T4/5 location

and medial edge of the scapula atthe end of the spine.

2.1.2. Special subgroups (BogdukChallenge) 33 patients total

One patient, who was allocated to theneedle only protocol, had a surpris-ingly different reaction as she wasbeing needled. She was a 32-year-oldfemale with onset after a gymnasticinjury involving a fall onto a flexed neckand sacrococcygeal area at age 14.This resulted in two weeks of partialtotal body paralysis, but she was ableto return to the sport despite pain.

Physically needling the ligamentsmassively exacerbated her pain andthe author switched to the full Xylocaine/steroid injectate with immediate ben-efit. Since injection (30 January 2004)she has experienced a 90% reductionin pain, full restoration of mobility, andhas only required right gluteal triggerpoint injection and gentle general spi-nal manipulation. She is now able tofully backbend to the floor, and enjoysa fully restored quality of life.

Two other patients who receivedneedling only are worthy of mention. A74-year-old, former RAF male para-trooper, with internally fixed left ankleand damaged knee from a jump injuryin World War 2, suffered from intrac-table bilateral lower limb edema, de-spite all treatments attempted by hiscardiologist. He had restricted restingspinal posture in 20 degrees flexion,and was seemingly unable to extend.He was unable to sit or stand still formore than a few minutes. After treat-ment, he was totally pain free, theedema resolved, and normal posturewas restored at follow-up one weeklater. This has been maintained withfurther PSIS and S1 injections twoweeks and one month later.

An 85-year-old male with Parkin-son’s Disease had the typical shufflinggait, tilted forward 25 degrees, inabilityto stand or sit still for more than a fewminutes, and limited exercise toler-ance. Following needling injection heis almost fully upright, his gait is im-proved, his tremor is diminished, andhe is able to walk daily for exercise. Herequired re-injection of the left PSISand left trochanteric area six weeks


May 2004 23

later and continues to improve.All others in the 33 patient subgroup

have maintained their improvement (75-100% on each patient’s own evalua-tion), with only seven requiring local-ized re-treatment, and four requiringmanagement of other musculoskeletalproblems.

2.1.3. Other notable resultsTwo patients, a 19-year-old female

competitive ice and roller skater, and a30-year-old female former gymnast,presented complaining of very wide-spread pain, with signs of multiplediscrete complex regional pain syn-dromes (CRPSs). They both had apast history of injury involving the coc-cyx and sacrum. Following the au-thor’s modified injection protocol, bothrecovered and have minimal persistingproblems. The 20-year-old subse-quently fell in December 2003 whiledelivering pizzas, suffering a severeleft gluteal hematoma, and reactivationof her widespread pain. Immediate re-injection relieved this again, and shenotes reactivation appears after dis-tance running on hard surfaces, butnot with other low-impact exerciseactivities.

Five patients (four female and onemale all over 65 years) indicated thatthey had been suicidal prior to treat-ment, and claimed they would havekilled themselves if treatment failed. Allhave been successfully managed, withcontinuing quality of life improvement.

A 32-year-old female part-Aboriginehad been totally disabled with backpain, and had received multiple as-sessments and treatment programs atMonash, Sydney, and Brisbane painand back clinics without success, thusleaving her an iatrogenic, drug-de-pendent person suffering persistentdisabling pain. Her initial benefit fromthe very first set of injections wasprofound, with almost complete initialrelief, and she has now reduced herprescribed oxycodone and liquid mor-phine intake from over 140 mg daily to10 mg twice daily, and is almost fullyweaned after 75 days! Her back painis negligible and well tolerated, and shecan now manage her other pain bysimple analgesics. She is further re-ducing her opiate requirements, asher underlying chronic pelvic inflam-

matory disease is being correctly di-agnosed and managed.

The previously described T9 para-plegic patient had a standard paraspinalligament injection series before Christ-mas 2003, which provided benefit ini-tially for one week. After long discus-sions, a second series was done, butincluded interspinous ligament injec-tions from the tip of the coccyx up to theT12/L1 level, with extensiveparasacrococcygeal ligament injec-tions as well. At the same time punchbiopsies were carried out on his midleft shin, producing no pain, only theexpected spinal reflex movements.

Two days later he had throbbing andpain perception at the biopsy sites.One week later he had lost all swellingof his lower limbs, and had recoveredpain perception to both legs and feet.A noticeable feature was a feeling hisbig toe was being painfully wrenchedoff, when caught slightly on the furni-ture. Previously there was merely anawareness of movement, even withovert tissue damage and bleeding fromminor trauma.

He also reported a total loss of thecramping and burning pain in his limbsfor the first time in 27 years, suggest-ing to him that they were not “phantompains” of central origin. Other benefitshave included improved bowel andbladder function, improved sleep, andimproved sense of general well being.To date the benefits have persisted formore than nine weeks, and show nosigns of diminishing. This well exceedsclaims by critics of only limited dura-tion of effect with the injected steroid.

It is such cases, and in fact theauthor’s own personal experience as apatient himself, which have helped toformulate the new model.

DiscussionThe hypothesis and model presented

in Part 1 of this paper evolved fromobservation of the clinical cases re-ported above. The Blomberg protocoland explanation given at the 2002 Aus-tralian Association of MusculoskeletalMedicine Annual Scientific Meeting inMelbourne did not satisfy the author,and failed to appreciate the impor-tance of looking at the whole functionalhuman body. A different explanationwas required for what was clinically

observed.The hypothesis and model in Part 1

were created to explain these observa-tions.

When tissues are damaged, injured,or in need of repair, the whole bodyresponds to the multiple sensory andnoceptive afferents, and via autonomicefferents, which alter vascular andother tissue level responses, the bodyattempts to correct, compensate, orrepair the perceived tissue problems.Compared with the usual singledermatomal sensory/motor input/out-put systems, the primary autonomicresponse consists of one efferent pre-ganglionic axon activating many levelsof postganglionic axons.

A publication by Japanese research-ers8, 9 demonstrated that single level L5or L6 nociceptive input resulted inautonomic/sympathetic outputs affect-ing the L1 to S3 levels bilaterally.

CLBP may be associated with thesemultiple peripheral signs and symp-toms of dysautonomia, now recog-nized by the author, and appears toresolve following the injections, withpatients spontaneously reporting suchimprovements. The improvements alsooccurred when “needling” alone wasused.

The autonomic activation mecha-nism may be an explanation for howCLBP causes the observed second-ary pedal edema that appears unre-sponsive to medication, but was ob-served to ameliorate after the author’smodified injection protocol in the spe-cific group of 33 patients.

Similarly, this autonomic activationmay be one of the mechanisms under-lying complex regional pain syndromes(CRPSs), carpal tunnel syndrome, lat-eral and medial elbow pain and relatedconditions, shoulder pain syndromes,pruritis ani, finger joint swelling andarthritis, and other peripheral joint dis-comfort. These have improved or amel-iorated completely in many patients,when their CLBP was treated with theauthor’s described protocol.

While undergoing Blomberg-styleinjections for his own back pain anddysfunction, the author was confrontedwith the Bogduk question and chal-lenge of what was the operative com-ponent of the injections? The chal-lenge raised by Bogduk resulted in the



simple mini-pilot study performed. Theresults indicated that the active multiple“needling” of the ligaments maybe asignificant factor in the treatment, with32 out of 33 results being successful,and essentially the same. These re-sults needed to be explained.

The one significantly abnormal re-action, to needling alone, in the 32-year-old gymnast described previouslymay be a guide to how the modeloperates. Her injuries occurred at age14 and by the age of presentation shehad learnt to ignore and over-ride theback pain to function and look after herchildren, but not with the same suc-cess observed in older patients.

When injected by the needle only,the active pain pathways were initiallyfurther activated, resulting in percep-tion of extreme pain. However, follow-ing reversion to all three components,with Xylocaine and steroid injected,she obtained the same effective sup-pression of her pain inputs, switchingoff her feedback or “wind up”. Thisallowed her to be able to increase heractivity levels, increasing her A-betainputs, and reduced her perceivedpain.

As Pavlov noted during his identifi-cation of his Reflex of Freedom,10 theunexpected and exceptional clinicalresult can often increase the knowl-edge of the whole response, or providea basis for a totally different and unex-pected interpretation and explanation.

In the older needle-only low backpain patients, the established condi-tioned reflexes were more success-fully moderated from higher centers,and any pain increase from the initialinjection was absent or much lessmarked. Yet the overall result wasessentially the same, with no diminu-tion in clinically significant effect. Otherpatients’ responses to injections andrecorded results have reinforced andconfirmed these observations.

In the paraplegic patient described,27 years of swollen legs, burning andcramping pain, gut and bladder dys-function, poor sleep patterns, and lossof general sensory perception belowT12 have all changed. This result alonedemanded a better explanation andunderstanding of how those signs andsymptoms developed and persisted,and why they should change so dra-

matically following injections some 27years later.

He had been taught during his initialhospitalization period that he wouldhave to learn to live with his crampsand burning pain in the lower limbs,because they were “phantom painsonly in his head”. He had success-fully done this for 27 years, and toler-ated the lack of any significant sensoryfeeling below T12. He also sufferedchronic swollen lower limbs, ischemictoes, gut dysfunction, and bladder ir-ritability, which he had accepted aspart of the spinal injury syndrome.

The protocol that he had learnt wasvery similar to the current evidence-based back and pain clinic protocols,that require patients to learn to livewith and overcome the pain, or morecorrectly to increase their efferent,central modulating output, to act on thespinal posterior horn cells.3

This man’s amazing results after 27years of living with these signs andsymptoms seriously challenges theevidence-based medical protocols.Perhaps the “base” in those methodsmay be at fault, and this new hypoth-esis and model will encourage alterna-tive thinking and experimentation basedon simple anatomy, physiology andbiochemistry?

The “needling” action appears toreduce the combined afferent inputsfrom T12 to the coccyx, up to themedulla, brain stem, and associatednuclei. The resultant autonomicefferents have significantly decreasedand the secondary effects of theseextensive un-modulated A-delta and Cfiber inputs (“wind up”) have beenreduced. This can readily be visual-ized on an outline plan of the auto-nomic nervous system, by followingthe paths activated by adrenalin/no-radrenalin in the flight/fight or fear/freeze pathways and the specificchanges caused to the function of thedifferent organs or tissues.

The author suggests that the aboveclinically-based model may also helpto explain the long-term patient-per-ceived “failure” of many back clinic,zygapophysial joint local anesthetic/steroid injections, and pain clinicprotocols, which often fail to appreci-ate the whole functional human body,the autonomic system effects, and the

benefits obtained from the Blombergprotocol.1 General practice and familymedicine doctors, who by default haveto manage CLBP and other chronicpain problems over the longer term,frequently observe the many failedresults. Patients often lose heart andfail to return to their specialists andclinics, and so are lost to follow up.

It raises a challenge to the appropri-ateness of the current back and painclinic protocols, which teach pain pa-tients simply to “learn to live with thepain,” and to get on with activities ofdaily living. Such patients often believethat those back and pain clinics do notbelieve or understand their genuinepain, and feel despondent becausethey then believe that their pain prob-lem is “in their brain”.

The above results strongly suggestthat their pain is a genuine physiologi-cal effect, which can now be remediedby the Blomberg or modified protocols,coupled with adequate follow-up andreactivation of the many normal activi-ties that they have reduced or ceased.Those activities decrease their A-deltaand C fiber inputs, improve muscleactivity, and thus self-esteem and qual-ity of life, which assists in preventingrecurrence of their pain syndromes.

The above model has evolved to tryand explain the clinical observations.

The overall results have been re-markable and often unexpected, fur-ther supporting Blomberg’s findings(1), but the results published above, nowplace a challenge before every mus-culoskeletal physician, orthopedic sur-geon, neurosurgeon, rheumatologist,or family physician, to consider offer-ing the Blomberg protocol or the au-thor’s modification, prior to any otherinvasive intervention for the treatmentof acute or chronic low back pain.

A set of Blomberg ligamentous injec-tions first is far less invasive or damag-ing than a discectomy, laminectomy,or other spinal surgery, yet promisesa high chance of achieving success-ful, sustainable pain relief and return offunction. Invasive procedures can bereserved till later if still needed.

The above “birth to death” modelprovides a plausible construct fromwhich to consider an explanation ofhow and why the Blomberg protocolsprovide such good clinically observed


May 2004 25

results. The current modified protocolhas only been in use for a relativelyshort period of time, and long-termfollow-up of the patients will be per-formed. The results to date identify theimmediate need for further controlledstudies for validation or repudiation ofthe proposed model’s hypothesis andresults.

The most important single thing thatall patients reported was the improve-ment to their quality of life.

The above model is a synthesis frommany reductionist observations, andfurther illustrates the benefits of return-ing to first principle, basic medicalsciences. The human is a single wholefunctioning human body, slowly evolvedto survive and function, while respond-ing to noceptive warnings of injury ordamage, as it “degenerates” in re-sponse to age and fatigue failure. It hasbeen possible to create the new modeland hypothesis that improves the man-agement of CLBP and other acute orchronic pain and dysfunction prob-lems.

After all the human body, like anyother species, does survive, function,reproduce, and enjoy life before dy-ing, as a single entity, and not as acomplex of seemingly unrelated sys-tems, organs, tissues, cells and meta-bolic processes currently described ingreat detail in the medical literature!Pain and especially CLBP affects thewhole functional human body and notjust the low back or localized areas.

Professor Ivan Pavlov has shown usthe correct pathway to use, by observ-ing and understanding how the WHOLEhuman functions in the real world ofhigh volumes of ever changing externaland internal stimuli.

2.2. Future developmentsSuccessful evaluation of this man-

agement of CLBP and associated syn-dromes using these methods will re-quire the development of standardizedquestionnaires, examination, and in-jection protocols, with post-injectionassessments for evaluation of outcomesimmediately post-treatment and longerterm. This might be implemented byinterested musculoskeletal physicians,general practitioners, family physi-cians, or any other interested medicalpractitioners, so that multi-center trials

can be supported by those who man-age the largest number of CLBP andassociated pain patients in the com-munity.

AcknowledgmentsAnastasia (0-4yrs), Elliot (0-2yrs)

and Alexander (0-6/12 months), whomI observed during their growing andlearning processes, as they respondedto and learnt about the internal andexternal stimuli in their worlds. Thishelped me to formulate the model andhypothesis.

Sarah-Jane, Jean, & Donna, whoseCRPS Type 1 responses forced areconsideration of the pathophysiol-ogy involved in these persistent painsyndromes.

Phyllis G who challenged me in No-vember 2002, and proffered her backas my first case. This opened a wholenew world of management and con-cepts, from which this paper hasevolved.

Also the other patients, who haveprovided the observable changes, sup-porting the model and hypothesis.

Professor Nikolai Bogduk, whosechallenges and assistance have beenvital in the production of the final con-cept, and for his challenge regardingwhich components of the treatment areactive.

Drs Daryl Wall, Scott Masters, DavidRoselt, Professor Ken Miles in the UK,and all the others who listened andhelped forge the model and hypoth-esis.

My wife and daughter, whose CRPSType 1 and Chronic Fatigue Syn-drome (CFS) have now been partiallyexplained. They have been through thesaga since 1995, and have been amaz-ingly supportive, appropriately critical,and yet demanding of simple commonsense explanations.

References1. Blomberg S, Hallin G, Grann K, et al.Manual Therapy with steroid injection; anew approach to treatment of low backpain. A controlled multicenter trial with evalu-ation by orthopedic surgeons. Spine 1994;19 (5): 569-77.

2. McKay AB, Wall D. The Orienting Re-sponse and the Functional Whole HumanBody. Aust. Musculoskeletal Med 2003;8(2): 86-99.

3. The Pathophysiology of Pain. NorthRyde, NSW; Astra Pharmaceuticals PtyLtd.

4. Tichelen P, Rousie-Baudry. CervicalgiesSecondaires aux Desordres Posturaux.La Revue Medecine Orthopaedique 1995;42: front page.

5. McKay AB, Brownlea A. Self Help HealthCare: Active Preventive Medicine. Aust FamPhys 1987; 16(11): 1682-85.

6. McKay AB, Forbes JA, Bourner K. Em-powerment in General Practice: The Trilo-gies of Caring. Aust Fam Phys 1990; 19(4):513-20.

7. McKay AB. Chronic Low Back Pain andPain: The Hypothesis and Model. AustralasMusculoskeletal Med 2004; 9(1): 14-19.

8. Takahashi Y, Hirayama J, Nakajima Y, etal. Electrical Stimulation of the rat Lumbarspine induces reflex action potential nervesto the lower abdomen. Spine 2000; 25(4):411-17.

9. Takahashi Y, Morinaga T, Nakamura S,et al. Neural connection between the ven-tral portion of the lumbar intervertebral discand groin skin. J Neurosurg 1996; 85(2):323-28.

10. Pavlov IP. Reflex of Freedom. Lectureson Conditioned Reflexes. Vol. 1. New York;International Publishers, 1928: 282- 86.

11. Bogduk N. Clinical Anatomy of theLumbar Spine and Sacrum. 3rd ed. ChurchillLivingstone: 121.



This review is based on aMedline search of the last fouryears. I have not assessed

the quality of the papers. I have lookednot just at risk factors for onset, but alsorisk factors for “acute becomingchronic” (prognostic risk factors). Itincludes all forms of neck pain, not justmotor vehicle related whiplash, andcommonly but not always includesshoulder pain and sometimes arm pain.The literature frequently does not sepa-rate out these latter components.

There has been a burgeoning litera-ture in the last five to ten years on riskfactors for neck pain, including pro-spective, cross-sectional, retrospec-tive, and cohort studies and these havebeen undertaken at clinics by postalsurveys and by telephone surveys.These studies are based around indus-try and occupational arenas, and thereare community-based studies such asgeneral practices, and tertiary clinics.

There is a variable quality of thestudies as is always the case and, whilstthis is not assessed in any great depthfor this descriptive overview, the follow-ing difficulties should be borne in mind:biases, confounders, drop-outs, end-points, control groups, return rates, etc.Often univariately significant factorsdisappear on multivariate analysis(Bogduk).

There are many conflicting data,especially in the realm of psychosocialissues, and as Bogduk stated in 1999“factors that pertain to neck pain aredifferent from those that pertain to backpain”, but does that statement still applyin 2004?

Incidence and prevalence of neckpain• 34.4% Finland office workers,

n=180/232, annual incidence• 29% one-month period prevalence,

n=5752 GP register adults• 47% one-year prevalence, Hong

Kong academic staff• 34% one-year prevalence, nurs-

ery school teachers• 28% cumulative annual incidence,

high school students• 14.4% over a three-year period,

n=1334 adults• 17.9% one-year cumulative inci-

dence, n=7669 on a GP register, UK• 31% one-month incidence, n=314

hospital nurses in Japan

Recovery is often poor. Only 4% ofpatients sick-listed with neck pain hadno present discomfort 12 years later(Sweden), n= 213. Compare this withabout 25% in an average back paingroup with no present discomfort.

Of children with neck pain at base-line, 20% had widespread pain at 12months.

“At risk” occupations• Dental professionals• ERCP endoscopists, 46% preva-

lence (cross-sectional survey)• Physical therapists – lifetime preva-

lence 91%• Bus drivers, especially after more

than 10 years’ employment• Wheelchair users 66%• Fighter pilots, (high performance)

50% reported in-flight or immediatepost-flight neck pain

Risk factorsFor the purposes of this paper these

have been grouped as follows:

A. Physical Risk B.PsychosocialFactors Risk Factors1. Work 1. Job factorsenvironment2. Work patterns 2. Social factors3. Work movements 3. Psychological

factors4. Injury factors 4. Health issues5. Miscellaneous

A. Physical risk factorsWork environment

These risk factors have been de-scribed in the literature variously aspoor physical environment, keyboard

placement, and poorly adjustable seats.For bus drivers, odds ratio (OR) = 3.52,and similar results for truck drivers.

Work patternsThis includes patterns which entail

insufficient work breaks, high quantita-tive work demands, relative risk (RR) =2.14, increased duration of employ-ment (for example, bus drivers workingfor more than 10 years showed an ORof 3.43), and long work hours (for ex-ample, working a lot of overtime).

Work movements• Neck flexion and rotation• Neck flexion sustained• Shoulder movements – repetitious• Working at or above shoulder height• High force (RR 2.0), high repeti-

tiveness (RR 1.8), or both (RR 2.3),especially in monotonous manualwork

• Prolonged desk sitting (RR 2.01),especially with forward head pos-ture (RR 1.63)

• VDU users, but a negative study fortyping per se

Injury factors• Past history of neck/shoulder in-

jury, RR = 1.7, 1.97• Other musculoskeletal (MSK)

strains/pains• Severity of initial pain• Radiation of initial period of pain

beyond shoulders• Pressure tenderness in muscles• Motor dyscontrol of neck/shoulder

muscles in acute injury

MiscellaneousCauses include macromastia (un-

controlled study), and absent headrestraint position in a motor vehicle.

B. Psychosocial risk factorsThese have been grouped as:

1. Job factors2. Social factors3. Psychological factors

Chronic Neck Pain: Risk Factors andPreventionDr Geoffrey Speldewinde, Rehabilitation, Pain and Musculoskeletal Physician, Canberra

This paper is a synopsis of a presentation on Risk Factors for Chronic Neck Pain presented at the Australian Associationof Musculoskeletal Medicine Annual Scientific Meeting held in Sydney in November 2003.

May 2004 27

4. Health issues

Job factors• Low job control• Low job security• Low skill discretion• Low job satisfaction• High job demands causing work

stress, RR = 1.20-2.14• Poor training opportunities• Low decision authority, RR 1.60

Social factors• Low co-worker support, RR 2.43• Low supervisor support• Other people causing negative emo-

tions• Ethnicity/migrant worker groups

Psychological factors• Passive coping style• Maladaptive suppressive coping be-

haviour• Catastrophising• Fear-avoidance behaviour• “Perceived general tension”• Recent development of adverse

working conditions, RR 2.1-3.7 (vsendemic adverse conditions)

• History of personal physical, sexual,or domestic abuse

• “Psychosocial demands”• Psychological distress (depression,

poor mental health score, OR 1.68)• Personality factors – NO SUPPORT• Overall, psychosocial variables are

more predictive than biomedical orbiomechanical factors (Linton1)

Health issues• Low self-reported general health• Unsatisfactory leisure time; for ex-

ample, additional domestic work-load – males

• Low physical exercise levels• Genetic influences (twin study, Nor-

way)• Prior neck/shoulder injury, RR =

1.7 – 1.97• Other MSK pains; for example,

headaches, RR 2.3-2.8• Pressure tenderness in muscles• Obesity• Smoking• Increasing age (four studies posi-

tive, one study negative)• Female gender (nine studies, but

one also showed that women hadworse conditions than men, RR =

1.8-1.98

Neck pain preventionAdequate prevention strategies re-

quire knowledge of risk factors, riskgroups, and trends. Determining riskfactors allows one to determine factorsthat may be amenable to interventionand then assess the effectiveness ofsuch interventions. Good public healthmeasures are built on an adequateepidemiological base.

The studies suggested the followingstrategies for prevention of neck pain:• CBT (six standard sessions) was

more effective than simple informa-tion delivery in reducing subse-quent sick-leave three-fold, fear-avoidance behaviour and days withpain in non-patients who were ex-periencing neck or back pain.

• A software program that stimulatedworkers with neck pain (NP) to takebreaks and do simple exercises:More than 55% vs 35% “recov-ered”; More than 20% vs 42% de-teriorated.

• EXERCISE showed a stable “mod-erate benefit” in preventing neckpain – Linton literature review onPREVENTION.

• There were NO data to support“ergonomic interventions” in thesame review.

• Regular 20 minutes “microbreaks”best reduced discomfort, with noloss of productivity.

• VDU operators reduced staticelectromyographic (SEMG) load onthe trapezii when lighting was im-proved, optometric corrections weremade, and the option of having thewhole forearm and hand supportedon tabletop was instituted, the ben-efit of which was sustained at two-year review.

• Regular weight training for fighterpilots seems helpful.

• In motor vehicles, the fitting of headrestraints close to the head, orbetter ACTIVE head restraints, wasassociated with lower neck injuryclaim rates.

ConclusionsNeck pain is common and endemic

in the community across all ages andall occupations. Some ages and occu-pations are at higher risk, and it has

been shown that physical as well aspsycho-social factors are operating ina broad spectrum of various contribut-ing factors.

Prevention strategies are availableand supportable, including sensiblework environments for “fit” people, whocan find their workplace an enjoyableplace to be, having driven in vehicleswith good quality head rests, and inyears to come when we start flying towork, by avoiding excessive G-forces!

Reference1. Linton SJ, van Tulder MW. Preventiveinterventions for back and neck pain prob-lems: what is the evidence? Spine 2001;26(7): 778-87. Review PMID: 11295900.

Chronic Neck Pain: Risk Factors and Prevention


Abstract

Cervical arthroplasty involvesreplacement of the interver-tebral disc space with a pros-

thetic device designed to maintainmotion. The interest in cervical arthro-plasty has increased of late because ofthe perceived shortcomings of cervicalfusion surgery. The Bryan® cervicaldisc prosthesis is the only currentlyavailable cervical disc prosthesis. Overthe past four years, over 5,500 im-plants have been surgically placed inpatients who predominantly had neuralcompression. The use of arthroplastyfor the management of neck pain isbeing examined. The long-term impli-cations of arthroplasty are not knownbut in the short-term hospital stays areshort, motion is maintained, hip graftcomplications are avoided and a cervi-cal collar is not required. The realissues relate to longevity of the im-plants, wear and particle debris, andpotential protection of adjacent seg-ments from degeneration. It will take atleast 10 years of careful follow-up be-fore the answers to these questionsare derived.

