Aamm Nov2008

ISSN 1324-5627 Australasian Musculoskeletal Medicine

• Risk factors for overuse tendinopathy

• Personal injury claims

• Discography

• Pain conundrums

• Treating inferior heel pain with vitamin D3 dermal cream

• An alernative sacroiliac joint injection technique

• Meralgia paresthetica

• Complementary pain management

• Paraspinal nerve injection Vol. 13 No.2 Nov 2008 Australian Association of New Zealand Association of Musculoskeletal Medicine Musculoskeletal Medicine Office Bearers Office Bearers Contents President President Editorial ...... 55 Dr Michael Oei MBBS, Dip Phys Med, M Dr Gary Collinson MBChB, Dip Musc Med, Med Phys Med, Cert Man Med, FACPM FAFMM, Cert Spinal Inj From the AAMM President ...... 58 MM & Golf Injury Clinic, 37a Wolseley Rd, 4 Kinross St, Blockhouse Bay, Auckland Mosman, NSW 2088 Ph: +64 9 6271024, Fax: +64 9 6271181 From the NZAMM President ...... 59 Ph: +61 2 8302 1180, +61 2 9969 2198 Fax: +61 2 8302 1195 Honorary Secretary Risk factors for overuse Dr Charlie Ng MBChB, Dip Musc Med, Dip tendinopathy ...... 60 Vice-President Sports Med, FAFMM, Cert Spinal Inj Personal injury claims ...... 66 Dr Geoffrey Harding MBBS, Dip Musc Med, 24 Green Lane East, Remuera, Auckland Ph: +64 9 523 4681, Fax: +64 9 523 4682 FAFMM Discography ...... 69 1st Flr, 67 Brighton Rd, Sandgate, Qld 4017 Ph: +61 7 32695522 Honorary Treasurer Pain conundrums ...... 72 Fax: +61 7 3269 6407 Dr Clemens Franzmayr Specialist for Con- servative Orthopoedics 1975 Treating inferior heel pain with Honorary Secretary 15 Frank St, Christchurch vitamin D3 dermal cream ...... 75 Dr David Roselt MBBS, Dip Musc Med, Ph: +64 3 352 7761, Fax: +64 3 352 7762 FRACGP, FAFMM An alternative sacroiliac joint 26 Crofton St, Bundaberg 4670 injection technique ...... 78 Phone +61 7 4152 2888 Past President (ex officio) Fax +61 7 4153 3245 Dr Peter McKenzie BSc, MBChB, Dip Obs, Meralgia paresthetica ...... 82 Dip Musc Med, FRNZCGP, FAFMM Honorary Treasurer 217 Bridge St, Nelson Complementary pain Dr Margaret Taylor BSc, MBBS, FACNEM, Ph: +64 3 548 3455, Fax: +64 3 546 8962 management ...... 87 FIBCT Paraspinal nerve injection ...... 95 PO Box 570, Fullarton SA 5063 Diploma Convenor (co-opted) Ph/fax: +61 8 8338 3778 Journal abstracts ...... 103 Dr Jim Borowczyk BSc, MBChB, Dip Musc Med, MRCP, FAFMM IASP world congress ...... 115 Committee Members 256 Papanui Rd, Merivale, Christchurch Dr Quet-Fui Ho MBBS, Grad Dip Mus Med Ph: + 64 3 355 0342, Fax: +64 3 355 7071 Educational activities ...... 117 PO Box 436, Melville Plaza, Melville WA6153 Ph: 08 9353 2140 Fax: 08 9353 2141 Censor in Chief (co-opted) Dr Mark Johnston MBChB, M Med Pain Dr Chris Homan MBBS, FRACGP, Med, Dip Mus Med, FAFMM, Cert Spinal Inj FACRRM, DRANZCOG, Grad Dip Mus Med 394 Hibiscus Coast Highway, Orewa 3/400 Gregory Terrace, Spring Hill Qld 4000 Ph: +64 9 426 1260, Fax: +64 9 426 1136 Ph: 07 3839 7600 Fax: 07 3236 5228 Committee Members Dr Roland Loeve MBBS, FRACGP, Mike Cleary MBChB, Dip Anaes, Dip Obs, FAFMM, Grad Cert Pain Medicine Dip Musc Med, Dip Occ Med, FRNZGP, PO Box 554, Tamworth NSW 2340 FAFMM Ph: 02 6766 7047 Box 3010 Onerahi, Whangerei Fax: 02 6761 3400 Ph: +64 2 132 3336, Fax: +64 9 459 4455

Dr Jennie Wright BMBS, FRACGP, Grad Lucy Holtzhausen MBChB, Dip MSM Dip Mus Med, Grad Cert Med Acupuncture Auckland Family Medical Centre Bayside Family Medical & Musculoskeletal 94 Remuera Rd, Auckland Brighton Rd, Glenelg SA 5045 Ph: +64 9 524 6249, Fax: +64 9 524 5230 Ph: 08 8295 1890 Australasian Musculoskeletal Medicine is Fax: 08 8295 6808 John MacVicar published by the Australian Association of 6 Bryndwr Road, Christchurch Musculoskeletal Medicine for medical prac- Immediate Past President Ph: +64 3 366 8436, Fax: +64 3 366 8436 titioners interested in the etiology and Dr Michael Yelland MBBS, Dip Musc Med, management of musculoskeletal disorders. PhD, FRACGP, FAFMM Opinions expressed are those of the au- School of Medicine, Logan Campus, thors and not necessarily those of the editor Griffith University, Meadowbrook, Qld 4131 or the Association. Editorial comment may reflect the opinions of the editor alone. Ph +61-7-3382 1358 Fax +61-7-3382 1338 Contributions on any relevant topic are Webmaster AAMM website: www.musmed.com welcome for submission to the editor, Dr Dr Victor Wilk MBBS, M Med Pain Med, Dip David Roselt NZAMSM website: www.musculoskeletal.co.nz 26 Crofton St, Bundaberg 4670 Musc Med, FAFMM Phone +61 7 4152 2888 441 Bay St, Brighton, Vic 3186 AFMM website: www.afmm.com.au Fax +61 7 4153 3245 Ph: +61 3 9596 7211 Email [email protected] Fax: +61 3 9596 7871 FIMM website: www.fimm-online.org

54 Australasian Musculoskeletal Medicine Editorial

rofessor Nik Bogduk is retiring from clinical pract- naire, and the need for any other care was recorded. ice in Newcastle and also I believe from the After treatment, median pain scores did NOT improve. PMasters in Pain Medicine at the University of Physical functioning, social functioning, and vitality did Newcastle. He has advanced the understanding of pain NOT improve. One patient out of 30 restored their desired and its assessment and management like no other per- ADLs. The majority of patients (25/30) restored NO activ- son, and has been truly a giant in our own time. He has ity. These outcomes did not improve at the three- or six- written a vast number of original papers and been on the month reviews. Four patients previously unemployed re- editorial board of anything worth reading. He has certainly turned to work, but six patients previously employed advanced the cause of evidence-based medicine world- actually ceased work. This was a net gain of unemployed wide and has led the good fight in Australia. We all owe him patients, totally at odds with the results reported in the a tremendous debt for his wonderful leadership and his literature. All patients required some form of continuing enormous energy and productivity. He will be very sorely care from their general practitioner. Anyone working at the missed. We hope that he will still join us when he can, and coalface would not be at all surprised by these results. that we will see him in the very near future. Importantly the sample size in this latest audit was The Australian Association of Musculoskeletal Medi- similar to that used in the original studies that promoted cine (AAMM) had its 38th annual scientific functional restoration as the Holy Grail for return to work meeting with another combined conference with the in patients with chronic low back pain. New Zealand Association of Musculoskeletal Medicine Statistically and clinically the outcomes in the audit are (NZAMSM), the Australasian Faculty of Musculoskeletal completely dissonant with the published claims of 80% Medicine (AFMM) and the Australian College of Physical success rate for functional restoration programs. The 95% Medicine (ACPM) 17-19 October 2008, coinciding with confidence intervals of a success rate of zero are 0-11%, the Melbourne Spring Racing Carnival and the Caulfield which fails to reach the lower limit 95% confidence interval Cup. of 80%, which is 66%. The results are completely incom- Melbourne was beautiful as always with a short walk to patible with the literature supporting functional restora- Fitzroy St, St Kilda for restaurants, Chapel St, South tion, which is still recommended by various practice guide- Yarra, for restaurants, cafes, and shopping, or a quick lines as the preferred, indeed the only, treatment en- tram ride on St Kilda Rd into the city centre to satisfy any dorsed for low back pain in many centers. need. I bought my wife some more peppermint tea at T2 These results warn that what is achieved in the real in the city to stay in the good books. world of conventional practice using functional restoration The weather was so good I thought I had stayed in may not even approach the purported outcomes estab- Queensland. Beautiful one day, perfect the next, a big lished in the literature as the benchmarks. Evidence from surprise really. Melbourne was full of that southern research is certainly not translating into standards of multicultural charm we have come to know and love, with practice, and many of us have been very unimpressed by barely an underbelly to be seen. similar observations with our own patients attending these Back pain and sciatica – New paradigms in manage- programs. Obviously, citing the evidence is no substitute ment was a huge success all round. for auditing the outcomes of individual programs in differ- Assessment, conservative evidence-based manage- ent public pain clinic settings or private programs used to ment, interventional procedures and surgery were all the treat workers’ compensation patients. Musculoskeletal go and were examined in detail. pain medicine practitioners and general practitioners at The lack of efficacy of public pain clinics was high- the coalface should audit their own local public pain clinic lighted, with some recent audit results presented from the services. Professor Bogduk suggested at the conference Newcastle experience. There was massive discrepancy that it might be hypocritical to follow such guidelines when in published results regarding the efficacy of functional doing so condemns patients to failure, despite complying restoration touted in studies and systematic reviews.1, 2 with these widely accepted clinical practice guidelines. The purported success rate of functional restoration in The Sebel Hotel, Albert Park, Queens Road, Melbourne, terms of return to work is 80%, with 95% confidence formerly the Carlton Crest, the scene of the historic 1984 intervals of 66% to 94%. AAMM meeting, is well located, and handy to the local In the Newcastle public pain clinic audit, with data offerings. collected by a research nurse not involved in the patient’s An AFMM meeting and winery lunch and afternoon on care, there was assessment before and then immediately Tuesday 14 October 2008 kicked off at 9.30 am. The bus after treatment, and at three months and at six months up to the bush picked up several stragglers on the way and follow up. This involved using a visual analogue scale for after a fruitful informal meeting and visiting several wineries pain, the SF36 for function, a patient-specified functional to taste the fruit of the vine, we had a wonderful lunch at outcome assessment based on four activities of daily Yeringberg Station Winery and restaurant, one of the living (ADLs) impaired by pain that the patients most oldest wineries in Australia. We went to the very scenic dearly wanted restored, a treatment helpfulness question- and impressive TarraWarra Museum of Art in Yarra Glen

November 2008 55 Editorial

that consists of three galleries – two to display the muse- usual. Thanks to all involved. um’s extensive collection and one to host temporary The AFMM held a retreat in conjunction with the NZ Pain exhibitions. We stopped for a palate cleanser and platter Society Meeting 12-15 March 2008 in Auckland, with on the way home at Domaine Chandon. It’s fair to say that involvement of AFMM fellows in presentations, and was a a great time was had by all. great success. Other meetings were held in Christchurch An AFMM workshop on the Wednesday featured inter- with a third planned for November 2008 in Auckland. ventional techniques at Metro Spinal Clinic. This was There are ongoing plans to again apply to the AMC for followed by drinks and sushi very kindly provided at the specialist recognition under the Rudd government which Vivian residence for those willing and able to attend. The has now been up and running for some 12 months. grand piano got a serious workout, with John Malloy and The 2020 submission was made prior to the summit but David Vivian providing some unexpected entertainment no reply has been received to date. and brought the dark horses out of hiding. Thanks very There is still interest in forming an alliance of the four much, David Vivian, for all your trouble for this wonderful organizations to enhance organization and to give secre- day. tarial support, at least. This is progressing steadily. Joint A working morning for Faculty with a meeting to discuss educational meetings are planned in the future. amalgamation was held at Mirka at Tolarno on Fitzroy Please read Michael Oei’s AAMM President’s Report for Street on the Thursday morning where we were made to the full details of developments. Michael worked tirelessly feel very welcome. Lunch was enjoyed very much by with Victor Wilk, David Vivian, Steve Jensen, NZAMSM those not golfing in the afternoon. Mirka was described in President Peter McKenzie, and the rest of the executive The Age as a professionally run restaurant with a sense of on the Melbourne program, along with Kate Ryall and folly and a place in history. Dianna Crebbin from DC Conferences. Thanks to all for a The pre-conference Thursday afternoon featured golf at job very well done. Royal Melbourne Golf Course for the lucky few brave NZAMSM President Peter McKenzie provides an up- enough to accept the challenge. Lunch prior to hit-off was date on the latest developments on the NZ scene across included in the Vivian golfing package and was a highlight the Tasman. Please read his informative report in this for the tried and true and they were truly tested. It was a edition of the journal. great success. The Australian Pain Society (APS) 29th Annual Scien- A group of 20 or so of us descended on Mirka again that tific Meeting will be celebrating the 30th Anniversary of the night after sampling Fitzroy St and its many delights. The APS at the Sydney Convention and Exhibition Centre evening menu and the international wine list were irresist- Sunday 5 - Wednesday 8 April 2009. The theme will be ible, as it turned out. We knew it was a great place after The Pain Continuum: Making Pain History. Three ex- lunch and they were able to accommodate us at very short cellent keynote speakers have accepted an invitation to notice and again did not disappoint, with a great night speak – Rolf Detlef-Treede from Germany, Patrick Mantyh enjoyed by those imbibing. from the USA, and PP Chen from Hong Kong. It should be The main combined conference started on Friday, and well worth supporting, so please mark your diaries.3 ran until lunch time Sunday. The welcome reception was The AAMM Annual Scientific Meeting is planned for July a blast and a few of us went out to dine and enjoy some live 2009 on the Gold Coast. A local Queensland subcommit- music in the vibrant Melbourne cultural scene. A few tee of co-opted insiders is working with your executive and diehards but mostly accompanying partners attended the representatives of all four organizations to plan another Caulfield Cup. Others descended on the National Gallery memorable and informative combined conference. of Victoria for some art and colour. Most registrants were James Gaida and Jill Cook from Deacon University transfixed by the concurrent workshops at the conference have provided a great overview of risk factors for on the Saturday afternoon. There was a nice roll out of tendinopathy, highlighting that there are intrinsic or pre- physios and other health professionals and interested disposing factors and extrinsic mostly environmental fac- parties who served to swell the numbers and make the tors, usually involving repetitive loading. These combine meeting successful from a social and financial perspec- to make an athlete susceptible to injury, and all it takes is tive. an inciting event, a certain manoeuvre, a collision, or a The conference dinner was held on the Saturday night session of hill running, for presentation with clinical at the hotel and was a mixed bag before the power went tendinopathy. out. But as usual a great time was had by all, with Jay Govind, Senior Staff Specialist, Occupational and entertainment by Doctors Harding, Nevin, Vivian, Malloy, Pain Medicine, Canberra Hospital, examines issues with and Keightley providing much entertainment before we personal injury claims and their management that are were consigned to emergency lighting by the storm. It was disturbing, to say the least. The existence of chronic axial at times amusing and at others stimulating, with diners pain is denied with the publication of the International joining in for some of the singing as appropriate. The Association for the Study of Pain’s (IASP) monograph on company and comradery was a highlight of the evening as Back Pain in the Workplace. This monograph has defined

56 Australasian Musculoskeletal Medicine Editorial

chronic low back pain not as a “medical problem,” but as paresthetica as part of his diploma studies in muscu- a problem of “activity intolerance”. Paradoxically, the loskeletal medicine, and it is presented in this edition of the same monograph advocated that the “medical manage- journal. ment” should not be “pain contingent” but rather “time Breck McKay has written a very interesting piece on contingent”. The taskforce recommended that those who complementary pain management, emphasizing the im- fail to achieve restoration of function and return to work portance of taking an exhaustive history and conducting a were to be reclassified as “unemployed.” It seems the thorough physical examination, and treating the whole IASP Task Force is promoting itself as “a self-appointed patient. surrogate gatekeeper to a non-medical system principally Breck, Scott Masters, and I have written a paper looking ensconced in claims management, cost containment, and at musculoskeletal pain and the role of paraspinal nerve cost reduction.” injection. We have found these injections to be very useful Victor Wilk expands further with his critique of the value as an office procedure since Stefan Blomberg visited our of discography in diagnosing discogenic pain after the Melbourne annual scientific meeting in 2002 as keynote great debate in Melbourne with Nik Bogduk. Local tender- speaker. We first heard about using local anesthetic and ness on physical examination can mislead the unwary. steroid injections to the parasacrococcygeal paraspinal Victor still believes internal disc disruption is a real entity nerve regions from Stefan’s paper, which was published and MRI can certainly be of value in the assessment in Spine in 1994.4 Paraspinal nerve injections are of value process. Discography, however, has a high false positive for acute spinal pain, and for chronic spinal pain that may rate and the risk of significant morbidity at least. Please be associated with radiculopathy or radicular pain. Some- read carefully this interesting and insightful review of the times there are elements of somatic pain and radicular evidence, with some practical case study material in- pain and/or features of radiculopathy in a patient’s pain cluded. presentation. There are limitations in sensitivity and John Lyftogt has provided a provocative and thought- specificity with history, but it is by far the best guide. provoking article about the relative merits of central nerv- Physical examination, and imaging, which does not show ous system sensitization versus peripheral nervous sys- pain per se, do not fully overcome diagnostic uncertainty, tem autonomy in terms of explaining chronic or persistent which remains an issue. There can certainly be mixed pain. He argues against the reigning paradigm of “pain presentations. Relieving somatic pain components can management” for people with chronic neuropathic pain provide pain relief and relieve patient suffering and help when there are well-documented alternatives available clarify the diagnosis. Any significant radicular symptoms that may offer a cure or at least address the pain scores or signs should be assessed and treated in their own right. and attempt to reduce them. There can be somatic components with radicular symp- In a subsequent paper, John Lyftogt has explored the toms and signs as the nerve root sleeves are innervated use of vitamin D3 dermal cream to treat inferior heel pain, by the sinuvertebral nerve, a recurrent branch of the also known as plantar fasciitis or even policeman’s foot in ventral ramus, as are the intervertebral discs, and these some parts, with impressive results. John explains that can be a source of somatic pain.5 this may be viewed as an example of a peripheral neuro- There are some abstracts from the recent literature and pathic pain syndrome due to persistent neuropathic in- comment which I hope readers will find stimulating and flammation of the medial calcaneal branches of the tibial informative. Any feedback on these abstracts and com- nerve. Vitamin D3 may be viewed as a neurosteroid with ments is welcome. Please address any correspondence neuroprotective properties. John highlights the lack of to the editor. efficacy and potential morbidity such as plantar fascia Geoff Harding continues as vice-president, master of rupture associated with the use of corticosteroid injection ceremonies, and entertainer extraordinaire. Thanks very in this setting. It is a condition resistant to most interven- much Geoffrey. He is still the onsite co-ordinator in Aus- tions and this is the first report of two patients responding tralia for the Otago Diploma of Musculoskeletal Medicine. favorably to twice daily applications of vitamin D3 Margaret Taylor, our treasurer, has again coordinated transdermal cream for this difficult-to-treat condition. Be educational activities. Thanks for all your wonderful ef- sure to read this important paper examining the role of forts, Margi, ably assisted by your assistant Martin. vitamin D deficiency in contributing to, and offering a David Vivian continues as co-editor of the journal and means of treating, some forms of neuropathic pain. played a very important role in organizing the Melbourne Paul Quin, current president of the Australasian Faculty conference, as did Victor Wilk, Steve Jensen, Michael of Musculoskeletal Medicine (AFMM), has produced a Oei, and the executive and committee. Thanks David, wonderfully clear account of his method of sacroiliac joint Steve, and Michael, and all who were involved. injection that should improve the reproducibility of the Victor Wilk continues his invaluable role as web master, technique while minimising patient discomfort and expo- committee member, and master debater. Thanks very sure time under fluoroscopy. much, Victor, for all of your efforts. Mark Bailey has produced a very nice review of meralgia I look forward very much to seeing readers in July 2009