IntroductionSurgery for spinal disorders has been

performed for over 50 years. Tradition-ally, the indications for spinal surgeryfor degenerative disease have been forneural compression. Simple laminec-tomy has been complemented by an-terior procedures where totaldiscectomy is performed. A variety ofprocedures are performed after this,including no placement of implants, ormore commonly intervertebral bonegrafting and sometimes plating. Sur-gery for primary axial neck pain is lesswell defined. Cord compression due tospondylotic disease termed cervicalspondylitic myelopathy (CSM), andacute disc herniation, are commonspinal disorder with controversy overthe role and timing of surgical interven-tion as well as the optimal treatment.1-

3,6-9,15,19,20 Over the past 50 years, vari-

ous combinations of anterior and pos-terior instrumented surgeries have beendevised and refined and continue to beutilized. In the absence of arthrodesis,kyphotic deformity is always a fearedcomplication.5,17 The problem withinterbody or posterior cervical fusion isthat typically a reduction in effectivemotion occurs and there are significantmorbidities associated with bone graftharvest.16 Coupled with this, the inci-dence of adjacent segment deteriora-tion, requiring reoperation, has beenquoted as being as high as 3% peryear.14 Consequently, there has beena more recent emphasis on surgicaltechniques such as cervicallaminoplasty or cervical disc arthro-plasty to maintain motion, avoid de-formity, reduce adjacent segmentstresses, and allow for an adequatedecompression without having to usebone graft. The precise indications forarthroplasty are currently being ex-plored and the biomechanics andchanges with disease assessed.

HistorySpinal arthroplasty has a relatively

short history. The aims of the idealintervertebral disc prosthesis have in-cluded preservation of normal motion,ease of implantation, ease of revision,minimal wear, longevity, ease of revi-sion and ease of postoperative imaging.All these goals have been achieved ina variety of permutations over the past40 years. Despite the ease of accessin the cervical spine, spinal disc re-placement surgery has historicallyconcentrated on the lumbar spine.7,8,10

Fernstrom11 in 1966 introduced anintracorporal endoprosthesis that con-sisted of a stainless steel ball insertedinto the centre of a lumbar disc afterlaminectomy. Although Fernstrom fo-cused on lumbar discs prostheses, healso placed these prostheses in thecervical spine. Cummins more recentlyhas described his experience with theCummins artificial cervical joint.7 Thisprosthesis was basically a stainless

steel ball-and-socket joint. A majorshortcoming of this design has beenthe inability to instrument more thanone level. They described implantationof 22 devices, designed within theirunit, in 20 patients. Two patients werelost to follow up. Of the 18 remainingpatients, x-rays demonstrated no move-ment at the level of implantation in twopatients. This rate of failure to preservenormal motion can be considered un-acceptably high. Wigfield et al23 modi-fied the Frenchay joint to allow morephysiological motion. They publisheda pilot study in 2002 in which the devicewas implanted in 15 patients. The studydemonstrated that implantation of thedevice is safe, and that motion is wellpreserved with the modified device inthe short term. Follow up reports stillsupport these conclusions.24 Pointillartdescribed a prosthesis in 2001 thatallowed motion between a titaniumbased prosthesis with a carbon sur-face that articulated with the inferiorendplate of the vertebra above the pros-thesis.18 However eight of ten patientsfused within two years. New prosthe-ses are expected to become availableover the next few years.

The Bryan® cervical disc prosthesis(Medtronic-Sofamor Danek, Memphis,TN, see Fig. 1) was first reported asbeing used for the management ofcervical spondylotic disease in 2002by Goffin et al12 and subsequently bySekhon.22 This cervical disc prosthe-sis consists of a polyurethane nucleus

Cervical Arthroplasty for the Treatment ofCervical Spine DiseaseJonathon F Parkinson, MB, BS; and Lali HS Sekhon,* MB, BS, PhD, FRACS; Department ofNeurosurgery and Spinal Injuries Unit, Royal North Shore Hospital and the University of Sydney

Figure 1. The Bryan disc prosthesisshowing the milled endplates thatallow for an interference fit of theprosthesis

May 2004 29

designed to fit between two titaniumalloy shells. Each shell has an outertitanium porous coating to encouragebony ingrowth and long-term stability.A polyurethane sheath surrounds thenucleus and is attached to the shellswith titanium wire, forming a closedcompartment. Sterile saline is placedinto the prosthesis and titanium alloyseal plugs provide for its retention. Thisprosthesis requires precise milling forits placement and the technique aimsat meticulous centering of the prosthe-sis. Multiple levels can be instrumentedbut must be visualized on fluoroscopy.Goffin et al12 described the use ofcervical arthroplasty in an attempt tomaintain cervical motion and avoid ar-throdesis after decompression. In theirstudy, 60 patients underwent singlelevel anterior cervical decompressionand placement of an artificial disc pros-thesis. Of note is that 93% of Goffin’spatients had radiculopathy predomi-nantly. They reported follow up at 12months, with clinical success reportedat between 85% and 90%. No subsid-ence of the devices was noted andpossibly two patients had device mi-gration. No spondylotic bridging oc-curred at the implanted disc space.Range of motion was preserved and nodevice had been explanted or surgi-cally revised. They have subsequentlyreported on three-year results in thisgroup and a similar one-year follow upon bi-level replacements, with equallyacceptable results.13

IndicationsThe commonest indication for cervi-

cal arthroplasty is as an intervertebraldisc replacement after total discectomyis performed. A typical case is shown inFigs. 2 a and 2b. Acute disc herniationsneed to be distinguished from cervicalspondylotic disease. Over time, thelarge and varied range of motion of thisregion places stresses on the cervicalspine, resulting in inevitable degen-erative changes, including desicca-tion of the discs, disc bulging, facetjoint hypertrophy, narrowing of facetjoints, and hypertrophy of ligaments.This process, ubiquitous in the adultpopulation, is known as cervical spondy-losis. The above changes may result innarrowing of the spinal canal or of theintervertebral foramen (or both) and

subsequently com-pression of the spinalcord or cervical nerveroots respectively mayensue. Acute cervicaldisc herniation, unlikespondylotic disease,tends to affect ayounger populationgroup. They may beassociated withtrauma, particularlywith acute hyper-flexion, rotation, orboth. The anulus fibro-sis and posterior lon-gitudinal ligament maytear, allowing part ofthe nucleus pulposusto herniate into the spi-nal canal or intervertebral foramen.Again either the cervical spinal cordand/or the cervical nerve roots may beinvolved. However, unlike the case withspondylosis, it is the nerve roots thatare most commonly affected. Fre-quently an acute disc herniation maybe superimposed upon existing spondy-litic change to cause a clinical prob-lem.

Cervical nerve root compression typi-cally results in neck pain and arm painin a radicular distribution. The mostcommonly affected cervical nerve rootsare C6 and C7. Paraesthesia mayaccompany the pain and these aretypically dermatomal in distribution.Associated sensory loss, typically topain and temperature, again in adermatomal distribution, is not uncom-mon. Weakness and hyporeflexia (thatis, lower motor neuron weakness) mayalso be present. The onset of thesesymptoms may be sudden or insidiousand progressive. A chronic episodicpresentation is more commonly causedby spondylitic change; however, anacute onset can imply either an acutedisc herniation or spondylitic change.The presence or absence of traumacan be an important differentiating fac-tor.

Cervical cord compression due todegenerative disease can present witha variety of syndromes. Most com-monly patients describe stiffness inthe upper and lower limbs and difficultywith fine movements in the hands.Examination generally reveals weak-

ness below the level of compression,with hypertonicity and exaggerateddeep tendon reflexes including an ex-tensor plantar response. Sensorychanges tend to be less marked. Otherspinal cord syndromes which may beassociated with cervical cord com-pression include central cord syndrome,Brown-Sequard syndrome and ante-rior spinal artery syndrome. Typicallywith acute cervical disc herniation thesesyndromes will develop rapidly. Anepisodic and insidious onset impliesspondylosis as the cause. Cord com-pression and myelopathy or root com-pression and radiculopathy can occurconcurrently in either acute cervicaldisc herniation or cervical spondylo-sis.

When looking at axial neck pain, theselection of patients becomes more

Figure 2. Preoperative (a) axial CT and (b) sagittal MRscans of the cervical spine showing typicallyspondylotic or disc bulges causing neural compressionin a patient ideal for cervical arthroplasty

Cervical Arthroplasty for the Treatment of Cervical Spine Disease


difficult. Arthroplasty is not suitable forpatients who have neck pain where thecause is thought to be myofascialdisease, facet degeneration, or de-formity. Neck pain related to degenera-tive disc disease is the only aetiologypotentially treated with this interven-tion. Sekhon reported in seven pa-tients that, if surgery was performed forcervical decompression of the spinalcord, neck pain often improved.21 Allthese patients had surgery for neuralcompression and the improvement inneck pain was an incidental finding. Inpatients with neck pain as their pri-mary symptom, selection is the key.CT scanning, static and dynamic fluor-oscopy, MR scanning, and possiblymultilevel provocative discography areall used to try and localize at least onepainful disc segment. However, asidefrom exclusion, there is no clear diag-nostic test. SPECT scanning with CTdoes not appear to have the samesensitivity in the cervical spine as itdoes in the lumbar spine and subtlespondylotic disease in facet joints doesnot appear to be as readily defined onCT. Subtle deformity plays a greaterrole in potential complications aftersurgery than in the lumbar spine and,with current designs, particularly in thecase of unconstrained devices such asthe Bryan® prothesis, surgery is bestavoided if kyphosis is present. Studiesare currently underway to evaluate pri-mary axial neck pain and its potentialcorrection with arthroplasty but at themoment ideal candidates are thosewith a single degenerative disc on MRscanning, negative cortisone facet in-jections, negative bone SPECT scans,minimal posterior element facetspondylotic disease on CT, normalcervical lordosis or a straight cervicalspine and motion on dynamic filmswith no evidence of instability. The roleof discography is unclear.

InvestigationsPlain x-rays, CT, MR, and bone scan-

ning all play a role in the work-up ofpatients for potential cervical arthro-plasty. Plain x-ray is often the firstinvestigation utilised by clinicians.Particular features of interest in thissetting are the overall balance of thecervical spine, deformity, if any, andany potential instability on dynamic

films. Coupled withthis, motion must bedemonstrated atany levels wherearthroplasty is con-templated. Asidefrom lack of motionor instability, othercontraindications tocervical arthro-plasty include ac-tive infection, an in-ability to visualizethe disc space onlateral x-ray, oste-oporosis, or ossifi-cation of the poste-rior longitudinal liga-ment (OPLL).

Computed tom-ography is also auseful investigation,primarily as it allowsfor accurate pre-operative planningof prosthetic size.The Bryan® discranges in size from14 mm to 18 mmand occasionally insmall individuals thesmallest prosthesisavailable is too largeand arthroplasty innot advisable. It is likely that smallerprostheses will be available in the future.

Surgical techniqueThe initial portion of surgery where

cervical arthroplasty is performed isidentical to that for an anterior cervicaldecompression and fusion. Implanta-tion of the Bryan® disc uses a simplegravitational reference system to iden-tify the centre of the disc space. Aseries of levels and plumb lines helpdetermine the centre of the implanta-tion site. This will change with futureincarnations and different implants.The reciprocating vertebral bodies aremilled to precision to match exactly theimplants convex outer surface. Bonyingrowth occurs into the roughenedouter surface over time. This tight fitprovides stability to the endplate. Theend result is shown in Fig. 3, withpostoperative images shown in Fig. 4.The current procedure is very depend-ent on intraoperative fluoroscopy.

Wear and particle debrisIn a situation analogous to hip and

knee arthroplasty, there have beenconcerns raised in terms of the longev-ity of cervical implants, potential parti-cle and wear debris and the complica-tions that may occur with these. Again,the Bryan® cervical disc prothesis ap-pears to be the most robust and mostthoroughly tested. Anderson et al pub-lished their data last year on theirbiomechanics of the prosthesis andwear characteristics.4 Using cervicalspine motion simulators, they reportedminimal wear at 10 million cycles ofmotion, with 500,000 – 1,000,000 cy-cles being deemed equivalent to oneyear of normal cervical motion. Animalstudies showed the polyethylene in-sert led to wear particles of a smallersize than that seen after hip and kneearthroplasty, but in the absence of aninflammatory reaction. No osteolysiswas seen and they felt that the wear

Figure 4. Postoperative (a) lateral extension and (b) flexionfilms showing the normal motion at the level of thearthroplasty. The titanium shells but not the inner nucleusare visualized on this imaging.

Figure 3. Intraoperative image of the Bryan disc prosthesis


May 2004 31

characteristics were acceptable. Noone knows how long the Bryan® discprosthesis will last. Estimates suggestsurvivals of at least 10 years but pos-sibly as high as 20-40 years, quitedifferent to those seen after large syno-vial joint surgery. To date no implanthas been removed because of devicefailure and particle debris seems onlyto be of theoretical concern.

The futureIt is possible, that the current pros-

theses available will not be the sameused in 5-10 years. Refinements intechniques, clarification of indications,as well as improvements inbiomaterials, should be realised overthe next 10-20 years. The trueincidences of adjacent segment dis-ease need to be further realised and atsome stage in the future, facet jointreplacement may also be possible.

ConclusionsCervical arthroplasty has arrived, yet

caution needs to be exercised in itsuse. The ideal patient has a soft discherniation with normal lordosis. Thelimitations and indications are currentlybeing defined. Long-term data are stillneeded. As newer prostheses becomeavailable and more data are made avail-able on the results of current designs,we will become more adequatelyequipped to use a powerful new tool inthe management of cervical spine dis-ease.

References1. Adams CB, Logue V. Studies in cervicalspondylotic myelopathy. I. Movement of thecervical roots, dura and cord, and theirrelation to the course of the extrathecalroots. Brain 1971; 94: 557-68.

2. Adams CB, Logue V. Studies in cervicalspondylotic myelopathy. II. The movementand contour of the spine in relation to theneural complications of cervical spondylo-sis. Brain 1971; 94: 568-86.

3. Adams CB, Logue V. Studies in cervicalspondylotic myelopathy. 3. Some functionaleffects of operations for cervical spondyloticmyelopathy. Brain 1971 94: 587-94.

4. Anderson PA, Rouleaux J P, Bryan VEand Carlson CS. Wear analysis of theBryan Cervical Disc prosthesis. Spine2003; 28(20): S186-S94.

5. Butler JC, Whitecloud TS3.Postlaminectomy kyphosis. Causes andsurgical management. Orthop Clin.NorthAm 1992; 23: 505-11.

6. Carol MP, Ducker TB. Cervical spondy-litic myelopathies: surgical treatment. JSpinal Disord 1988; 1: 59-65.

7. Cummins BH, Robertson JT, Gill SS.Surgical experience with an implanted arti-ficial cervical joint. J Neurosurg 1998; 88:943-48.

8. David T. Lumbar disc prosthesis. EurSpine J 1993; 1: 254-59.

9. Ebersold MJ, Pare MC, Quast LM. Sur-gical treatment for cervical spondylitic my-elopathy. J Neurosurg 1995; 82: 745-51.

10. Enker P, Steffee A, McMillin C, et al.Artificial disc replacement. Preliminary re-port with 3-year minimum follow up. Spine1993; 18: 1061-70.

11. Fernstrom U. Arthroplasty withintercorporal endoprosthesis in herniateddisc and in painful disc. Acta Chir ScandSuppl 1966; 357: 154-59.

12. Goffin J, Casey A, Kehr P, et al. Prelimi-nary clinical experience with the BryanCervical Disc Prosthesis. Neurosurg 2002;51: 840-45.

13. Goffin J, Van Calenbergh F, Van Loon J,et al. Intermediate follow-up after treatmentof degenerative disc disease with the BryanCervical Disc Prosthesis: single level andbi-level. Spine 2003; 28(24): 2673-78.

14. Hilibrand AS, Carlson GD, PalumboMA, et al. Radiculopathy and myelopathy atsegments adjacent to the site of a previousanterior cervical arthrodesis. J Bone JointSurg Am 1999; 81: 519-28.

15. Kumar VG, Rea GL, Mervis LJ, et al.Cervical spondylotic myelopathy: functionaland radiographic long-term outcome afterlaminectomy and posterior fusion.Neurosurg 1999; 44: 771-77.

16. Malloy KM, Hilibrand AS. Autograft ver-sus allograft in degenerative cervical dis-ease. Clin Orthop 2002; 394: 27-38.

17. Orr RD, Zdeblick TA. Cervicalspondylotic myelopathy. Approaches tosurgical treatment. Clin Orthop 1999; 359:58-66.

18. Pointillart V. Cervical disc prosthesis inhumans: first failures. Spine 2001; 26: E90-92.

19. Satomi K, Nishu Y, Kohno T, HirabayashiK. Long-term follow-up studies of open-door expansive laminoplasty for cervicalstenotic myelopathy. Spine 1994; 19: 507-10.

20. Saunders RL, Bernini PM, Shirreffs TGJr, Reeves AG. Central corpectomy forcervical spondylotic myelopathy: a con-secutive series with long-term follow-upevaluation. J Neurosurg 1991; 74: 163-70.

21. Sekhon LH. Cervical arthroplasty in themanagement of spondylotic myelopathy. JSpinal Disord Tech 2003; 16: 307-13.

22. Sekhon LHS. Two level artificial discplacement for spondylotic cervical myelopa-thy: J Clin Neurosci 2004; 11(4): 412-15.

23. Wigfield C, Gill S, Nelson R, et al.Influence of an artificial cervical joint com-pared with fusion on adjacent-level motionin the treatment of degenerative cervicaldisc disease. J Neurosurg 2002; 96(1Suppl): 17-21.

24. Wigfield C, Gill SS, Nelson RJ, et al.The new Frenchay artificial cervical joint:results from a two-year pilot study. Spine2003; 27: 2446-52.

*For correspondence and requests forreprints: Clinical A/Prof. Lali Sekhon,[email protected]



Abstract

We evaluated the effective-ness of 300 mW, 830 nmlaser in the management

of patients with chronic neck pain, ingeneral practice, between May 1998and June 1999. Data were obtainedfrom 78 patients who rated self-as-sessed improvement of symptoms ona Visual Analogue Scale (VAS). Anaverage improvement of 67.5% wasfound in 48 patients who reported apositive response to treatment. Numberof treatments was the only factor thatcorrelated with a positive response,reaching a plateau by 15. Low LevelLaser Therapy (LLLT) using this wave-length and power of infrared laser mayprovide a non-drug, non-invasive optionfor the management of neck pain. Thisstudy lends support for a randomizedcontrolled trial to further evaluate thistherapy.

IntroductionThe use of Low Level Laser Therapy

(LLLT) in pain management is contro-versial.1 The outcomes of randomizedcontrolled trials vary widely2,3 and stud-ies are difficult to compare because ofthe many different laser devices inclinical use. There are no standardizedtreatment protocols and reviews of theliterature attempt to combine trials usinglaser devices of different wavelengths,power, and energy densities beingapplied for varying lengths of time innumerous different conditions.4,5 Fur-thermore, parameters used or meth-ods of application are often reported ininsufficient detail to permit them to bereproduced.6,7

The variety of laser parameters andtechniques of application have thwartedeven the most well-intentioned attemptsat systematic review. The CochraneCollaboration made one of the most

assiduous attempts at assembling theavailable data of laser use in rheuma-toid arthritis, and concluded that fac-tors such as wavelength, treatmentduration of LLLT, dosage, and site ofapplication may all influence the effec-tiveness of laser.8 The same heteroge-neity of reported techniques and wave-lengths clouds the review of the use ofLLLT in other areas of clinical medi-cine.9 In particular, there have beenlimited studies using 830 nm laser inmanagement of painful musculoskel-etal conditions. This is the first pub-lished report in which a 300 mW con-tinuous wave (cw), 830 nm laser hasbeen used.

Notwithstanding the uncertainty ofthe available evidence, the proponentsof LLLT argue for a strong, positiveeffect in routine clinical practice.10

Therefore, there is a need for highquality, methodologically sound trials,using appropriate treatment protocols.As a preliminary step in designingsuch a trial, a retrospective, question-naire-based study of patients who hadreceived laser therapy for chronic neckpain was undertaken.

Chronic neck pain was selected forstudy as it a common cause of painand disability in the community. Treat-ment in general practice is usuallylimited to the use of analgesics andanti-inflammatory agents with their at-tendant risks.11

A self-administered questionnairewas used to determine whether therewas a clinically useful effect of 300mW, 830 nm laser and, if so, the sizeof that effect and other factors that mayhave influenced response to treatment.

The chair of the Ethics Committeeindicated that formal ethical approvalwas not required. Audits of generalpractice are part of the ongoing QualityAssurance (QA) activities of the Royal

Australian College of General Practi-tioners for vocationally registered gen-eral practitioners.

Subjects and methodsThe study was conducted in a gen-

eral (primary care) practice in Sydney,Australia. This practice offers Low LevelLaser Therapy as a routine part ofprimary care for acute and chronicmusculoskeletal conditions.

Patients were predominantly self-referred, with a small percentage beingreferred from other medical practition-ers. Many of the patients who attendedthe practice had typically tried manyother modalities of treatment such asacupuncture, physiotherapy, chiro-practic, naturopathy, and osteopathybut had failed to gain any long-lastingbenefit. A number had attended painclinics and had undergone interven-tional procedures such as cervicalzygapophyseal joint injections. Pa-tients had usually been extensivelyinvestigated by other medical practi-tioners prior to their attending the prac-tice. Further investigations were notroutinely performed unless there wereclear indications such as fever, weightloss, or other unexplained symptoms.The survey included patients with work-related neck pain, neck pain followingcar accidents, and those involved inlitigation.

The sampling frame was all patientswho had attended the practice for painmanagement between May 1998 andJune 1999.

Patients were recruited for the studyif they had marked on a pain diagramany part of the neck as the site of painat their first visit and had been treatedwith LLLT on at least one occasion.Patients were excluded if their painwas part of a systemic disease, suchas rheumatoid arthritis, or was part of

Efficacy of 300 mW, 830 nm laser in thetreatment of chronic neck pain: a survey in ageneral practice setting*Roberta T Chow, MB BS (Hons), FRACGP (Castle Hill Medical Centre, NSW); Leslie Barnsley, BMed (Hons),PhD, Grad Dip Epi, FRACP, FAFRM (RACP) (Department of Rheumatology, Repatriation Hospital, Con-cord,); Gillian Z Heller, PhD (Department of Statistics, Macquarie University); Philip J Siddall, MB BS, MMed(Pain), PhD (Pain Management and Research Centre, University of Sydney, Royal North Shore Hospital)

* First published in the Journal of Musculoskeletal Pain, Vol 11, No. 3, 2003, Editor: Dr I Jon Russell. Haworth Press,www.HaworthPress.com. Published here with that journal’s kind permission.

May 2004 33

a pain syndrome involving other areas.Questionnaires were mailed to 133

patients, with two subsequent reminderletters being sent to those who had notresponded at intervals of one monthfollowing the first letter. The time be-tween patients completing treatmentand receiving the questionnaire variedfrom one to 18 months.

QuestionnaireThe questionnaire was developed by

the author (RC) and aimed to deter-mine whether patients had benefitedfrom laser therapy or not and, if theyhad improved, to what extent, using aVisual Analogue Scale (VAS). Patientswere also asked to select the primarycause of pain from a list provided: workinjury, motor vehicle accident (MVA),arthritis, trauma (not work or car acci-dent related), no obvious cause andother. There were two patients who didnot complete this section.

Response to treatmentEach patient was asked to indicate,

by selecting from “yes”, “somewhat”,or “no” options whether or not theirsymptoms had improved following thelaser treatment. They were then askedto indicate along a Visual AnalogueScale to what extent their symptomshad changed since the completion oftreatment, where 0 was no change atall and 10 was complete relief of pain.

To provide assessment of the inter-nal consistency of the answers to thequestionnaire, the VAS scores werecompared to the categorical (that is,no, somewhat, and yes) results. Be-cause of the overlap between “some-what” and “yes”, these responses wereconsidered to represent a positive re-sponse to treatment (Fig. 1). Theywere therefore analyzed together, pro-viding a dichotomous outcome, that is,a “no” response or “yes” response.

“No” responses“No” responses were unambiguous.

Of those who returned the question-naire, 30 patients, 8 males and 22females, stated that they had no re-sponse to treatment. They are referredto as non-responders. Two patients inthe “no” group indicated that they wereworse at the end of treatment.

Response ratesFifty-one replies were received (38%)

after the first mailing and a further 27responses were received following twosubsequent letters. Seven question-naires were returned as unable to bedelivered. Therefore, of 126 possiblerespondents, 78 returned question-naires: a response rate of 62%.

Treatment protocolThe following treatment protocol was

used in all patients.