November 2008 57 Editorial

at the Gold Coast. The committee, with other Queensland rehabilitation for chronic back pain: systematic review. Br Med J members co-opted, will endeavour to put together another 2001; 322: 1511-16. highly memorable event academically, pragmatically, func- tionally, and socially as always. 3. APS Newsletter, June 2008. http://www.apsoc.org.au/owner/ files/4t0r8y.pdf . Please remember to spread the word to all of your medical, nursing, and allied health colleagues and we 4. Blomberg S, Hallin G, Grann K et al. Manual therapy with should have another successful and highly enjoyable steroid injections – a new approach to treatment of low back pain: event to look forward to and attend. a controlled multicentre trial with an evaluation by orthopedic surgeons. Spine 1994; 19: 569-77. 1.Mayer TG, Gatchel RJ, Kishino N et al. Objective assessment of spine function following industrial injury. A prospective study 5. Bogduk N. Clinical Anatomy of the Lumbar Spine and Sacrum. with comparison group and one-year follow-up. Spine 1985; 10: 3rd ed. Edinburgh; Churchill Livingstone, 1997. 482-93.

2. Guzman J, Esmail R, Karjalainen K et al. Multidisciplinary David Roselt

From the AAMM President

hope everyone attending the combined annual Roselt, Margaret Taylor, Peter McKenzie, Jennie Wright, scientific conference of musculoskeletal medicine at and Rod Ayscough for their contributions. Last but not IAlbert Park, Melbourne, on 16-19 October 2008 least, I would like to congratulate Kate Ryall from DC found it as stimulating and interesting as I did. Unfortunately, Conferences for doing such a wonderful job and making I was too unwell to appreciate fully both the conference this conference a success. and the social functions. At the AGM held on 17 October 2008, it was proposed From all the feedback, the conference program was that we form an alliance between the musculoskeletal very well received by all delegates. Most of the delegates organizations rather than an amalgamation. This will have were very impressed by the calibre of the speakers and to be worked out by the respective presidents. rated them very highly. The conference was a success in The next combined conference is likely to be held at the uniting all the musculoskeletal organizations together, Gold Coast in July 2009, to allow enough time before the with the aim of working more closely as a group. Apart Spine in Action conference in Auckland, New Zealand on from the educational success, it also achieved a financial 26-30 March 2010. profit, which is a great bonus. This is why it’s so important As the year 2008 is drawing to a close, I wish you all a that we should continue to have a joint conference with very peacef,ul Christmas holiday and a very fruitful and AFMM, ACPM, and NZAMSM. A successful conference happy New Year 2009. Finally I look forward to meeting all like this will not happen without the hard work of the old and new AAMM members at the next conference at the organizing committee, who have spent countless hours in Gold Coast. preparing for it. Once again I would like to thank Victor Wilk, Steven Jensen, David Vivian, Geoff Harding, David Michael Oei

58 Australasian Musculoskeletal Medicine From the NZAMSM President

his year has seen the continuing development of Plans for a flagship Spine in Action conference to be musculoskeletal medicine. The role of the held in Auckland in March 2010 are well advanced, with TNZAMSM continues to evolve and change. four keynote European speakers confirmed. The possibility of becoming part of a larger Australasian Two AFMM retreats have been held this year, the first in musculoskeletal organization is being considered, with association with the NZ Pain Society (colleagues were discussions between the four organizations underway, asked to contribute) and the second in Christchurch. A that is, NZAMSM, AAMM, AFMM, and ACPM. third is planned for Auckland in November. What is being considered is the formation of an umbrella Planning for further practical sessions is under active organization – possibly called the Australasian College of consideration and members will be notified accordingly. Musculoskeletal Medicine – to which the above four The NZAMSM remains a CME provider for the RNZCGP organizations will be affiliated. With time a merger may and various educational activities have been organized by occur. members in their own regions, the largest being the The aim is to find commonality and to speak with one Auckland Roadshow. Musculoskeletal teaching sessions voice on all maters pertaining to musculoskeletal medi- have also been incorporated into the GP registrar training cine. program. The role needs to be clearly defined but could include: Jim Borowczyk continues as convener of the Otago 1) Unification of the present separate bodies. Musculoskeletal Diploma. He has developed a new paper 2) Research MSMX 711 Pain Assessment which is now available. Jim 3) Organizational and secretarial is also looking into the possibility of offering a Masters in 4) Registrar training Pain Medicine through Otago. This would replace New- 5) Accreditation and re-accreditation of Fellows castle’s program as Nik Bogduk is looking towards retire- 6) Political voice ment. 7) More conjoint conferences. Being involved in and offering academic studies of the 8) Education, including GPs and colleagues. highest order helps give musculoskeletal medicine status and credibility. It also helps build bridges with other Hopefully, the formation of such a body will help achieve medical colleagues. Australian specialist recognition. Ian Holding has the position of GP liaison at the Depart- It could be argued that loss of autonomy may occur. NZ ment of Orthopaedics and Musculoskeletal Medicine. already has specialist status so why bother. However, Nationalistic differences continue to beset FIMM, with musculoskeletal medicine in NZ is struggling. Member- its continuing existence in doubt. NZAMSM is continuing ship of the NZAMSM is dropping, mainly through retire- dialogue but we did not send a delegate to their annual ment. The vast majority of active members are Fellows meeting this year as we felt the cost could not be justified and the distinction between NZAMSM business and AFMM with the present uncertainties. A written statement has business is increasingly blurred. The paramount concern been sent representing our views, that is, the continuation of both the NZ and Australian Medical Councils is the small of a global musculoskeletal organization would be worth- numbers. A larger unified body would go some way while but the direction it takes would need to have continu- towards addressing these concerns ing relevance to us. Holding conjoint conferences continues to be very successful. This started in Palmerston North last year and Peter McKenzie continued in Melbourne this year.

November 2008 59 Risk Factors for Overuse Tendinopathy

James E Gaida, Physiotherapist, School of Exercise and Nutrition Sciences, Deakin University ([email protected]) Jill L Cook, Associate Professor, Centre for Physical Activity and Nutrition Research, Deakin University

nism but also the environment – firmness of the surface, Introduction interaction with other players, and also factors such as the endinopathies limit physical activity, are often stage of the game at which the injury occurs (that is, 89th long-standing, and are difficult to treat. A thor- minute of a soccer match). Tough understanding of the risk factors for tendinopathy is important for several reasons. First, it makes screening for these factors possible among high- risk populations (that is, athletes). Second, prophylactic treatment can be devised, evaluated and applied among Predisposing factors the high-risk individuals. Third, knowing which factors increase the risk of tendinopathy gives insight into the (intrinsic risk factors) underlying mechanisms. And finally, treatment can be directed toward modifying the factors that have precipi- Age tated the injury. The underlying assumption is that ad- Generally the incidence of tendinopathy increases with dressing these underlying factors will improve treatment age.2,3 While young athletes often develop tendinopathy outcomes and prevent recurrences. as a consequence of overload, with increasing age the It is only possible to apply the label “risk factor” if loading threshold required to incite a tendon injury de- measurement takes place prior to injury. Much of our creases. This association is more evident for some ten- current knowledge about tendinopathy is derived from dons than others. For example, in the general community cross-sectional and case-control studies. As such, we rotator cuff problems are relatively rare below the age of know little about risk factors for tendinopathy – our knowl- 50 but become common from that age onward.4 Similarly, edge is of factors associated with tendinopathy. The Achilles tendinopathy incidence peaks during middle age, exception is situations where a strong case can be made particularly among men.5 It is well known that the mechani- that the variable of interest cannot change as a result of cal properties of many tissues decline from middle age the injury (that is, genetics). onward. The increased incidence of tendinopathies may be related to altered tissue properties or to cumulative loading history, which increases with each passing year.

Bahr model Gender Bahr and Holm have presented a thorough and compre- Gender biases are evident for some tendinopathies, hensive model of musculoskeletal injury risk factors.1 while others are equally represented. In males there are While the basics of this model are outlined here, interested much higher incidences of Achilles,6 patellar and (hip) readers are directed to the original article. Briefly, factors adductor tendinopathy.7 Conversely, gluteus medius that increase the likelihood of injury are risk factors for that tendinopathy presents almost exclusively in women.8 injury. These factors may either occur within the individual Upper limb tendinopathies such as medial and lateral (intrinsic) or they may come from the external environment elbow and rotator cuff are approximately equally repre- (extrinsic). In the Bahr model, intrinsic factors make an sented.3 These findings may relate to biomechanical athlete predisposed to injury. In their paper the authors differences between men and women – for example, stress that being predisposed to injury is rarely, in itself, pelvis shape and gluteus medius tendinopathy. More enough to lead to an injury. The next step toward injury likely, however, is that for the other tendinopathies, it is the involves the extrinsic factors – these are laid on top of the hormonal and metabolic differences that influence ten- intrinsic factors and create an athlete who is now suscep- dons and affect the incidence of injury.9 tible to injury. The final piece of the puzzle, once the athlete has been “prepared” for injury by being both predisposed and susceptible, is the inciting event. The inciting event Genes may be, for example, a particular manoeuvre, a collision Achilles tendinopathy with another athlete, or a session of hill running. The Knowledge of genetic factors associated with Achilles inciting event encompasses not only the injury mecha- tendinopathy is much more advanced than for any other

60 Australasian Musculoskeletal Medicine Risk Factors for Overuse Tendinopathy

tendon. Seminal work by Jozsa and co-workers demon- nation for this apparent contradiction is that once the strated associations between tendon injury and ABO inhibiting effect of estrogen is removed after menopause, blood grouping.10 It is now thought that the association tendons have a greater capacity to adapt to loads.17 Thus, with ABO grouping is due to genetic linkage between the although it is acknowledged that estrogen affects ten- ABO gene [9q34] and other closely associated genes. dons, disagreement exists as to whether the effect is The South African group have shown that the gene for the positive or negative. alpha chain of collagen type V (COL5A1, [9q34]) and the gene for tenascin-C (TNC, [9q32-q34]) are linked to Achil- les tendon injuries.11-14 Biomechanics Achilles tendinopathy Rotator cuff tendinopathy A host of case-control studies have identified In comparison, only one study has investigated genetic biomechanical factors related to Achilles tendinopathy. influences for rotator cuff tendinopathy. A 2004 paper These include excessive hindfoot movement,18-21 which is showed a 4.65 relative risk (95% CI 2.42 to 8.63) of thought to cause a whipping mechanism in the Achilles symptomatic full-thickness rotator cuff tears in full first- tendon. Arch height22,23 as well as increased forefoot degree siblings of probands compared with spousal con- varus,20 knee range of motion24 and electromyographic trols.15 While this paper did not investigate tendinopathy patterns of the muscles controlling the foot and ankle19,25 specifically, it could be argued that painful rotator cuff also differ between individuals with tendinopathy and tears are an endpoint of rotator cuff tendinopathy. Further controls. research is required into the influence that genetics plays Interestingly, the only two longitudinal studies investi- in rotator cuff tendinopathy, with COL5A1 and TNC being gating biomechanical risk factors for Achilles tendinopathy likely starting points. have produced conflicting results. Kaufman studied 334 males enrolled in Navy SEAL training and found that Race reduced dorsiflexion range was the only factor predicting A recent study covering 6.8 million person-years of the 30 cases of tendinopathy.26 In contrast Mahieu fol- military service and 4,451 tendon ruptures showed the lowed 69 military recruits during six weeks of basic training effect of race on these injuries.6 The increased risk of and found that increased dorsiflexion range in conjunction quadriceps tendon rupture among blacks was 2.89 (95% with decreased plantarflexion strength was a predictor for CI 2.42 to 3.44), for the patellar tendon 4.52 (95% CI 3.94 the 10 cases of tendinopathy.27 A key difference between to 5.19) and for the Achilles tendon 3.58 (95% CI 3.31 to these cohorts is that the Navy SEAL trainees were ath- 3.88). The authors hypothesized that these differences letes who increased their training, while Mahieu’s cohort may be attributable to racial differences in tendon me- was unaccustomed to physical training. From a clinical chanical properties, ABO blood grouping (higher preva- standpoint, the first group is probably most informative. lence of type O in blacks) or body weight. Thus, in trained athletes it is important to address limited dorsiflexion while poor control of dorsiflexion may be a factor when untrained individuals suddenly start running Estrogen long distances. Again, scientific evidence supporting the Following early work2 which showed a spike in the efficacy of these interventions is lacking, although clini- incidence of Achilles tendon problems in women aged 50 cally good results are seen.28 and over (that is, menopause), Cook and co-workers investigated the influence of estrogen on tendons.16 They Patellar tendinopathy compared the tendons of post-menopausal women taking A host of small case-control studies have investigated hormone replacement (HRT) with those not taking HRT, differences in lower-limb biomechanics in relation to patel- who were either active (golfers) or non-active. Active lar tendinopathy. They have shown alterations in run- women had more tendon abnormalities than did non- ning,29 jumping, and landing mechanics both at the knee30,31 active women, but active women on HRT had less tendon and the ankle.30,32 At times the findings have been contra- abnormality (p=0.056) and thinner tendons (p<0.05) than dictory and currently have limited clinical utility. did active women not on HRT. Using these data, the A longitudinal study of 138 physical education students authors argued that estrogen offers protection against provides us with some useful insights.33 Over two years, tendon injuries and the spike in tendon injuries with meno- 19 students developed patellar tendinopathy. Looking pause is due to the sudden loss of circulating estrogen. back over the data the investigators found that those who In contrast, Danish researchers argue that estrogen is went on to develop tendinopathy had lower hamstring and harmful to tendons. They note that men’s but not women’s quadriceps flexibility at the beginning of the study. Thus, patellar tendons respond to prolonged running by increas- a good starting point when treating patellar tendinopathy ing in cross-sectional area. Additionally, they note that is to examine and address any muscle inflexibility. We post-menopausal women have larger Achilles tendon await scientific evidence to support the efficacy of this cross-sectional area than do young females. Their expla- intervention.

November 2008 61 Risk Factors for Overuse Tendinopathy

Another factor linked to patellar tendinopathy is a de- of a poor outcome following the same treatment is a high creased range of ankle dorsiflexion.34 As with muscle HbA1c (poorly controlled glucose).43 The lower rates of inflexibility of the thigh, limited dorsiflexion may be im- success for these interventions in diabetes should be proved through intervention and training under physi- considered when recommending treatments to patients. otherapy guidance.