EquipmentAll patients were treated with a

Diolase (Diolase Corporation of Moun-tain View, California USA) 830 nm, 300mW, continuous wave, hand-held semi-conductor laser with a power density of0.67 watts/cm2.

Technical aspects of laser applicationThe laser was applied with firm pres-

sure to all tender areas in the neck,without specific identification of theunderlying anatomical structure. Thelaser hand piece, which was held atright angles to the skin, was centeredover each area of maximum tender-ness. The laser beam has a fusiformshape 15 mm in length and 3 mm at itswidest diameter and is emitted fromthe diode located in the hand piece.

Laser was applied to each tenderarea until sensitivity to palpation wasreduced or for a maximum of 30 sec-onds, whichever came first. The aimwas to reduce tenderness on palpationduring the course of the treatment. Ifthere was no response within 30 sec-

onds, laser application to that areawas ceased and other areas weretreated. Once treated, tender areaswere repalpated and, if still tender,were treated again. If there was nochange in the patient’s response aftera total treatment time of 30 minutes,treatment was ceased.

Patients were instructed to avoidany activity which exacerbated thepain between treatments. General ad-vice was given with regard to maintain-ing correct posture and attending toergonomic factors in the work place.These strategies were utilized to as-sist in the overall management of thepatient’s pain.

Patients continued to take whatevermedication they had been prescribedwhen they presented for laser therapy.This included analgesics, anti-inflam-matory, and pain-modulating medica-tion and drugs for other, unrelatedmedical conditions. Intake of analge-sics in this patient group varied fromthose who took medication on an as-needed basis to those who took regu-lar pain medication.

Over the course of treatment pa-tients were free to use whatever anal-gesic medication they felt was neces-sary to control the symptoms. Thosewho were on pain-modulating drugswere asked to continue.

Patients were advised that a positivebenefit would be likely to occur afterthe first or second treatments. If therewas no substantial response by thesecond or third treatments, then addi-tional treatments were unlikely to im-prove symptoms.

Distribution of Yes/Somewhat scores

0

2

4

6

8

10

12

14

1 2 3 4 5 6 7 8 9 10

VAS

Nu

mb

er o

f p

atie

nts Yes

Somewhat

Figure 1. Distribution of yes/somewhat responses and VAS scores

Efficacy of 300 mW, 830 nm laser in the treatment of chronic neck pain


This protocol was modelled on thatused in several previously publishedcase series.12,13 In these case series,a 100 mW, rather than 300 mW laserwas used. This is the first publishedreport in which the more powerful 300mW continuous wave laser has beenused.

Statistical analysisComparisons of continuous variables

across groups were made using inde-pendent-samples t-test when the vari-ables were normally distributed (age)and Mann-Whitney U-tests when thevariables were not normally distributed(for example, number of treatments).Chi-square was used to test for asso-ciation of categorical variable. The pro-gram SSPS Version 10 was used foranalysis.

ResultsWe analyzed data from 78 patients

who returned the questionnaire. Thisgroup consisted of 58 females and 20males who are referred to as partici-pants. We also compared data from 55patients (33 females and 22 males)who did not return the questionnaire,referred to as non-participants.

Demographics of participants and non-participants

The participant group was signifi-cantly older than the non-participantgroup, 51.3 years compared with 43.5years (p<0.001). There were no signifi-cant gender differences between thetwo groups (p=0.061). Patients in theparticipant group had completed sig-nificantly more treatments, mediannumber 7 (range 1-32) compared witha median number of 3 (p<0.001) in thenon-participant group (Table 1). Non-participants were significantly more

likely to have attributed their pain to anMotor Vehicle Accident (MVA) (p<0.05)(Table 2).

Demographics of the participants: Re-sponders and non-responders

Data were compared between thosewho reported an improvement with treat-ment, referred to as “responders” andthose who did not report any benefitfrom treatment, referred to as “non-responders”. Of the participant group,48 out of 78 patients (61.5%) indicatedthey had experienced positive responseto laser therapy (95% CI 50.7%-72.3%).

Age, gender, and number of treat-ments in responders and non-re-sponders

There was no statistically significantdifference in age between responders(mean 49.9 years, range 30-69) andnon-responders (mean 51.7, range 21-76) (Table 3).

There was no difference betweenmales and females in the likelihood ofa positive response to LLLT (p=0.87)and those who did respond did so in thesame number of treatments (p=0.3).

The median number of treatments forresponders was 8 (range 1-32) and fornon-responders was 4 (range 1-14)(Fig. 2). There was a statistically sig-nificant difference between the numberof treatments given to the respondersand non-responders (p<0.002).

There were a small number of pa-tients in this group where the number oftreatments was very much greater thanthe average. Four patients had be-tween 29 and 32 treatments each.These outliers all had work or caraccident-related neck pain.

Participants Non-participants Total p valuesMale 20 (26%) 22 (40%) 42 (32%) p = 0.061Female 58 (74%) 33 (33%) 91 (68%)Average age 51.3 years 43.5 years p < 0.001

(range 21-76) (range 26-76)Median number 7 3 p < 0.001of treatments (range 1-32) (range 1-6)

Table 1. Demographics of participants and non-participants

Table 2. Suspected cause of pain in the participant and non-participant groups

Cause of pain Participants Non-participants TotalWork Injury 23 (30%) 11 (20%) 34MVA * 15 (20%) 21 (38%) 36Other non-work injury 4 (5%) 7 (13%) 11Arthritis 10 (13%) 4 (7%) 14Other 24 (32%) 12 (22%) 36Total 76 (100%) 55 (100%) 131

Table 3. Demographics of responders and non-responders

Responders Non-responders p valuesMedian number of 8 (1-32) 4(1-14) p<0.002treatments (range)Males 12 (60%) 8 (40%) p = 0.87Females 36 (62%) 22 (38%)Mean age (range) 51.7 years 49.9 years p = 0.50

(21-76) (30-69)

Figure 2. Comparison of number of treatments in responders and non-responders


*P<0.05

May 2004 35

Cause of pain and response to treat-ment

There was no statistically significantdifference between responders and non-responders with regard to the cause oftheir pain. Seven out of 10 patients with“arthritis” experienced a benefit fromtreatment and 16 out of 23 patents withwork-related neck pain reported ben-efit from laser therapy. Nine out of 15patients with MVA-related neck painexperienced some benefit. Those withpain related to a non-MVA injury wereleast likely to benefit but the number inthis group was very small. Two pa-tients did not complete this section ofthe questionnaire.

Extent of response to treatmentPatients indicated, on a Visual Ana-

logue Scale, to what extent their symp-toms had changed since the comple-tion of treatment, where 0 was no changeat all and 10 was complete relief of pain.Patients who responded positively ex-perienced an average of 67.5% im-provement in symptoms as measuredby a Visual Analogue Scale (Fig. 3).

Number of treatments and responseto treatment

The relationship between the numberof treatments and eventual response totreatment was assessed. There is rapidlinear increase up to approximately

eight treatments, thereafter the prob-ability of positive response slows andthen plateaus at approximately at 15treatments.

Fig. 4 depicts the probability of even-tual response to number of laser treat-ments. Data points are circles. Thesolid line is a loess curve which is anon-parametric smoother.14

The graph shows an increasing prob-ability of response to LLLT with anincreasing number of treatments.

DiscussionWe found that 300 mW, 830 nm

laser was effective in 62% of patientswith chronic neck pain surveyed in aprimary care medical centre. The prob-ability of responding positively to treat-ment correlated with increasing numberof treatments, plateauing at 15. Aver-age self-reported improvement was67.5%, which is a clinically usefuleffect.

Age and gender did not alter poten-tial response to treatment and this hasbeen demonstrated in previous studiesof laser therapy.15 Numbers were toosmall to make a statistical analysis ofwhether or not certain conditions weremore likely to respond to laser therapy;however, data suggest that the great-est benefit occurred in patients withneck pain associated with “arthritis” ofthe spine and work-related pain. Theleast benefit was in the group who hadno clearly definable cause.

The only factor demonstrated to havea positive association with responsewas increasing number of treatments.Probability of response was greatestfor the first eight treatments, leveling offgradually to reach a plateau at 15treatments. This number would be thatrecommended for a complete courseof treatment.

The difference in median number oftreatments in the responders was eightand in the non-responders was four.This was a significant difference andmay underlie the importance of com-pleting an appropriate course of treat-ment to obtain the maximum benefit.This is further corroborated by the factthat the median number of treatmentsin the non-participants was three.

A number of factors may be respon-sible for patients persisting with treat-ment. It is plausible that patients who

Figure 3. Percentage of improvement following laser therapy

Figure 4. Probability of response to laser therapy and number of treatments



responded early in the course of treat-ment persisted with the therapy, be-cause of their positive initial response.Conversely, patients who did not re-spond rapidly did not persist with anyadditional treatments. It is not knownwhether persisting with treatment, ifthere is no initial early positive re-sponse, will produce a delayed butultimately beneficial effect. Moreover,early response to initial treatmentsmay be a prognostic indicator of sus-tained benefit from LLLT.

Only one non-responder completedwhat would be regarded as a full courseof 14 treatments, experiencing a short-term response after each treatmentthat was unsustained over the courseof treatment. In the future a trial inwhich 15 treatments is given may an-swer this question of delayed response.There were a small number of patients,all females, who had a dramatic andpositive response to treatment afterone treatment. These rapid respond-ers required only one or two treatmentsto resolve their symptoms significantly.This spectrum of response to lasertherapy from extreme responsivenessto complete unresponsiveness hasbeen recognised in a previous study oflaser.16 The mechanism for this is un-known.

Another factor operating as a barrierfor patients to persist if response isslower than anticipated may be thecost of treatment. At our medical cen-tre the cost of treatment was bornedirectly by patients except for thosewho were insured by either workerscompensation or third party insurance.There was no pensioner discount forthe consultation and the cost of lasertherapy was not covered by any thirdparty provider. This may have servedas a disincentive for patients to con-tinue treatment unless they perceiveda real benefit occurring at the initialstages of treatment. This factor wouldbe eliminated in a formal trial wherethere would be no cost to the patient.

There have been limited studies onthe treatment of neck pain using lasertherapy. Two studies have used pulsedlasers of 904 nm wavelength, thoughSoriano et al17 treated patients withacute cervical pain and Ceccherelli etal18 used laser for stimulation of acu-puncture points. A more recent study

by Ozdemir, 2001,19 used 50 mW, 830nm, continuous wave laser, thought tobe the most appropriate for muscu-loskeletal pain. This is the first study inthe literature using 300 mW, 830 nmlaser.

The mechanisms underlying an an-algesic effect of laser in chronic painremain to be fully elucidated althougha number have been postulated. Whilethe underlying mechanism is unknown,it has been demonstrated in animalstudies that laser therapy results in aselective reduction of A delta and Cfibre activity.20 Analgesia may alsooccur due to the release of endog-enous opioids following laser stimula-tion.21 Anti-inflammatory effects havebeen demonstrated both in-vitro22 andin-vivo23, 24 and a direct effect onmotoricity of lymph vessels,25, 26 reduc-ing interstitial fluid at the site of inflam-mation, has been described. Increasedfibroblast activity and laying down ofcollagen in damaged ligaments mayalso contribute to long-term pain reliefassociated with laser therapy.27, 28

While the results of the study aresuggestive of a clinically useful effectthe limitations of this survey must beconsidered. This was explicitly an au-dit of practice and was not intended tobe a formal trial; therefore there is nocontrol group. Since the aim of a con-trol group is to eliminate placebo ornon-specific response, these resultsraise the question as to whether apositive response rate to treatment ofmore than 67.5% is likely to be due toplacebo response.

The entire questionnaire had notundergone extensive evaluation, butkey items in the questionnaire haveestablished validity, for example,VAS.29 Patients were familiar with thistool, as they had been required to fill ina pain diagram and a VAS at eachtreatment visit. All patients, who se-lected “yes” and “somewhat” as a posi-tive response to treatment, consist-ently indicated improvement on theVAS. The positive correlation betweenthese responses adds to the internalvalidity of the questionnaire.

We achieved a response to theaudit of 62% which is less than ideal.However, even if all the non-partici-pants were non-responders, 36.1% ofthe entire group would still have had a

positive response, still constituting aclinically useful effect in a difficult-to-treat condition.

As this was a retrospective analysiswe had access to information concern-ing those patients who failed to re-spond to the audit questionnaire. Con-sideration of factors which may haveled to non-response bias revealed thatnon-respondents were younger(p<0.001), had fewer treatments(p<0.001) and were more likely to havebeen injured in a car accident (p<0.05).The Saskatchewan health survey ofneck pain prevalence demonstrated apreponderance of younger males in itsgroup of questionnaire non-respond-ents.30 A trend of higher rates of ques-tionnaire return by older women, alsoseen in our survey, was demonstratedin the Saskatchewan study but did notreach significance. How these factorsmay have influenced the return of thequestionnaire and their response tothe treatment is not clear and would bea matter for further study.

Even if a worst case scenario isassumed, with none of those who failedto return the audit questionnaire expe-riencing any benefit at all, over one-third of surveyed patients would haveexperienced a positive outcome. Manywithin this group of patients had multi-ple prior unsuccessful treatments withother modalities. The phenomenon of“extinction of placebo response” orplacebo “sag”, a form of conditionedresponse to multiple failed treatmentsin which placebo response is elimi-nated, may make this level of responsemore significant than it otherwise mightappear.31

There are several other issues aris-ing from this audit which would beaddressed in a randomized controlledtrial, which were not and could not beanswered in this retrospective analy-sis. These include the effect of painseverity and duration of pain on re-sponse to laser, the effect of concomi-tant medications on the response tolaser therapy, and adverse effects oflaser therapy.

ConclusionThis audit demonstrated a clinically

useful response in a notoriously refrac-tory group of patients. Despite thelimitations, there is no reason to be-


May 2004 37

lieve that the results of this audit areseverely compromised. It revealed apositive response to 300 mW, 830 nmlaser therapy in 62% of patients treatedfor neck pain due to a variety of causes.LLLT may offer an additional non-drugmodality in the management of pa-tients with chronic neck pain in generalpractice. This rate of response, in thisdifficult group of patients, would justifyfurther scrutiny of the technique and isworthy of further study in a randomizedcontrolled clinical trial.

References1. Basford JR. Low Intensity Laser therapy:Still not an established clinical tool. Lasersin Surg and Med 1995; 16: 331-42.

2. Saunders L. The efficacy of low-levellaser therapy in supraspinatus tendinitis.Clin Rehab 1995; 9(2): 126-34.

3. Vecchio P, Cave C, King V, et al. Adouble-blind study of the effectiveness oflow-level laser treatment of rotator cufftendonitis. Br J Rheumatol 1993; 32(8):740-42.

4. Gam AN, Thornsen H, Lonneberg F. Theeffect of low-level laser therapy on muscu-loskeletal pain: a meta-analysis. Pain 1993;52: 63-66.

5. Bjordal JM, Greve G. What may alter theconclusion of reviews? Phys Ther Re-views 1998; 3: 121-32.

6. Toya S, Motegi M, Inomata K, et al.Report in a computer-randomised doubleblind clinical trial to determine the effective-ness of the GaAlAs (830 nm) diode laser forpain attenuation in selected pain groups.Laser Ther 1994; 6: 143-48.

7. Oa RM, De Palma F. Clinical Efficacy oflow power laser therapy in osteoarthritis.Physio Research Int 1999; 4(2): 141-57.

8. Brosseau L, Welch V, Wells G, et al. LowLevel Laser Therapy for Osteoarthritis andRheumatoid Arthritis: A meta analysis. JRheumatol 2000; 27(8): 1961-69.

9. Flemming K, Cullum N. Laser Therapyfor venous leg ulcers. Cochrane Databaseof Systematic Reviews 2000: 2.

10. Tuner Jan, Hode L. Low Level LaserTherapy - Clinical Practice and ScientificBackground. 1st ed. Sweden: AB PrimaBooks, 1999: 318-36.

11. Hoving L, Gross AR, Gasner D, et al.

Critical Appraisal of Review Articles in theeffectiveness of conservative treatment forneck pain. Spine 2001; 26(2): 196-205.

12. Wong E, Lee G, Zucherman J, et al.Successful management of female officeworkers with “repetitive stress injury” or“carpal tunnel syndrome” by a new lasertreatment modality - application of low levellaser. Int J Clin Pharmacol Therapeutics1995; 33(4): 208-11.

13. Lee G, Wong E, Mason D. New con-cepts in pain management and in the appli-cation of low-power laser relief ofcervicothoracic pain syndromes. Am HeartJ 1996; 132: 1329-34.

14. Cleveland WS. Robust locally weightedregression and smoothing scatterplots. JAm Statistical Assoc 1979; 74: 829-36.

15. Simunovic Z, Trobonjaca T, TrobonjacaZ. Treatment of medial and lateral epicondyli-tis - tennis and golfer’s elbow - with low levellaser therapy: a multicenter double blind,placebo-controlled clinical study on 324 pa-tients. J Clin Laser Med and Surg 1998;16(3): 145-51.

16. Logdberg-Andersson M, Mutzell S,Hazel A. Low Level Laser Therapy of Ten-donitis and Myofascial Pains - a randomizeddouble-blind controlled study. Laser Ther1997; 9: 79-86.

17. Soriano FA, Rios R, Pedrola M, et al.Acute cervical pain is relieved with GalliumArsenide (GaAs) Laser Radiation. A Dou-ble-Blind preliminary study. Laser Ther1996; 8: 149-54. .

18. Ceccherelli F, Altafini L, Lo Castro G, etal. Diode laser in cervical myofascial pain:a double blind study versus placebo. ClinJ Pain 1989; 5(4), 301-304.

19. Ozdemir F, Birtane M, Kokino S. Theclinical efficacy of low-power laser therapy onpain and function in cervical osteoarthritis. ClinRheumatol 2001; 20: 181-84.

20. Wesselmann U, Lin SF, Rymer WZ.Selective Decrease of Small Sensory Neu-rons in Lumbar Dorsal Root GangliaLabeled with Horseradish Peroxidase afterNd:YAG Laser Irradiation of the Tibial Nervein the Rat. Experimental Neurol 1991; 111:251-62.

21. Laasko EL, Cramond T, Richardson C,et al. Plasma ACTH and Beta-endorphinlevels in response to low level laser therapy(LLLT) for myofascial trigger points. LaserTher 1994; 6(3): 133-42.

22. Sattayut S, Hughes F, Bradley P. 820nm Gallium Aluminium Arsenide LaserModulation of Prostaglandin E2 productionin Interleukin I stimulated myoblasts. LaserTher 1999; 11(2): 88-95.

23. Campana VR, Moya M, Gavotto A, et al.The relative effects of He-Ne Laser andMeloxicam on experimentally induced inflam-mation. Laser Ther 1999; 11(1): 36-42.

24. Palma J, Juri H, Campana V, et al..Blockade of inflammatory signals by laserradiation. Lasers in Surg and Med 1999;suppl 3(1): 11.

25. Lievens P. The influence of laser treat-ment on the lymphatic system and on woundhealing. Laser 1988; 1(2): 6-12.

26. Lievens PC. The Effect of a CombinedHeNe and I.R. Laser Treatment on the Regen-eration of the Lymphatic System During theProcess of Wound Healing. Lasers in MedScience 1991; 6(193): 193-99.

27. Enwemeka CS, Rodriquez OO, GallNG, et al. Morphometrics of Collagen FibrilPopulations in He:Ne Laser Photo-stimulated Tendons. J Clin Laser Med andSurg 1990; 8: 47-51.

28. Enwemeka CS, Reddy GK. The Bio-logical Effects of Laser Therapy and otherPhysical Modalities on Connective TissueRepair Processes. Laser Ther 2000; 12:22-30.

29. McDowell I, Newell C. Measuring Health:A Guide to Rating Scales and Question-naires. 2nd ed. New York: Oxford Univer-sity Press, 1996: 341-46.

30. Cote P, Cassidy JD, Carroll L. TheSaskatchewan health and back pain sur-vey: the prevalence of neck pain and re-lated disorders in Saskatchewan adults.Spine 1998; 23: 1689-98.

31. Peck C, Coleman G. Implications ofPlacebo Therapy for Clinical Research andPractice Management. Theoretical Med1991; 12, 247-70.



In this article I have used trials andclinical reports where possible,and otherwise I have used my

own clinical experience. Practical de-tails have been included to enable amusculoskeletal medicine practitionerto carry out treatments without furtherinstruction. This can be achieved be-cause the solution used is benign and,in conjunction with the rest of muscu-loskeletal and sports medicine, is veryeffective. A useful, inexpensive text-book is Diagnosis and Injection Tech-niques in Orthopedic Medicine by TADorman and TH Ravin. It is publishedby Williams and Wilkins and is avail-able from Dorman’s website.1

Inflammation is necessary for heal-ing

Prolotherapy has been described asthe use of growth factors or growthfactor stimulation to promote tissuerepair or growth.2 This is of great benefitin ligamentous strain, where collagenfibres are stretched and undergo aplastic change but do not necessarilytear sufficiently to incite the inflamma-tory process that is responsible fornormal healing (cell rupture releasescytokines, which attract polymorphs,macrophages then fibroblasts, whichform procollagen).3

Using a needle with hypertonic glu-cose or some other irritant, we canstimulate the inflammatory cascaderesulting in increased collagen fibrilnumber, diameter,4 and junctionstrength.5 It is possible that the resultis also due to the mechanical trauma ofthe needle at the enthesis.

As the procollagen matures into col-lagen and shrinks (losing water), liga-ments, tendons, and joint capsulesbecome thicker and stronger. Move-ment in lax ligaments stimulates painmechanoreceptors, and it is thoughtthat the pain relief with successivetreatments of prolotherapy is due tothe stability created by this connectivetissue repair.

The use of prolotherapy in low backpain6-13 and whiplash14 has been exten-sively reported.

This article will review current prac-tice in other joints.

Joint injury is a major risk forosteoarthritis

A joint is only as strong as its weak-est ligament. Ligamentous weaknessallows excessive mobility in a jointwhich is conducive to increased wearand tear. This is the major factor in thedevelopment of osteoarthritis (OA). Ahealthy joint has a coefficient of frictionless than a skater on ice. The study bySutton et al showed that lifetime regularexercise does not increase knee OAbut a prior knee injury increases therisk eight times.15

Similarly, Gelber used a longitudinalstudy of 1337 medical school gradu-ates from 40 years previously, andfound that knee injury before age 22tripled risk of arthritis in that knee –typically by the mid-fifties. The riskrose to five fold if they also had a laterinjury.16

Prolotherapy, with its ability to stabi-lize joints, can be used to prevent OAshortly after the injury, or at any time inthe decades of instability that lead toOA.

Strained entheses are tenderThe techniques of prolotherapy in

the neck and back are best learned byobservation, but there are some princi-ples that are universal, and by experi-menting in simple peripheral joints apractitioner can easily achieve goodresults. Bogduk says that “Injectionsinto tender attachment sites for liga-ments are a simple treatment that GPscan perform.”17

Strained entheses are usually ten-der, so in assessing where to treat, theexaminer’s thumb is an excellent guide.For example, in the common sprainedankle, it is usually easy to find theinsertion of the calcaneo-fibular liga-ment on the calcaneus and inject 0.5-1 cc at that point.

The injury will be greatest to theligaments on the outside of the joint.For example, the medial ligaments ofthe knee will be more injured in a valgusinjury, so we use our knowledge ofanatomy to search for tender points atthe insertion of the pes anserinus, andthe upper edge of the medial tibialplateau.

Injections into jointsThirdly, the solution is often injected

into the joint cavity as well as thesurrounding ligaments. This is a diffi-cult concept for most practitioners atfirst, as they are concerned that it maycause fibrosis in the joint. Actually theproliferant solution is also effective inpromoting growth factors in osteocytesand chondrocytes.2 It can be used totreat OA and other cartilage and intra-joint pathologies. The solution usuallyused in joints is 25% glucose withlignocaine. Three to four treatmentsare more effective and longer lastingthan using Hyalan in osteoarthritis,and much less expensive.

Reeves’ study of OA in knees18

used only 10% glucose in order to havea non-inflammatory solution, to ensurethe trial was properly double blind. Inpractice, he uses the usual 25% intothe joint and 15% to the ligamentsaround the joint. He treated 38 kneesdevoid of cartilage in at least one com-partment. There was a significant dif-ference in the glucose group by 12months in:• pain - 44% decrease• swelling - 63% decrease• knee buckling - 85% decrease• flexion range - 14% increase com-

pared to the lignocaine only group.

Osteoarthritic x-ray findings stabi-lized or improved, and eight of 13 withanterior cruciate ligament (ACL) laxitywere no longer lax after 12 months;that is, the anterior displacement dif-ference (ADD) was less than 2 mm asmeasured on a goniometer. He hassince published a three-year follow-upstudy of 16 patients with ACL laxitytreated with 10 or 25% glucose, de-pending on patient preference. At threeyears, pain at rest, pain with walking,and pain with stairs had decreased by45%, 43%, and 35%, respectively.ADD was normal in six knees by sixmonths, nine were normal by 12months, and 10 were normal at threeyears.19

Ongley, Dorman et al reported aseries20 of five very severely unstableknees treated with injections of theP2G solution into the insertions of the

Prolotherapy for Peripheral JointsDr Margaret Taylor, Musculoskeletal Physician, Adelaide

May 2004 39

anterior and posterior cruciate liga-ments according to the technique de-scribed by Cyriax,21 and also along theligaments. This variously named P2G,P25G, or Ongley solution, is a strongsolution of phenol 2.5%, glucose 25%,and glycerine 25%, added to an equalvolume of 0.5% lignocaine. Theseknees had massive anterior displace-ment distances of 7-13 mm (mean 9.4mm) at 90 degrees of flexion. Ninemonths after a series of prolotherapytreatments, this was improved to 4-8mm (mean 6.2 mm), and the patientswere able to run, play tennis, bicycle,etc, which they had been unable to do.

Treatment for OA of the knee isusually 5-6 cc of 15 or 25% glucosewith lignocaine into the joint, and 0.5cc to tender points on the medicalcoronary ligament (medial joint line),trying to contact both the upper edge ofthe tibial plateau and the lower edge ofthe femur. The insertion of the pesanserinus on the medial tibia will prob-ably have 3-5 exquisitely tender points,which also need 0.5 cc each. Occa-sionally, the lateral ligaments will betender instead. Four to six treatmentswill be necessary, and there should bevery significant pain relief, sufficient toremain off non steroidal anti-inflamma-tory drugs (NSAIDs) indefinitely inmiddle-aged patients. The elderly willprobably need regular treatments, per-haps every 2-3 months, but should alsobe able to avoid these dangerous drugs.

Rheumatologist Dr Steven Hall toldthe AAMM Annual Scientific Meeting(ASM) on Low Back Pain in GeneralPractice in Melbourne in 1997 thatNSAIDs caused more death and dis-ability than any other drugs. He statedthis is not taken seriously enough,particularly in the elderly.

Not only are NSAIDs dangerous inthe elderly, they also reduce thestrength of the healing ligament. Inanimals given ibuprofen during tendonrepair, the strength of flexor tendonswas decreased at four weeks from 12newtons to 2.5 newtons.22 In an Aus-tralian Army study of acute anklesprains, piroxicam reduced pain andtime to resume training, but at days 3,7, and 14 there was greater instabilitymeasured on the anterior draw test.23

During prolotherapy, it is usual to usesimple analgesics instead of NSAIDs

for this reason.Recurrent dislocation of the patella

should be treated at a few spots (whichwill be tender) at the medial side of thepatella, at both upper and lower attach-ments. The whole tibial insertion shouldbe injected.

The tibial insertion is also the site forOsgood-Schlatter disease. Kidd re-ported a series of six knees in fourmales.24 The teenagers responded inone or two treatments with completepain relief. A 26-year-old with a 12-yearhistory did not. He had bony ossiclesin the tendon.

Sporting injuries should be treatedindividually, according to the type ofinjury and the points of tenderness.Theoretically, prolotherapy is usuallyreserved for chronic injuries that arenot healing. However, there is no rea-son why the glucose solution cannotbe used to increase growth factor pro-duction in the acute injury and hastenhealing. In Europe, lignocaine alone isused, according to the principles ofneural therapy. It is theorized that thestrong polarization of cell membranesenhances cell function. This wouldcertainly be kinder in an acute injury,but consideration could be given tousing the glucose solution after a fewdays in an athlete who is very keen toget back to sport.

Ankles and feetProlotherapy is very useful to the

practitioner with a good knowledge ofanatomy of the feet, as it is easy to findthe strained ligaments by palpation.As well as sprained ankles, strainedAchilles tendon insertions, etc, youcan also relieve:• metatarsalgia• hammer toes and calluses - treat

the outside of the curves• calcaneal spurs• Morton’s neuromas - treat the liga-

ments between the metatarsalheads from the plantar or dorsalsurface, depending on comfort

• bunions - treat the tender points onthe medial side of the joint and put1 cc into the joint

• tired, aching feet - treat the tendermedial arch joints.

Pubic symphysisInstability after vehicle accidents,

sports injuries, and during and afterpregnancy can be treated with prolo-therapy. The joint is actually quite alarge fibrous structure. It is often verytender in a severe pelvic injury, and thepatient may be unaware of it. A sacro-iliac belt may be useful during thetreatment period to facilitate healing.Chakraverty reports a case in whichthe SI joint needed treatment as well,for an excellent result.25 Treatment dur-ing pregnancy is not contra-indicated,and can be very effective in the weeksbefore birth, even though the levels ofrelaxin are still high.

Groin injuriesGroin pain referred from the lumbar

spine is more common than a trueligamentous or muscle lesion of theadductors. If there is no tendernesslateral to the spines of L4 and L5, thevery localized insertion sites of theadductors on the pubic ramus can befound by looking for tenderness. Theycan be treated several times as needed.Of course, other musculoskeletal medi-cine approaches may also be used.Muscles that have been reflexly inhib-ited by pain may need to be retrainedwith specific exercises, and self- per-petuating increased muscle tone maybe addressed. It has been noted thatwhen the underlying ligaments aretreated, and the pain is removed, mus-cles begin to function fully again, andthese problems often correct them-selves.

Temporomandibular joint (TMJ)pain and increased tone can be re-lieved by injecting the usual proliferantsolution into the joint and tender liga-ment insertions on the zygoma and themandible in small amounts to a total ofabout 1 cc. This solution consists ofglucose 50%, lignocaine 2%, and nor-mal saline in a ratio of 3:1:6 producinga solution with 15% glucose content.As usual, the number of treatmentsvaries with the age of the patient andthe chronicity of the condition. Onewoman in her thirties with a shorthistory needed only two treatments. A75-year-old man who had been able toeat pureed food only for many yearsneeded six treatments in 1994, provid-ing full relief for three years. Anotherfive treatments in 1997 led to his re-

Prolotherapy for Peripheral Joints


maining pain free in 2004.

ShoulderThe easiest structure to treat is the

acromioclavicular (AC) joint. A fibrousjoint, easily located and treated, itneeds about 3-5 cc of 15% or 25%solution in 2-3 spots. Two to five treat-ments are needed depending on theseverity of the disruption. The com-monest shoulder structure to treat isthe supraspinatus attachment on thehumerus.26 You may even need to treatat the musculotendinous junction,medial to the AC joint, with the armelevated.27 Most commonly though,the tender point is easily located on thehumerus, and treated with 1 cc of 15%solution.

Other shoulder lesions also respondto prolotherapy:• Subacromial impingement may be

due to anterior or posterior rotatorcuff lesions, as well as the suprasp-inatus - treat their insertions on thehumerus if also tender.

• Both ends of the coraco-acromialand coraco-clavicular ligaments.

• The insertion of the short head ofbiceps on the inferior edge of thecoracoid.

• Recurrent shoulder dislocation -treat along the anterior edge of theglenoid and use 5 cc into the joint.One sports physician, who hadserious doubts as to the use ofintra-articular prolotherapy, saw arecurrent post-traumatic disloca-tion with bilateral Bankhart lesionsof the capsule on x-ray. The patienthad read about prolotherapy andinsisted on trying it. After two treat-ments all the laxity and apprehen-sion tests normalised on the treatedshoulder.

• The origin of the deltoid on theacromion and insertion on the hu-merus.

Theoretically, only partial tendon orligamentous tears should respond toprolotherapy. However, it is surprisingthe relief possible in elderly patientswith advanced age related changes onultrasound scanning. One 70-year-oldwoman had “a full thickness tear withretraction of the anterior to mid fibres ofthe supraspinatus tendon. The poste-rior fibres are intact… Early

degeneration…at the superior marginof the AC joint.” Four treatments in1999 gave her complete relief of pain,until two falls in 2001 and 2002. Twotreatments each time restored her pain-free state. It is always worth a trial oftwo treatments, bearing in mind theneed for withdrawal from NSAIDs, astheir inhibition of the inflammatory proc-ess is considered to be disadvanta-geous to the result of prolotherapy.However, there has been no studyproving this to date.

ElbowThree recent studies cast doubt on

the use of steroid in lateral epicondyli-tis.28-30 Although steroid injections dowell at six weeks, after a year only 69%had a successful outcome, comparedto 91% for physiotherapy, and 83% foraspirin or NSAID.

Steroids and inflammationAre musculotendinous lesions which

result from an injury inflammatory innature? The general consensus now isthat they are not. If so, why do steroidinjections work at all? Cyriax sug-gested injecting 1 cc of steroid in 20droplets “by a series of half withdraw-als and insertions”.31 This is similar tothe acupuncture technique, periostealpecking.

Trauma is a very effective way ofinitiating the (inflammatory) healingcascade even in the presence of thesteroid. It is likely that in non-inflamma-tory lesions, lignocaine would workequally well alone.

Steroid injections are not totally be-nign. The decrease in pain is due todecreased cytokines, which also de-creases ligament and bone repair.

Effects of corticosteroid include:• Decreased uptake of calcium by

bone, possibly weakening the fibro-osseous junction

• Inhibition of growth hormone (im-portant for soft tissue and bonerepair)

• Inhibition of synthesis of protein,collagen and proteoglycans in car-tilage by inhibition of chondrocyteproduction

• Inhibition of fibroblastic productionof collagen, ground substance andangiogenesis

• Other side effects, for example,

atrophy of overlying skin, psycho-sis, etc.

Studies have shown that even afterone steroid injection, cartilage remainsbiochemically and metabolically im-paired. In an animal knee study, tibialchondrocyte count/mm decreased withintra-articular steroid. The decreasewas even more significant if the animalwas also exercised.32 This is relevantin athletes who hate to stop training.

One US Naval study on 137 acromio-clavicular joint injuries compared corti-costeroid injections with those treatedconservatively with a sling, with sixmonths to 3.5 years follow-up. Thecorticosteroid treated first degreestrains had a marked increase in theamount of long-term degeneration inphysical findings, x-ray, and pain.33

This is not a complete review ofcorticosteroids, but the fact there issomething else to offer other than ster-oids is exciting.

Wrist and handReeves also produced a double-

blinded trial in the use of prolotherapyin OA of the fingers and thumb.34

Thirteen patients with 74 OA jointswere injected on medial and lateralaspects of each joint with 10% glucoseand lignocaine, and 14 patients with 76OA joints were treated with lignocainealone. Pain VAS at rest, with move-ment, and with application of grip, im-proved more in the glucose group, butwas only significantly better with grip.Flexion range increased by 8 degreesin the glucose group, and decreasedby 8 degrees in the placebo group. Youcan view this and Reeves’ other twostudies in full on his website: http://www.integrativemedicineresearchonline.com/prolotherapy_research.html.

ConclusionConsider glucose first, instead of

steroid for musculoskeletal pain, toencourage inflammation instead ofsuppressing it, and promote connec-tive tissue repair and healing.

References1. www.dormanpub.com

2. Reeves KD. Prolotherapy: Basic Sci-


May 2004 41

ence, Clinical Studies and Technique. InPain Procedures in Clinical Practice, ed-ited by Ted A Lennard. 2nd ed. Hanley andBelfus Inc, 2000.

3. Banks AR. A Rationale for Prolotherapy.J Orthopaed Med 1993;13: 54-59.

4. Klein RG, Dorman TA, Johnson CE.Proliferant Injections for Low Back Pain:Histological Changes of Injected Ligamentsand Objective Measurements of LumbarSpine Mobility Before and After Treatment.J Neurolog Orthop Med Surg 1989; 10:123-26.

5. Liu YK et al. An insitu study of the influ-ence of a sclerosing solution in rabbit me-dial collateral ligaments and its junctionstrength. Connect Tiss Res 1983; 11: 95-102.

6. Ongley MJ, Klein RG, Dorman TA, et al.A new approach to the treatment of chroniclow back pain. Lancet 1987; 2: 143-46.

7. Klein RG, et al. A Randomised Double-Blind Trial of Dextrose-Glycerine-PhenolInjections for Chronic Low Back Pain. JSpinal Dis 1993; 6: 22-33.

8. Dhillon GS. Prolotherapy in lumbo-pelvicpain. Australas Musculoskeletal Med 1997;2(2): 17-20.

9. Yelland M. Prolotherapy injections forchronic low back pain: Results of a pilotcomparative study. Australas Musculoskel-etal Med 2000; 20-23.

10. Yelland MJ, Glasziou PP, Bogduk N, etal. Prolotherapy injections, saline injections,and exercises for chronic low back pain: arandomised trial. Spine 2004; 29: 9-16.

11. Dechow E, Davies RK, Carr AJ, et al. Arandomised, double-blind placebo-control-led trial of sclerosing injections in patientswith chronic low back pain. Rheumatol1999; 38: 1255-59.

12. Frost W. Case Study: Sacro-iliac prob-lems and the benefit of prolotherapy overtime. J Orthop Med 1994;16: 96-97

13. Dorman TA, Cohen RE, Dasig D, et al.Energy efficiency during human walkingbefore and after prolotherapy. J OrthopMed 1995; 17: 24-26.

14. Dorman TA. Whiplash Injuries: Treat-ment with Prolotherapy and a new hypoth-esis. J Orthop Med 1999; 21; 19-21.

15. Sutton AJ, Muir KR, Mockett S, et al. Acase-control study to investigate the rela-

tion between low and moderate levels ofphysical activity and osteoarthritis of theknee. Ann Rheumat Dis 2001; 60: 756.

16. Gelber AC, Hochberg MC, Mead LA, etal. Joint injury in young adults and risk forsubsequent knee and hip osteoarthritis.Ann Intern Med 2000; 133(5): 321-28.

17. Bogduk N. Management of chronic lowback pain. Med JAust 2004; 180: 79-83.

18. Reeves KD, Hassanein K. Random-ised prospective double-blind placebo-con-trolled study of dextrose prolotherapy forknee osteoathritis with or without ACL lax-ity. Altern Therapies 2000; 6(2): 68-80-

19. Reeves KD, Hassanein KM. Long termeffects of dextrose prolotherapy for ante-rior cruciate ligament laxity. Altern TherHealth Med 2003; 9: 58-62.

20. Ongley MJ, Dorman TA, Eek BC, et al.Ligament instability of knees: A new ap-proach to treatment. Manual Med 1988; 3:152-54.

21. Cyriax JH, Cyriax PJ. Cyriax’s Illus-trated Manual of Orthopaedic Medicine.2nd ed. 1983, pp. 101-103.

22. Kulick MI, Smith S, Hadler K. Oralibuprofen: evaluation of its effect onperitendinous adhesions and the breakingstrength of a tenorrhaphy. J Hand Surg[Am]. 1986; 11(1): 110-20.

23. Slatyer MA, Hensley MJ, Lopert R. Arandomized controlled trial of piroxicam inthe management of acute ankle sprain inAustralian Regular Army recruits. TheKapooka Ankle Sprain Study. Am J SportsMed 1997; 25(4): 544-53.

24. Kidd RF. Treatment of Osgood Schlatterdisease by prolotherapy, a case report. JOrthop Med 1993; 15: 62-63.

25. Chakraverty RC. A case of osteitispubis secondary to unilateral sacroiliac jointinstability treated with prolotherapy. J OrthopMed 2003; 25: 10-13.

26. Cyriax, op cit, p.43

27. Cyriax, op cit, p. 45.

28. Newcomer KL, Laskowski ER, IdankDM, et al. Corticosteroid in early treatmentof lateral epicondylitis. Clin J Sport Med2001; 11: 214-22.

29. Smidt N, Assendelft WJ, van der WindtDA, et al. Corticosteroid injections for lat-eral epicondylitis. Pain 2002; 96: 23-40.


30. Smidt N, van der Windt DA, AssendelftWJ, et al. Corticosteroid injections, physi-otherapy, or a wait-and-see policy for lat-eral epicondylitis: a randomized controlledtrial. Lancet 2002; 359:657-62

31. Cyriax, op cit, p. 44.

32. Gogia PP, Brown M, al-Obaidi S. Hy-drocortisone and exercise effects on ar-ticular cartilage in rats. Arch Phys MedRehabil 1993; 74(5): 463-67.

33. Bergfeld JA, Andrish JT, Clancy WG.Evaluation of the acromioclavicular jointfollowing first- and second-degree sprains.Am J Sports Med 1978; 6(4): 153-59.

34. Reeves KD, Hassanein K. Randomisedprospective placebo controlled double-blindstudy of dextrose prolotherapy forosteoarthritic thumb and finger (DIP, PIPand trapeziometacarpal) joints: Evidenceof clinical efficacy. J Altern Comp Med2000; 6(4): 311-20.


Introduction

During 2001 and 2002, theHealth Insurance Comm-ission was concerned about

the unexplainable increase in shoulderultrasound imaging compared to ultra-sound imaging of other musculoskel-etal structures, as seen in Fig I. Theadvent of more specialised imagingequipment may in part explain thisincrease, but the important questionsto ask concern whether such imagingis best practice and whether it im-proves management.

Shoulder pain is third behind backand neck pain as a musculoskeletalreason for presentation to general prac-tice.1,2 Despite the fact that 50 – 60%of acute shoulder pain resolves in 8 –10 weeks, many patients present withthe anticipation of requiring some kindof imaging.

The reason that pain may persistbeyond three months is strongly re-lated to personality traits, coping style,and occupational factors.3,4

Data are available that indicate thatplain radiography for shoulder pain isuninformative and because ultrasoundis operator dependent, there is a widerange of reliability that can be placedon the results.5 In the best studies,ultrasound has high sensitivity andspecificity for detecting rotator cuff tears,with a significant proportion beingasymptomatic.6

ProposalIn view of this, a proposal concerning

the imaging for shoulder pain in generalpractice was presented to the Depart-ment of Health and Ageing. This pro-posal was in three parts.

Stage 1This stage correlated what was writ-

ten on the request form with what wasreported by the radiologist. Four radiol-ogy practices with expertise in muscu-loskeletal ultrasound were approachedin Sydney, Melbourne and Adelaide toprovide a sequential sample of requestsand reports during a six-week period.This resulted in 329 requests and re-

ports being analysed.The demographics were 176 females

and 150 males, with three showingneither age nor gender. The averageage for females was 56.7 years andthat for males 52.1 years. The perti-nent findings were:• Eighty per cent (263) of reports

listed pathology of some kind in thesymptomatic shoulder but no com-parison was made with the asymp-tomatic side.

• Thirty-four per cent (113) of requestshad no contributory history for theradiologist.

• Tears were found in 37% (123) ofpatients. Eighty-nine (72%) werepartial and 34 (28%) were com-plete. The average age for partialtears was 63.1 years while that forcomplete tears was 73.6 years.There were no comments on thereports that tears correlated withthe patient’s symptoms.

• When a diagnosis was made (169or 51%) on the request form theagreement with the report was only51%, that is, 86/169 or 25% overall.

• No report mentioned that in theprocess of the dynamic ultrasoundinvestigation whether the patient’spain was reproduced.

Recommendations arising from StageI included:• More clinical details to be recorded

on the request form.• All ultrasounds to include both sides

and comment by the radiologist asto whether pain was reproduced.

• Further study needed to determinewhat the practitioner does with theimaging findings.

Stage IIThis was a retrospective study from

the University of Adelaide’s databasecomparing the outcome of 100 pa-tients who had imaging with 100 whohad no imaging.

There were 17,733 patient visits re-corded from July 1, 2000, to October31, 2002, of which 1867 visits or 11%had shoulder pain. One hundred andeighty-three (84 with imaging and 99without imaging) were selected on arandom basis for the case notes review.Overall, one in four patients with imagingand one in 16 patients without imagingprovided the data for this report.

Study conclusions1. There was no indication from his-

tory or clinical examination thatwould enable the study to identify

Management of Shoulder Pain in GeneralPracticeNorman A Broadhurst, Department of Musculoskeletal Medicine, Flinders University, SA

Figure 1. Musculoskeletal ultrasound costings: 2001/2002

May 2004 43

why imaging was ordered. How-ever, there were significant statis-tical parameters identified whichwould indicate the likelihood for aperson to have imaging.

• Age 45-60 (p-value 0.009)• Pain on activity (p-value 0.001)• Pain present 5-13 weeks (p-value

0.002)2. The presence of comorbidities has

no influence on whether a patientwas to have shoulder imaging ornot.

3. Approximately half the patients hadsome documentation about thecause of the pain and little aboutseverity and location.

4. The decision to image subsequentlyinvolved multiple visits, with theimaged groups averaging 5.4 visitsand the non-imaged group 1.7 vis-its. Imaged at first visit was 69%and a further 20% at the secondvisit, with ongoing pain as the mainreason at the second visit. There isno information from the notes as tohow the results of imaging impactedon management.

5. A physical examination was re-corded at the first visit in 75% ofpatients. It is of some concern that17% of patients had no record of aphysical examination, with 12% ofpatients referred for imaging with-out a physical examination beingrecorded.

6. Imaging revealed some pathologyin 75% of patients, which is similarto Stage I (80%). Again, there wasno evidence to indicate that anycorrelation was made between thepathology and the patient’s symp-toms. Neither was there any evi-dence of a comparison with thenon-symptomatic shoulder.

7. The imaging reports indicated that23% of shoulders were normal, whichreflects the results of Stage I (20%).When a diagnosis was proffered bythe GP, the correlation with theimaging report was 25% which re-flects Stage I (25%). Although sub-acromial pathology was the mostfrequent problem reported, it rarelyappeared in the GP diagnosis.

8. Of those who had imaging, 92%was for ultrasound either alone(60%) or in conjunction with plainfilms (32%).

9. When medication was prescribedit was more likely to be NSAIDs,with the imaging group more likelyto receive this type of medication(55% versus 30%, p=0.001). How-ever, there was no indication fromthe clinical notes as to the efficacyof the treatment. This is likely areflection of the clinical assess-ment as to the severity of the pres-entation. Assurance and advicewere more likely to be given to theimaging group (57% versus 39%).

10.The subacromial space was the areareported with most pathology (62%).Tears were next with 13%, A/C joint8%, tendonitis 8%, and capsulitis2%. No comment was made regard-ing correlation with symptoms.

11.Referral to a specialist was morelikely to occur if the patient hadimaging (45%) compared to non-imaging (6%). Similarly more refer-rals to physiotherapy came fromthe imaged group (32%) comparedto the non-imaged group (23%).

Project deficiencies1. Two major omissions from the clini-

cal record were the mention ofoccupation (50%) and the recordof when pain first occurred (40%).

2. Given the inadequacies of a retro-spective study, 70 – 80% of pa-tients have no mention of their shoul-der pain after four months from firstpresentation.

3. No mention in the clinical recordcould be found of the benefit orotherwise the specialist or the physi-otherapist had on the outcome.

4. There was no indication of howimaging affected management orwhat management could be recom-mended following imaging.

Stage III A program of academic detailing is

being conducted in two Divisions ofGeneral Practice. Approximately 100GPs will look at imaging before andafter the detailing, as well as includingan outcome profile.

DiscussionIn considering the results of the data

gathered from Stages I and II a fairconclusion would be that managingshoulder problems in general practice

has room for improvement. This isespecially true in relation to the use ofimaging modalities which, apart from“red flag” conditions, is rarely requiredfor diagnostic purposes.

On the basis of Stages I and II as wellas the National Musculoskeletal Medi-cine Initiative, the age of the averageperson presenting with shoulder painwill be in his/her early fifties. Generallyat this age there are significant degen-erative changes in the musculoskel-etal system, much of which is asymp-tomatic or does not require a medicalconsultation. The duty of the GP is totake the relevant history and performan adequate history to glean sufficientinformation which will allow eliminationof “red flag” conditions followed by anappropriate management plan. Suc-cessful outcome depends partly on thenatural course of the varieties of shoul-der dysfunction and where in this paincontinuum the patient presents. Aknowledge of shoulder anatomy andbiomechanics, as well as an apprecia-tion of the reliability of tests reputed toidentify some pathologies, adds fur-ther to the successful resolution of thepresenting complaint in a high percent-age of cases.

Pathology was reported in 80% ofshoulders imaged and this must alertthe practitioner to the fact that thepresence of pathology does not neces-sarily mean a cause of symptoms. Thecorrelation of symptoms, anatomy, andexamination need careful assessmentand should be adequate at first consul-tation to formulate a management planwithout the necessity for referral and/orimaging.

The incidence of one-third of requestshaving no contributory information mustbe considered an omission and thereasons need clarification. How muchis “let’s x-ray” a function of “I don’tknow”, or perhaps shoulders are poorlyappreciated and resolution is due tonatural events rather than medical in-tervention.

Tears in the rotator cuff are morecommon with age and how much theseare related to symptoms is a cause forcontinuous debate. Many patients arediagnosed with complete tears and areonly marginally impaired in their ADLs.Recommendation for a reconstructionin a patient over 70 years must be

Management of Shoulder Pain in General Practice


considered against many social anddomestic issues, not the least of whichis whether the dominant arm will be outof action for several months.

It is not acceptable medical prac-tice to assess only the symptomaticshoulder – the asymptomatic shouldermust be examined in the same detailbefore a satisfactory management plancan be implemented as currently rec-ommended in the Medical BenefitsSchedule (2002, p. 415).

A correct diagnosis implies subse-quent appropriate management; yetwhen a diagnosis was made, the rel-evant pathology was shown in only10% of patients. Does this mean thata noticeable proportion of patients goon to chronic states or that no matterwhat we do the patients get better andall we add is palliative care?