Lateral epicondyle tendinopathy When performing the backhand stroke in tennis, novice players strike the ball with a greater degree of wrist flexion Mechanisms compared with expert players. Computer models have shown that this strategy involves substantial eccentric Diabetes contraction of extensor carpi muscles. It is hypothesized The underlying mechanisms that increase the risk of that the repeated eccentric contractions overload the tendinopathy in diabetes are not well understood. Most extensor origin.35 likely, elevated glucose levels are responsible through their ability to cause non-enzymatic cross-linking of collagen. This non-enzymatic glycosylation increases the stiff- Diabetes ness of tendon and other connective tissue, potentially Achilles tendinopathy explaining the increased injury risk.44 Another possibility is Diabetes is consistently associated with tendinopathy that the metabolic environment associated with diabetes throughout the body. In the Achilles tendon, those with (increased proinflammatory cytokine expression) alters diabetes have thicker tendons36 and more frequently have the protein expression of the cells (tenocytes) that build disorganized collagen on ultrasound.37 A recent case and maintain the tendon extracellular matrix. series showed that diabetes was more common than expected in young males with painful Achilles tendinopathy.38 Adiposity Adiposity is a factor that has only recently come to Knee attention as a potential risk factor for tendinopathies. At the knee, asymptomatic MRI changes affecting the Recent work by both our group based in Melbourne and quadriceps tendon are much more common in diabetes.39 others internationally highlights the importance of stored The clinical significance of these changes was not dis- fat in relation to tendinopathy.45 For example, among elite cussed, and is difficult to determine. male volleyball players waist circumference (a proxy for abdominal adipose tissue) was the only factor able to Hand discriminate those with patellar tendon abnormalities from Tendinopathies affecting the hand and wrist are associ- those with normal tendons.46 This factor was superior to ated with either poor glucose control or overt diabetes.40,41 body weight, training schedule, and a host of other factors It has been suggested that a tendon disorder of the hand considered. Similarly, high BMI is a very strong risk factor should prompt the physician to examine glucose toler- for pathology affecting the rotator cuff tendons47,48 and the ance.41 Thus, tendon problems in the hand may be the first medial epicondylar attachment of elbow tendons.3 We sign of incipient diabetes. have recently outlined the reasons a mechanical hypothesis is insufficient in explaining these findings.45 Briefly, as Elbow only the lower limb tendons are weight bearing, the At the elbow, a study with more than 10,000 participants association between adiposity and tendinopathy in both found that diabetes was associated with both medial the upper and lower limbs supports, an alternative, sys- (golfer’s elbow) and lateral epicondyle pain (tennis el- temic hypothesis. Interested readers are directed to a bow).3 recent paper discussing this matter.45

Shoulder In a study investigating factors associated with rotator cuff tendinopathy among more than 4,000 participants, insulin treatment for diabetes was associated with a Susceptible factors (extrinsic relative risk of 12.8 (95% CI 2.6 to 62.7) for tendinopathy among men.4 risk factors)

Treatment Load Finally, a diagnosis of diabetes is a strong predictor of The most widely recognized factor that makes individu- poor outcome following steroid injection for trigger fin- als susceptible to tendinopathy is repetitive loading. This ger,42 while in diabetes with trigger finger the best predictor is why high rates of patellar tendinopathy are seen in

62 Australasian Musculoskeletal Medicine Risk Factors for Overuse Tendinopathy

volleyball players,49 and Achilles tendinopathy in middle perately required to address this knowledge shortfall. distance runners.50 It also appears as if training surfaces A number of the listed factors are non-modifiable (that is, are important, with much higher rates of patellar age, gender); however, knowledge of these factors will tendinopathy among volleyball players who train on as- allow the clinician to identify cases that don’t fit the usual phalt compared with sprung wooden floors.51 Similarly, presentation. These atypical cases may prompt the search runners who perform running sessions in sand, or fre- for underlying diseases such as seronegative arthropa- quently use hill running for training report higher rates of thies or other rheumatologic disorders.66,67 Achilles tendinopathy.52 By the same token, tennis elbow Conversely, knowledge of modifiable factors allows the is common in tennis; golfer’s elbow common in golfers; clinician to educate their patients and to encourage them adductor tendinopathy common in AFL players; rotator to engage in risk factor reduction. This knowledge also cuff tendinopathy common in pitchers53 and swimmers.54 directs the clinician when interviewing the patient with the Also, workers who are exposed to heavy manual la- view to understanding the factors that have led to the bour,55 repetitive movements,56-58 particularly above the injury. And finally, when modifiable risk factors are identi- level of the shoulder57,59 are at high risk of upper limb fied during the examination, these factors can be ad- tendinopathies. Similarly, awkward shoulder postures48 dressed either by the treating doctor or by appropriate and vibration60 appear to be detrimental. referral.

Tobacco Tobacco exposure both as cigarettes and snuff/snus seems to play an important role in increasing the risk of References tendinopathies. This has been reported for the shoulder,60 1. Bahr R, Holme I. Risk factors for sports injuries – a methodo- lower limb injuries,61 wrist and hand symptoms,62 and for logical approach. Br J Sports Med 2003; 37(5): 384-92. both medial and lateral epicondylar pain.3 2. Maffulli N, Waterston SW, Squair J et al. Changing incidence of Achilles tendon rupture in Scotland: a 15-year study. Clin J Sport Med 1999; 9(3): 157-60. Medication Exposure to certain medications also appears to in- 3. Shiri R, Viikari-Juntura E, Varonen H, Heliovaara M. Preva- crease the risk of tendinopathies and associated condi- lence and determinants of lateral and medial epicondylitis: a tions. In some circumstances it may be appropriate to population study. Am J Epidemiol 2006; 164(11): 1065-74. switch to an alternative medication, while in other cases the medication must be continued and the tendon problem 4. Miranda H, Viikari-Juntura E, Heistaro S et al. A population managed as far as possible.63 For example, if study on differences in the determinants of a specific shoulder fluoroquinolone antibiotics induce Achilles tendinopathy a disorder versus nonspecific shoulder pain without clinical findings. Am J Epidemiol 2005; 161(9):847-55. different class of medication may provide similar antibiotic cover while avoiding further exacerbation of the tendon 5. Alfredson H, Lorentzon R. Chronic Achilles tendinosis: recom- 64 problem. Similarly, if tendinopathy is associated with mendations for treatment and prevention. Sports Med 2000; initiation or change in statin medication, avoiding a rapid 29(2):135-46. increase in dosage or changing the class of statin may be appropriate.65 6. Owens B, Mountcastle S, White D. Racial differences in Change is inappropriate if patients are being treated tendon rupture incidence. Int J Sports Med 2007; 28(7): 617-20. with a metalloproteinase inhibitor (such as Marimastat) for inoperable cancers. In these cases the development of 7. Holmich P. Long-standing groin pain in sportspeople falls into three primary patterns, a “clinical entity” approach: a prospective musculoskeletal side effects such as frozen shoulder and study of 207 patients. Br J Sports Med 2007; 41(4): 247-52; Dupuytren’s contracture are associated with improved discussion 52. survival.63 8. Connell DA, Bass C, Sykes CA et al. Sonographic evaluation of gluteus medius and minimus tendinopathy. Eur Radiol 2003; 13(6):1339-47.

Conclusion 9. Miller BF, Hansen M, Olesen JL et al. Tendon collagen It is clear from the evidence presented that our knowl- synthesis at rest and after exercise in women. J Appl Physiol 2007; 102(2): 541-46. edge of true risk factors for overuse tendinopathy is limited. In many cases, we cannot be certain whether the 10. Jozsa L, Balint JB, Kannus P et al. Distribution of blood factors cross-sectionally associated with tendinopathy groups in patients with tendon rupture. An analysis of 832 cases. were present prior to injury or whether they developed after J Bone Joint Surg Br 1989; 71(2): 272-74. the injury. Carefully controlled longitudinal studies are des-

November 2008 63 Risk Factors for Overuse Tendinopathy

11. Mokone GG, Gajjar M, September AV et al. The guanine- injuries. Am J Sports Med 1999;27(5): 585-93. thymine dinucleotide repeat polymorphism within the tenascin-C gene is associated with achilles tendon injuries. Am J Sports Med 27. Mahieu NN, Witvrouw E, Stevens V et al. Intrinsic risk factors 2005; 33(7): 1016-21. for the development of achilles tendon overuse injury: a prospective study. Am J Sports Med 2006;34(2): 226-35. 12. Mokone GG, Schwellnus MP, Noakes TD, Collins M. The COL5A1 gene and Achilles tendon pathology. Scand J Med Sci 28. Kountouris A, Cook JL. Rehabilitation of Achilles and patellar Sports 2006; 16(1):19-26. tendinopathies. Best Pract Res Clin Rheumatol 2007;21(2): 295- 316. 13. September AV, Cook J, Handley CJ et al. Variants within the COL5A1 gene are associated with achilles tendinopathy in two 29. Grau S, Maiwald C, Krauss I et al. What are causes and populations. Br J Sports Med 2008:doi:10.1136/bjsm.2008. treatment strategies for patellar-tendinopathy in female run- 048793. ners? J Biomech 2008;41(9):2042-46.

14. September AV, Schwellnus MP, Collins M. Tendon and 30. Bisseling RW, Hof AL, Bredeweg SW et al. Are the takeoff ligament injuries: the genetic component. Br J Sports Med 2007; and landing phase dynamics of the volleyball spike jump related 41(4): 241-46. to patellar tendinopathy? Br J Sports Med 2008:doi:10.1136/ bjsm.2007.044057. 15. Harvie P, Ostlere SJ, Teh J et al. Genetic influences in the aetiology of tears of the rotator cuff. Sibling risk of a full-thickness 31. Richards DP, Ajemian SV, Wiley JP, Zernicke RF. Knee joint tear. J Bone Joint Surg Br 2004; 86(5): 696-700. dynamics predict patellar tendinitis in elite volleyball players. Am J Sports Med 1996;24(5): 676-83. 16. Cook J, Bass SL, Black JE. Hormone therapy is associated with smaller Achilles tendon diameter in active post-menopausal 32. Richards DP, Ajemian SV, Wiley JP et al. Relation between women. Scand J Med Sci Sports 2007; 17(2): 128-32. ankle joint dynamics and patellar tendinopathy in elite volleyball players. Clin J Sport Med 2002;12(5): 266-72. 17. Magnusson SP, Hansen M, Langberg H et al. The adaptabil- ity of tendon to loading differs in men and women. Int J Exp Pathol 33. Witvrouw E, Bellemans J, Lysens RJ et al. Intrinsic risk 2007; 88(4): 237-40. factors for the development of patellar tendinitis in an athletic population. A two-year prospective study. Am J Sports Med 18. Clement DB, Taunton JE, Smart GW. Achilles tendinitis and 2001;29(2): 190-95. peritendinitis: etiology and treatment. Am J Sports Med 1984; 12(3): 179-84. 34. Malliaras P, Cook J, Kent P. Reduced ankle dorsiflexion range may increase the risk of patellar tendon injury among 19. Donoghue O, Harrison A, Coffey N, Hayes K. Functional data volleyball players. J Sci Med Sport 2006;9(4): 304-9. analysis of running kinematics in chronic Achilles tendon injury. Med Sci Sports Exerc 2008; 40(7):1323-35. 35. Eygendaal D, Rahussen FT, Diercks RL. Biomechanics of the elbow joint in tennis players and relation to pathology. Br J 20. Kvist M. Achilles tendon injuries in athletes. Ann Chir Gynaecol Sports Med 2007;41(11): 820-23. 1991; 80(2):188-201. 36. Akturk M, Ozdemir A, Maral I et al. Evaluation of Achilles 21. Kvist M. Achilles tendon injuries in athletes. Sports Med tendon thickening in type 2 diabetes mellitus. Exp Clin Endocrinol 1994; 18(3): 173-201. Diabetes 2007;115(2): 92-96.

22. Haglund-Åkerlind Y, Eriksson E. Range of motion, muscle 37. Batista F, Nery C, Pinzur M et al. Achilles tendinopathy in torque and training habits in runners with and without Achilles diabetes mellitus. American Orthopaedic Foot and Ankle Society tendon problems. Knee Surg Sports Traumatol Arthrosc 1993; [and] Swiss Foot and Ankle Society. Foot Ankle Int 2008;29(5): 1(3-4): 195-99. 498-501.

23. McCrory JL, Martin DF, Lowery RB et al. Etiologic factors 38. Holmes GB, Lin J. Etiologic factors associated with sympto- associated with Achilles tendinitis in runners. Med Sci Sports matic achilles tendinopathy. Foot Ankle Int 2006;27(11): 952-59. Exerc 1999; 31(10): 1374-81. 39. Altinel L, Kose KC, Degirmenci B et al. The midterm effects 24. Azevedo LB, Lambert MI, Vaughan CL et al. Biomechanical of diabetes mellitus on quadriceps and patellar tendons in variables associated with achilles tendinopathy in runners. Br J patients with knee arthrosis: a comparative radiological study. J Sports Med 2008:doi:10.1136/bjsm.2008.053421. Diabetes Complicat 2007;21(6): 392-96.

25. Baur H, Divert C, Hirschmuller A et al. Analysis of gait 40. Gamstedt A, Holmglad J, Ohlson CG, Sundstrom M. Hand differences in healthy runners and runners with chronic Achilles abnormalities are strongly associated with the duration of diabe- tendon complaints. Isokinet Exerc Sci 2004;12(2): 111-16. tes mellitus. J Intern Med 1993: 189-93.

26. Kaufman KR, Brodine SK, Shaffer RA et al. The effect of foot 41. Leden I, Jonsson G, Larsen S et al. Flexor tenosynovitis structure and range of motion on musculoskeletal overuse (FTS): a risk indicator of abnormal glucose tolerance. Scand J

64 Australasian Musculoskeletal Medicine Risk Factors for Overuse Tendinopathy

Rheumatol 1985;14(3): 293-97. sample of workers in France (the Pays de la Loire study). Occup Environ Med 2006;63(11):1754-61. 42. Rozental TD, Zurakowski D, Blazar PE. Trigger finger: prognostic indicators of recurrence following corticosteroid injec- 56. Frost P, Bonde JP, Mikkelsen S, Andersen JH, Fallentin N, tion. J Bone Joint Surg Am 2008;90(8): 1665-72. Kaergaard A, et al. Risk of shoulder tendinitis in relation to shoulder loads in monotonous repetitive work. Am J Ind Med 43. Kameyama M, Funae O, Meguro S, Atsumi Y. HbA1c values 2002;41(1): 11-18. determine the outcome of intrasheath injection of triamcinolone for diabetic flexor tenosynovitis. Diabetes Care 2006;29(11): 57. Miranda H, Viikari-Juntura E, Martikainen R, Takala EP, 2512-14. Riihimaki H. A prospective study of work related factors and physical exercise as predictors of shoulder pain. Occup Environ 44. Avery NC, Bailey AJ. Enzymic and non-enzymic cross- Med 2001;58(8): 528-34. linking mechanisms in relation to turnover of collagen: relevance to aging and exercise. Scand J Med Sci Sports 2005;15(4): 231- 58. Tanaka S, Petersen M, Cameron L. Prevalence and risk 40. factors of tendinitis and related disorders of the distal upper extremity among U.S. workers: comparison to carpal tunnel 45. Gaida JE, Cook JL, Bass SL. Adiposity and tendinopathy. syndrome. Am J Ind Med 2001;39(3): 328-35. Disabil Rehabil 2008: doi:10.1080/09638280701786864. 59. Svendsen SW, Gelineck J, Mathiassen SE, Bonde JP, Frich 46. Malliaras P, Cook JL, Kent PM. Anthropometric risk factors LH, Stengaard-Pedersen K, et al. Work above shoulder level and for patellar tendon injury among volleyball players. Br J Sports degenerative alterations of the rotator cuff tendons: a magnetic Med 2007;41(4): 259-63. resonance imaging study. Arthritis Rheum 2004;50(10): 3314- 22. 47. Wendelboe AM, Hegmann KT, Gren LH et al. Associations between body-mass index and surgery for rotator cuff tendinitis. 60. Stenlund B, Goldie I, Hagberg M, Hogstedt C. Shoulder J Bone Joint Surg Am 2004;86-A(4): 743-47. tendinitis and its relation to heavy manual work and exposure to vibration. Scand J Work, Envir and Health 1993;19(1): 43-49. 48. Werner RA, Franzblau A, Gell N et al. A longitudinal study of industrial and clerical workers: predictors of upper extremity 61. Heir T, Eide G. Injury proneness in infantry conscripts tendonitis. J Occup Rehabil 2005;15(1): 37-46. undergoing a physical training programme: smokeless tobacco use, higher age, and low levels of physical fitness are risk factors. 49. Lian O, Engebretsen L, Bahr R. Prevalence of jumper’s knee Scand J Med Sci Sports 1997;7(5): 304-11. among elite athletes from different sports: a cross-sectional study. Am J Sports Med 2005;33(4): 561-67. 62. Zetterberg C, Ofverholm T. Carpal tunnel syndrome and other wrist/hand symptoms and signs in male and female car 50. Kujala UM, Sarna S, Kaprio J. Cumulative incidence of assembly workers. Int J Ind Ergon 1999;23(3): 193-204. achilles tendon rupture and tendinopathy in male former elite athletes. Clin J Sport Med 2005;15(3): 133-35. 63. King J, Zhao J, Clingan P, Morris D. Randomised double blind placebo control study of adjuvant treatment with the 51. Ferretti A, Puddu G, Mariani PP, Neri M. Jumper’s knee: an metalloproteinase inhibitor, Marimastat in patients with inoper- epidemiological study of volleyball players. Physician and able colorectal hepatic metastases: significant survival advan- Sportsmed 1984;12(10): 97-106. tage in patients with musculoskeletal side-effects. Anticancer Res 2003;23(1B): 639-45. 52. Knobloch K, Yoon U, Vogt PM. Acute and overuse injuries correlated to hours of training in master running athletes. Foot 64. Khaliq Y, Zhanel GG. Fluoroquinolone-associated Ankle Int 2008;29(7): 671-76. tendinopathy: a critical review of the literature. Clin Infect Dis 2003;36(11): 1404-10. 53. Wang H, Lin J, Pan SL, Wang TG. Sonographic evaluations in elite college baseball athletes. Scand J Med Sci Sports 65. Marie I, Delafenetre H, Massy N et al. Tendinous disorders 2005;15(1): 29-35. attributed to statins: A study on ninety-six spontaneous reports in the period 1990-2005 and review of the literature. Arthritis 54. Sein ML, Walton J, Linklater J, Appleyard R, Kirkbride B, Rheum 2008;59(3): 367-72. Kuah D, et al. Shoulder Pain in Elite Swimmers: Primarily Due to Swim-volume-induced Supraspinatus Tendinopathy. Br J Sports 66. Ames PR, Longo UG, Denaro V, Maffulli N. Achilles tendon Med 2008:doi:10.1136/bjsm.2008.047282. problems: Not just an orthopaedic issue. TIDS 2008: 1-5.

55. Melchior M, Roquelaure Y, Evanoff B, Chastang JF, Ha C, 67. Benjamin M, McGonagle D. The anatomical basis for disease Imbernon E, et al. Why are manual workers at high risk of upper localisation in seronegative spondyloarthropathy at entheses limb disorders? The role of physical work factors in a random and related sites. J Anat 2001;199(Pt 5): 503-26.

November 2008 65 Personal Injury Claims: Quo Vadis?