The finding that the non-imaging pa-tients visited the GP less frequentlythan the imaged patients (1.7 v. 5.4visits) is interesting and may imply thatthe non-imaged patients were sufferingless or had less pain at the first pres-entation. It also may be due to differentdisease and personal reasons whichneed more clarification. Patients whohad imaging were more likely to have along consult at first visit, have moremedication and be referred, thus add-ing further costs to management.

The statistically significant factorsfor the GPs to order imaging were age(45-60), pain on activity, and pain longerthan six weeks. None of these factorsreflect clinical competence in manag-ing shoulder pain, which means thatthis study cannot help provide clinicalbased guidelines for appropriatenessof shoulder imaging.

For the most part, medication in-volved a mild analgesic and NSAIDs,the latter being prescribed more fre-quently when imaging was ordered.Self-treatment exercises did not ap-pear in the case notes so it may be thatany exercise regime was left for thephysiotherapist to institute. Level Imeta-analyses support the use of ex-ercises, NSAIDs and intra-articular in-jections in the acute presentation.7 Itwould not be difficult for GPs to learn afew non-specific stretches to be taughtto patients which could be implementedat the first visit. This would be a worth-while service as many patients do not

have “extras” cover, waiting lists atpublic hospitals are long, and in somerural areas physiotherapists are non-existent.

Referrals to specialists were to or-thopaedic specialists but there is noindication in the case notes of theproportion which needed surgery. It isnoted that all the patients referred to aspecialist had imaging at the first visitprior to seeing the specialist. Althoughit is common practice to order someimaging which the patient takes to thespecialist it might, if referral is neces-sary, be more economical to ask whatimaging would be helpful prior to thespecialist consultation.

Practice recommendations• In the absence of “red flags” the

average person presenting with ashoulder problem in general prac-tice is 50 years of age.

• At first consultation explanation,reassurance, stretches, analgesicsand NSAIDs are indicated.

• Review in 2-4 weeks when injec-tions or physiotherapy may be indi-cated.

• Referral may be required if adequateprogress is not achieved.

• If ultrasound imaging is contem-plated, compare the other side, andconsider whether pain or symp-toms are reproduced during theultrasound examination.

• Guidelines for imaging of shoulderdisorders similar to the Ottawa rulesfor knee and ankle are needed.

SummaryThe National Musculoskeletal Medi-

cine Initiative has established that evi-dence based practice has less than10% of patients being referred or imagedfor shoulder pain. With shoulder painpresenting to general practice in 7-32% of presentation, it becomes achallenge for AAMM to actively pursue2(c) of the Articles of Incorporation: “ toeducate physicians, other health pro-fessionals and the general public in thediagnosis and management of muscu-loskeletal disorders”.

There are few areas left in generalpractice that can be termed hands-onactivity. The peace and joy to solveand manage problems is what com-forts physicians and, while the knowl-

edge base is readily accessible, acontinuous effort by each generationof the AAMM executive has to bedirected in upskilling programs.

The author welcomes any discus-sion on how this could be implemented.

References1. Cailliet R. Shoulder Pain. 2nd ed. Phila-delphia: FA Davis, 1981.

2. van der Heijden G J, van der Windt D A,Kleijnen J, et al. Steroid injections for shoul-der disorders: a systematic review ofrandomised controlled trials. Br J Gen Pract1996; 46: 309-16.

3. van der Windt DA, Koes BW, Boeke AJ,et al. Shoulder disorders in general prac-tice: prognostic indicators of outcome. BrJ Gen Pract 1996; 46: 519-23.

4. van der Heijden GJ. Shoulder disorders:a state of the art review. In: Croft P, BrookesPM (eds). Bailliere’s Clinical Rheumatol-ogy 1999; 13: 287-309.

5. Fraenkel L, Shearer P, Mitchell P, et al.Improving the selective use of plain radio-graphs in the initial evaluation of shoulderpain. J Rheum 2000; 27: 200-204.

6. Dinnes J. Loveman E, McIntyre L, WaughN. The effectiveness of diagnostic test forthe assessment of shoulder pain due tosoft tissue disorders: a systematic review.Health Technology Assessment 2003; 7:15-66.

7. Australian Acute Musculoskeletal Guide-lines Group. Evidence-based managementof Acute Musculoskeletal Pain. Brisbane:Australian Academic Press P/L, 2003: 119-54. On-line www.nhmrc.gov.au/publica-tions.

8. Australasian Faculty of MusculoskeletalMedicine. Report on the NationalMusculoskeletal Medicine Initiative. New-castle: University of Newcastle, August,2001, Section III E.

Management of Shoulder Pain in General Practice

May 2004 45

The Orphan OrganDr Peter Jackson, Musculoskeletal Physician, Brisbane

Introduction

Musculoskeletal medicine hasbeen called the bastard childof medicine, and muscle

tissue the orphan organ.Skeletal muscle, even without its sub-

tending nervous system, must be thelargest human organ but is generallytreated with disinterest when it comesto pain-generating mechanisms.

There are decades and institutesdedicated to bones and joints but hardlya mention of the organ system thatmakes bone and joints function – skel-etal muscle.

Cardiac muscle has been graspedwith alacrity by cardiologists, the uterusby gynecologists, the detrusor by bothurologists and gynecologists and thesphincter muscles by gastroenterolo-gists, urologists and gynecologists, butnone of the classical medical specialtiesappears to take interest in the patho-physiology of muscle.

It would appear that muscle tissue isthe red-brown stuff that needs to becut, burned, stretched, and retractedto access the zygapophysial joint ordisc or alternatively the grainy greystuff of images to be dismissed whilststudiously staring at the white or blackstuff of bone, cartilage, or disc.

Modern medical practitioners haveno difficulty in accepting that problemswith cardiac muscle may cause a spe-cial pain called angina. Until fairlyrecently the pathophysiology of an-gina was not known. Modern medicalpractitioners have no problem withaccepting that the uterus can be thesource of pain or that there can bevarious forms of colicky pain resultingfrom dysfunctional smooth muscle.However, there is general scepticismthat skeletal muscle can be the sourceof pain.

This is despite the great complexityof skeletal muscle, much more com-plex than the repetitive contraction ofthe cardiac muscle or peristalsis ofhollow organ smooth muscle. For ex-ample, skeletal muscles are both theengine and brake of the locomotorsystem, and in fact a muscle such asthe quadriceps can be engine andbrake at the same time. Skeletal mus-cles can perform complex movements

as seen in gymnastics and dance orthe prolonged stillness required of amicrosurgeon or watchmaker. Skel-etal muscle is important not only formovement and posture but also for theexpression of emotion – witness facialexpressions during laughing, crying,anger, and grief.

Muscle painTerminology for muscle pain is con-

troversial. There have been numerousdescriptions over time, such as fibro-sitis, rheumatism, and myogelosis. Oneof the current terms is myofascialpain. This is the term I shall use in thisarticle to attempt to explain one currentparadigm. To date, there is noBogdukian evidence to support theparadigm, and this evidence may be along time coming because of the diffi-culty in performing randomized con-trolled trials and lack of research andfunding. Pharmaceutical companieshave not been able to find a product tosupport, other than Botulinum type Atoxin, a fairly recent development. Also,there are clinical difficulties in locatingthe manifestations of myofascial pain.

There is no undergraduate trainingand very little postgraduate training inthe clinical assessment of myofascialpain. For those interested in myofascialpain, there is no teacher or examiner.It is a skill that the interested persongradually acquires over a long period.However, myofascial pain is eitherprimarily or secondarily associatedwith most of humanity’s aches andpains, including those commonlytreated with surgery, powerful drugs,and expensive psychological and psy-chiatric interventions. Individuals whohave suffered both cancer pain andmyofascial pain or fractured bonesand myofascial pain frequently remarkthat myofascial pain is the more severeand distressing

Considerations of myofascial painMyofascial pain can be considered

a local or regional pain syndrome.Generally, myofascial pain is not wide-spread.

When a person with myofascial painis given a pain diagram, he or shemarks the area with a dot, dash, line,

or localised hash. There may be avague myotomal appearance to thepain diagram from trigger points in thescalene group of muscles, gluteusminimus anterior and posterior, andpiriformis, to name a few.

Current thinking is that myofascialpain develops as the result of a sickneuromuscular junction, making it atrue neuromuscular disorder and, infact, a mini pathoanatomical entity thatcan respond to target-specific treat-ment.

Myofascial pain is one form of softtissue pain that should be distinguishedfrom the other common form of softtissue pain, namely fibromyalgia.Myofascial pain can coexist withfibromyalgia and it may be that thenociceptive drive emanating from col-lections of sick neuromuscular junc-tions results in central sensitizationthat is thought to be at the heart of theetiology of fibromyalgia.

A cluster of loci of sick motor endplates (a myofascial trigger point)causes shortening of muscle whichresults in joint stiffness, a cardinal signof the condition. Fibromyalgia, on theother hand, is characterised byhypermobility.

These loci result in a condition ofweakened, centrally inhibited musclewithout atrophy.

The muscles in which the triggerpoint loci are found develop induratedtight bands. This is not true musclespasm as in muscle guarding associ-ated with an inflamed viscus, such asan appendix, ovary, or gall bladder.The alpha motor neurones and theiraxons are electrically silent. Thus theterms “muscle spasm”, “muscle ten-sion” and “tension headache” are in-appropriate and best avoided. Like-wise, the rubric of mechanical backpain does not make sense unless it ishypothesised that tight muscle bandsthat cross the motion segment causehypomobility of the zygapophysial andintervertebral joints.

The combination of local muscle tight-ness and motor weakness results inmotor imbalance. This is very com-monly seen in the many painful stiffshoulders that defy classic diagnosticlabelling.


When the loci are active, they spon-taneously refer familiar pain to associ-ated joints or entheses, causing themistaken impression of joint disease.The intervertebral joints are most com-monly affected. If the reported pain isnot familiar, another etiology must beconsidered.

Dysfunctional motor end plate locimay be quiescent or latent and referpain only when stimulated, usually bysome sort of pressure. Latent triggerpoints may still cause ropy induratedmuscle bands and muscle fatigue,weakness, and incoordination in theabsence of pain.

Autonomic components of the nerv-ous system are also involved, and seenin scleral injection, excess lachrym-ation, vasomotor rhinitis, and certainpilomotor activity. For example, stimu-lation of a mid trapezius trigger pointmay cause “gooseflesh” over the lat-eral upper arm.

Afferent nociceptive information frommany neck muscles enters the spinalcord at C 0-3 which is adjacent toautonomic nuclei in the medulla.

PathophysiologyA trigger point nodule is considered

to be a cluster of numerous micro-scopic abnormal loci of dysfunctionalmotor end plates scattered through itssubstance.

These spontaneously release exces-sive acetylcholene at rest.1 This hasbeen identified by electromyographyas “end plate noise”.

The small packets of acetylcholenecause shortening of nearbysarcomeres without propagation ofaction potentials along the entire lengthof the muscle cell.

Acetylcholene results in depolarisa-tion of the post junctional membranewhich opens up receptor channels,resulting in miniature end platepotentials. Nonphysiological levels ofacetylcholene cause increased in-gress of Ca++, resulting in localized,prolonged supercontraction of sub-end plate sarcomeres, and swollenmitochondria and sarcoplasmic re-ticulum.

Miniature end plate potentials are theconsequence of small, spontaneoussynaptic depolarizations of muscle cellmembranes in the end plate region in

the absence of electrical activity in thealpha motor neurone. Miniature endplate potentials are always sub-thresh-old, and are caused by random re-lease of single packets of acetylcholenefrom presynaptic nerve terminals.

Miniature end plate potentials areevinced by electromyography as endplate spikes and they occur at activemyofascial trigger points. Miniatureend plate potentials are short-lastingmembrane potentials caused byacetylcholene packet summation.

A normal end plate potential causedby the firing of an alpha motor neuroneis normally super-threshold and makesthe muscle cell membrane fire an ac-tion potential.

Contractures in many muscle cellsproduce a palpable taught band. Algo-genic substances are released in theregion of the dysfunctional motor endplates as found by a novel acupunctureneedle containing a U tube with aspecial terminal membrane.2

This could account for local andreferred pain and autonomic nervoussystem stimulation.

For some time there has been acomforting thought that myofascial trig-ger points were part of a simple painafferent-efferent loop, which becamea self-perpetuating vicious cycle. Itwas thought that nociceptive trafficsensitized the spinal segment, which inturn caused the resident alpha motorneurones to fire spontaneously, result-ing in a tight band containing triggerpoints. The afferent limb is now thoughtto be provided by the sympatheticnervous system. It is known that no-radrenaline causes abnormalacetylcholene release which, in turn,causes sustained sarcomere contrac-tion.

There is a significant differencebetween algogenic substances at ac-tive and latent trigger points.3

Testing methodsBench-side testing methods for in-

vestigating myofascial trigger pointshave included the following:• Specific needle EMG• Surface EMG• Ultrasound, which can capture a

local twitch response caused by nee-dle penetration of a trigger point

• Algometry.

Obviously, none of these modalitiesare available to doctors who practiseoutside multidisciplinary or institution-alised medicine.

PrevalenceThose who have taken the time have

found the prevalence of myofascialpain in general medical practice to be30%, in a pain medicine centre, 85-93%, head and neck pain clinic 55%,and in a lumbo gluteal orthopaedicclinic, 21%.4

EtiologyOne of the problems of convincing

sceptics about myofascial trigger pointsis its uncertain etiology.

Trigger points are said to be causedby direct stimuli, including:• Acute overload of muscle• Overwork fatigue including pro-

longed abnormal postures• Radiculopathy• Gross trauma.

Indirect stimuli include:• Other trigger points• Visceral disease• Joint dysfunction• Emotional distress, possibly by

means of increased circulatingnoradrenaline levels.

All these phenomena are mediatedvia the central nervous system, and areunder the influence of supra-spinalactivity and the descending inhibitorypathways that that are subject to en-dogenous seratoninopathy, althoughthis point is conjecture.

Strong afferent nociception fromprimary trigger points spread in theinternuncial neurons to adjacent seg-ments, causing efferent activity result-ing in secondary or satellite triggerpoints.

CircuitryMuscles have connections via the

primary afferent neurone to the sen-sory transmission cells in the dorsalhorn. These connections are continu-ously active and are called effectiveconnections. They also have connec-tions that relay deep referral and ten-derness with sensory transmissionneurones of other usually distal mus-cles. These are normally silent, andare called ineffective connections.Likewise, they have silent or ineffec-

The Orphan Organ

May 2004 47

tive connections with the sensory trans-mission neurones of skin and subcu-taneous tissue that are associated withcutaneous referral and hyperesthesia.Finally, there are silent connectionsbetween inactive receptive fields onthe cell membranes of the sensorytransmission neurones of the triggerpoint-containing muscle and distal mus-cles. This substrate is the basis of thedistal referral of active or stimulatedtrigger points to distal muscle in thevaguely myotomal distribution men-tioned above, and to the overlyingcutaneous tissue.5

In the neck, the opposite is true.Sensory disafferentation from manyneck muscles, particularly the trape-zius and sternomastoid, enters thespinal cord at the C0-3 segments andinterfaces with the cervico-trigeminalnucleus. This results in various formsof headache, sometimes associatedwith autonomic phenomena as out-lined in the introduction.

Interrater reliabilityInterrater reliability has attracted

criticism, which is not surprising giventhe lack of teaching, knowledge ofanatomy, and clinical skill required.Nevertheless, a study by Gerwin et al6

provided the following kappa scores:• .84 for spot tenderness• .88 for familiar pain recognition• .85 for palpable band• .69 for referred familiar pain• .44 for local twitch response

Myofascial pain syndrome andfibromyalgia syndrome

Frequently there is confusion aboutthese two common conditions.

Essentially, myofascial pain fromtrigger points• does not have a female preponder-

ance• is regional rather than widespread

general pain• has local tenderness rather than

widespread tenderness• is associated with hard ropy mus-

cles, not soft doughy muscles• is associated with reduced range of

motion not hypermobility• is examined for characteristic trig-

ger points not tender points• has an immediate response to in-

jections of trigger points rather than

a delayed or poor response to simi-lar injections

• has responded to Botulinum A toxin,whereas fibromyalgia sufferershave not.

The neuromuscular junctionSensory and autonomic nerves and

blood vessels accompany motor nervefibres to the neuromuscular junction.

The endplate region of muscle isdetected electromyographically by aninitial negative deflection of the wave-form followed by a positive first deflec-tion.

End plates are found in the mid-region of each muscle fibre, and havea characteristic topography for eachmuscle.

When special intracellular needleelectrodes are used, trigger pointsdisplay characteristic low voltage spikes(end plate or acetylcholene noise),interspersed with high-voltage nega-tive deflection wave forms (end platespikes) that are interpreted as mini endplate potentials with intermittent sum-mation to form the high amplitudespikes.7 Whilst this waveform is char-acteristic, it is not pathognomonic as itmay differ only in amplitude and fre-quency from the normal situation.

Trigger pointsTrigger points have been identified

using needle EMG and acetylcholenestaining. A trigger point appears tocontain a number of dysfunctionalmotor end plates scattered, albeit con-centrated, amongst normal motor endplates. The concentration of dysfunc-tional end plates has been called an“active locus”. A number of active locimake up a trigger point.

Trigger point regions tend to occurwhere end plate zones cross tautbands.

Muscle midbellies usually containthe highest concentration of motor endplates. For this reason, it is importantto be able to visualise the anatomy ofmuscle in a three-dimensional way.

Ultramicroscopy of active loci re-veals closely spaced sarcomeres di-rectly under the motor end plate whichappear like a contraction knot. Thesarcomeres on either side of the con-traction knot are widely spaced as ifstretched. On some occasions the

sarcolemma is devoid of contractileelements, and appears empty.

A closely concentrated collection ofthese contraction knots is called thecentral trigger point, and a number ofthese are found in the taut band. Ateither end of the taut band is a localisedenthesopathy. This can be thought ofas an attachment trigger point, al-though these have not been studiedmicroscopically to identify whether theyhave a unique morphology.

It is comforting to think that triggerpoints cause taut bands; however, tautbands can occur in the absence oftrigger points, and an alternative viewis that these bands are a precursor totrigger points.8

This trigger point complex must beunderstood for clinical reasons. Forexample, when a patient is asked topoint to the centroid of his/her pain, heor she will point to the attachmenttrigger point, not the central triggerpoint of which the patient will be una-ware. Yet, this is the most importantproblem to treat and to prevent recur-rence.

A common example is the glutealgroup of muscles, which has the proxi-mal enthesis on the iliac crest andespecially on the tuberosity. This isjuxtaposed to the sacroiliac junctionand joint and the distal enthesis on thegreater trochanter of the femur. Pain inthese regions is exceptionally com-mon. Multiple megalitres of steroidshave been expended in the manage-ment of this pain, which can be consid-ered a collection of attachment (trac-tion) trigger points. The patient almostnever points to the central trigger point,which is usually much more tender topalpation and much more important totreat. Other common examples are thetrapezius, deltoid, wrist extensors,quadriceps, and abductor hallicis.Failure to identify and treat centraltrigger points may be a principal rea-son for the less-than-spectacular re-sults obtained from published trials onthe efficacy of trigger point therapy.

TreatmentIn the Australasian context, muscle

pain is treated, from a non-pharma-ceutical musculoskeletal perspective,in various ways:• Mobilisation with impulse

The Orphan Organ


• Trigger point injections using localanesthetic

• Prolotherapy using local anestheticand glucose

• Acupuncture• Nesfield’s procedure• Blomberg’s technique using local

anesthetic and steroid• Thermocoagulation of the medial

branches of the posterior primaryrami, or of the anulus fibrosis.

Most purport to work in differentways. However, with the exception ofmobilisation with impulse, all have afinal common pathway in that sharpobjects pierce muscle cells andentheses.

It is possible that muscles crossingzygapophysial or intervertebral jointsdevelop taut bands, resulting in spinalsegments developing a functionally ab-normal position that various practition-ers call the “chiropractic lesion”, “theosteopathic lesion”, “joint blockage”,“somatic dysfunction”, or “minor in-tervertebral dysfunction”. Mobilisationwith impulse may work by acutelystretching the taut bands beyond thephysiological limit. This therapy is mosteffective in acute spinal pain but lesseffective in chronic spinal pain, possi-bly because it cannot address thedeactivation of trigger points as effi-ciently as in the acute situation.

The use of local anesthetic has neverbeen considered therapeutic, but it isused as a mercy procedure. The typeof anesthetic used, ester or amide,short- or long-acting, has no bearingon outcome measures.

A recent study9 on the efficacy ofprolotherapy in chronic low back painconcluded that significant and sus-tained reductions in pain and disabilityoccurred with ligament injections, irre-spective of the solution injected or theconcurrent uses of exercises.

Nesfield’s procedure uses a 32-34mm thin scalpel blade to incise para-vertebral and gluteal muscles in a non-discriminating way but in areas thatare known to harbour myofascial trig-ger points.

Injectable steroids are popular andused intuitively because of the asso-ciation of pain with inflammation. How-ever, there is no evidence thatmyofascial pain is associated with in-flammation, and studies of their use

have been disappointing.Blomberg’s technique has been re-

cently popularized for injecting theparasacrococcygeal region andsacrospinous and sacrotuberous liga-ments. These are enthetic regions ofthe gluteus maximus and longhead ofhamstring, with trigger points that cancause lumbo-gluteal pain, includingpain referred to the lumbosacral junc-tion, sacroiliac joint, coccyx, and pos-terior thigh.

It has been suggested that steroidinjections10 unintentionally impale trig-ger points, thereby unknowingly inac-tivating them during joint injections.The relief of pain thus obtained wouldfurther reinforce the incorrect conclu-sion that inflammation of tissues in-cluding joints is responsible for pain.

Likewise, steroid injections ofzygaphophysial joints and the synovialsacroiliac joints pass through manycentral and attachment trigger pointsbefore the solution is injected and thismay be one of the reasons why thistreatment is sometimes effective.

It would appear that success in treat-ing myofascial trigger points is due tothe mechanical deactivation (destruc-tion) of the active loci of dysfunctionalmotor end plates. It occurs irrespec-tive of the injectate, whether it be thevarious types of steroid, local anestheticeither long- or short-acting, and thevarious forms of prolotherapy addi-tives. The cataract blades used inNesfield’s procedure also destroy rela-tively superficial trigger points, as dodry needles when they are placedspecifically into the collections of ac-tive loci and not just into the variousacupuncture points as drawn on themeridians unless they actually overlaythe central or attachment trigger points.

Post-isometric relaxation techniques,using the neurophysiological Golgi ten-don reflexes augment the effect bystretching the sarcomeres immediatelyafter the active loci have been ablated.

An emerging therapy is the use ofBotulinum A toxin, which is showingpromising results in early trials and hasface validity.11

This may herald the third wave ofinterest in musculoskeletal medicine inAustralia, and it is important that thefew and the willing grasp this opportu-nity whilst it is possible.

References1. Proceedings of the New Zealand Asso-ciation of Musculoskeletal Medicine, An-nual Scientific Conference 4th-7 Sep 2003.Muscle Pain.

2. Ibid.

3. Ibid.

4. Mense S, Simons DG. Muscle Pain.Understanding its Nature, Diagnosis, andTreatment. Lippincott Williams & Wilkins;2001: 206. Table 8-1.

5. Baldry PE. Myofascial Pain andFibromyalgia Syndromes. A Clinical Guideto Diagnosis and Management. ChurchillLivingstone; 2001: 26. Figure 2.3.

6. Mense S, Simons DG. Muscle Pain.Understanding its Nature, Diagnosis, andTreatment. Lippincott Williams & Wilkins;2001: 223. Table 8-2.

7. Ibid, pp. 234, 237, 240.

8. Ibid, pp. 246-47, 250-51.

9. Yelland MJ, Glasziou PP, Bogduk N, etal. Prolotherapy Injections, Saline Solu-tions, and Exercises for Chronic Low BackPain: A Randomized Trial. Spine 2004; 29:9-16.

10. Travell JG, Simons DG. Travell&Simons’ Myofascial Pain and Dysfunc-tion. The Trigger Point Manual. Vol. 1.Williams and Wilkins; 1982: 436.

11. Proceedings of the Use of BotulinumToxin for the Treatment of Back and NeckPain. February 2004

Further reading1. Davidoff RA. Skeletal muscle tone andthe misunderstood stretch reflex. Neurol1992; 42: 952.

2. Lewitt K. The needle affect in the relief ofmyofascial pain. Pain 1997; 6: 83-90.

3. Dvorak J, Dovrak V. Manual MedicineDiagnostics and Therapeutics. GeorgeTheime; 1984.

4. Korr I M. Proprioceptors and SomaticDysfunction. 1976 AAO Yearbook.

5. Jackson PMC. Case Commentary OnLow Back and Leg Pain. Australas Muscu-loskeletal Med. 1997; 2(2): 38.

The Orphan Organ

May 2004 49

In patients with osteoarthritis, thereis often uncertainty about the ef-fectiveness of anti-inflammatories

versus analgesics. An Individual Medi-cation Effectiveness Test (IMET) is asimple, but rigorous way of comparingthe effectiveness of these two classesof medications to ensure that patientsare receiving the most appropriatetreatment. It is a randomised, double-blind crossover trial for individual pa-tients that offers the highest level ofevidence about the effectiveness ofmedications. The University of Queens-land is now providing IMETs compar-ing celecoxib with extended releaseparacetamol for osteoarthritis.