Jayantilal Govind MBChB, M Med, FAFOEM, Director and Senior Staff Specialist, Occupa- tional and Pain Medicine, ACT Health at Canberra Hospital; Australian National University, Canberra ([email protected])

takeholders who have a vested interest in the ment, including medical care and returning the injured management of personal injury claims and more worker to work – be it pre-injury, alternative or even Sso in the management of chronic axial pain notional work that would expedite case-closure.7 Case coincidentally demonstrated an acute attitudinal change managers have multiple roles. Within the ambit of a single with the publication of the International Association for the claim, they serve multiple stakeholders simultaneously. In Study of Pain’s (IASP) monograph on Back Pain in the their “administrative” role, case managers process claims, Workplace. By denying the reality of chronic axial pain, pay wages and bills. As “watchdogs” they monitor health this monograph defined chronic low back pain not as a care services and the “medical necessity” thereof. In a “medical problem,” but as a problem of “activity intoler- “supportive” role they liaise and co-ordinate the passage ance”.1 Yet paradoxically, the same monograph advo- of the claim with the legal fraternity, health care and cated that the “medical management” should not be “pain rehabilitation providers, the employer and the worker. contingent” but rather “time contingent.” The rationale for Throughout, case managers are accountable either to the this was not articulated, and evidentiary basic science – as insurer or to government instrumentalities that administer one would expect in cardiorespiratory and other medical the relevant Act. disorders – was conspicuously absent. The taskforce Nomogenic disorder is a newer kind of impairment and further recommended that those who fail to achieve res- disability created by such a rigid and inflexible system.8 toration of function and return to work were to be reclas- Analogous to an iatrogenic disorder, nomogenic disorder sified as “unemployed.” Despite its irony, it is a sad describes those psychopathologic disorders in which the commentary for the premier scientific body in pain medi- law and its application play an etiologic role.8 This is further cine to deny the existence of chronic axial pain, to encour- exacerbated by unique pressure placed on health care age unemployment and its psychosocial upheavals and providers, such that their traditional role as a healer has for this Task Force to promote itself as a self-appointed been transformed into that of a “medical police”. The surrogate gatekeeper to a non-medical system principally process also undermines the quality of health care per- ensconced in claims management, cost containment, and missible, devalues the (treating) doctor-patient relation- cost reduction. ship and hinders access to unbiased clinical assess- Yet the medical profession cannot totally abrogate the ment.9 Many claimants say they have experienced a loss need for cost containment. In 1992 the total cost of of esteem, self-worth and dignity: a traumatic separation occupational injuries in California was at least A$20 bil- from the workplace and an exposure to an overwhelming lion2 and by 2000 Washington State outlaid $472.4 million range of health care professionals. Inappropriate and for medical care only.3 Commensurate with the rapid ineffectual treatment is said to prolong absence from expansion of Health Maintenance Organizations (HMOs), work, causing financial loss, anger and stress anxiety, physicians so affiliated had a greater tendency to classify whilst adversarial medical consultations could lead to claims as compensable under workers’ compensation disenfranchisement.10 than did other physicians.4 Levied too, is the indictment of With its newly found epiphany, some stakeholders in- self-referral by physicians outside the bounds of “medical cluding insurers, government instrumentalities and necessity”.5 Self-referrals were associated with costly and anointed members of the health care profession dictate excessive administration of inappropriate multimodal the management of work related injuries according to treatments, generating positive revenue enhancement “evidence based guidelines”, but fail (or refuse) to appre- but negative medical outcomes – causing Congress to ciate that inherent within such mantra is: pass legislation prohibiting the referral of Medicaid and · a failure to define the level or hierarchy of evidence, or Medicare patients for any of the 11 designated health that, services – from clinical labs to prosthetic supplies – with · evidence can be conjured to suit self-interests; which the referring physician had a financial relationship.5 · an absence of validation of most published guidelines, In most Western societies, changes in Workers’ Com- and, pensation legislation induced an inflexible system of case · problems associated with insurance-funded research.11 management. Defined as a set of “logical steps and a Published guidelines rely heavily on randomized control process of interaction within a service network which trials for their conclusions, irrespective of quality and assures that a client receives needed services in a sup- validity, and what is not universally known is that policy portive effective efficient and cost-effective manner”6 case- makers legitimized randomized controlled trials (RCTs) management is primarily pre-occupied with cost contain- so that the medical profession could be regulated.12 Au-

66 Australasian Musculoskeletal Medicine Personal Injury Claims: Quo Vadis?

thors of putative “evidence based guidelines” have carefully omitted “integrating individual clinical expertise ... Conclusion and ... compassionate use of individual patient’s predica- In the USA, approximately 48 million patients suffer from ments, rights and preferences”13 in making decisions chronic pain and they suffer needlessly, because al- about patient care. By a process of selective conceptual- though the technology is available, 90% cannot access ization, third party funders and legislators have hijacked it.10 What is at stake here is the erosion of the real standard the principles of evidence based medicine, principally and of care.28 Recognizing a constitutional right to adequate solely to contain costs, as aptly exemplified in a recent pain relief has the potential to remedy any inequalities.29 publication by the Bone and Joint Decade Task Force on In a throw-away society, when bad evidence happens to Neck Pain.14 good treatments30 the “injured worker suffers the same Insurers do this by refusing to reimburse the costs of fate as the plastic cup”.31 treatment that are not “medically necessary” and by refusing to pay more for the treatment of a particular problem than the predetermined average cost of treating that problem within a particular patient population.15 Rather than judiciously incorporating the current best evidence, References pre-eminent in the postulations of guideline authors is the 1. Fordyce WE (ed). Back Pain in the Workplace. Task Force on rationing – and not rationalizing16,17 of health care18,19 To be Pain in the Workplace. International Association for the Study of trustworthy and accepting, authors of guidelines must Pain. Seattle; IASP Press, 1995, p.xiii. demonstrate the legitimacy of their process through clini- 2. Leigh JP, Cone JE, Harrison R. Cost of occupational injuries cal governance.20 and illness in California. Preventive Med 2001; 32: 393-406. No system of injury compensation can function without the expert evidence of physicians, irrespective of qualifi- 3. Wickizer TM, Franklin G, Gluck JV, Fulton-Keoe D. Improving cations.21 Under most workers’ compensation systems, a quality through identifying inappropriate care: the use of guide- caveat to reimbursement is that treatment must be appro- line based utilization review protocols in the Washington State priate, reasonable and medically necessary. The concept Workers’ Compensation System. J Occup Environ Med 2004; of “medical necessity” actually functions as a principle of 46: 198-204. allocation and gate-keeping22 – because insurance companies fear that funds will be siphoned into a bottomless 4. Butler RJ, Hartwig RP, Gardner H. HMOs, moral hazard and cost shifting in workers compensation. J Health Econ 1997; 6: pit. Thus, pre-emptively, insurers and third party payers 191-206. rely on “utilization management/review” boards to reduce the consumption of “unnecessary and inappropriate” health 5. Baer N. Fraud worries insurance companies but should care services.23 Traditionally, insurers’ decisions are based concern physicians too, industry says. Can Med Assoc J 1997; on the idea that without the service harm will come to the 156: 251-56. patient and with that service potentially beneficial outcome will result. Setting such threshold is illusionary 6. Kenny DT. Case management in occupational rehabilitation: because patients and providers, insurers and courts have would the real case manager please stand up? Aust J Rehabil different values and objectives.24 Whilst clinical facts may Counselling 1995; 1: 104-17. determine “medical necessity”, ethically and morally, phy- 7. Franche RL, Baril R, Shaw W et al. Workplace-based return- sicians so engaged must demonstrate transparency about to-work interventions: optimizing the role of stakeholders in the grounds for decisions and procedures for revising the implementation ad research. J Occup Rehabil 2005; 15: 525-42. decisions in light of challenges to assure “accountability for reasonableness”.25 8. Hayes B, Solyom CA, Wing PC, Berkowitz J. Use of psycho- In many Australian jurisdictions, such decision-making metric measures and nonorganic signs testing in detecting process is delegated to “approved medical specialists” nomogenic disorders in low back pain patients. Spine 1993; 18: and in at least one Australian state it appears that medical 1254-59. expertise has been conferred by Parliamentary decree in 9. Niemeyer LO. Social labelling, stereotyping and observer bias preference to a university degree. In this way the “hired- 26 in workers compensation: the impact of provider patient interac- gun” is legitimized. However, a trend to hold expert tion on outcome. J Occup Rehabil 1991; 1: 251-69. witnesses liable for their professional errors is gaining momentum.27 10. Roberts-Yates C. The concerns and issues of injured workers in relation to claims/injury management and rehabilitation: the need for new operational frameworks. Disability and Rehab 2003; 25: 898-907.

11. Merskey H, Teasell RW. Problems with Insurance-Based research on chronic pain. Med Clin Nth Am 2007; 91: 31-43.

November 2008 67 Personal Injury Claims: Quo Vadis?

12. Oakley A. Experimentation and social interventions: a forgot- Accessed 17.04.08. ten but important history. Br Med J 1998;317: 1239-42. 29. Benson SW. The pain of irresponsible pain management. 13. Sackett DL, Rosenberg WMC, Gray JAM et al. Evidence Oncology Issues 2003 (July/August): 21. based medicine: what it is and what it isn’t: it’s about integrating individual clinical expertise and the best external evidence. Br 30. Carr DB. When bad evidence happens to good treatments. Med J 1996; 312: 71-72. Reg Anesth Pain Med 2008; 33: 229-40.

14. Carragee EJ, Hurwitz EL, Carroll LJ et al. Treatment of Neck 31. Kryspin J, Phillips H. Personal injury compensation: the cure of Pain. Spine 2008; 33: S153-S169. that fails. Humane Medicine Health Care. www.humanehealthcare. com/Article.asp?art_id=343. Accessed 20.01.07. 15. Weinman BP. Freedom from Pain. Establishing a constitutional right to pain relief. J Legal Med 2003; 24: 495-539.

16. Ratmell JP. Rational use of new modalities for the treatment of back pain. www.com/asa2005/rcl-_SOURCE/131_Ratmell.pdf. Accessed 31.07.2007. Suggested readings 1. Tucker KL. Provider accountability for inadequate pain man- 17. Bogduk N. Evidence-informed management of chronic low agement. In Weiner RS (Ed). Pain Management. A practical back pain with facet injections and radiofrequency neurotomy. guide for clinicians.6th ed. American Academy of Pain Manage- Spine J 2008;8: 56-64. ment, 2002, pp.935-38.

18. Gibson JNA, Waddell G. Surgery for degenerative lumbar 2. Hogerzeil HV, Samson M, Casanovas JV, Rahmani-Ocora L. spondylosis: updated Cochrane Review. Spine 2005; 30: 2312- Is access to essential medicines as part of the fulfilment of the 20. right to health enforceable through the courts? Lancet 2006;368:305-11. 19. Gibson JA, Waddell G. [Letter in Response]. Spine 2006; 31: 1402-140. 3. Mendelson G, Mendelson D. Medicolegal aspects of pain management. Pain Reviews 1997; 4: 244-74. 20. Samanta A, Samanta J. Evidence-based medicine. A clinical governance tool for rationalising or rationing health care? Clin 4. Hyman CS. Pain management and disciplinary action: how Governance 2005; 10: 308-13. medical boards can remove barriers to effective treatment. J Law Med Ethics 1996; 24: 338-43. 21. Duncan, G. Workers’ Compensation and the Governance of Pain. Economy and Society 2003, 32: 449-77. 5. Furrow R. Pain management and provider liability: no more excuses. J Law Med Ethics 2001; 29: 289-51. 22. Sabin JE, Daniels N. Determining “medical necessity” in mental health practice. The Hastings Centre Report 1994; 24: 6. Shapiro RS. Health care provider’s liability for inappropriate file://H:\CM5.htm. Accessed 08.02.08. pain management. J Law Med Ethics 1996;24: 360-64.

23. Wickizer TM, Lesler D. Utilization management: issues, 7. Weinman BP. Freedom from pain: establishing a constitu- effects and future prospects. Ann Rev Pub Health 2002; 23: 233- tional right to pain relief. J Legal Med 2003; 24: 495-539. 54. 8. Shapiro RS. Liability issues in the management of pain. J Pain 24. Glassman PA, Model KE, Kahan JP et al. The role of medical Symptom Management 1994; 9:146-52. necessity and cost effectiveness in making medical decisions. Ann Intern Med 1997; 126: 152-56. 9. Abraham I, Killachey-Jones B. Lack of evidence-based research for idiopathic low back pain. The importance of a specific 25. Daniels N. Accountability for reasonableness. Br Med J diagnosis. Arch Intern Med 2002;162: 1442-48. 2000; 321: 1300-1301. 10. Havighurst CC, Hutt PB, McNeil BJ, Miller W. Evidence: its 26. Meister M, Masella R. Have gun will travel: the role of the meaning in health care and in law. J Health Politics, Policy and expert witness before and during litigation. Seminars Orthodon- Law 2001; 26: 195-215. tics 2000; 8: 234-37. 11. Langworthy J, Clow W, Breen. Low back pain: barriers to 27. Hansen M. Experts are liable, too. Am Bar Association J effective clinical governance. Clin Governance 2005; 10: 281- 2000; 86: 17-18. 90.

28. Fisher P. Defending the real standard of care. Fam Pract 12. Daniels N. Justice, Health and Healthcare. Am J Bioethics Manag. 2008; 15(2).www.medscape.com/view article/570383. 2001;1: 2-16.

68 Australasian Musculoskeletal Medicine Discography - Making the Diagnosis by Provocative Means. Part 2.

Dr Victor Wilk MBBS, Grad Dip Mus Med, Masters Pain Med, Medical Director Brighton Spinal Group, Melbourne ([email protected])

Introduction consultations and comments in italics below: n the November 2007 issue of Australasian Musc- 01/10/2008 (Wednesday) 9:16 am with Dr Victor Wilk uloskeletal Medicine we looked at the correlation (VW) Ibetween lumbar disc morphological changes and Medical initial consultation pain in the general population. We know that there are certain changes in the disc seen on MRI that do correlate HISTORY: WC injury 7/7/08 official date, but gradual with pain, but are nonetheless present in significant pro- onset of low back and left leg pains at work. No specific portions of the normal population. We also examined trauma though, and no time off work. Some tingling was some of the key evidence questioning the validity of felt in the left foot, dull ache throughout whole left leg. No provocative discography as the gold standard in diagnos- real shooting/electric shock pains in the left leg. Pains bad ing discogenic pain. at night – can’t lie on his back at night. Some back pain in Since then we have had the “great debate” on discogra- addition to leg pains, but leg pain is worse. Physiotherapy phy (between Professor Nikolai Bogduk and me) at the was not making any difference. Pain was there most of annual scientific meeting of Australasian Musculoskeletal time – worse bending forwards, unable to lift anything Medicine in Melbourne in October 2008. The debate heavy. continues and the jury is still out as to whether there is a clinical role for discography. In this article I will examine the WORK: His job is systems operator – administration job principle of provoking pain to make a specific diagnosis. managing all computers in the store and checking pricing. Sitting on and off.

PAST HISTORY: WC injury 12 years ago at Woolworths when doing lots of heavy lifting – order writer at the time – Finding the nociceptor on the day of injury he was squatting down doing orders There are a few aspects of musculoskeletal medicine and waddling along the isles when he stood up and twisted practice that differentiate it from mainstream medicine. and felt sharp pains across the back worse on the right The taking of a detailed pain history including the assess- side, but with no leg pains. He was off work for one month, ment of biomechanical factors leading to pain and assess- recovering with lots of physio over 6 months. Occasional ing the quality of the pain are important. We also put a lot pains since. of emphasis on trying to find the source of pain by performing a more careful detailed examination looking FAMILY HISTORY: Nil relevant for abnormal mobility and tenderness. Over the years, these tender spots near the spine have been described GENERAL HEALTH: Weight ~ 100 kg – the same over the variously as paravertebral muscle spasm, facet joint ten- last 8 years derness, zones of irritation, tendonitis and enthesopathies, myofascial trigger points, interspinous ligament pain, HOBBIES: Likes bush walking – but he can’t get far, walks iliiolumbar ligament strain and, more recently, nerve en- the dogs, 3 sons – 14, 15, and 17 trapment (greater occipital nerves in the upper neck, cluneal nerves over the iliac crests). TREATMENTS: Traction, interferential (IF), massage, The diagnosis in each of these examples relies on home exercises finding the tender spot and reproducing the patient’s pain. The site and quality of the pain and the texture of the MEDICATION: Nil underlying tissues lead to the hypothesis of a likely nociceptor. The reproduction of the exact same pain is said to INVESTIGATION: CT scan lumbar 29/8/08 – moderate be proof of the diagnosis. However, what I have discov- left postero-lateral disc prolapse L5/S1 ered over the years (and argued recently) is that provoking pain alone is not specific enough to make a diagnosis. Let EXAM: Physical: Height: 178 cm; Weight: 110 kg; BMI: me explain by way of example in a real patient I have seen 34.72; Abdominal obesity. Walks with slight limp, F=60, recently – Mr GD, aged 48. Here are my actual notes of E=10, SB = 15 bilaterally, HIPS ok, SLR supine left 40*,

November 2008 69 Discography - Making the Diagnosis by Provocative Means

right 60*, slump test positive for left calf pain and tingling tender over the left Post Superior Iliac Spine (PSIS), in foot on the left side only. Neurology – reflexes ok, power reproducing the ache into the left leg. ok, sensation ok, palpation of back – no spasm, but was tender over the left L5 region. PLAN: Injection of a total of 3 ml 1% xylocaine with adrenaline with a 25 g 38 mm needle to the left PSIS 80 ASSESSMENT: Most likely moderate left L5/S1 prolapse mm needle to a depth of 40 mm. This reproduced the exact with some radicular pain features, but no radiculopathy. leg pain on contacting bone – pre-injection pain was level 5 out of 10, and increased to 10 with tingling in the left foot. PLAN: Recommended epidural injection of local anesthetic Post-injection pain after 5 mins was slightly worse. The left and corticosteroid. leg pain increased to 6 out of 10. Mr GD was asked to keep Interesting points to note: firstly, the slightly atypical a pain diary (Figure 1). history of radicular pain – the leg pain is dull/aching in quality, but on balance with the story of leg pain radiating Figure 1. Pain chart for injection PSIS with 1% xylocaine. to the foot, leg pain greater than back pain and associated pins and needles in the foot, it sounds like it may be Left buttock Left calf radicular. The examination findings confirm a moderate Pre-injection 2 5 restriction of straight leg raise worse on the affected side, On bone contact 10 10 with some increased distal leg pain on slumping. Neuro- 5 mins after 4 6 logical tests reveal no radiculopathy, but there is confirma- 15 mins 8 8 tion on the CT scan of an appropriate disc prolapse. I 30 mins 9 8 thought it would be reasonable to proceed to an epidural 60 mins 10 8 corticosteroid injection. 90 mins 10 8 2 hours 10 8 09/10/2008 (Thursday) 10:17am with Dr VW Left L5/S1 Transforaminal epidural injection under fluor- When I reviewed him 2 weeks after the epidural injection oscopy Mr GD stated that he had good pain relief for one week suggesting the diagnosis of disc prolapse was correct – PROCEDURE: Left L5/S1 Transforaminal epidural injec- but the effects were not long lasting. The examination tion under fluoroscopy (L5 nerve root) 22 g x 127 mm revealed more prominent tenderness at the left PSIS – needle to depth 115 mm. Position checked on AP and about 4 cm lateral to the midline at the level of L5/S1 lateral films. Some nausea was felt during positioning of approximately. This area is commonly tender in many the needle, but this settled. Contrast Ultravist 240 showed patients presenting with low back pain. As his pain was good position with good epidural spread. 1 ml 1% xylocaine somewhat atypical I thought it may be worth trying a local + 1 ml Celestone Chronodose was injected slowly. Pain injection there. In this case when the needle contacted was 7 out of 10 before injection in the left buttock and leg. bone it elicited a severe sharp pain response with repro- After injection the pain eased to level 0 in the left buttock duction of the area of leg pain to a level of 10 out of 10 and but with only slight relief in left calf. Mr GD was asked to bringing on the tingling in the foot. I am quite sure the keep a pain diary, and see Dr VW in 2 weeks. needle tip was nowhere near any nerve roots having Straightforward epidural injection but his immediate performed an epidural one week previously. pain response is also atypical – one would expect ? hope On the basis of provocation testing one would have to for complete relief of the calf pain as well as the buttock rate this latter PSIS injection as being very specific for his pain. One interpretation may be that some of the calf pain pain, and yet the local anesthetic failed to block the pain. is somatic referred pain from the disc itself which we Why is this so? cannot anesthetize or from some other structure. The explanation for this common phenomenon comes from theories of convergence of neural pathways in the 22/10/2008 (Wednesday) 8:04am with Dr VW, for 25 dorsal horn. The same pathways that give rise to referred minutes pain patterns are also responsible for convergence of pain Medical review from nociceptive sources. In acute inflammation, peripheral sensitization occurs where there is an increase in HISTORY: Was really good for one week post epidural – release of inflammatory mediators and an enlarged field of then pain recurred last 3 days – today almost as bad as hyperalgesia results. Typically with any moderate to se- before. The tingling present in the foot was now back vere pain there is also likely to be an element of central again. sensitization where the modulating neurones deep in the dorsal horn become more sensitive to peripheral stimuli. EXAMINATION: Walking with a mild limp, F=60, E=15, SB These two phenomena often combine in low back pain = 20 bilat – better than before injection, Hips ok, SLR syndromes. A regional hyperalgesia results. Aage Indahl supine left 50* now, palpation revealed he was quite published his PhD in 1999 showing the interaction be-

70 Australasian Musculoskeletal Medicine Discography - Making the Diagnosis by Provocative Means

tween the disc, zygapophysial joints and the paraspinal some morphological changes on MRI scans. There may muscles and how they interplay to cause regional func- be some emerging therapies that will help these condi- tional disturbance. It is still very relevant and worth a tions. I would advocate that any new therapies be trialled read.1,2 on patients with a specific condition diagnosable on MRI In some patients, pain can be very localized to one scan. In the research setting all patients with the condition segment and there may be very localized superficial would receive the active or control therapy and all could tenderness, some reactive protective muscle tightness also receive discography. It is only in this way that we can and a possible deeper joint/disc problem. In other cases discover whether discography has any extra predictive pain may be more widespread. Anesthetizing the pain is value over and above MRI. At the present time all we know the best way to confirm a diagnosis – it is the only true gold is that if we see something abnormal in the disc on MRI, standard. However, even this gold standard has to take then that disc is more like to be painful when provoked with into account the placebo response. a needle. We must continue to keep an open mind in relation to the interpretation of findings on physical examination. I have had the odd great success in alleviating pain of several years’ duration by the simple injection of local anesthetic Further research into a tight band of tender muscle. However, I hesitate to This lack of specificity of discography has led one make the diagnosis of myofascial trigger points in every researcher, Dr Richard Derby in the USA, to investigate patient I see with local muscle tenderness and spasm. I what proportion of provocative positive discs may be believe it is important to carefully examine for alterations responsive to local anesthetic injected into the disc.3 Of 39 in local tissue texture and to try to reproduce the patient’s subjects with positive discograms, only 51% gained mod- pain by palpation or movement. We just need to keep in est relief with injection of 4% lidocaine into the nucleus mind the effects of regional hyperalgesia and the possible pulposis. Criteria for relief included a reduction of pain > 2 differential diagnoses. on a 0 to 10 pain scale on sitting. However none of the In my opinion the only case that can be made for subjects achieved improvement in other functional scores. discography in clinical practice is where the surgeon has Some would argue that they didn’t gain pain relief because made the decision to operate irrespective of the discogra- the anulus may have been largely intact and the local phy findings and that they are testing adjacent levels to agent couldn’t reach the outer anular nociceptive nerves. help plan the extent of surgery. The argument for using This may well be the case – we just don’t know. However, discography to avoid surgery does not hold in the real most of these discs had significant grade 3 or above world. A significant number of patients suffer increased anular fissures and one would expect some anesthetic pain for up to one year post discography. I have had two infiltration into the outer anular tears where the pain is patients aggravated by the procedure to the degree that thought to be generated. they ended up having fusion operations they didn’t need I believe this study adds weight to the evidence of a large and they continue to suffer with long-term disability. false positive response to discography. If we use the strict criteria of 90-100% relief of pain used to diagnose zygapophysial joint pain, false positives in the study above approach 100%. References 1. Indahl A. Low back pain – a functional disturbance. University of Oslo, Norway 1999.

Conclusion 2. Indahl A, Kaigle AM, Reikeras O, Holm SH. Interaction between the porcine lumbar intervertebral disc, zygapophysial As I have stated previously, I am a believer in the joints and paraspinal muscles. Spine 1997; 22 (24):2834-40. concept of internal disc disruption and primary discogenic pain. Some cases may not yet have developed MRI 3. Derby R. Discogenic pain - evolving standards of practice. changes – these cannot be diagnosed at present. How- Presentation, ISIS Annual Scientific Meeting, Las Vegas, 2008. ever, in the majority of cases, discogenic pain will show

November 2008 71 Pain Conundrums: Which Hypothesis? Central Nervous System Sensitization versus Peripheral Nervous System Autonomy

Dr John Lyftogt, Christchurch, New Zealand

he two hypotheses, central nervous system (CNS) vibration or tickle now connect to a different second-order sensitization and peripheral nervous system cell in the spinal cord. Their activity now may produce a T(PNS) autonomy are at first glance irreconcilable. burning pain instead of a tickle. In an article in the CNS sensitization is the reigning paradigm in main- Lancet, Loeser and Melzack3 conclude that “The brain stream pain medicine. It is shared by most members of the contains widely distributed neural networks that create an medical scientific community. image of self through genetic programmes and memories PNS autonomy is not recognized despite convincing of past experience. Afferent inputs act on this neuromatrix scientific and clinical evidence. It has yet to establish a and produce output patterns that lead to the report of pain. paradigm status and would require a scientific revolution Stress can change the interactions between the or paradigm shift for it to gain acceptance, as predicted by neuromatrix and peripheral stimuli, as can learned expe- Thomas Kuhn.1 riences and expectation.” However, a growing body of scientific evidence, old and As a consequence of the above concepts, the memory new, is addressing anomalies in the CNS sensitization of the injury leading to chronic pain and CNS sensitization concepts that have been ignored or dismissed. are now generally considered useful in the “management” Historically, ideas culminating in the CNS sensitization of chronic pain by increasingly complex multidisciplinary theory started with the Melzack-Wall article in 19652 on the teams. Gate Control Theory, which “emphasized the mecha- One anomaly in the CNS sensitization theory is its nisms of the CNS controlling the perception of a noxious impotence in curing chronic pain, despite more than 40 stimulus and thus integrated afferent, upstream proc- years of millions of dollars of research unraveling the esses with downstream modulation from the brain”.3 The mysteries of the CNS. Loeser and Melzack3 admit to this current definition of pain endorsed by the International when they conclude their article in 1999 by saying, “In both Association for the Study of Pain (IASP) is a logical clinical and basic research, we are rapidly gaining useful outcome of this theory: “Pain is an unpleasant sensory information that will lead to more effective care for those and emotional experience associated with actual or po- who suffer pain”. In the introduction to the third edition of tential tissue damage, or described in terms of such The Textbook of Pain, Wall and Melzack6 express the damage”.4 hope that in their next edition they will be able to announce According to Howard L Fields,5 “The pain pathway we to the world a cure for chronic pain. This inability to cure are all familiar with normally begins with tissue damage, chronic pain has led mainstream medicine to build up an inflammation, and traumatic injury. It starts with impulses immutable conviction that any health professional claim- out in the periphery. These are propagated to the spinal ing the opposite is deluding himself or herself and his or cord, cross in the contralateral spinothalamic tract, deliv- her patients. Popularized books on the management of ered to the thalamus and then widely distributed to the chronic pain by reputable and leading specialists thus cortex. Injury to a peripheral nerve somehow causes an warn patients seeking a cure for their chronic pain to be increase of activity in this pathway somewhere along this wary because offering a cure is akin to deception.7 A pathway.” He goes on to say that this increase of activity further anomaly is the belief there is no demonstrated could come from either greater activity in the nociceptors pathology in the PNS satisfactorily explaining chronic in the periphery or by removal of some sort of inhibition in pain. This view is detailed in the introduction to Wall and the CNS releasing the transmission neurons from inhibi- Melzack’s Textbook of Pain6 in 1997. tion. Further, he argues that these neurons are now The last 40 years of basic research into the PNS has spontaneously active and produce a pain signal. Animal shown the opposite. Since Jancso et al. published their studies have shown that these nerves themselves be- Direct Evidence for Neurogenic Inflammation and its Pre- come pain generators. It is also known that damage to vention by Denervation and by Pretreatment with Capsai- selectively large myelinated fibers will cause central fibers cin in 19678 a growing number of scientists have system- to fire more to any peripheral stimulus. There is also atically unraveled the PNS response to injury. Bennett in evidence that damage to peripheral nerves results in 19999 summarized this: “Painful peripheral neuropathies spontaneous activity in second-order neurons. Injury to begin with nerve injury caused by disease or trauma. This peripheral nerves can also possibly cause “rewiring” in the injury will result in an inflammatory reaction, a neuritis that spinal cord where fibers from the periphery normally will mobilize the immune system.” Subsequent changes responding to light touch producing the sensation of may result in more slowly developing mechanisms of

72 Australasian Musculoskeletal Medicine Pain Conundrums: Which Hypothesis?

abnormal pain that underlie the chronic phase of painful in cholinergic and adrenergic nerves. The intimate con- neuropathy. nection between sensory and autonomic nerves is par- Douglas Zochodne from the Neuroscience Research ticularly poignant in children born with congenital insensi- Group in Calgary10 examined the role of the microenviron- tivity to pain in hereditary sensory and autonomic neu- ment and microcirculation of the injured and regenerating ropathy (HSAN type I-IV). The absent or abnormal periph- peripheral nerve trunk and concluded in his seminal paper eral nerves are the reason for severe disfiguring sequelae on peripheral nerve response to injury: “Better under- of trauma, inability to repair tissue or adequately mobilize standing of these and other events in injured nerve trunks the immune system, often leading to death from infection is needed to help solve the two cardinal problems of during childhood. The recent finding of opioid receptors on peripheral nerve injuries: peripheral sensory axons15 led to some speculation that 1) functional disability from impaired regeneration, and these µ opioid receptors (MORs) may have an anti- 2) the development of disabling neuropathic pain.” nociceptive action. This motivated Zochodne et al,16 to Peripheral nerves respond to injury in a unique way. examine the function and expression of local MORs Instead of ischemia, peripheral nerves develop increased associated with the chronic constriction injury (CCI)17 endoneurial blood flow. Trauma-induced ischemia in all model of sciatic neuropathic pain in rats. Low dose mor- other tissues may lead to cell death and release of phine was injected percutaneously near the nerve. They arachidonic acid, stimulating COX I, COX II, and 5-LOX concluded that their positive findings “may provide a pathways upregulating prostaglandin production and tis- therapeutic direction for the treatment of certain focal sue inflammation. Peripheral nerve injury leads to “dump- neuropathic lesions in humans”. ing” of calcitonin gene related peptide (CGRP), substance Successful treatments of painful peripheral neuropa- P (SP) and nitric oxide (NO) from nervi nervorum, the thies or chronic recalcitrant pain have been described in extensive innervations of the connective tissue of periph- the literature. Whether one goes along with the rationale eral nerve trunks, the epi-perineurium. CGRP, SP, and for these treatments is less relevant. After all, clinicians NO are vasodilators with CGRP and SP also potent would consider it unethical to cease treatment with lithium upregulators of vascular permeability of the vasa nervorum carbonate or chlorpromazine simply because the mode of and neighboring blood vessels. The result is a rapid action is unknown. By 1965 George Hackett18 had pub- increase in the endoneurial blood flow and neurogenic lished the results of prolotherapy treatment of 1800 cases inflammation of the nerve trunk itself and the surrounding of chronic low back pain, with an 82% success rate and a tissues. This forms the basis of the Triple Response 12-year follow up. He published 16 articles and one book described by Lewis in 192711 with the well-known “line, on his treatment. Also in 1965 Melzack and Wall published wheal and flare”. Lewis also identified the Axon Reflex, their Gate Control Theory of Pain. Their Textbook of Pain, showing axonal impulses travelling in an orthodromic (to published in 1997, does not reference prolotherapy. Nei- CNS) and antidromic direction. In 1901 Bayliss12 found ther does it reference neural therapy. This treatment was that stimulation of the dorsal root ganglion (DRG) resulted developed in Germany in the 1940s by Drs Ferdinand and in peripheral vasodilatation. He postulated afferent and Walter Huneke. Lidocaine is used to treat chronic pain by efferent conduction. Some 20 neuropeptides and targeting postulated “interference fields” that cause “blocks” neurotransmitters are known to be involved in neurogenic in the autonomic nervous system leading to chronic pain. inflammation.13 Most of these have been cloned, including This treatment is highly successful and practised widely in their antagonists, their receptors, and receptor antago- Germany and Spain by more than 5000 medical practi- nists. Evidence of pivotal roles for specific neuropeptides tioners. Most of the literature is in German and this may be is lacking, hence no drug treatment has yet been devel- the reason there is little knowledge of this treatment in the oped against neurogenic inflammation and the concept of English-speaking world. neuromodulation is rationalizing the impasse. It has also The growing scientific evidence supporting the view that been found that some neuropeptides (CGRP, peptide YY neuropathic pain syndromes are caused by unremitting - PYY - and neuropeptide Y - NPY) can be released from peripheral neurogenic inflammation involving the auto- non-neuronal cells and also in a paracrine fashion from nomic and sensory nerves may lead to renewed interest neurons. Some anti-inflammatory neuropeptides such as in prolotherapy and neural therapy as these treatments melanocyte-stimulating hormone (MSH), vasoactive in- are effective and seem to target the PNS. The author has testinal peptide (VIP) and pituitary adenylate cyclase- now treated more than a 1000 patients with subcutaneous activating polypeptide (PACAP) may be released to termi- prolotherapy targeting neurogenic inflammation of periph- nate inflammation under physiological conditions. Thus eral nerve trunks in much the same way as Zochodne’s neuromediators are not all pro-inflammatory but regulate percutaneous near nerve injections with low-dose opioids. all phases of the inflammatory response. Published results19-21 are promising for recalcitrant lum- The complexity of responses of the peripheral nervous bago, shoulder, knee, elbow pain, and achillodynia. system was also highlighted by Burnstock in 1976.14 He Patients with chronic neuropathic pain will continue to introduced the concept of co-transmission in the auto- suffer needlessly if physicians remain fixed on the reigning nomic nervous system with neuropeptides also contained paradigm that can suggest only “pain management” when

November 2008 73 Pain Conundrums: Which Hypothesis?

there are well-documented alternatives available that may and Microcirculation. Biomed Rev 1997; 8: 37-54. offer a cure. 11. Lewis T. Released substances the cause of the triple response. In: The blood vessels of the heart and their responses. London; Shaw and Son.

12. Bayliss WM. On the origin from the spinal cord of the vaso- References dilator fibers of the hind-limb, and on the nature of these fibers. 1. Kuhn T. The Structure of Scientific Revolutions. 1962. J Physiol 1901; 26: 173-209.

2. Melzack R, Wall PD. Pain Mechanisms: A New Theory. 13. Brain SD, Cox HM. Neuropeptides and their receptors: Science 1965; 150: 971-79. Innovative science providing novel therapeutic targets. Br J Pharmacol 2006; 147: S202-S211. 3. Loeser J D. Melzack R. Pain: an overview. Lancet 1999; 353: 1607-09. 14. Burnstock G. Do some nerve cells release more than one transmitter? J Neurosci 1976; 1: 239-48 co-transmission. 4. Merskey H, Bogduk N. Classification of Chronic Pain. Seattle: International Association for the Study of Pain Press, 1994, 15. Coggeshall RE, Zhou S, Carlton SM. Opioid receptors on p.210. peripheral sensory axons. Brain Res 1997;764: 126-32.

5. Fields H L. Power Point presentation Medscape Family 16. Truong W, Cheng C, Xu Q et al. µ Opioid Receptors and Medicine 2007. Analgesia at the Site of a Peripheral Nerve Injury. Ann Neurol 2003; 53: 366-75. 6. Wall PD, Melzack R, eds Textbook of Pain. 3rd ed. Edinburgh; Churchill Livingstone, 2004. 17. Bennett GJ, Xie YK. A peripheral mononeuropathy in rat that produces disorders of pain sensation like those seen in man. 7. Nicholas M, Molloy A, Tonkin L, Beeston L. Manage your pain: Pain 1988;33: 87-107. practical and positive ways of adapting to chronic pain. Sydney; Australian Broadcasting Corporation Books, 2001. 18. Hackett G. Ligament and Tendon Relaxation Treated by Prolotherapy. 3rd ed. Springfield, IL; Charles Thomas, 1958. 8. Jancso N, Jancso-Gabor A, Szolcsanyi J. Direct Evidence for Neurogenic Inflammation and its Prevention by Denervation and 19. Lyftogt JA. Prolotherapy for recalcitrant lumbago. Aust Mus- by Pretreatment with Capsaicin. Br J Pharmac Chemother 1967; culoskeletal Med 2008; 13(1): 18-20. 31: 138-51. 20. Lyftogt J. Subcutaneous prolotherapy treatment of refractory 9. Bennett GJ. Does a neuroimmune interaction contribute to the knee, shoulder and lateral elbow pain. Aust Musculoskeletal genesis of painful peripheral neuropathies? Proc Natl Acad USA Med 2007; 12(2): 110-12. 1999; 96(14): 7737-38. 21. Lyftogt J. Subcutaneous Prolotherapy for Achilles 10. Zochodne D. Local Events within the Injured and Regener- tendinopathy: The best solution? Aust Musculoskeletal Med ating Peripheral Nerve Trunk: The Role of the Microenvironment 2007; 12(2): 107-109.