How does the celecoxib vs extendedrelease paracetamol IMET work?

During the IMET, the patient under-goes three pairs of two-week treatmentperiods – a total of 12 weeks. Duringone treatment period of each pair, thepatient takes celecoxib and a placebo,and during the other period they takeextended release paracetamol and aplacebo. This means that both thedoctor and the patient remain blindedto the active medication at all times,which reduces bias in judging theeffectiveness of the medications.

The patient records their pain, stiff-ness and functional levels and anyother adverse effects in a symptomdiary throughout the IMET. Upon com-pletion of the IMET, the IMET unitmatches the timing of each activetreatment with the results and sendsthe doctor a report. This can be usedto make informed decisions about fu-ture management.

Which patients would benefit?This IMET is most useful in patients

on regular anti-inflammatories or anal-gesics who are uncertain about theeffectiveness of their medication. It isopen to adults with osteoarthritis painfor at least one month where long-termuse of anti-inflammatories or analge-

Individual Medication Effectiveness TestComparing Celecoxib with ExtendedRelease Paracetamol for OsteoarthritisDr Michael Yelland, Senior Lecturer in General Practice, University of Queensland

sics are indicated. It is important thatthere are no contraindications tocelecoxib or extended release para-cetamol and that they have not had adepot corticosteroid injection in thelast two months. They are available topatients anywhere in Australia at nocost to them or their doctors.

For further informationContact the IMET service on (07)

3346 4835 or 1800 038 464, or [email protected], or Dr MichaelYelland on (07) 32755444 or [email protected].


Low back pain is a topic inmedicine that hasn’t enjoyedthe publicity that it deserves.

With its limited coverage in medicalcurriculae and hospital and GP trainingprograms, one would be forgiven forthinking it must be an uncommon orunimportant complaint. Yet it is a popu-lar topic in the media where cure claimsabound. It is the leading cause ofdisability in the workplace and a verycommon cause of presentation tohealthcare providers, often non-medi-cal practitioners.

The authors seek to readdress manyof the common misconceptions aboutlow back pain by presenting an ap-proach to diagnosis and managementfirmly supported by evidence. Manyreaders may be surprised to hear that

the evidence base for low back pain isstronger than for most other commonconditions, but amongst this evidencelays little support for the traditionalorthopaedic approach. The evidence ispresented with great clarity and linksvery logically with the algorithms fordiagnosis and management. Thesealgorithms gravitate towards precisiondiagnosis and treatment of the ana-tomical sources of back pain whenconservative therapy has failed.

It is essential reading for:1. People involved in musculoskeletal

medicine and medicolegal work2. Rehabilitation providers3. Physical therapists4. Workcover and other insurance pro-

viders5. Independent medical assessors.

It is a monumental task to coverthis huge topic in 200 pages.Professor Cailliet has, however,

been writing on this topic for the lastthree decades and has a knack forsimplifying complex subjects. He haspreviously found a receptive audienceof over one million people. Undoubt-edly, there is a thirst for knowledge inthis field as it is a common reason forseeking healthcare, but one ignored inlarge by undergraduate training andhospital medicine, especially in Aus-tralia. A great pity indeed as a recentMJA article1 revealed musculoskeletaldisability to be the commonest causeof disability across all age groups inAustralia.

In the Decade of the Bone and Jointit is encouraging that this black hole ofmedical education is receiving increas-ing attention. Professor Cailliet’s bookwould be most attractive to the novicewith little previous exposure to the

Book Reviews:Medical Management of Acute and Chronic Low BackPain. An Evidence-Based Approach, by N Bogduk and BMcGuirk

Medical Orthopaedics. Conservative Management ofMusculoskeletal Impairments, by Renee Caillet

It would be a very useful referencetext for general practitioners and su-persedes most other books in thisarena, which all too often are laced withopinion and hyperbole. Especially use-ful are the sections on history, imagingand management. These sections willsave a lot of nail biting amongst prac-titioners who are scared of missingdangerous conditions or who think theyneed to routinely refer low back painpatients to orthopaedic surgeons orrheumatologists. Health economistsmay also find the concepts in this bookinformative as cost savings abound inthis billion dollar heath expenditure pit.

- Review by Dr Scott Masters, Mus-culoskeletal Medicine, Caloundra

field. It is easy to read, well illustrated,and directive. The perspicacious reader,however, will be left unfulfilled. Theperipheral joints are touched on sobriefly I was left wondering why theauthor bothered at all. No mention wasmade of tendinopathies or frozen shoul-der syndrome and the knee chapterwas five pages long.

On the positive side there is reason-able coverage of low back and neckpain with the importance of ruling outred flags, avoiding rest, confident ex-planation, attention to psychosocialfactors and limiting radiological expo-sure emphasised. Chronic regional pain(CRP) and fibromyalgia are awarded achapter each. Both are syndromeswhose pathophysiology are yet to beunravelled but describe a group of pa-tients who seek help frequently andwidely. Dissemination of quality infor-mation about both these topics is vitaland this book helps in that task.

Strangely there is little referencethroughout the text to the level of evi-dence for statements. Instead we aregiven statements such as “therapistsagree”, “exercises are desirable” and“salicylates are of value”. I suspectmany readers would like to know moreabout the effect size of treatmentsrather than these global type procla-mations.

1. Giles LC, Cameron ID, Crotty M.Disability in Older Australians. MJA2003: 179: 130-33.

- Review by Dr Scott Masters, Mus-culoskeletal Medicine, Caloundra

May 2004 51

Journal Abstracts

This section aims to update the reader with some of the more significant musculoskeletalresearch published in the last year which is listed on the Medline and CINAHL databases.

NECKYlinen J, Takala EP, Nykanen M,Hakkinen A, et al. Active neckmuscle training in the treatment ofchronic neck pain in women: arandomized controlled trial. JAMA2003; 289(19): 2509.

Context. Active physical training iscommonly recommended for patientswith chronic neck pain; however, itsefficacy has not been demonstrated inrandomized studies.

Objective. To evaluate the efficacy ofintensive isometric neck strength train-ing and lighter endurance training ofneck muscles on pain and disability inwomen with chronic, nonspecific neckpain.

Design. Examiner-blinded random-ized controlled trial conducted betweenFebruary 2000 and March 2002.

Setting. Participants were recruitedfrom occupational health care sys-tems in southern and eastern Finland.

Patients. A total of 180 female officeworkers between the ages of 25 and 53years with chronic, nonspecific neckpain.

Interventions. Patients were ran-domly assigned to either 2 traininggroups or to a control group, with 60patients in each group. The endurancetraining group performed dynamic neckexercises, which included lifting thehead up from the supine and pronepositions. The strength training groupperformed high-intensity isometric neckstrengthening and stabilization exer-cises with an elastic band. Both train-ing groups performed dynamic exer-cises for the shoulders and upper ex-tremities with dumbbells. All groupswere advised to do aerobic and stretch-ing exercises regularly 3 times a week.

Main outcome measures. Neck painand disability were assessed by avisual analog scale, the neck and shoul-der pain and disability index, and theVernon neck disability index. Interme-diate outcome measures includedmood assessed by a short depressioninventory and by maximal isometricneck strength and range of motionmeasures.

Results. At the 12-month follow-upvisit, both neck pain and disability haddecreased in both training groups com-pared with the control group (P<.001).Maximal isometric neck strength hadimproved flexion by 110%, rotation by76%, and extension by 69% in thestrength training group. The respectiveimprovements in the endurance train-ing group were 28%, 29%, and 16%and in the control group were 10%,10%, and 7%. Range of motion hadalso improved statistically significantlyin both training groups compared withthe control group in rotation, but onlythe strength training group had statis-tically significant improvements in lat-eral flexion and in flexion and exten-sion.

Conclusions. Both strength and en-durance training for 12 months wereeffective methods for decreasing painand disability in women with chronic,nonspecific neck pain. Stretching andfitness training are commonly advisedfor patients with chronic neck pain, butstretching and aerobic exercising aloneproved to be a much less effective formof training than strength training.

Comment: This study reports goodresults for both strength and endur-ance training exercises for chronic neckpain in women. Other RCTs have nothad such good results. The authorsspeculate that there may be severalreasons for this. Firstly, they excludedpeople with fibromyalgia and includedonly those motivated for rehabilitation.One hundred and eighty people wereselected for the trial but no informationwas given on how many applicantswere rejected and the reasons for theirexclusion. This would have been valu-able information on the utility of thistreatment. The exercises were rela-tively low-tech involving theraband anddumbbells and being performed athome after initial supervision. – ScottMasters

Sterling M, Jull G, Vicenzino B,Kenardy J. Characterization of

acute whiplash-associated disor-ders. Spine 2004; 29(2):182-88.

Study Design. An experimental studyof motor and sensory function andpsychological distress in subjects withacute whiplash injury.

Objectives. To characterize acutewhiplash injury in terms of motor andsensory systems dysfunction and psy-chological distress and to comparesubjects with higher and lesser levelsof pain and disability.

Summary of Background Data. Mo-tor system dysfunction, sensory hy-persensitivity, and psychological dis-tress are present in chronic whiplashassociated disorders (WAD), but littleis known of such factors in the acutestage of injury. As higher levels of painand disability in acute WAD are ac-cepted as signs of poor outcome, fur-ther characterization of this group fromthose with lesser symptoms is important.

Materials and Methods. Motor func-tion (cervical range of movement [ROM],joint position error [JPE], activity of thesuperficial neck flexors [EMG] during atest of cranio-cervical flexion), quanti-tative sensory testing (pressure, ther-mal pain thresholds, and responses tothe brachial plexus provocation test),and psychological distress (GHQ-28,TAMPA, IES) were measured in 80whiplash subjects (WAD II or III) within1 month of injury, as were 20 controlsubjects.

Results. Three subgroups were iden-tified in the cohort using cluster analy-sis based on the Neck Disability Index.Those with mild, moderate, or severepain and disability. All whiplash groupsdemonstrated decreased ROM andincreased EMG compared with thecontrols (all P < 0.01). Only the mod-erate and severe groups demonstratedgreater JPE and generalized hyper-sensitivity to all sensory tests (all P <0.01). The three whiplash subgroupsdemonstrated evidence of psychologi-cal distress, although this was greaterin the moderate and severe groups.Measures of psychological distressdid not impact on between group differ-ences in motor or sensory tests.


Journal Abstracts

Conclusions. Acute whiplash sub-jects with higher levels of pain anddisability were distinguished by sen-sory hypersensitivity to a variety ofstimuli, suggestive of central nervoussystem sensitization occurring soonafter injury. These responses occurredindependently of psychological dis-tress. These findings may be impor-tant for the differential diagnosis ofacute whiplash injury and could be onereason why those with higher initial painand disability demonstrate a pooreroutcome.

Comment. This study from the Uni-versity of Queensland PhysiotherapyDepartment analysed 80 whiplash pa-tients looking to see if it was possibleto divide them into subgroups for prog-nostic value. They found the main dis-tinguishing feature between patientswith severe levels of pain and disabilityand those with mild levels was gener-alised hypersensitivity to a range ofstimuli. This suggested that centralsensitisation occurred soon after in-jury. This sensitisation was unrelatedto levels of psychological distress. Thepaper suggests that addressing thesensitisation issue early in WAD pa-tients may provide new answers to man-agement issues. – Dr Scott Masters

Miettinen T, Leino E, Airaksinen O,Lindgren KA. The possibility to usesimple validated questionnaires topredict long-term health problemsafter whiplash injury. Spine 2004;1; 29(3):E47-51.

Study Design. A prospective follow-up study.

Objectives. To evaluate the relationof the state of health before the acci-dent and the significance of the symp-toms reported soon after the injury tothe situation 3 years after the injury. Toevaluate the possibility of using simplevalidated questionnaires to predict long-term health problems after the injury.

Summary of Background Data. Awhiplash injury is generally benign inits natural course. However, some ofthe patients have diverse and prolongedsymptoms. Although several prognos-tic factors have been suggested for thepoor recovery, in most cases the fac-tors leading to prolonged disability re-

main unclear.Methods. In collaboration with traffic

insurance companies, we gatheredinformation of neck injuries that oc-curred in traffic accidents in Finland in1998. After the insurance companyreceived a notification of a neck injuryand consent from the injured party toparticipate in the study, they sent theinformation to the research team. Thefirst inquiry was sent to the patients assoon as possible. One- and three-yearfollow-up questionnaires were postedto those who responded to the firstinquiry. A total of 144 persons returnedthe 3-year follow-up questionnaires andform the material of this study.

Results. A poor state of health orfrequent neck pain or headache beforethe accident did not have any signifi-cant relation to the poor outcome 3years after the accident. The extent ofneck pain and lower back pain reportedsoon after the accident was signifi-cantly associated to a poor outcome inthe follow-up. The Neck Disability Indexquestionnaire was significantly relatedto the poor outcome after 3 years.

Conclusions. The subjective experi-ence of a notably decreased level ofactivity because of the neck pain whensupplemented by the enhanced scoreof Neck Disability Index questionnairepredicts well poor outcome in long-term follow-up and can be used as atool to identify persons who are at riskto suffer long-term health problemsafter whiplash injury.

Comment. The interesting result ofthis Finnish study is the lack of rela-tionship between premorbid health andoutcome. The other results confirmprevious studies associating poor out-comes with initial pain and disabilitylevels. – Dr Scott Masters

HEADACHEGovind J, King W, Bailey B, BogdukN. Radiofrequency neurotomy forthe treatment of third occipital head-ache. J Neurol Neurosurg Psychia-try 2003; 74(1): 88-93.

Objective. To evaluate the efficacy ofa revised technique of percutaneousradiofrequency neurotomy for third oc-cipital headache.

Methods. The revisions included us-

ing a large gauge electrode, ensuringminimum separation between the threeelectrode placements, and holding theelectrode in place by hand. The revisedtechnique was used to treat 51 nervesin 49 patients diagnosed as sufferingfrom third occipital headache on thebasis of controlled diagnostic blocks ofthe third occipital nerve. The criteria forsuccessful outcome were completerelief of pain for at least 90 days asso-ciated with restoration of normal activi-ties of daily living, and no use of drugtreatment for the headache.

Results. Of the 49 patients, 43 (88%)achieved a successful outcome. Themedian duration of relief in these pa-tients was 297 days, with eight pa-tients continuing to have ongoing relief.Fourteen patients underwent a repeatneurotomy to reinstate relief, with 12(86%) achieving a successful outcome.The median duration of relief in thesepatients was 217 days, with six pa-tients having ongoing relief. Side ef-fects of the procedure were consistentwith coagulation of the third occipitalnerve and consisted of slight ataxia,numbness, and temporary dysaesthe-sia. No side effects required interven-tion, and they were tolerated by thepatients in exchange for the relief ofheadache.

Conclusions. Use of the revised pro-cedure greatly improved the rather lowsuccess rate previously encounteredwith third occipital neurotomy. Althoughthe relief of headache is limited in dura-tion, it is profound and can be reinstatedby repeat neurotomy. No other form oftreatment has been validated for thiscommon form of headache.

Comment. The clinical researchinto RFN continues from Newcastlewith an updated technique for the 3rd

occipital nerve. The superior resultswith this technique suggest it shouldbe standard for anyone performing theprocedure. To date however, there isno formal accreditation procedure forRFN, and its usage around Australiaremains very operator dependent. – DrScott Masters

LOW BACK PAINFritzell P, Hagg O, Jonsson D,Nordwall A. Cost-Effectiveness of

May 2004 53

Lumbar Fusion and NonsurgicalTreatment for Chronic Low BackPain in the Swedish Lumbar SpineStudy. A Multicenter, Randomized,Controlled Trial From the SwedishLumbar Spine Study Group. Spine2004; 29 (4): 421-34.

Study Design. A cost-effectivenessstudy was performed from the societaland health care perspectives.

Objective. To evaluate the costs-effectiveness of lumbar fusion for chroniclow back pain (CLBP) during a 2-yearfollow-up.

Summary of Background Data. A fulleconomic evaluation comparing costsrelated to treatment effects in patientswith CLBP is lacking.

Patients and Methods. A total of 284of 294 patients with CLBP for at least2 years were randomized to eitherlumbar fusion or a nonsurgical controlgroup. Costs for the health care sector(direct costs), and costs associatedwith production losses (indirect costs)were calculated. Societal total costswere identified as the sum of direct andindirect costs. Treatment effects weremeasured using patient global assess-ment of improvement, back pain (VAS),functional disability (Oswestry), andreturn to work.

Results. The societal total cost perpatient (standard deviations) in thesurgical group was significantly higherthan in the nonsurgical group. Swedishkroner (SEK) 704,000 (254,000) vsSEK 636,000 (208,000). The cost perpatient for the health care sector wassignificantly higher for the surgicalgroup, SEK 123,000 (60,100) vs 65,200(38,400) for the control group. All treat-ment effects were significantly betterafter surgery. The incremental cost-effectiveness ratio (ICER), illustratingthe extra cost per extra effect unitgained by using fusion instead of non-surgical treatment, were for improve-ment. SEK 2,600 (600-5,900), for backpain. SEK 5,200 (1,100-11,500), forOswestry. SEK 11,300 (1,200-48,000),and for return to work. SEK 4,100 (100-21,400).

Conclusion. For both the societyand the health care sectors, the 2-yearcosts for lumbar fusion was signifi-cantly higher compared with nonsurgi-cal treatment but all treatment effectswere significantly in favour of surgery.

The probability of lumbar fusion beingcost-effective increased with the valueput on extra effect units gained byusing surgery.

Comment. Hats off to the Swedishdoctors who ran this study as it was avery comprehensive look at cost-ben-efit of surgical versus non-surgicaltreatments for chronic LBP. An as-sumption seems to be made in thisstudy that these patients had discogenicpain. No mention of any diagnostic testsis mentioned. Considering it was Swed-ish, I wondered whether these patientshad been through Dr Blomberg’s “StayActive” clinic before surgery. – Dr ScottMasters

Pauza KJ, Howell S, Dreyfuss P, etal. 2003 Outstanding Paper Award.Nonoperative Science. A random-ized, placebo-controlled trial ofintradiscal electrothermal therapyfor the treatment of discogenic lowback pain. Spine 2004; 4 (1): 27-35.

Background Context. Intradiscalelectrothermal therapy (IDET) is a treat-ment for discogenic low back pain theefficacy of which has not been rigor-ously tested.

Purpose. To compare the efficacy ofIDET with that of a placebo treatment.

Study Design/Setting. Randomized,placebo-controlled, prospective trial.

Patient Sample. Patients were re-cruited by referral and the media. Noinducements were provided to any pa-tient in order to have them participate.Of 1,360 individuals who were preparedto submit to randomization, 260 werefound potentially eligible after clinicalexamination and 64 became eligibleafter discography. All had discogeniclow back pain lasting longer than 6months, with no comorbidity. Thirty-seven were allocated to IDET and 27 tosham treatment. Both groups weresatisfactorily matched for demographicand clinical features.

Methods. IDET was performed usinga standard protocol, in which the pos-terior anulus of the painful disc washeated to 90 C. Sham therapy con-sisted of introducing a needle onto thedisc and exposing the patient to thesame visual and auditory environmentas for a real procedure. Thirty-two

(85%) of the patients randomized tothe IDET group and 24 (89%) of thoseassigned to the sham group compliedfully with the protocol of the study, andcomplete follow-up data are availablefor all of these patients.

Outcome Measures. The principaloutcome measures were pain and dis-ability, assessed using a visual ana-logue scale for pain, the Short Form(SF)-36, and the Oswestry disabilityscale.

Results. Patients in both groupsexhibited improvements, but meanimprovements in pain, disability anddepression were significantly greaterin the group treated with IDET. Morepatients deteriorated when subjectedto sham treatment, whereas a greaterproportion showed improvements inpain when treated with IDET. Thenumber needed to treat, to achieve75% relief of pain, was five. Whereasapproximately 40% of the patientsachieved greater than 50% relief of theirpain, approximately 50% of the patientsexperienced no appreciable benefit.

Conclusions. Nonspecific factorsassociated with the procedure accountfor a proportion of the apparent efficacyof IDET, but its efficacy cannot beattributed wholly to a placebo effect.The results of this trial cannot be gen-eralized to patients who do not fit thestrict inclusion criteria of this study, butIDET appears to provide worthwhilerelief in a small proportion of strictlydefined patients undergoing this treat-ment for intractable low back pain.

Comment. A minimally invasive in-tervention for the management ofdiscogenic back pain would be veryhandy indeed. The results of the firstplacebo-controlled trial into IDET havethus been eagerly awaited and haveconfirmed that the procedure is supe-rior to placebo intervention. However,it is evident that a large part of the effectis nonspecific and probably just re-lated to “having an intervention”. Theauthors warn that no other surgicalprocedure for discogenic pain has un-dergone placebo-controlled trial andsuggest that this should be compulsorybefore any acceptance as a legitimateintervention. Time will tell whether thedisc replacement surgeons take up thechallenge. – Dr Scott Masters

Journal Abstracts


Yelland MJ, Glasziou PP, Bogduk N,Schluter PJ, McKernon M. Prolo-therapy injections, saline injections,and exercises for chronic low-backpain: a randomized trial. Spine 2004;29(1): 9-16; discussion 16.

Objectives. To assess the efficacyof a prolotherapy injection and exer-cise protocol in the treatment of chronicnonspecific low back pain.

Design. Randomized controlled trialwith two-by-two factorial design, triple-blinded for injection status, and single-blinded for exercise status.

Setting. General practice.Participants. One hundred ten par-

ticipants with nonspecific low-back painof average 14 years duration wererandomized to have repeated prolo-therapy (20% glucose/0.2% ligno-caine) or normal saline injections intotender lumbo-pelvic ligaments andrandomized to perform either flexion/extension exercises or normal activityover 6 months.

Main outcome measures. Pain in-tensity (VAS) and disability scores(Roland-Morris) at 2.5, 4, 6, 12, and 24months.

Results. Follow-up was achieved in96% at 12 months and 80% at 2 years.Ligament injections, with exercises andwith normal activity, resulted in signifi-cant and sustained reductions in painand disability throughout the trial, butno attributable effect was found forprolotherapy injections over saline in-jections or for exercises over normalactivity. At 12 months, the proportionsachieving more than 50% reduction inpain from baseline by injection groupwere glucose-lignocaine: 0.46 versussaline: 0.36. By activity group theseproportions were exercise: 0.41 ver-sus normal activity: 0.39. Correspond-ing proportions for >50% reduction indisability were glucose-lignocaine:0.42, versus saline 0.36 and exercise:0.36, versus normal activity: 0.38.There were no between group differ-ences in any of the above measures.

Conclusions. In chronic nonspe-cific low-back pain, significant andsustained reductions in pain and dis-ability occur with ligament injections,irrespective of the solution injected orthe concurrent use of exercises.

Comment: This study by Michael

Yelland and colleagues from the Uni-versity of Queensland and the Univer-sity of Newcastle found no attributableeffects of the glucose-lignocaine andexercise components of the prolo-therapy treatment.

However, 20% of patients in theprolotherapy group with very persist-ent pain for average duration 14 yearsachieved complete relief from theirpain at 12 months follow-up. Another26% achieved greater than 50% re-duction in pain from baseline. Nine percent achieved zero disability scores.The trend was in favor of prolotherapyfor all measures, but did not reachstatistical significance.

The median of minimal acceptablereductions to make treatment worth-while nominated by patients was 25%for pain and 35% for disability. At 12months, the proportion of all partici-pants who achieved this was 55% forpain, and 54% for disability.

The absence of effect of sagittalloading exercises contrasts with ef-fects seen in other trials of exercise.Sagittal loading has less effect onmuscles such as quadratus lumborumand piriformis, and also otherligamentous and capsular structures,which may be important, and maybenefit from the addition of a rotationalcomponent to the stretching.

The trial’s success rates in treatingpain and disability are at least as goodas reported outcomes for spinal cordstimulation,1 surgery,2 or multidiscip-linary treatment.3

Possible causes of the effects ob-tained include regression to the mean.This is less likely to be an adequateexplanation given the chronicity of thepain, and the fact that trial applicantswith acute exacerbations of their painwere excluded from entry.

The similarity in results between thegroups raises the question of themechanism being a needling effect,independent of any injectant used.

There is evidence that six treatmentsis more effective than the three treat-ments used in the trial by Dechow et al,in which there was no change in meanpain or disability in either group at sixmonths.4 This suggests that the numberof treatments may be very important.The other two randomized, double-blind trials of prolotherapy for chronic

low back pain,5, 6 have utilized sixtreatments, saline and lignocaine con-trols respectively, and initial manipula-tion as a co-intervention.

Possibly there is some cumulativeeffect of the needling treatment, or is itthat the patient with chronic pain isresponding to confident treatment froma caring doctor?

There was a high incidence of tran-sient, minor adverse effects, espe-cially an initial increase in pain andstiffness, headaches, nausea,diarrhea, and other symptoms, sopatients need to be forewarned aboutthese. Interestingly, there was no dif-ference in the incidence of these ad-verse effects between the active treat-ment group and the saline control group,irrespective of allocation to exercise ornormal activity.

1. Turner JA, Loeser JD, Bell KG. Spinalcord stimulation for chronic low back pain:a systematic literature synthesis.Neurosurg 1995; 37: 1088-95.

2. Fritzell P, Hagg O, Wessberg P, et al.2001 Volvo Award Winner in Clinical Stud-ies: Lumbar fusion versus nonsurgical treat-ment for chronic low back pain: a multicenterrandomized controlled trial from the Swed-ish Lumbar Spine Study Group. Spine 2001;26: 2521-32.

3. Guzman J, Esmail R, Karjalainen K, etal. Multidisciplinary rehabilitation for chroniclow back pain: a systematic review. BMJ2001; 322: 1511-16.

4. Dechow E, Davies RK, Carr AJ, et al. Arandomized, double-blind, placebo-control-led trial of sclerosing injections in patientswith chronic low back pain. Rheumatol1999; 38:1255-59.

5. Ongley MJ, Klein RG, Dorman TA, et al.A new approach to the treatment of chroniclow back pain. Lancet 1987; 2: 143-46.

6. Klein RG, Eek BC, Delng WB, et al. Arandomized double-blind trial of dextrose-glucose-phenol injections for chronic lowback pain. J Spinal Disord 1993; 6: 23-33.

- Dr David Roselt

KNEERaynauld J-P, Buckland-Wright C,Ward R, et al. Safety and efficacy oflong-term intraarticular steroid in-jections in osteoarthritis of the knee:

Journal Abstracts

May 2004 55

a randomized, double-blind, pla-cebo-controlled trial. ArthritisRheum 2003; 48 (2): 370-77.

Objective. To evaluate the safetyand efficacy of long-term intraarticular(IA) steroid injections for knee painrelated to osteoarthritis (OA).

Methods. In a randomized, double-blind trial, 68 patients with OA of theknee received IA injections of triamci-nolone acetonide 40 mg (34 patients)or saline (34 patients) into the studyknee every 3 months for up to 2 years.The primary outcome variable wasradiologic progression of joint spacenarrowing of the injected knee after 2years. Measurements of minimum jointspace width were performed by anautomated computerized method onstandardized fluoroscopically guidedradiographs taken with the patient stand-ing and with the knee in a semi-flexedposition. The clinical efficacy meas-ure of primary interest was the painsubscale from the Western Ontarioand McMaster Universities OA Index(WOMAC). Efficacy measures of sec-ondary interest were the total score onthe WOMAC, physician’s global as-sessment, patient’s global assessment,patient’s assessment of pain, range ofmotion (ROM) of the affected knee,and 50-foot walking time. Clinical symp-toms were assessed just before eachinjection.

Results. At the 1-year and 2-yearfollow-up evaluations, no differencewas noted between the two treatmentgroups with respect to loss of jointspace over time. The steroid-injectedknees showed a trend toward greatersymptom improvement, especially at 1year, for the WOMAC pain subscale,night pain, and ROM values (P = 0.05)compared with the saline-injectedknees. Using area under the curveanalyses, knee pain and stiffness weresignificantly improved throughout the2-year study by repeated injections oftriamcinolone acetonide, but not saline(P < 0.05).

Conclusion. Our findings supportthe long-term safety of IA steroid injec-tions for patients with symptomaticknee OA. No deleterious effects of thelong-term administration of IA steroidson the anatomical structure of the kneewere noted. Moreover, long-term treat-ment of knee OA with repeated steroid

injections appears to be clinically ef-fective for the relief of symptoms of thedisease.

Comment: This study from Mon-treal, Quebec, in Canada, is a majorlandmark double blind controlled triallooking at an important intervention forknee pain. Knee OA is a conditioninvolving degradation and repair ofcartilage, bone, and synovium.

There can be secondary compo-nents of inflammation. Clinically thereis gradual onset of pain, stiffness, andloss of joint range of movement. Thereis some evidence from animal modelsof OA to suggest steroids exert protec-tive effects, reducing severity of carti-lage lesions, and the size ofosteophytes.

Pain relief is still a major goal intreatment. There have been concernsthat relieving the pain with steroids maylead to overuse, and aggravate jointand cartilage damage, or lead to tissueatrophy, especially if used repeatedlyas a definitive treatment. Intra-articu-lar steroids have been used for morethan 40 years, but some clinicianshave restricted their use to when obvi-ous joint effusion is present, for fear ofside-effects.

Published studies on long-term ef-fects have been missing, with moststudies restricted to follow-up of onlyseveral weeks. This is despite the factin vitro and in vivo studies in experi-mental models have shown a reductionin progression of structural damage.

This important two-year, double blind,saline controlled study showed long-term injections of IA steroids over twoyears did not have a deleterious effecton knee anatomy. A strong trend to-wards greater clinical improvement inthe IA group was shown over normalsaline. The difference was statisticallysignificant for pain and stiffness whenarea under the curve (AUC) analysiswas made. It is more appropriate forcapturing long-term differences in ef-ficacy between the groups. RepeatedIA injections of steroid for pain reliefwere not associated with accelerateddisease progression, and appear to besafe. There were no infections or acuteflares following steroid injections in thisstudy. - Dr David Roselt

Journal Abstracts

Arroll B, Goodyear-Smith F. Corti-costeroid injections for osteo-arthritis of the knee: meta-analysis.BMJ 2004; 328: 869-73.

Objectives. To determine the effi-cacy of intra-articular corticosteroidinjections for osteoarthritis of the kneeand to identify numbers needed totreat.

Data sources. Cochrane controlledtrials register, Medline (1966 to 2003),Embase (1980 to 2003), handsearches, and contact with authors.

Inclusion criteria. Randomized con-trolled trial in which the efficacy ofintra-articular corticosteroid injectionsfor osteoarthritis of the knee could beascertained.

Results. In high quality studies, thepooled relative risk for improvement insymptoms of osteoarthritis of the kneeat 16-24 weeks after intra-articularcorticosteroid injections was 2.09 (95%confidence interval 1.2 to 3.7) and thenumber needed to treat was 4.4. Thepooled relative risk for improvement upto two weeks after injections was 1.66(1.37 to 2.0). In the statistically signifi-cant studies the numbers needed totreat to get one improvement was 1.3 to3.5 patients.

Conclusion. Evidence supports shortterm (up to two weeks) improvement insymptoms of osteoarthritis of the kneeafter intra-articular corticosteroid in-jection. Significant improvement wasalso shown in the only methodologi-cally sound studies addressing longerterm response (16-24 weeks). A doseequivalent to 50 mg of prednisone maybe needed to show benefit at 16-24weeks.

Comment: This important meta-analysis comes from the Departmentof General Practice and Primary HealthCare, University of Auckland, and ishot off the press. Ten per cent ofpeople in Western Europe aged 55 orover will have painful disablingosteoarthritis (OA) of the knee, with aquarter being severely disabled. Simi-lar figures are likely to apply in Aus-tralia. Without joint replacement, treat-ment aims include pain relief and im-provement of function. This is the firstmeta-analysis looking at this topic, andthe first to show benefits of such injec-tions in improvement of symptoms ex-


tending beyond 16 weeks. Trials haveoften used one injection at low dose inthe past. The authors also felt thatsubjective pain scales may be an in-sensitive outcome measure in this set-ting. They felt that improvement insymptoms was a better measure thanincreases in range of movement orpain reduction.

The study highlights the therapeuticutility of this approach with low clini-cally significant numbers needed totreat, and validates this conservativeoffice-based treatment approach thatmay have been underutilized to date. Itincluded the study of Raynauld et al1

that showed preservation of joint spaceat two years. Overall, no important sideeffects were encountered in the trialsother than transient redness and dis-comfort.

The studies were small; however,statistical significance was achieved.The authors went to great lengths toidentify all available research to mini-mize the impact of possible publicationbias, where negative trials are notpublished, possibly leading to overes-timation of positive benefits.

The evidence suggests that a dose of20 mg of triamcinolone, which is equiva-lent to 25 mg of prednisolone, wasefficacious in terms of pain control attwo weeks. The only study using 40 mgwith injections repeated every threemonths found benefit for night pain andstiffness at 24 months based on areaunder the curve analysis.1 This sug-gests doses of 50 mg equivalent ofprednisolone is needed to obtain ben-efit out to 16-24 weeks. No evidence todate supports promotion of diseaseprogression by corticosteroid use.

One study found predicting benefitwas not possible.2 Another found thatif synovial fluid could be aspirated,there was a better response.3 Thisoccurred only in the intervention grouphowever, so it was not just a differencein the accuracy of needle placement,and suggests increased efficacy whenclear evidence of synovitis and inflam-mation is present. The use of jointlavage in addition to corticosteroidinjection probably warrants furtherstudy.

1. Raynauld J, Buckland-Wright C, WardR, et al. Safety and efficacy of long-termintra-articular steroid injections in

Journal Abstracts

osteoarthritis of the knee. Arth Rheum2003; 48: 370-77.

2. Jones A, Doherty M. Intra-articularcorticosteroids are effective in osteoarthritisbut there are no clinical predictors of re-sponse. Ann Rheum Dis 1996; 55: 829-32.

3. Gaffney K, Ledingham J, Perry JD. Intra-articular triamcinolone hexacetamide inknee osteoarthritis: factors influencing theclinical response. Ann Rheum Dis 1995;54: 379-81.

- Dr David Roselt

Bachmann LM, Haberzeth S, SteurerJ, ter Riet G. The accuracy of theOttawa knee rule to rule out kneefractures: a systematic review. AnnIntern Med 2004; 140 (2): 121- 24.

Background. The Ottawa knee rule isa clinical decision aid that helps ruleout fractures and avoid unnecessaryradiography.

Purpose. To summarize evidence aboutthe accuracy of the Ottawa knee rule.

Data Sources. Relevant English- andnon-English-language articles wereidentified from PreMEDLINE andMEDLINE (1966-2003), EMBASE(1980-2003), CINAHL (1982-2003),BIOSIS (1990-2003), the CochraneLibrary (2002, Issue 3), the ScienceCitation Index database, reference listsof included studies, and experts.

Study Selection. Articles were in-cluded if they reported enough infor-mation to determine the sensitivity andspecificity of the Ottawa knee rule fordetecting fractures confirmed eitherradiologically or in combination withfollow-up.

Data Extraction. Two reviewers in-dependently extracted data on studysamples, the ways that the Ottawa kneerule was used, and methodologicalcharacteristics of studies.

Data Synthesis. Of 11 identifiedstudies, 6 involving 4249 adult patientswere considered appropriate for pooledanalysis. The pooled negative likeli-hood ratio was 0.05 (95% CI, 0.02 to0.23), the pooled sensitivity was 98.5%(CI, 93.2% to 100%), and the pooledspecificity was 48.6% (CI, 43.4% to51.0%).

Conclusion. A negative result on anOttawa knee rule test accurately ex-cluded knee fractures after acute knee

injury. However, because the rule iscalibrated toward 100% sensitivity andactual fracture prevalence is usuallylow, large-scale, multi-centered stud-ies are still needed to establish thecost-effectiveness of routinely imple-menting the rule.

Comment: This systematic review isfrom Zurich University, Switzerland.

The Ottawa knee rule, developed in1995 by Stiell et al, has been validatedin several clinical settings, and 1 con-sists of five “yes-no” items, asking1. Is the patient 55 years or older?2. Is there isolated tenderness of the

patella?3. Is there tenderness of the head of

the fibula?4. Is there inability to flex the knee to

90 degrees?5. Is there inability to bear weight,

both immediately, and in the emer-gency department, for four steps?

Patients with at least one positiveanswer are considered to have posi-tive indication of knee fracture, andradiology is advised. There is evi-dence that an all-negative answer ishighly effective in excluding fracture,without having to resort to unneces-sary radiology, which is the purpose ofthe exercise. Even modest values forspecificity can markedly reduce thenumber of unnecessary radiographs.The threshold for the Ottawa knee ruleis calibrated towards very high sensi-tivity to avoid false negatives and missedfractures. There will still be a substan-tial proportion of false positives, whichwill be excluded by plain radiographyor CT if indicated which remains thecriterion standard for diagnosing bonyfractures.

The pooled negative likelihood ratiowas 0.05% (CI, 0.02 to 0.23) in adults.The study in children found a negativelikelihood ratio of 0.16 (CI, 0.02 to1.04). In the studies assessing theOttawa knee rule in adults, the prob-ability of fracture after a negative testresult, assuming a fracture prevalenceof 7%, based on previous studies, was0.37% (CI, 0.15% to 1.48%).

In children, the probability was 2%(CI, 0.3% to 12%); hence the ruleshould not be relied on here.

The authors suggest there is stillneed for more validation studies, and

May 2004 57

then an independent replication of theprevious cost-effectiveness study.

Most knee injuries result from a di-rect blow, a fall, or a twisting injury.Blows and falls, blunt injuries, accountfor 25% of knee injuries, but more than80% of all knee fractures.2 The inci-dence of fracture after a blunt injury isfour times higher than with a twistinginjury, so injury mechanism has somepredictive value, but was not consid-ered by most of the studies examinedby this review.2

1. Stiell IG, Greenberg GH, Wells GA, et al.Derivation of a decision rule for the use ofradiography in acute knee injuries. AnnEmerg Med 1995; 26: 405-13.

2. Expert Panel on Musculoskeletal Imaging.American College of Radiology ACR Ap-propriateness Criteria. Acute Trauma tothe Knee. Accessed at www.acr.org/dyna/?id=apperit&pdf=0365-374_acute_trauma_to_knee_ac on 22 August 2003.

- Dr David Roselt

Journal Abstracts


(Editor’s Note: The following documenthas been edited from a PowerPointpresentation given by the chairman ofthe Education Committee to the Gen-eral Assembly at Montreux, Switzer-land. Any unintentional misunderstand-ing or any errors of interpretation arethe sole responsibility of the Secre-tary-General.)

This is not a long report, al-though it is pleasing to statethat the Education Commit-

tee has never been better prepared toset prioritized goals and reach them.We are pleased with the standard ofthe work achieved and the effort under-taken by all committee members.

Members of the Education Commit-tee, September 2002Marcus Hanna (Austria), vice-chairmanAssisted by Prof Hans TilscherGuido Brugnoni (Italy)Egon Frolich (Germany)Prof Joan Garcia Alsina (Spain)Marc-Henri Gauchat (Switzerland)Prof Michael Kuchera (USA)Jukka Manevaara (Finland)John Tanner (UK)Marie Jose Tessandier (France)Assisted by Jean Yves MaigneProf Norm Broadhurst (Australia/NewZealand)Glen Gorm Rasmussen, chairman

Changes to the committee occurredin the summer of 2003 as follows:Massino Groppi (Italy) replaced GuidoBrugnoni; Matthias Psczolla (Germany)replaced Egon Frolich; Jehan Lecocq(France) replaced Marie JoseTessandier.

As chairman I would like to thankthose retiring for their diligent work andcontribution to the Education Commit-tee of the FIMM.

The year in general had both goodand bad aspects. Good news: not toomuch money spent. Bad news: too littlework done.

Unfortunately it costs a lot of moneyfor workshops and the ultimate pro-gression of goals is reached through

the combined aspects of the work-shops. With limited finances the speedof reaching goals is unfortunately slow.

During the year a subcommittee wasestablished to review both the glossaryand the inventory. The importance ofdefinite terms has been emphasisedby Scientific Chairman Jacob Patijn.Those serving on the subcommittee onthe Glossary are Michael Kuchera,Jehan Lecocq, Matthia Psczolla, JoanGarcia Alsina.

Planning of EC program for comingyear• Revision of strategy and long-range

aims of the EC• Redefining future tasks• Further development of Masters

course• Interactive internet working groups• Hands-on workshops on diagnos-

tic and therapeutic procedures• Defining tasks for Scientific Com-

mittee essential to the EC• Implementing results from the SC

into the education programs• Further work on glossary/inventory

– inventory of diagnostic and thera-peutic procedures, including reli-ability and validity.

• Definition of manipulable lesion• Co-operation with SC in establish-

ing the Academy• CD Rom edition of tests and tech-

niques

Budget problems for the Educa-tion Committee

The last workshop in Vienna 2002had expenses of CHF 12,314 and thebudget for EC 2002/3 was CHF 8,000.

The lowest cost for a workshop inBratislava 2003 was estimated to beCHF 12,000. Following discussion withthe president and treasurer, this work-shop was cancelled.

The estimated budget for the 2004EC function is about CHF 20,000. There-fore, a workshop may not be possible.

Costs for mini-meetings, internetactivities, and co-ordination functionsestimated to be CHF 10,000.

Planning of the EC for 2003• No workshop was possible• President of FIMM together with

the SC chairman and the EC chair-man met in Amsterdam, June 20-21, for revision of strategy.

• Following the meeting the EC mem-bers requested for their opinion onthe future tools and goals of thecommittee.

• Much more work to be done viaemail and later blackboard/chat onthe internet.

• Propositions were sent out to ECmembers:• Further work on the FIMM Glos-

sary with translation into differ-ent languages

• Second and improved curricu-lum of the basic EducationCourse (300 hours)

• Planning a Master’s Degree(eventually a joint venture withuniversities)

• Collection of programs from thedifferent schools via internet

• Preparing intervention for the dif-ferent schools to participate withposters and workshops at theFIMM Congress in Bratislava,September 2004

• Further development of the in-ternational exchange program

• Inventory of diagnostic tests andtherapeutic techniques, includ-ing CD Rom and video

• Definition of segmental dysfunc-tion/manipulable lesions

• Definition of manual/muscu-loskeletal medicine educationon diagnostic and therapeuticstrategies

• Establishing instructionalcourse on reproducibility by theSC

• A request for any other informa-tion from EC members

Results of questionnaire• Glossary subcommittee (four-lan-

guage presentation)• Inventories to include video/CD Rom• Improved version of curriculum• Collection of various national pro-

Education Committee ReportMontreux, September, 2004

Dr Glen Gorm Rasmussen, Chairman Education Committee

May 2004 59

grams• Definition of segmental dysfunc-

tion/manipulable lesion• Definition of manual/musculoskel-

etal lesion• Masters degree• Diagnostic/therapeutic strategies• Instructional course on reproduc-

ibility• Posters/workshops in Bratislava

There were two negative responses:1. Defining of segmental dysfunction2. Reworking the curriculum

Therefore, it was decided to set upworkshops on the positives.

What FIMM needsResearchEducationOrganizationMoney

Optimal working conditionsOne meeting of EC per yearActive working groupsSociety assistance

Top PriorityBasic curriculumAdvanced curriculumUniversity/Masters degreeEBM attitude orientated educationGlossary and definitionsActive participation of EC and Societyschools in Bratislava

ConclusionI wish to thank my colleagues and

friends in the EC for all of the enthusi-asm and hard work that they haveundertaken. Special thanks go to JacobPatijn of the SC for his ongoing adviceand help.

It is the aim of the EC to make alleducation in manual/musculoskeletalmedicine evidence based and to workwith the SC to produce a spinal coursefor reproducibility.

Our ultimate aim is to have a univer-sity-based Masters degree.

Education Committee Report


The past year has been anextremely busy one for me inmy role as secretary-general

of the FIMM. I have a number of itemsto report and some observations for theGeneral Assembly. The very size androle of the FIMM is changing. Indeed,the basis of these changes will have abearing on the future role of the secre-tary-general’s office. All the executiveofficers of FIMM will also have an evolv-ing and changing role, one which willrequire more devotion of time and ef-fort. Therefore, I intend to divide thisstatement into two parts, one concern-ing what has occurred in the past yearand the other about changes I seeoccurring in the office of secretary-general.

At the outset I would like to thank ourpresident, Bernard Terrier, for all hishelp, and also my deputy, MichelDedee. They have each given me sup-port and have been vital in the produc-tion of the FIMM News. Any office in anorganization like the FIMM has to beone of team management. With aninternational group of this magnitude,the singular role of the individual is farless important than the total teamapproach. To advance M/MSM in theinternational arena requires cohesionand a common direction. There remaindifferences in philosophy betweenmember nations and a unified approachis required to overcome obstacles thatare present or may arise, just throughbeing associated. Simply, the wayforward must be by a universal evi-dence-based scientific approach. Inthe evolving world of medicine, pastdogma is justifiably dead.

Year achievementsNew membersNew applicantsCommunication with member socie-tiesUp-dating society executive addressesFIMM NewsletterDistribution of FIMM research materialSwiss society back-up office

A brief summary of each of these

Secretary-General AGM Address, 2003Montreux, Switzerland

achievements is listed.New members

South Korea and Canada have beenwelcome as new FIMM member soci-eties.

I have had good contact with theirexecutive Board and look forward toeven better inter-medical contact in thefuture. There is little point in havingmember nations if we cannot worktogether.

South Korea has made a proposalthat will be discussed during the courseof this AGM.

New applicantsJapan and Bulgaria have indicated

that they wish to join FIMM. It is goodto see an expansion of FIMM and evenbetter to see contact with Asia. I havehad a chance to review some materialfrom Japan and can say that theirsociety appears well advanced in botheducation and science associated withM/MSM. Likewise, I have had goodemail communication with Bulgaria.

Communication with member so-cieties

Every effort to contact all membersocieties of the FIMM has been under-taken. This has not always been suc-cessful. I have tried to reach eachmember society and advise them ofhow the FIMM is trying to liaise betterwith members. The FIMM newsletterhas been sent to most members. Ihave offered all member societies thechance of asking the FIMM executivefor help in training their own members,have offered to advertise their societyconferences, and indeed advertise anyeducational programs they run. Theaccent has been placed on the FIMMbeing present to help if required.

Updating society executive ad-dresses

This has been extremely difficultbecause of changes in positions andaddresses of their executive officers.The FIMM has not been notified inmost cases and tracking down the newdetails has been difficult. In fact, it took

me 11 months of writing, emailing,phoning, and annoying my colleaguesfor details. This work would not havebeen necessary had member societyexecutives let me know of their elec-tion results and any changes in ad-dress contact. Yes, I am complaining,but as a parent society the FIMMcannot function adequately withoutthese details. Remember, the FIMM isyour society. I am only doing the jobyou have given me and co-operationmust be reciprocal.

FIMM newsletterThis year the newsletter was pro-

duced for the first time. The aim of thenewsletter is to give better communi-cation to all members and to be aformat for providing information thatarises from the EC and SC. It couldbecome a vehicle for publishing scien-tific work that arises from the proposedAcademy. We will try to advertisemember society coming events com-pletely free of charge. In addition itwould be useful to list member websiteaddresses. The FIMM newsletter isnot designed to mirror image the FIMMNews and should be seen as a helpfuladdition to what the FIMM is trying todo in regard to better communicationwith all member societies. You arerequested to forward me any materialthat your society would care to havepublished.

Distribution of FIMM research ma-terial

All members of the SC have beenrequested to publish in their own Soci-ety journals work that originates fromthe SC. Richard Ellis is doing a fine jobin achieving this through the Journal ofOrthopaedic Medicine. As secretary-general I have forwarded considerablematerial to some member societies.We also have continual coverage inAustralasian Musculoskeletal Medi-cine. Further material is published inthe FIMM newsletter. The office ofsecretary-general now has a signifi-cant role to play in communication, afield not previously developed to its full

Ron Palmer, Secretary-General FIMM, September 2003, Montreux

May 2004 61

potential. This role will continue toexpand in the future.

Swiss society back-up officeThe office of secretary-general is

vital for the proper functioning of theFIMM and, for that matter, any largeinternational society. It should be ap-parent to all that in the event of injury ordeath, there would be confusion in a“hand-over” and both valuable informa-tion and time would be lost. It would befoolish to think any individual couldefficiently manage any executive officealone. On this basis there has been aneffort to establish a back-up office toensure these problems do not arise.Fortunately, our president has agreedand gratefully the Swiss society hasundertaken this role. All relevant mate-rial I email to Bernard Terrier and hethen passes this on to the Swiss soci-ety. It is my opinion that this practiceshould continue in the future.

Future developmentFunctional changes have already

taken place in the office of the secre-tary-general. These changes in thisrole will continue. I wish to reflect onthis matter as I see it as a hugedeveloping problem in the future.

The lack of time is the prime problem.I have no idea how anyone in a full-timemedical practice could possibly de-vote sufficient time to this job and stillhold his family together and run a full-time medical position. I speak fromconsiderable experience after one yearin this office.

As you are all aware, I was involvedin a serious accident that effectivelyhalted my private practice and teach-ing career. These very factors haveenabled me to find the time to devote tothe role of secretary-general. A con-servative estimate would be 15 hours aweek spent on FIMM work, a little morewhen publishing the FIMM News andthe newsletter. This does not take intoaccount time for research work withthe Scientific Committee.

I foresee a management problemwith running the proposed Academyfor the same basic reasons. It will beimpossible to devote the time neededto function effectively. Any internationalsociety, or for that matter, any largeindustrial company, would have ex-

actly the same strategic problems. Anexample is the Australian Medical As-sociation. It has 34,000 members,about the same size as the FIMM butwithout the multinational connectionsand the widely differing views held bythose members. Here there is a full-time secretarial staff and paid officials.

I see the role of secretary-generalbecoming a paid full-time position. Itwould also incorporate managing theday-to-day functions of the Academy.These changes may take time to evolve;yet we should all be aware that it isgoing to happen.