74 Australasian Musculoskeletal Medicine Treating Inferior Heel Pain with Vitamin D3 Dermal Cream: A clinical report on two case histories

Dr John Lyftogt, Christchurch, New Zealand

Abstract nferior heel pain, also known as plantar fasciitis, is a peripheral neuropathic pain syndrome due to persist- Ient neurogenic inflammation of the medial calcaneal branches of the tibial nerve. Vitamin D3 is considered to be a neurosteroid with neuroprotective properties. This is the first report of two patients responding favorably to twice daily applications of vitamin D3 transdermal cream for this difficult-to-treat condition.

Introduction Inferior heel pain, also known as plantar fasciitis or policeman’s foot, is common both in runners and non- runners. Incidence has been estimated at 10-15% of all patients presenting with foot pain and 10% in runners. The incidence peaks between 40 and 60 years in the general population and earlier in runners. In 30% the pain presents bilaterally.1 Figure 1. Cutaneous innervations, plantar aspect R foot It is a condition resistant to most interventions and often treated with corticosteroid/local anesthetic injections. This treatment is painful and likely to be ineffective or harmful.2 A number of observational studies found a high rate of plantar fascia rupture and other complications associated Methods and results with corticosteroid injections, which may lead to chronic Prospective recovergrams5 were recorded for each disability in some people.2 patient, monitoring weekly VAS pain scores. One telephone follow up survey with a mean length of 47 Patients were instructed to massage a small amount of months on 100 people treated conservatively found that vitamin D3 transdermal cream into the painful area twice 82 people had resolution of symptoms, 15 had continued daily and after activity, followed by heat application where symptoms, and three had had to change work status and possible. had limited activity.2 The vitamin D3 transdermal cream consisted of chole- The author has treated more than 30 patients with calciferol (25(OH) D3) 12.000 IU/gram. inferior heel pain with subcutaneous prolotherapy with Both patients were monitored for serum vitamin D and encouraging results (unpublished). However, repeated calcium levels at the end of treatment. Vitamin D and plantar injections are distressing and infection occurs serum calcium levels were all in the normal range. infrequently unlike treatment with subcutaneous prolo- At the time of writing this report both patients were therapy elsewhere. running pain free, although still using the cream. Earlier Vitamin D3 has recently been shown to have suspected experimental clinical experience suggests that it is pru- analgesic properties in neuropathic pain.3 Inferior heel dent to continue the vitamin D3 transdermal cream until all pain is best viewed as a neuropathic pain syndrome4 pain and tenderness has resolved. caused by persistent neurogenic inflammation of the medial calcaneal branches of the tibial nerve (see Figure 1). The author postulated that local application of a vitamin Patient 1 D3 transdermal cream may have analgesic effects in the History: MM, age 46, female, elite masters middle dis- treatment of disabling pain of this self-limiting but recalci- tance runner with 2-month history of right inferior heel pain trant condition. treated initially with subcutaneous prolotherapy, compli-

November 2008 75 Treating Inferior Heel Pain with Vitamin D3 Dermal Cream

cated by infection, complaining of inability to run, difficulty walking, and pain at rest. Past history of bilateral peripatellar pain treated with failed surgical decompression, Achillodynia. VAS: visual analogue scale 0= no pain 10= worst imaginable pain

Year Month 06 07 08 09

08 Day 12 19 26 03 10 17 24 31 07 14 21 28 04

8 x

7 x

6 x

5 xxx

4 x

3 x

2 xxx

1 xx

0 Weeks Patient 2 History: JF, age 24, female, fitness trainer with 8-month history of left inferior heel pain, complaining of inability to run, difficulty walking, affecting work. Has prior treatment with physiotherapy and podiatry without effect. Past history of bilateral Osgood Schlatter Disease, right medial shin splints and peripatellar pain VAS: visual analogue scale 0= no pain 10= worst imaginable pain

Year Month 08 09 10

08 Day 15 22 28 12 19 26 03

7 x

6 x

5 x

4 x

2 x

1 x

0 x Weeks

76 Australasian Musculoskeletal Medicine Treating Inferior Heel Pain with Vitamin D3 Dermal Cream

Discussion Conclusion Policeman’s foot or inferior heel pain is a painful periph- This is the first report of disabling and recalcitrant eral neuropathy precipitated by nerve injury6 to the medial neuropathic pain of the inferior heel, also known as calcaneal branches of the tibial nerve. The local milieu of policeman’s foot or plantar fasciitis, responding favorably the injured nerve will determine the likelihood of regenera- to twice daily applications of vitamin D3 transdermal tion and the development of neuropathic pain.4 Current cream. Two patients were treated and no side effects or research is suggesting a role for vitamin D in nerve repair. complications were observed. Further research into this Vitamin D is best known for its role in calcium metabo- promising and safe treatment is warranted, with particular lism and bone health, but new roles are continually being focus on the long-term beneficial effects of vitamin D3 discovered. Vitamin D is now described as a pleiomorph transdermal cream on peripheral neurogenic inflamma- seco-steroid hormone, with actions on 200 genes in at tion either in combination with subcutaneous prolotherapy least 16 different tissues. Vitamin D receptors (VDR) have or on its own. been identified in the cell nucleus and membrane, giving rise to respectively nuclear and cytoplasmic signalling pathways.7 Recent investigations have considered the mechanisms underlying the neuroprotective effect of vita- References min D and its receptors in the nervous system8 and the 1. Frater C, Vu D, Vander Wall H et al. Bone Scintigraphy Predicts effect of vitamin D on the nervous system and skeletal Outcome of Steroid Injection for Plantar Fasciitis. J Nuclear Med muscle.9 2006; 47(10): 1577-80. Rheumatologists in the UK have for many years been 2. Crawford F. Plantar heel pain and fasciitis. Br Med J Clin Evid. aware of the extremely high prevalence of hypovitamino- 2005; 13: 1533-45. Review. sis D in Indo-Asian patients, associated with high scores for musculoskeletal pain and low clinical scores for gait 3. Macfarlane GJ, Palmer B, Roy D et al. An excess of widespread and muscle strength.10 pain among South Asians; are low levels of vitamin D implicated? A growing number of articles have been published in the Ann Rheum Dis 2005;64(8): 1217-19. last five years connecting vitamin D with musculoskeletal 4. Zochodne D. Local events within the injured and regenerating pain.11,12,3 peripheral nerve trunk: the role of the microenvironment and micro- Most recently a research letter published in the April 14, circulation. Biomed Rev 1997; 8: 37-54. 2008, issue of Archives of Internal Medicine13 reported that vitamin D supplementation reduced pain levels in 5. Watson P. The Recovergram. Aust Musculoskeletal Med 2000; 5(2): 24-28. patients with diabetic neuropathy. The authors concluded “Vitamin D insufficiency is under-recognised and may be 6. Bennett GJ. Does a neuroimmune interaction contribute to the a significant contributor to neuropathic pain in Type II genesis of painful peripheral neuropathies? Proc Natl Acad Sci USA Diabetes. Vitamin D supplementation may be an effective 1999; 96(14): 7737-38. ‘analgesic’ in relieving neuropathic pain.” It is now well documented that the skin has a unique role 7. www.vitaminDcouncil.com 14 in the vitamin D endocrine system. It is the only site of 8. Klueff AV, Erimin KO, Tohimaa P. Mechanisms of neuroprotective vitamin D photosynthesis and plays a central role in action of vitamin D 3. Biochem (Mosc) 2004;69 (7): 738-41. obtaining a sufficient vitamin D status. The skin is also capable of synthesizing the active vitamin D metabolite 9. Nakagawa K. Effect of Vitamin D on the nervous system and the calcitriol (1, 25(OH) (2) D (3)) due to the presence of 1α skeletal muscle. Clin Calcium 2006;16: 1182-87. hydroxylase, although this reaction is heat labile. The skin 10. Serhan E, Newton P, Ali HA et al. Prevalence of hypovitaminosis itself is an important target organ for calcitriol where it D in Indo-Asian patients attending a rheumatology clinic. Bone regulates growth and differentiation of many cell types. 1999;25(5): 609-11. Vitamin D receptors (VDR) on cutaneous nerves may influence neurotrophin release, Ca2+ regulation and 11. de Torrente de la Jara G, Pecoud A, Favrat B. Musculoskeletal neuroimmunomodulatory effects of calcitriol. pain in female asylum seekers and hypovitaminosis D3. Clinical review. Lesson of the week. Br Med J 2004; 329: 156-57. Transdermal creams with bioidentical steroid hormones have a well established use in hormone replacement 12. Al Faraj S, Al Mutairi K. Vitamin D deficiency and chronic low back therapy. pain in Saudi Arabia. Spine 2003;28(2): 177-79. It is postulated that the application of a transdermal cream with the prohormone vitamin D3 (25(OH)D(3)) near 13. Paul L, Chen R. Vitamin D as an analgesic for Patients with Type neuropathic cutaneous nerves will upregulate the local 2 Diabetes and Neuropathic Pain. Arch Intern Med 2008;168: 771- 72. production of calcitriol and result in a neuroimmune modu- latory effect more effective than oral vitamin D supplemen- 14. Reichrath J. Vitamin D and the skin: an ancient friend, revisited. tation. Exp Dermatol 2007;16(7): 618-25.

November 2008 77 An Alternative Sacroiliac Joint Injection Technique

Dr Paul Quin, Full-time musculoskeletal and interventional pain medicine, Auckland; current president, Australasian Faculty of Musculoskeletal Medicine

ith the increasing performance of sacroiliac procedure, given a relevant information pack, and queried joint injections, both for diagnosis and treat- about allergy to shellfish, crayfish, etc. If an allergy is W ment of sacroiliac joint nociception, there is a present, the patient is given a prescription for pred- suspicion that a significant number of attempted proce- nisolone, cetirizine hydrochloride (Razene) 10 mg and dures fail in their intent. If the confirmation of intra-articular ranitidine to be taken over the 24 hours prior to the entry is the demonstration of an arthrogram with contrast procedure to obviate cross-sensitivity responses to iodo- medium, it is likely that there is a significant percentage of contrast. failures which may not show up in the literature. Anecdotal After informed consent is obtained, the patient is posi- reporting suggests that 10-50% of sacroiliac joint injec- tioned squarely prone on a C-arm fluoroscopic table, tions may not succeed which may skew outcome data generally lying flat with no pillow underneath the trunk. from sacroiliac joint reports. Rosenberg1 et al. reported in The C-arm x-ray beam is set entirely vertically with no a double blind study of 39 joint injections in 37 patients that cranial, caudal, or oblique angulation, and the inferior intra-articular injection was successful in 22 joints – a aspect of the SIJ is visualized on the screen (Figure 1). failure rate in technique of 40.5%. With the x-ray tube perpendicular to the table, the target The sacroiliac joints have been shown to be richly is identified with a metal pointer and that position is innervated and identified as sources of low back pain and marked on the skin with a skin pen. The target is the distal referred somatic buttock, groin, and leg pain. Therefore, 1 cm of the SI joint, and if more than one joint cavity is seen the injections have face validity. Providing the sacroiliac on the image intensifier, the correct target is the medial joint injections are controlled, the technique has also one (Figure 2). construct validity. If the “gold standard” of diagnosis is Usual sterile technique practice is observed and the injections of local anesthetic into the sacroiliac joint space patient is swabbed appropriately with antiseptic solution – to demonstrate pain relief, then technique failure be- we tend to use iodophor. The skin is anesthetized with comes relevant. xylocaine 1% solution at the site previously marked. Very Owing to its complex configuration, the sacroiliac joint anxious patients are offered Entenox gas for pain relief has typically been difficult to enter, especially as a blind and to aid relaxation. A 22-gauge, 5-inch straight or 10° office procedure, and even when using fluoroscopic guid- curved-tip spinal needle is advanced perpendicular to the ance. The plane of the joint is curved in three dimensions, fluoroscopic table through the skin and directed down and the posterior aspect of the joint is located medially as towards the SIJ for 20-30 mm (Figures 3 and 4). compared with the anterior aspect of the joint, which is positioned more laterally. The net plane of the joint is from postero-medial to antero-lateral. Usual fluoroscopy has utilized obliquity of the fluoroscopic tube in a medial or lateral direction to attempt to obtain a good target for needling. Unfortunately this may give the visual impression that the joint is well aligned, whereas, in fact, only a portion of the joint may be demonstrated, and which portion is demonstrated is uncertain.

The SIJ injection technique The following technique was originally described by Dussault et al. 2 in 2001 in Radiology and I have used it for SIJ injections since November, 2003. I describe it as I practise it in Auckland. The patient is advised in detail about the procedure when it is first considered. He or she is shown what is done on a skeleton of the pelvis, shown a slideshow of the Figure 1

78 Australasian Musculoskeletal Medicine An Alternative Sacroiliac Joint Injection Technique

The tube is then angled about 20°-25° by moving it in a cephalic direction to displace the postero-inferior portion of the SI joint in a caudad direction (Figure 5). This allows the accessible posterior aspect of the joint to be clearly differentiated from the inaccessible anterior aspect of the joint, which moves cephalad on the image. After moving the tube into the cephalic position (20°- 25°), the needle is then directed toward the posterior SI joint, which appears to be easily visible (Figure 6). If using a curved-tip needle, the tip of the needle is

Figure 2

Figure 5

Figure 3

Figure 4 Figure 6

November 2008 79 An Alternative Sacroiliac Joint Injection Technique

Figure 9

Figure 7

Figure 10

posterior aspect of the SIJ became more accessible with his technique. In his diagrams (Figure 8), a single medial metallic dot (solid arrow, P) is positioned on the postero- inferior SI joints, and then two slightly larger metallic dots located more laterally (open arrow, A) are affixed to the antero-inferior aspect of the SI joints. The view in Figure 8 is that with the x-ray tube perpendicular. When the image intensifier moves cranially, objects which are nearer or closer to the image intensifier move relatively in an opposite (caudad) direction to those more distant objects which appear to move in the same direction. This will separate the objects in the view. With the x- ray tube angled 20° by moving cephalad, the posterior aspects of the SI joints (solid arrow, P) project inferiorly Figure 8 and are now well outlined (Figure 9). The anterior aspects of the SI joints (open arrow, A) project superiorly and are oriented in a cephalic direction, and the convex portion of more difficult to identify. Angling the x-ray beam by moving the curve is oriented downward (closest to the joint). The it in a cephalic direction, the posterior aspect of the caudal curved-tip needle may be advanced either vertically or end of the SI joint is clearly depicted as separate from the angled 10° downward to compensate initially for the 10° remainder of the joint. curve until the needle reaches the joint. As the needle This allows easy placement of a needle directly into this contacts the firm tissues on the posterior aspect of the portion of the joint. As the joint is entered posteriorly, the joint, it is maneuvered through the ligaments and capsule needle may sometimes need to be oriented in a cephalic into the joint by advancing it about 5–10 mm, usually by direction to remain in the joint. This is best obtained with angling the needle tip slightly laterally to follow the natural the 10° curved-tip needle, with the curve directed cepha- curve of the joint. It often seems a surprise to feel how far lad (Figure 10). one must traverse to enter the joint. Intra-articular position The failure rate of this technique may well be less than is confirmed by injecting 0.2–0.5 ml of contrast material that of other techniques. My personal experience sug- through the needle to obtain an arthrogram (Figure 7). gests that I am failing to obtain an arthrogram with contrast Dussault demonstrated in his original article how the relatively less frequently than before. Some SIJs have

80 Australasian Musculoskeletal Medicine An Alternative Sacroiliac Joint Injection Technique

surrounding osteophytes which may confound the tech- • Tilt the image intensifier 20-25° down by moving it nique. cephalad but it must not be either medially or laterally I suspect that temporary leg weakness lasting 15 min- displaced. The posterior aspect of the SIJ is then clearly utes or so and up to two hours may be more frequent. It is separated from the anterior aspect and is located likely that, as the sciatic nerve is at the same level as the medially compared with the anterior joint which is more inferior SIJ, some leakage of bupivacaine onto the sciatic laterally placed. nerve may occur at times. In general, advantages include (a) no premedication • If using a 10° curved tip, centre the bevel on the required; (b) reproducible technique; and (c) low failure convexity of the curve. The tip of the curved needle is rate, and short x-ray exposure time – 36-328 seconds orientated in a cephalic direction and the convexity (mean 108 seconds) in a teaching unit (original article). orientated downward (closest to the joint). The curved My main source of unsuccessful SIJ entry was self- tip may be advanced either vertically or angled 10° deception. For a while I thought I was getting a superior downwards initially to compensate for the 10° curve view at 10–15° of cephalad image intensifier movement until the needle reaches the joint. but I started to have an increased failure rate. However, I was obtaining enough success to delude myself into • Advance the needle about 5-10 mm to pierce the thinking I was performing satisfactorily. It took me about ligaments and capsule. The needle tip is then angled six weeks and a few failed arthrograms to re-read and slightly laterally to follow the curve of the joint. review the technique. The minimum cephalad movement should produce an angle of 20°. • Inject the contrast slowly to confirm the position in the To make a 10° curved tip needle, bend the terminal 1 cm joint. Contrast runs up and into the anterior sacroiliac of the sterile 22 gauge needle with the stylus in situ into a joint. If having difficulty with a straight needle, the tip of 10° convexity while holding the tip with a sterile swab. The the needle can be bent about 10° and reinserted with bevel must face the convexity (outside) of the curve. the concavity of the curve pointing cranially, as indicated above.

• If in the joint, inject 0.5-1.0 ml bupivacaine + 1 ml Summary of sacroiliac joint triamcinolone into the joint SLOWLY. injection technique • Lie the patient on his or her stomach with vertical x-ray and screen. References

• Mark the skin over the distal 1 cm of the sacroiliac joint 1. Rosenberg JM, Quint TJ, de Rosayro AM. Computerized and apply local anesthetic to the skin. tomographic localization of clinically-guided sacroiliac joint injections. Clin J Pain 2000:16: 18-21. • Insert a 22 gauge x 5 inch needle and start to advance 2. Dussault RG, Kaplan PA, Anderson MW. Fluoroscopy-guided the needle toward the posterior joint without any an- Sacroiliac Joint Injections. Radiol 2000; 214: 273-77. gling, cephalic, caudad, or oblique.

November 2008 81 Meralgia Paresthetica: a Review

Dr Mark J Bailey, Resident Medical Officer, Christchurch, New Zealand

Introduction Anatomy eralgia paresthetica is a syndrome of pain or The lateral femoral cutaneous nerve (LFCN) is a sen- dysesthesias, or both, in the anterolateral thigh, sory branch of the lumbar plexus and is usually derived Mknee, and sometimes buttock secondary to from the posterior roots of L2 and L3. In addition, an L1 irritation of the lateral femoral cutaneous nerve. The first branch may contribute to the nerve, although this is rare. case of meralgia paresthetica was described by German Sympathetic afferent and efferent fibers are also present neuropathologist Martin Bernhardt in 1878 and then again within the nerve.9 It emerges at the lateral border of the more fully in 1895.1 Vladimir Roth, a Russian neurologist psoas major just above the crest of the ilium. It then takes also published a paper in 1895 after noticing the syndrome an oblique course across the anterior surface of the iliacus in cavalrymen who wore their belts too tightly.2 Hence it before exiting the abdomen near the inguinal ligament and was originally known as the Bernhardt-Roth syndrome. entering the proximal thigh. This exit point has traditionally Roth coined the term meralgia paresthetica from deriva- been described as 1 cm medial to the anterior superior tives of “meros” – thigh, and “algos” – pain. Sigmund Freud iliac spine (ASIS), but in fact this has been found to be presented his own affliction and also the first bilateral case highly variable. A study of 104 LFCNs in 52 cadavers10 report in the same year.3 revealed the following five anatomical variations: Meralgia paresthetica has a variable presentation with Type A (4%) regards to both the nature of the symptoms and the area The nerve exited through the abdominal wall muscles 2- of skin affected. Patients may complain of pain, burning, 3 cm posterior to the ASIS across the iliac crest. This is the aching, tingling, numbness, and dysesthesias with or most superficial variation. without paresthesias involving pinprick and touch sensation. Sensory loss is variable and is not usually prominent. Type B (27%) The area of involvement varies in size and may affect The nerve was found superficial to the origin of sartorius anywhere from the distal anterolateral thigh/knee region and directly medial to the ASIS. Ten per cent of type B up to the proximal anterolateral thigh/buttock and groin nerves also had an additional branch that crossed the iliac region. It usually presents unilaterally but bilateral afflic- crest in a similar position to type A. tions are estimated to occur in 8-20% of cases. Bilateral cases may be seen more commonly in children.4 Most Type C (23%) series have demonstrated a male predominance.4-6 Fa- The nerve was located medial to the ASIS and just milial disposition has been suggested by some authors,4,7 beneath the inguinal ligament ensheathed in the tendi- although this does not appear to be a significant factor in nous origin of the sartorius muscle. Nine per cent of Type most of the literature. Patients often report an aggravating C nerves had an additional lateral branch that crossed the activity such as prolonged standing or positions involving iliac crest in a similar position to type A. hip extension. Sitting may exacerbate the symptoms in some cases and relieve them in others. Sleep disturbance Type D (26%) may feature in more severe cases. The nerve passed under the inguinal ligament medial to The incidence of the syndrome in the general population the tendinous origin of sartorius and then between the is almost impossible to estimate for a number of reasons. sartorius and iliopsoas muscles. Firstly, its variable severity: it is likely that severe cases eventually present to medical services but many milder Type E (20%) cases may not seek any help. Secondly, despite the The nerve was in the most medial location, embedded reasonably large collection of literature on the subject, it is in soft connective tissue on top of the iliopsoas muscle. likely that the condition is under-diagnosed by medical In addition, the series revealed that only 65% of cadav- personal mainly due to ignorance and poor understanding ers had symmetrical LFCN anatomy. of the condition. Indeed, a review of the literature reveals The LFCN divides into anterior and posterior divisions at that the incidence is described as both “common” and a variable distance from the ASIS. The anterior branch “uncommon”! One study estimated the incidence to be 4 penetrates fascia lata about 10 cm inferior to the ASIS to per 10,000.8 It is also interesting to note that the condition supply the skin over the anterolateral thigh down to the may present to family physicians, neurologists, knee. The smaller posterior branch innervates skin over neurosurgeons, orthopedic surgeons, anesthetists with the greater trochanter region.11 an interest in pain medicine, sports physicians, and plastic Interestingly, in many anatomy texts the area of skin that surgeons. It would seem very likely that some cases will the LFCN supplies is described as being the proximal two- also be seen by musculoskeletal physicians. thirds of the lateral thigh.12 However, as described above, more recent research has confirmed that the area of skin

82 Australasian Musculoskeletal Medicine Meralgia Paresthetica: a Review

Table 1. Suspected causes of LFCN irritation in the inguinal region4,14-21

Direct trauma Total abdominal hysterectomy Seatbelt Injury SLE Iliac crest bone graft Repetitive flexion-extension at the hip Appendicectomy Ascites Obesity Tight waist-belts/garments Pregnancy Excessive weight loss Pelvic fractures Cardiac catheterization (via femoral artery) Inguinal lymph node dissection Posterior spine surgery (prone position) Lower limb length discrepancy Long distance backpacking Posterior spine surgery (prone position) Cesarian section supplied by the LFCN extends right down to knee level. meralgia paresthetica remains idiopathic in a significant number of cases and isolating an exact cause often proves to be a challenge. Etiology Meralgia paresthetica may be caused by anything that irritates the LFCN along its course. The classically de- Diagnosis scribed lesion is that of entrapment of the nerve as it exits The diagnosis of meralgia paresthetica can usually be the pelvis in the inguinal region.13 It is postulated that this made on the patient’s history of pain and/or dysesthesias is a site where the nerve is subjected to compressive and in the LFCN territory, exacerbating activities and identifi- possibly traction forces. Table 1 shows suspected causes cation of possible causes. It may be possible to reproduce of nerve irritation at the inguinal region. the symptoms by pressing on the typical location of the Diabetes mellitus may be a risk factor for the develop- LFCN 1 cm inferomedial to the ASIS. Similarly, in a ment of LFCN entrapment at the inguinal region.14,15 The symptomatic patient, it may be possible to abolish their proposed mechanism is either secondary to intrinsic dia- symptoms with an injection of local anesthetic in this spot. betic neuropathy or due to the diabetic nerve swelling and Clearly, an awareness of the anatomical variability of the decreased axoplasmic transport, rendering it more sus- LFCN and consideration of more proximal entrapment is ceptible to external compression. However, other series essential when performing this diagnostic test. The pain is have not observed an increased occurrence of meralgia generally exacerbated by extending the hip with the pa- paresthetica in diabetes compared to that in the general tient prone and the knee flexed to 90° as this maneuver population.22 Other associated systemic diseases that places the LFCN under stretch.4,15 Other exacerbating have been reported include lead poisoning, alcohol abuse, activities may include the Valsalva maneuver and any- and “other” neuropathies.15 thing that increases intra-abdominal pressure. The ex- Dissections have revealed the frequent occurrence of amination may include assessment of light touch and pseudoganglions of the LFCN as it passes under the pinprick sensation to the area of skin supplied by the inguinal ligament.23 These pseudoganglions have not LFCN but, as objective sensory deficits are often absent, been observed in fetal cadavers, so it has been postulated this is not particularly reliable. Similarly, cutaneous stimu- that erect human posture and the angulated course of the lation by light touch to the lateral thigh may cause some LFCN as it exits the pelvis result in mechanical stresses on patients to report a dysesthetic sensation. Some clinicians the nerve leading to their development. However, the have also noted an area of hair loss on the lateral thigh that relationship of these pseudoganglions to meralgia appears to be secondary to the patient’s rubbing or paresthetica is not entirely clear as they are seen in both massaging of the leg.27 As the LFCN is a sensory nerve, symptomatic and asymptomatic individuals. there should be no associated motor weakness or reflex Although less common, more proximal irritation of the deficits. Nerve conduction studies may be utilized and LFCN can also lead to meralgia paresthetica. Potentially appear to be reliable with findings of prolonged latency or any structure that comes into contact with the LFCN along decreased conduction velocity.14 However, they are not its course from its origin to its exit from the pelvis can lead usually required except when the diagnosis is in doubt, to compression or traction irritation. To date some of the such as differentiation from lumbar radiculopathy. Stand- described causes have included meralgia paresthetica of ard nerve conduction tests may also miss a proximal spinal origin,24 malignant tumor of the psoas muscle,25 and entrapment of the LFCN. Recent studies have demon- compression of the LFCN beneath the iliacus fascia strated significant alterations in cutaneous silent periods secondary to infection or hematoma.26 The cause of of vastus medialis in subjects with meralgia paresthetica.28

November 2008 83 Meralgia Paresthetica: a Review

Cutaneous silent periods are brief interruptions of volun- not secondary to a traumatic cause and is summarized as tary contraction that follow strong electrical stimulation of in the chart below. a cutaneous nerve and are thought to be a protective reflex. Electromyography has no role in the diagnostic work up as there are no motor manifestations of meralgia paresthetica. Neurolysis versus transection The two major types of surgical treatment are neurolysis of the LFCN at the inguinal region and transection of the nerve in the suprainguinal region. Details of the neurolysis Management and transection procedures have been documented by To date, no gold standard treatment has been estab- Aldrich30 and Williams,27 respectively. The one randomized lished for meralgia paresthetica, but a recent series by series that appears in the literature placed patients into the Haim has established a useful algorithm that appears to two options and declared that transection produced supe- be practical and cost-effective.29 The algorithm has been rior outcomes.6 Another series also reported success with proposed for spontaneous meralgia paresthetica, that is, nerve transection in 23 out of 24 cases.27 In a small series,

INITIAL TREATMENT – a course of oral NSAIDs +/- analgesics, rest and avoidance of likely causes of nerve compression (for example, lose weight if obese, avoid tight garments). L (After 3 months of the above and still symptomatic) L DIAGNOSTIC TEST - Inject 5-10 ml of local anesthetic at a point 1 cm medial and inferior to the ASIS or point of maximal tenderness. L L POSITIVE TEST = relief of symptoms lasting more NEGATIVE TEST – retest 3-4 weeks later as above than 30 minutes. but to a wider area. L L If still negative reconsider diagnosis (or consider L intrapelvic causes). L CORTICOSTEROID THERAPY – treat the same site with corticosteroid injection (1 ml volume) and repeat on up to 3 occasions every 4-6 weeks as required. L (NON-RESPONDERS) L Further evaluation to rule out a more proximal compression (CT or MRI, additional ultrasound scan of pelvis in females). L L No intrapelvic cause found. Intrapelvic cause identified – definitive treatment as appropriate. L Offer SURGERY – Neurolysis versus Transection of the LFCN.

84 Australasian Musculoskeletal Medicine Meralgia Paresthetica: a Review

Ivins reported a high failure rate with neurolysis and also With regards to meralgia paresthetica of spinal origin, favored transaction.31 However, other operators have high rates of a success were obtained with 1-4 epidural found that neurolysis has a high rate of success,4,14 and injections of dexamethasone.24 arguments against transection include the potential de- The author developed bilateral meralgia paresthetica velopment of painful neuromas32 and the resulting sen- while training as an endurance athlete and after three sory loss, although it is a relatively unimportant territory. It years of symptoms had a failed LFCN neurolysis surgery. has been suggested that some of the anatomical varia- The symptoms were eventually brought under control with tions of the LFCN render neurolysis as technically difficult a yoga-based myofascial stretching program involving the and less likely to succeed.27 In addition, they felt that the lower back, pelvic, and thigh musculature. To my knowl- presence of a neurinoma results in a higher failure rate edge this type of therapy has not been described previ- with neurolysis and suggested this was an analogous ously in the literature. lesion to Morton’s neurinoma. In the presence of either of these findings, transection may be the procedure of choice. Ivins recommended that neurolysis should be offered to all pediatric patients and patients with less than one year of symptoms.31 He advised that transection should be References performed after failed neurolysis and as the procedure of 1. Bernhardt M. Uber isolirt im Gebiete des Nervus cutaneous first choice in patients who have been symptomatic for femoris externus vorkommende Parasthesien. Neurologisches more than one year. One consensus is that alleviation of Centralblatt 1895;14: 242-44. symptoms from a local anesthetic block in the inguinal region is essential before proceeding to surgical treat- 2. Roth VK. Meralgia Paraesthetica. Meditisinskoye Obozrainie Moskova 1895; 42: 678. ment. The choice between the two options seems to be dependent largely on the operator’s preference and famili- 3. Freud S. Ueber die Bernhardt’sche Sensibilitätsstörung am arity of a particular procedure as well as the patient’s Oberschenkel. Neurologisches Centralblatt 1895;14: 491-92. wishes with regards to preservation of sensory function. In the future more successful outcomes from neurolysis may 4. Edelson R, Stevens P. Meralgia Paresthetica in Children. J also be facilitated with the assistance of intraoperative Bone and Joint Surg 1994;76A(7): 993-99. somatosensory evoked potentials. A recent case demonstrated that during a LFCN release an intraoperative 5. Dureja GP et al. Management of meralgia paresthetica: a increase in amplitude of somatosensory evoked potentials multimodality regimen. Anesthes and Analges 1995;80(5): 1060- 61. in the nerve correlated with a favorable clinical outcome.33 Further investigation in this area would be useful. 6. van Eeten PV, Polder TW, Broere CAJ. Operative treatment of meralgia paresthetica: transection versus neurolysis. Neurosurg 1995; 37(5): 63-65.

7. Goldstein H. Meralgia paresthetica (Roth’s or Bernhardt’s Other treatments disease): with the report of five cases: three cases occurring in Other treatments that have been described in the litera- the same family. Am J Med Sci 1921;162(5): 720-35. ture but their efficacy and role in management is yet to be 8. van Slobbe AM et al. Incidence rates and determinants in established include anticonvulsant and nerve-stabilizing meralgia paresthetica in general practice. J Neurol 2004;251(3): drugs such as carbamazepine, gabapentin, and diphenyl- 294-97. hydantoin.5 Abdominal toning exercises could theoretically reduce 9. Reichert FL. Meralgia paresthetica: a form of causalgia pressure over the nerve at the inguinal region, but again relieved by interruption of the sympathetic fibers. Surg Clinics of this is of unproven value. Nth Am 1933;13: 1443. One case report in the literature reported the successful treatment of meralgia paresthetica with topical capsaicin 10. Aszmann OC, Dellon ES, Dellon AL. Anatomical Course of 0.025% cream applied to the area of skin supplied by the the Lateral Femoral Cutaneous Nerve and Its Susceptibility to Compression and Injury. Plastic and Reconstructive Surg 1997; LFCN.34 The proposed mechanism is desensitization of 100(3): 600-604. C-polymodal nociceptors and depletion of substance P in the nerve. There was no mention of an endpoint in this 11. Grossman MG. Meralgia paresthetica: diagnosis and treat- treatment, but it may be a useful non-invasive adjunctive ment. J Am Academy of Orthop Surg 2001;9(5): 336-44. therapy. Again, further investigation in this area would be useful. 12. Moore KL. Clinically Oriented Anatomy. 3rd ed. Williams and Alcohol rubs, diathermy, and ultrasound have also ap- Wilkins, 1992. peared as therapies in the older literature, but their effectiveness was not described.15 13. Wilkins RH, Rengachary SS, eds. Neurosurgery. Vol 2.

November 2008 85 Meralgia Paresthetica: a Review

McGraw-Hill, 1985. 24. Jiang G-X, Xu W-D. Meralgia paresthetica of spinal origin: brief report. J Bone and Joint Surg 1998;70-B(5): 843-44. 14. Nahabedian MY, Dellow A L. Meralgia Paresthetica: etiology, diagnosis, and outcome of surgical decompression. Annals of 25. Amoridis G et al. Malignant tumour of the psoas: another Plastic Surg 1995;35(6): 590-94. cause of meralgia paresthetica. Electromyog and Clin Neurophysiol 1993;33(2): 109-12. 15. Kitchen C, Simpson J. Meralgia paresthetica: a review of 67 patients. Acta Neurologica Scandinavica 1972;48(5): 547-55. 26. Traycoff RB. Pseudotrochanteric bursitis: the differential diagnosis of lateral hip pain. J Rheumatol 1991;18(12): 1810-12. 16. Baldini M, Raimondi PL, Princi L. Meralgia paresthetica following weight loss. Case report. Neurosurg Rev 1982;5(2): 27. Williams HW, Trzil KP. Management of meralgia paresthetica. 45-47. J Neurosurg 1991;74(1): 76-80.

17. Butler R, Webster MI. Meralgia paresthetica: an unusual 28. Tataroglu C et al. Cutaneous silent periods of the vastus complication of cardiac catheterisation via the femoral artery. medialis evoked by the stimulation of lateral femoral cutaneous Catheterisation and Cardiovascular Interventions 2002;56(1): nerve. Clin Neurophysiol 2005;116(6): 1335-41. 69-71. 29. Haim A et al. Meralgia paresthetica: a retrospective analysis 18. Goel A. Meralgia paresthetica secondary to limb length of 79 patients evaluated and treated according to a standard discrepancy: case report. Archives of Phys Med and Rehab algorithm. Acta Orthopaedica 2006;77(3): 482-86. 1999;80(3): 348-49. 30. Aldrich EF, van den Heever CM. Suprainguinal ligament 19. Yang SH, Wu CC, Chen PQ. Postoperative meralgia approach for surgical treatment of meralgia paresthetica: techni- paresthetica after posterior spinal surgery: incidence, risk fac- cal note. J Neurosurg 1989;70(3): 492-94. tors, and clinical outcomes. Spine 2005;30(18): E47-50. 31. Ivins GK. Meralgia paresthetica, the elusive diagnosis: 20. Paul F, Zipp F. Bilateral meralgia paresthetica after cesarian clinical experience with 14 adult patients. Annals of Surg section with epidural analgesia. J Peripheral Nervous System 2000;232(2): 281-86. 2006;11(1): 98-99. 32. Stevens H. Meralgia paresthetica. Archives of Neurol and 21. Boulware DR. Backpacking-induced paresthesias. Wilder- Psych 1957;77(6): 557-74. ness and Environmental Med 2003; 14(3): 161-66. 33. Salengros JC et al. Intraoperative somatosensory evoked 22. Jones RK. Meralgia paresthetica as a cause of leg discom- potentials to facilitate peripheral nerve release. Can J Anaesthes fort. Can Med Assoc J 1974; 111(6): 541-42. 2006;53(1): 40-45.

23. Edelson JG, Nathan H. Meralgia paresthetica: and anatomi- 34. Puig L, Alegre M, de Moragas JM. Treatment of meralgia cal interpretation. Clin Orthopaed and Related Research paresthetica with topical capsaicin. Dermatol 1995;191(1): 73- 1977;122: 255-62. 74.