Any international organization of thissize cannot effectively function withoutproper management. Lack of timemeans that no individual can hold downa medical position and then devotesufficient time to the FIMM activities toallow the society to run both effectivelyand smoothly. This of course meansthere has to be a change in the finan-cial side of the FIMM. I am aware thatmany would prefer to disregard thesethoughts. Burying your head in thesand will not make the matter passaway. I am aware that these are mat-ters for the FIMM executive to solve.However, I raise these points now forI personally have been faced with suchproblems, even though I am effectivelynot in practice. The role of secretary-general must continue to expand andtherefore the position will become un-tenable if its current situation contin-ues.

I have raised these points for you tothink about. I consider it part of myelected position to bring to your atten-tion problems that can occur. I thank theGeneral Assembly for appointing me assecretary-general and I hope that I cancontinue to serve you well for the re-mainder of my term.

Secretary-General AGM Address, 2003


Dr John Martin Bosler, ofTamworth, was one of the“founding fathers” of the

Australian Association of Musculoskel-etal Medicine, and was president of theAssociation from 1979 to 1983.

Many of our members will hold fondmemories of him, and of his work forthe Association.

Born in 1927 in Manly to parentsWinifred and Wilfred Bosler, Johnwas an active boy who joined the localScouts Brigade at age seven, and hada lifelong association with the move-ment. He married Joy Gregory in 1952.

John graduated in medicine from theUniversity of Sydney in 1953. Afterthree years as a resident and locum,he settled in Tamworth in 1956. He wasto practise there for the next 48 years,initially in general practice.

He was appointed an honorary sur-geon at Tamworth Base Hospital in1956, and honorary medical officer(surgeon) at that hospital in 1958.

In 1968, John was in a three-manpractice with Drs Doug Harbison andPeter Wakeford. Two would work whilethe third would take it in turn to traveloverseas pursuing their respectivemedical interests.

After four months’ study under DrJames Cyriax at St Thomas’s Hospital,London, that year, John returned andworked as a specialist in musculoskel-etal and manipulative medicine.

He went to congresses in Salzburg,Tokyo (presiding over the 6th ses-sion), Prague, Copenhagen, BadenBaden, Rotarua, and Zurich. He wasfortunate to be able to take the wholefamily along in 1968 and 1977. He alsopresented papers to numerous meet-ings of medical practitioners in variousstates of the Commonwealth of Aus-tralia.

He was appointed honorary medicalofficer (physical medicine) in 1970,honorary physician in physical medi-cine in 1974, and visiting physician inphysical medicine in 1978 at TamworthBase Hospital. In fact, he gave over 45years of service at the Tamworth BaseHospital. He was president of the North-ern District Medical Association for atime.

John was a long-standing member of

the Australian Association of Muscu-loskeletal Medicine (AAMM). He waschairman of the Committee for Re-search and Teaching for the Associa-tion from 1978 to 1983, and presidentof the Association for the years 1979to 1983. He was also a member of theBritish Association of ManipulativeMedicine, and a member of the Aus-tralian Rheumatism Association.

He was appointed specialist exam-iner for the Australian GovernmentHealth Service of the CommonwealthDepartment of Human Services andHealth, and for the CommonwealthDepartment of Veterans’ Affairs.

He was a lecturer on back pain forthe Barwon Division of General Prac-tice.

He was appointed medical refereefor the Medical Journal of Australia in1983, and presented papers at variousinternational conferences relating tophysical medicine and back pain.

He attended the Second Interdisci-plinary World Congress on Low BackPain in San Diego, USA, in November1995; the annual scientific meeting ofthe Australian Pain Society in the AyersRock Resort, NT, in April 1997; theannual scientific meeting of the AAMMon Low Back Pain in General Practicein Melbourne, Victoria, in August 1997;the 12th Triennial World Congress ofthe International Federation of Muscu-loskeletal Medicine (FIMM) atBroadbeach, Queensland, in April1998; the Third Interdisciplinary WorldCongress on Low Back and PelvicPain in Vienna, Austria, in November,1998; and the annual scientific meet-ing of the Australian Pain Society inMelbourne, Victoria, in March 2000.

As well as devoting himself to hispractice and the wider medical frater-nity, John was heavily involved with thecommunity of Tamworth, particularlySt John’s Church Tamworth, Rotary,and the Scouting Association.

John was featured in the WeekendMagazine of the local paper on Satur-day, December 6, 2003, with the head-ing “Pioneer doctor hangs up his shin-gle”.

John had planned to finally retirefrom his practice on December 12,2003, on his seventy-sixth birthday. He

was looking forward to spending moretime with his family in retirement, andespecially his grandchildren, Emilyand Nicholas Rose. John used to enjoyspending time at the Barrington Re-serve each year with his extendedfamily, and Christmas turn about inSydney and Tamworth.

However, tests revealed severe coro-nary occlusion, necessitating majorcardiac surgery in Sydney on Decem-ber 5, 2003. Although the surgery wasinitially successful, complications ledto John’s sudden death on ChristmasEve 2003.

He is survived by his wife, Joy, andhis children, Greg Bosler and DianaRose, and Adrian and Lez.

He will be sadly missed by all whoknew him.

- David Roselt

Vale Dr John Martin BoslerMB BS 1953 University of Sydney

May 2004 63

This meeting over four days insunny Canberra in early au-tumn was a coming together

of many groups and individuals treat-ing pain, the common foe. Rehabilita-tion and pain medicine specialistGeoffrey Speldewinde, the conferenceconvener, and the organizing commit-tee did a superb job in organizing theevent. They were ably assisted byconference secretariat, DC Confer-ences Pty Ltd, well known to AAMM.Geoffrey is a member of AAMM and aFellow of the AFMM. The meeting waswell sponsored by many companies,including Pfizer Australia, Allergan,Elsevier Australia, and Medtronic, toname but a few. Boots HealthcareAustralia was an important source ofexcellent coffee during the meeting.

Principal speakers included FabrizioBenedetti, who spoke about his re-search into the placebo effect. C Rich-ard Chapman, this year’s SunderlandLecturer, spoke about suffering, andthe emotional dimensions of pain, andits behavioral manifestations. ThomasGraven-Nielsen spoke on muscle painwith respect to referred pain and deeptissue hyperalgesia. Lorimer Mosley,this year’s Bonica Lecturer, from thePhysiotherapy Department at the Uni-versity of Queensland, spoke aboutpain and motor control.

My conference started with me jet-ting into Canberra late Sunday on awarm Canberra morning. I went to apre-conference workshop onneuromodulation in pain medicine,sponsored by Medtronic. This wasinteresting, with a lively talk by USneurosurgeon Ken Alo on his practiceand approach to pain management.

He was joined in the discussion byluminaries from the Australian painscene. Spinal cord stimulation is usedto control pain mediated by the spinalcord, irrespective of origin.1 It involvesthe introduction of electrodes into theepidural space. Neurosurgeons tendto use larger devices, implanted usingan open procedure. Anaesthetists use

Conference ReportPain in the Post-Modern Era: Keeping Pain Man-agement Relevant25th Annual Scientific Meeting of the Australian Pain Society, 7-10 March 2004, National Convention Centre,Canberra, ACT, Australia

epidural catheters for placement. Acurrent is delivered from an implantedstimulator that inhibits the pain percep-tion by induction of tingling in the areawhere the pain is felt. There are nocontrolled studies to date, but a sys-tematic review has been performedusing observational data.2

The day was rounded off by thewelcome reception at the NationalConvention Centre, then the musicalsoiree at a nearby hotel, where somememorable performances ensued.

A solid plenary session then concur-rent sessions on Monday morning waswell sustained by coffee and refresh-ments at the breaks, when the tradedisplays were vigorously supported.Networking and interaction with col-leagues and acquaintances old andnew was a prominent feature of theproceedings. Different practices andapproaches were canvassed, and strat-egies advanced. Possible journal arti-cles presented themselves. Lunch wasprovided on the three full days, andproved to be most convivial.

Monday concluded with a night onthe Tarago Express, which featured adinner dance with good food and wine,and much social interaction. The 1940sRailway Historical Society diesel-hauled train travelled to Tarago throughthe scenic Molongo Gorge. Wildlife,including birdlife and local kangaroos,were of interest, especially to overseasguests. Dessert was served on thereturn journey, supplemented by moredeep and meaningful discussion aboutlife in general.

The conference continued at a crack-ing pace on Tuesday opening with abrief history session from Chair Pro-fessor Tess Cramond introducing theSutherland Lecture.

Musculoskeletal medicine was wellrepresented by a topical concurrentsession after lunch chaired by JayGovind. Michael Yelland discussedhis randomized controlled trial of pro-lotherapy and exercise for chronic lowback pain published in Spine in Janu-

ary 2004. This is the basis of hiscurrent PhD thesis. Victor Wilk pro-vided a stimulating discourse on realoutcome measures for assessing suc-cess in treating musculoskeletal pain.Patients want pain relief, rather than tobe told to accept pain. The importanceof long-term follow-up was highlighted.Wade King outlined the evidence basefor the management of shoulder pain,acute and chronic. There is now asubstantial body of Level I and Level IIevidence on the methods used in thediagnosis and treatment of shoulderpain. Systematic reviews andrandomized, controlled trials have high-lighted the reliability, validity, and effi-cacy of current practices, endorsedby the recent NHMRC guidelines: http://www.nhmrc.gov.au/publications/synopses/cp94syn.htm

Many currently used practices arenot supported by the evidence base.There is often a clear difference be-tween assumed utility of common prac-tices and the results of Level I and LevelII studies, with respect to both diagno-sis and treatment of shoulder pain.

Other musculoskeletal pain medi-cine colleagues in attendance at themeeting included Geoff Speldewinde,Steve Jensen, Phillip Giles, AlexGanora, KE Khor, Susie Lord, TimMcCarthy, John Bastian, MichaelCreswick, Roger Watson, and GireshKanji from NZ. John Rosenthal, RajSundaraj, his daughter physiothera-pist Shona, and Milana Votrubec werealso in attendance.

The AGM business meeting filled inWednesday afternoon after afternoontea.

The gala dinner with three coursedinner and fine wines concluded theday, and was held in the Grand En-trance Hall at the impressive NationalMuseum of Australia from 7 pm. TheHorizons, Tangled Destinies, and Eter-nal Galleries were open exclusively forAPS Conference Delegates from 7 pmto 8 pm, after pre-dinner drinks. Amusculoskeletal pain medicine table


was procured and convened, andthought-provoking discussion ensued.Delegates then danced to the 10-pieceBig Brass Groove into the night. Agreat night was had by all.

Wednesday continued in similar vein.A plenary session on peripheral andcentral sensitization in musculoskel-etal pain by Thomas Graven-Nielsenwas followed by the Bonica Lecture,and an APRA PhD scholarship pres-entation on the analgesic properties ofalphadolone by Lara Winter fromMonash University.

Geoffrey Speldewinde then spokeeloquently on the role of reductionismin the treatment of chronic cervicalspinal pain. Jay Govind followed withprecision diagnosis and treatment forchronic lumbar spinal pain, furtherraising the profile of musculoskeletalpain medicine in this important forumwith another spell-binding presenta-tion.

Morning tea included a sub-commit-tee meeting to discuss the future AAMMAnnual Scientific Meeting planned forMarch 3-6, 2005, at Twin Waters,Sunshine Coast, Queensland. Chair-man Nell Karpin from DC ConferencesPty Ltd officiated. Other attendeesincluded Steve Jensen, Victor Wilk,Michael Yelland, and me.

The day was rounded out by freepapers after morning tea, then lunch,followed by more interesting topicalconcurrent sessions, and a plenarysession on the possible emerging roleof cannabinoids in pain management.

Unfortunately I had to leave early duringthis session to get the jet for home.

But it was followed by panel discus-sion, awards including prizes for thebest poster presentation, and plans forSydney 2005.

It was a brilliant meeting, and I’dthoroughly recommend attending thenext one.

The 26th Annual Scientific Meeting ofthe Australian Pain Society will be heldin Sydney in August 2005. It will be heldin conjunction with the InternationalAssociation for the Study of Pain(IASP) 11th World Congress on Pain,August 21-26, 2005, and should bewell worth attending, so mark it in yourdiaries, and keep the time free:

www.iasp-pain.org/05Cong.html.

References1. Bogduk N, McGuirk B. Pain Re-search and Clinical Management, Vol.13. Medical Management of Acuteand Chronic Low Back Pain. An Evi-dence-Based Approach. Elsevier Sci-ence, 2002

2. Turner JA, Loeser JD, Bell KG.Spinal cord stimulation for chronic lowback pain: a systematic literature syn-thesis. Neurosurgery 1995; 37: 1088-96.

- David Roselt

Conference Report

May 2004 65

The 33rd Annual Scientific Meet-ing (ASM) of the AustralianAssociation of Musculoskel-

etal Medicine (AAMM) had the themeof “A Pain in the Neck”. The two-dayscientific conference examined evi-dence-based medical research intoneck pain and associated disorders.The program followed the previouslypopular format of morning lectures andafternoon practical “hands-on” work-shops.

The results of the evaluation ques-tionnaires of the two-day AAMM ASMreveal that the plenary sessions andworkshops were rated as at least goodby an overwhelming majority ofattendees. The vast majority ofattendees were of the opinion that atthis year’s ASM, we reasonably metthe conference objectives, namely:• To improve assessment of neck

pain and whiplash-associated dis-orders

• To be able to differentiatecervicogenic headache from otherforms of headache

• To gain a better understanding ofhow to manage complex pain prob-lems

• To learn new injection techniques.A major criticism of the 2002 ASM

was that the time for open discussionwas too limited. This issue was activelyaddressed in the planning of this year’sASM, and so it was pleasing for theorganising committee to receive posi-tive feedback in this regard, formalisedin the written comments from someattendees in terms of “good discus-sion”.

AAMM remains a primary-care-based organisation, in contrast to theAustralasian Faculty of Musculoskel-etal Medicine, which is for those whowant to make musculoskeletal medi-cine their practising specialty, ratherthan just a special interest area. Basedon this premise, the major goal of theASM of the AAMM and its associatedworkshops over the years has been toteach and upgrade general practition-ers’ practical skills in musculoskeletalmedicine, including physical exami-

Conference ReportAustralian Association of Musculoskeletal Medicine 33rd An-nual Scientific Meeting, Sydney 27 – 30 November 2003

nation, and management techniques,such as manual therapy and injectiontechniques.

This year’s workshops covered theseareas well, with a beginner’s basicmanual therapy workshop run byMichael Cheswick, and for the moreadvanced, a counter-strain workshoprun by Philip Watson. Injections werewell covered by a prolotherapy work-shop, including use of cadavers tocover the practical aspects of thistechnique, run by Michael Yelland.The more theoretical aspects of inter-ventions with injections were admira-bly covered by David Vivian. Roundingoff the workshop aspect of the ASMprogram was a CBT/Indahl/Activationworkshop run by Scott Masters, RobertGassin, and Geoff Harding.

The lecture program was also wellreceived. The topics were diverse andinteresting – from presentation of theNHMRC guidelines for acute cervicalpain, in Nik Bogduk’s inimitable andentertaining style, to the revolutionarysurgical technique of cervical discreplacement surgery, presented byLali Sekhon. For my own part, it isalways a bonus to come away with afew pearls to use on return to myclinical practice. Les Barnsley’s pres-entation of acromioclavicular and ster-noclavicular joint pain referral patternsproximally to the neck fitted this billperfectly.

Backing onto our ASM, on Novem-ber 30, was a multidisciplinary sympo-sium on whiplash and associated dis-orders (WAD), organised primarily bythe Australian Physiotherapy Asso-ciation, with the organising committeealso comprising a representative fromAAMM, and also the Chiropractic andOsteopathic Council of Australia, andthe Faculty of Rehabilitation Physi-cians. Our ASM attendees were stronglyencouraged to attend this seminar aswell, and 68 did so.

Personally, I found the plenary ses-sions of this program interesting andsound. Nik Bogduk presented his verycompelling research pertaining to cer-vical zygapophysial joint pain diagno-

sis and treatment with radiofrequencymedial branch neurotomy, whichAAMM members are all familiar with.Gwen Jull is another familiar name toall those who follow the research in thisarea. Her presentation suggested thatthose with WAD and abnormal painprocessing can be detected early, andrequire a different therapeutic regi-men from those without abnormal painprocessing, confirming my own clini-cal impression. Philip Bolton’s work onbasic physiology and the probableinvolvement of the afferent input frommuscle spindles to explain some of theWAD symptoms, such as headache,dizziness, ataxia, and visual distur-bance, was stimulating. For me per-sonally, it was an honour to introduceJim Taylor and his work on the pathol-ogy of whiplash, a presentation worthtravelling across the continent for, ifyou have not heard it before. Speakingpersonally again, I found the breakoutsessions to be a little disappointing intheir scientific content and rigour, andin their presentation.

AAMM is committed to continuing toprovide training in musculoskeletalmedicine skills at its future ASMs, butis also very keen to utilize its teachingresources to run workshops at othertimes, through the divisions of generalpractice. In the past, a major barrier tothis goal has proven to be just gettingour foot in the door of the GP divisions.When we have managed to do so thefeedback from such ventures has beenvery positive. So this is an invitation toall AAMM members to influence theirown GP divisions to secure a slot ontheir educational timetable for muscu-loskeletal up-skilling.

- Dr Steve Jensen


The Red Flag Checklist sum-marizes historical features thatare the best guide to the pos-

sible presence of a “red flag” condition(serious cause, for example, fracture,cancer, infection) in a patient present-ing with acute low back pain. It can beadapted and should be incorporated inthe medical record.

“Red flag” conditions are fortunatelyrare, and best suspected on the basisof history or examination. Minor traumais not a risk factor for fracture unlessosteoporosis is present. This is veryrare under the age of 50 years, and theevidence base suggests patients pre-senting with osteoporotic fractures fromminor trauma are usually much older.Corticosteroid use increases the risk

Name: Low Back PainDOB MRN

Presence of Cardiovascular EndocrineTrauma Y N Risk factors? Y N Corticosteroids? Y NNight Sweats Y N Respiratory MusculoskeletalRecent Surgery Y N Cough? Y N Pain elsewhere? Y NCatheterization Y N Urinary NeurologicalVenipuncture Y N Hematuria? Y N Symptoms/signs Y NOccupational exposure Y N Retention? Y N SkinHobby exposure Y N Stream problems? Y N Infections? Y NSporting exposure Y N Reproductive Rashes? Y N(Overseas) travel Y N Menstrual problems? Y N G/TIllicit drug use Y N Haemopoietic Diarrhoea? Y NWeight loss Y N Problems? Y NHistory of Cancer Y NComments Signature:

Date:

Fig. 1. A checklist for “red flag” clinical indicators, suitable for inclusion in medical records used in general practice, developed byProfessor Nikolai Bogduk for the Australian National Musculoskeletal Medicine Initiative

Red Flag Clinical Indicatorsof osteoporosis presenting at an ear-lier age.

The pre-test probability of a generalpractice patient presenting with acutelow back pain due to cancer is 0.7%.Infection is the cause in less than0.01%.1

A positive response does not con-firm the presence of a “red flag” con-dition, but serves to alert the practi-tioner to its possible presence. It meansmore attention should be focused onhistory and examination for this fea-ture.

If all items are checked and re-sponses negative, the possibility of a“red flag” cause for the pain is ex-tremely unlikely. Further investigationis not indicated.

However, it is important to be vigilant,and the checklist can be revisited ateach review, and recorded for medi-colegal purposes.

For chronic low back pain, associ-ated features are of utmost importancein detecting “red flag” conditions. TheRed Flag Checklist serves just as wellfor chronic low back pain as it does foracute low back pain. Nil responses toall items again allow the practitionerand the patient to be reassured that aserious condition is extremely unlikelyto be the cause of the pain.

1. Bogduk N, McGuirk B. Pain Researchand Clinical Management, Vol. 13. MedicalManagement of Acute and Chronic LowBack Pain. An Evidence-Based Approach.Elsevier Science, 2002.

May 2004 67

Educational ActivitiesMASTERS, DIPLOMA, AND CERTIFICATE COURSES IN MUSCULOSKELTAL MEDICINE

FLINDERS UNIVERSITY DIPLOMA/CERTIFICATE IN MUSCULOSKELETAL MEDICINE

DATE TITLE/KEY VENUE PROVIDER CONTACT CME POINTSRESOURCEPERSON

1st Sem- MSME 704 Fortnightly University of Otago V. McGroggan Mixture of pointsester 2003 Pain, teleconferences Tel. +64 3 364 1086

MSME 708 on Tuesdays Fax +64 3 364 0909Clinical Email: veronica.mcgrogganTherapeutics @chmeds.ac.nz or

Geoff HardingTel. +61-7-32695522Fax +61-7-32696407Email: [email protected]: www.chmeds.ac.nz/go/dept-orthop

2nd Sem- MSMX 701 To be announced As above As above Mixture of pointsester 2004 Part 2 - Clinical including small

Diagnosis group points24/7/04 – MSMX 707 Fortnightly As above As above Mixture of points30/10/04 Musculoskeletal teleconferences

rehabilitation on Thursdays24/7/04 – MSME 710 Fortnightly As above As above Mixture of points

Recreational & teleconferencessports injuries on Thursdays

24/7/04 – MSMX 705 Fortnightly As above As above Mixture of points30/10/04 Regional teleconferences

disorders - on ThursdaysSpineMSMX 706Regionaldisorders -Limbs


2004 Masters in Pain Internet University of Louise McPherson N/ANew Medicine Newcastle Email: Louise.McPhersonenrolments @newcastle.edu.aufor 2005 -admin. liaison officerfrom 10/04

UNIVERSITY OF NEWCASTLE MASTERS IN PAIN MEDICINE



8/5/04 Explain pain - Physiotherapy Physiotherapy Maree Raymer N/A9am - 1pm Dr Lorimer Department, Royal Department, Royal Ph: 07 3636 8547

Mosely Brisbane and Brisbane and Email: Maree_Raymer@Women’s Hospital Women’s Hospital health.qld.gov.au

25-26/6/04 International Moscow, Russia Ministry of Health Organisers: Russian N/ACongress of Russian Federation, Federation, 119571 Moscow,Manual Russian League of Vernadsky prospect, 121Medicine Manual Medicine

Professionals & Dr Sergei V NikonovRussian Center of Mob: (095) 8 903 593 4496Manual Medicine Fax: (095) 434 3101

Email: [email protected] or [email protected]

31/7/04 - Advanced Sydney Margi Taylor Margi Taylor N/A1/8/04 Prolotherapy Ph/fax 08 8338 3778

Workshop Email: [email protected]

6-7/8/04 Basic Sydney URL: Prolotherapy for doctorsprolotherapy www.drmtaylor.com.auworkshop

17-19/9/04 Basic Adelaideprolotherapyworkshop

6-7/8/04 Pain is pain, Rydges Riverwalk CPM Training and CPM Training and CounsellingMelbourne suffering is Melbourne Counselling PO Box 188, Heidelberg 3084

optional: helping Ph: 1800 100 2929-10/8/04 people manage Wanganui Gardens Fax: 03 9479 1762Brisbane pain and Brisbane Email: bevans@cpmservices.

discomfort orgURL: www.cpmservices.org

13-14/8/04 The Epping ClubSydney Sydney15-18/9/04 14th Triennial Bratislava, Slovak Medical Sona Kozakova N/A

FIMM World Slovakia Association of Fax +421 2 554 24015Congr. Manual/ Myoskeletal or +421 2 554 15287Musculoskeletal Medicine & Email: [email protected]. & Pain: FIMM Website: www.FIMM2004.skEvidence & NewChallenges

7-9/10/04 Australian Alice Springs Sports Medicine Rainer WiltonConference of Australia Sports Medicine AustraliaScience and PO Box 237, Dickson, ACTMedicine in 2602; Ph: 02 6230 4650Sport Fax: 02 6230 5908

Email: [email protected]; URL: www.sma.org.au/ACSMS/2004/about/

29-31/10/04 AAMM Annual Adelaide AAMM A/Prof Norm Broadhurst TBAScientific Ph: +61 8 8295 1890Meeting Fax: + 61 8 8295 6808

Email: [email protected]

OTHER MUSCULOSKELETAL MEDICINE EDUCATIONAL ACTIVITIES

Educational Activities

May 2004 69


10-13/11/04 Interdisciplinary Melbourne Craig BosworthWorld Congress Exhibition Ph: +61 3 9534 3943on Lumbo- Convention Email:[email protected] Pain Centre com.au; Website: www.

worldcongresslbp.org3-6/3/05 AAMM Annual Sunshine AAMM Nell Karpin

Scientific Coast DC ConferencesMeeting - Pain Queensland PO Box 571, Crows Nestin the Elderly NSW 1585

Ph: 02 9954 4400Fax: 02 9954 0666

21-26/8/05 11th World Sydney International IASP Secretariat N/ACongress on Convention Association for the 909 NE, 43rd St, Suite 306Pain Centre, Study of Pain Seattle, WA 98105-6020 USA

Darling Ph: +1 206 547 6409Harbour Fax: +1 206 547 1703

Email: [email protected]: www.iasp-pain.com

27-28/8/05 International Sydney DC Conferences N/AConference on Convention PO Box 571, Crows NestOrofacial Pain Centre, NSW 1585and Tempero- Darling Ph: 02 9954 4400mandibular Harbour Fax: 02 9954 0666Disorders

Educational Activities

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