86 Australasian Musculoskeletal Medicine Complementary Pain Management Based on Anatomical, Physiological, and Neurological Concepts

Dr A Breck McKay, Bayside Medilink, Victoria Point, Qld (mckayabATbigpond.net.au)

referential meaning and so we lack any identical shared Introduction meaning for the words pain, ache, sore, and hurt. How- omplimentary pain management has been writ- ever, there is continuous learning from parents and peers ten about before1,2 but usually as a series of of the difference in attention that is paid to various forms Csummations of what has been used and the fact of injury or pain and how they are managed. For example, that they do work, based on treatment trials. Few, how- ignore it, apply a “Band-aid”, try a medicine, see a doctor, ever, have addressed the issue of how they may work, or go to bed to rest. from the basic anatomy, physiology, neurology, etc. To do It is obvious that pain is largely the person’s brain that one must go right back to the very beginning. What is perception which has been remembered or reactivated pain? after being sorted out from the massive chaos of afferent “Pain” is a very difficult concept to understand and is stimuli activating all parts of the brain structures continu- made even more difficult through lack of a shared lexicon ously during life. Therefore, it is unique to that person. between individuals. By definition: “Pain is an unpleasant In medicine we spend a lot of time collecting many sensory and emotional experience associated with actual shared words and details of the experience of pain from or potential tissue damage, or described in terms of such the patient, which forms the patient’s history. Unfortu- damage. Pain is always subjective. Each individual learns nately, because most health practitioners do not recog- the application of the word through experiences.”3 nize the importance of this stage of history taking and the And this is where the problem commences. Pain is a vagueness of such words, there is often only a brief record warning system to draw the attention to actual or impend- of the abbreviated words used to refer to pain, ache, ing harm to the tissues. Take out the sensory component soreness and hurt regarding the pain experience and, as and there is no pain perception, and take out the emo- a result, such histories are almost useless. tional component and similarly there is no pain experi- How can we make this better, simpler, and thus allow the ence per se. So both sensory and emotional components use of appropriate forms of complimentary pain manage- are needed at the same time for the brain to perceive that ment? the afferents are associated with the reactivation of the This involves understanding the mechanism of the previous memory of pain. stimulus to the body part that will finally be perceived as Based on its learnt memory, pain is only the brain’s pain. It is activation of the local receptors, then the nocic- perception that starts in utero, but is maximally activated eptive pathways and steps to the spinal cord, with modu- after birth and continues throughout life, where each lation and convergence, upward to the midbrain, and person has a completely unique experience of pain. finally to the brain areas. This was clearly detailed in my Yet, who can verbally share such sensory and emotion- previous article4 based on the booklet Pathophysiology of ally combined experiences and memories with other Pain produced by Astra-Zeneca,3 available to any doctor people? requesting it. (Telephone Australia 02 9978 3500, New The four most common words used to express such an Zealand 09 623 6300.) experience are pain, ache, sore, and hurt, but what do It is now possible to share some understanding of how these words mean to any individual? Each person has his and why different methods of complementary pain man- or her own personal experience of what these words agement work in overall pain management. mean, but can they expect or believe that their experience is the same as anyone else? If not, then why not? The answer is quite simple. Take the example of a gold- colored paper weight. When a patient is asked what color it is, he or she can tell you immediately and say “gold”. So Pain pathway elements and why does this occur? When they were very young, someone told them that management options the item that their eye and brain were perceiving was Most of these have little to no evidence based on blinded “gold”, and from that point on they hear others saying or randomized trials. In all cases, however, the most “gold”, and they tell others that it is “gold”, so the lexical important consideration is that the patient presents with a word “gold” has a very specific and continuously shared problem. The doctor or other healthcare practitioner, after meaning. taking a history and examination, applies a “black box” Now when a person suffers a pain, ache, soreness or (whichever management is utilized) and ideally the patient hurt, there is no similar sharing of the details, context or says “My problem is fully resolved!” That is a successful

November 2008 87 Complementary Pain Management

management outcome. Flotation Chamber treatment. How can this be achieved at What was wrong, what was actually done, plus how and home? By using 4-8 kg of swimming pool salt (it costs why it worked remain largely the subject of medical about A$6 for 25 kg bags) in their usual hot bath water, scientific examination and is mostly relevant to those in people can soak in this, then pat the water off and finally the healthcare profession, with the patient often remaining let the extra salt stay on their skin overnight. disinterested.

Promethazine: Cheap over-the-counter medication Balneotherapy Everyone knows that promethazine is an ideal treat- Considering the peripheral receptors (Figure 1), it can ment for allergy or insects stings, but look carefully at the be seen that trauma leads to changes in the cells of the diagram again (Figure 1). Histamine is released by the damaged tissues. The very first lecture in physiology told mast cell when traumatized, so this is one site for promet- us that if any cell membrane was damaged, K+ would be hazine action, that is, to reduce the dual histamine activa- released from intra- to extra-cellular and this would pro- tion of the A-delta and C fiber nerve endings. The dose is duce an electric current across the membrane, where patient dependent, and one should start at a low dose of adding many together produces an impulse in the special- 10 mg at night initially and increase slowly and gradually ized cells called nerves. At the same time, other sub- each night until the best effect is obtained without exces- stances, for example, prostaglandin (Pg) E, are also sive dry mouth or somnolence. See later for other uses of released to help trigger the nerve response. promethazine in histamine blockade in pain activated If this area were to be flooded with extra Na+, the pathways. imbalance of K+ would be reduced and less nerve stimulation due to the change would occur. It is not necessary to actually float in salty water because strong salty water Exercise, massage, yoga, tai chi, and related activities applied or sprayed on to the skin can work in the same – all free too! way. This is the simple principle behind balneotherapy or Looking at Figure 2, there are different receptor types in salt water bathing and is why people feel “refreshed” after tissues. A-alpha fibers relate to control-feedback involv- swimming in salt water or travel to the Dead Sea to float in ing muscle and tendons. the very salty water, or why people get such benefit from A-beta fibers are the fourth input after olfactory cranial

Figure 1. Reproduced with Figure 2. Reproduced with permission from AstraZeneca. permission from AstraZeneca.

88 Australasian Musculoskeletal Medicine Complementary Pain Management

nerve (CN) 1, optical CN 2, and auditory CN VIII for forwards. This results in over-working of the psoas mus- Pavlov’s Orienting Response5- 8 and are fast-conducting cles almost in isolation to the posterior back muscles, with impulses at 50 m/sec. overdrive by the quads and other leg muscles. This can A-delta fibers (myelinated) and C fibers are for aggravate pain and dysfunction, because the proximal nociception, mechanoreception, and thermoreception and psoas muscle fibers effectively surround the exiting lum- are slower conducting impulses at 15 m/sec and 1 m/sec, bar nerve rami. While in water, with feet on the bottom, the respectively. person should always walk sideways or backwards to On looking at Figure 3, the input of these fibers to the avoid pain exacerbation via excessive psoas muscle dorsal root ganglion and spinal cord are clearly illustrated. activity. Simple anatomy, biomechanics, and whole body Further, in considering the function of these nerves, touch function always help understanding of what should or A-beta fibers pass primarily and immediately to the higher should not be done. centers, because survival and function almost always over-rule pain. This is a very fast pathway, but there are also retrograde pathways (Figure 4) that enter the dorsal Downward modulation of dorsal horn mechanisms by horn at level V. These act as modulators or inhibitors of the higher centers incoming A-delta and C fibers in level V up to level 11 of This pathway is via the dorso-lateral funiculus (DLF) as the Rexed laminae. shown in Figure 3. This is the pathway that the current pain This gives rise to simple and effective methods of clinics try to enhance as their main method of dealing with reducing pain, by utilizing massage, exercise, tai chi, pain. The patient is taught that the “pain is in the brain and yoga, etc., which all act by increasing A-beta inputs to the they must learn to ignore it” and they are then taught how dorsal horn layers. to achieve this. Sadly, this is more akin to diversion therapy used in aged care homes, than true pain management. This is done utilizing classical Pavlovian conditioned Hydrotherapy reflex activation9 with the amplification of the output via the This works for a number of simple reasons. Once the DLF to the dorsal horn units. The level to which the pain body is two-thirds in water, much of the activity of the can be attenuated was demonstrated by the solo rock antigravity muscles reduces, the attachments of the mus- climber who had not notified others regarding his plans. cles and tendons to the periosteal areas are less strained He was trapped in a chasm by a boulder on his right hand. (reducing A-delta and C fiber inputs) and muscles can On day three he cut his right hand off with a penknife in relax more, allowing better flow of the synovial fluid be- order to survive.10 Similarly, in NSW, a young seven-year- tween the joint surfaces. This allows joint spaces to “open old lad came off a quad motorbike and suffered fractures more”, with less closely applied cartilage surfaces. In to his shoulder, clavicle, and ribs, and he had a collapsed addition, exercise enhances pain reduction, by the clear- lung. He walked two kilometers to get help11 because his ance of metabolic products, as well as increasing nutrient dad had collapsed near the motorbike. flow to cartilage normally in close contact and under The power of mind-over-pain occurs when survival and pressure. function have to be achieved and pain can be ignored in The one caveat for hydrotherapy is that, if the patient has their feet on the bottom of the pool, they should never walk

Figure 3. Reproduced with permission from AstraZeneca.

Figure 4. Reproduced with permission from AstraZeneca.

November 2008 89 Complementary Pain Management

the short term if needed. However, when chronic pain The other is the sympathetic nervous system that uses occurs due to continuing tissue damage or excessive adrenalin (flight, fight, fun) or noradrenalin (fear, freeze, ongoing nociceptor activity or accumulated damage over flight, fear) as its final neuromodulators at the alpha and longer periods of time, dorsal horn “wind up” may occur. beta adrenergic receptors. In all other synapses, pregan- The patient cannot continue this pain suppression path- glionic neurons, ganglia and postganlionic synapses it is way. Sleep deprivation often occurs, caused by histamine acetylcholine that predominates. release in the midbrain areas,12,13 giving rise to secondary On considering the overall mechanism it is easy to use reactive or relative “depression” due to increased adrena- the simplest concepts: line and nor-adrenaline compared to the serotonin levels A. Full belly (food) wine, comfort, and relaxation. Time to in the autonomic nervous system. Persistent and continu- digest, shift excess heat to the skin and to relax and the ing use of these methods of pain management via the DLF blood flow changes to achieve this. Parasympathetic can result in neuroplastic cerebral brain map changes, nervous system. with increased conscious awareness of some pathways Or and cerebral recognition of afferents being diminished or B. Threatened, alert, anxious, aroused, ready for flight/ ignored altogether in others. This is the amazing new area fight or fear/freeze. Sympathetic nervous system, via of brain neuroplasticity.14 Because pain is a warning adrenalin – fun, alert, or anxious, or noradrenalin – fearful, system for whole body function, persistent and accumu- scared, and often very jumpy. They have different effects lating pain afferents will eventually override all these on individual terminal receptors, giving differing outcomes. pathways modifications and become all-important or overt At the same time all this is happening, information again. travels to the midbrain areas, where there are immediate midbrain responses, often in less than 200 milliseconds,8 which activate the autonomic nervous system and whole body function via the midbrain and thalamus. One of these effects is the activation of the sleep centre by neuropeptides How the autonomic nervous activating histamine pathways of the tubero-mammillary bodies and causing wakefulness.12 sytem is involved, and how The hormone orexin or hypocretin is released by afferent nociceptive activation of the thalamus15,16 and is also to treat that associated with wakefulness and increased appetite, his- How many remember the complexity of the autonomic torically fulfilling an animal’s need to keep awake and eat nervous system (ANS) from medical school? If you step to allow rapid repair of damaged tissues after being back and look at it as a system with two operations, it injured. This is one reason why people in chronic long- becomes very simple (Figure 5). One is the term pain tend to put on weight. parasympathetic nervous system (cranial and caudal) Reduce their pain and they can and will lose weight. Not that primarily uses acetylcholine as its final neuromodulator. the other way around. “When you lose weight we can help you with your pain.” So how do we manage these problems by simple methods? Once again, the effect of promethazine becomes relevant. Promethazine blocks the histamine-activated pathways, thus allowing sleep to occur. At the same time promethazine is a general and mild anti-cholinergic so we have a modulation of both the sympathetic and parasympathetic nervous systems by this simple, over-the-counter drug, known best for its use in allergies and also to help children sleep. So promethazine has a triple action: 1. Working at tissue levels to stop activation of nociceptive fibers by histamine released from the mast cells in injury; 2. Blocking of the histamine pathways that prevent sleep; and 3. General peripheral ganglionic modulation of both sides of the autonomic nervous system. It is obvious to see why people taking promethazine complain of drowsiness. Their sleep depri- Figure 5. vation (caused by acute or persistent pain) be-

90 Australasian Musculoskeletal Medicine Complementary Pain Management

comes dominant and, as soon as the peripheral and It was considering autonomic nervous system function central histamine effects are blocked by promethazine, in the gut in pain and observing the benefit of the digestive the body naturally tries to catch-up on the missing sleep. enzymes that led Dr Daryl Wall and me to make longer- With continuing use of the promethazine, the dry mouth term observations on pain management, utilizing regular and drowsiness reduce as the sleep deprivation is also promethazine and pancreatic enzyme supplements. Dr reduced, allowing a dose gradually increasing over time. Wall’s comments, when I asked him if he had tried the Now we go back to the functioning of the autonomic combinations, are worthy of publication. He stated that nervous system, as mentioned above. When threatened prior to using the promethazine and pancreatic enzyme: or in pain, one of the body’s autonomically mediated “When I did a ward round, I saw tired patients in pain, and responses is to reduce blood flow to the skin (pallor, when I picked up their charts they were already on itchiness, aroused erector pilae) and also reduce blood maximum analgesic doses and getting side effects. Once flow to the gut, so that the maximum blood can be shunted we introduced the promethazine and pancreatic enzymes to the brain, heart, lungs, and muscles. Reduced blood as a regular management, I now see happy patients who flow to the gut results in reduced digestive processes, less have slept well and have little pain, but when I pick up their digestive enzymes, and disturbed peristalsis, often pro- charts I see that we are using only 1/3 to 1/5 of the pain ducing bloating, reflux, constipation, or diarrhea. medication. Another benefit is that our liver and kidney So it follows logically that oral medication for pain transplant patients are now using 1/3 to 1/5 of their management is often poorly digested, which is necessary immunosuppressant drugs – a massive financial saving before they can be adsorbed. So they are less effective, per week per patient.” This would be a wonderful study for often hanging around in the gut, causing many side effects some enthusiastic registrar. (ulceration, nausea, severe constipation, bloating). Another benefit from this is that many patients may be able to cease the expensive proton pump inhibitors that are not free of side effects and have much better digestion and fewer gut symptoms that were secondary to pain. Improving drug effectiveness by better digestion This method resulted from a patient I shared with Dr How other pain manage- Daryl Wall (associate professor of surgery, Princess Alexandra Hospital, Brisbane). The patient had gut sur- ments work gery for a small malignant pedunculated bile duct tumor. Exercise It was observed that her Panadeine Forte worked well This takes us back to the very first question asked: Why during the day when she took pancreatic enzymes to does a muscle not pull out of its attachments when the assist digestion post-gut surgery, but not at night. So the muscle is very active (Figure 6)? The answer is very patient took pancreatic enzymes at night and got much simple in principle. The muscle/tendon/ligament is at- better pain management. The dose is very simple: two tached to and through the periosteum (via Sharpey’s capsules of Creon or similar enzyme preparation with fibers) to the cortical bone. So when the muscle contracts, each dose of any analgesic medication. There are no dose the many receptors in the periosteal layer are immediately limits because it is only an enzyme preparation and not a activated, where the densest distribution of such drug and it is used for digestive dysfunction in gall bladder mechanoreceptors and nociceptors occur17 (Figure 7). disease, liver diseases, cystic fibrosis, adsorption disor- This activates feedback inhibition to the motor neurons ders, etc. They are readily available on general prescrip- opposing excessive muscles contraction, both from the tion. Many patients find extra doses at meal times also help spinal cord level and via afferent activation of higher with their previous poor digestion and gut dysfunction. centers, producing secondary efferent motor inhibition.

November 2008 91 Complementary Pain Management

At the same time the receptors in the muscle body (Golgi afferent nociception and allowing full muscle length to be body, etc.) are squeezed, adding to the feedback inhibi- restored. tion. This compression also impedes both arterial and venous flows, causing a relative lactic acidosis, hypo- oxygenation and forces anaerobic metabolism, resulting Chinese cupping or equivalent in further incremental acidosis. This may eventually cause This acts by causing reduced pressure under the hot a reflex increased blood flow as shown by plethysmogra- cup as it cools, which then sucks out fluid and blood into phy which is a whole of limb or body measure.18 the tissue. Blood in the tissues is very irritating, as anyone The way to reduce those effects is to reduce excessive who has had a good sprain or hematoma can attest, and muscle contraction and cause relaxation and lengthening, the remaining blood in the tissues is a persisting source of thus reversing the above. A-beta stimulation.

How is this done? Prolotherapy Yoga, tai chi, and many other programs work, at least, Yelland’s work,19 which showed that injected glucose partly by this method. solution was as effective as saline control begged a simple Simply consider the arm bending and straightening. As explanation. In my paper,6 I was faced with the fact that all it bends the brain and cerebellum make the flexor muscles three variations (needle + steroid + local anesthetic, contract, but also make the opposing extensors relax. The needle + local anesthetic, and needle alone) gave the opposite happens when the arm is again straightened. same result, even after one month, and in two cases the So exercise that encourages stretching in both direc- needle alone was still effective some 2.5 years later. The tions by alternate contraction and relaxation helps restore last cases were effectively simple dry needling. The nee- normal lengths and functions of the muscles involved. dle alone is not a placebo effect as there is active physical There is reduction in any excess activity via the A-delta damage to the entheses being carried out. So what was and C-fiber afferents to the dorsal horn. This also helps happening? reduce the afferents to the dorsal horn and higher centers In the model published in May 2004,6 the application of and thus reduces the brain’s perception of pain. This is Chaos Theory was used to explain how and why the what so many pain management programs emphasize, original cases presented and were interpreted. As Bogduk20 but fail to simply and adequately explain – exercise is so suggested: “Chaos Theory explains intricate situations important. It also helps reduce relative “depression”. Many with a complex differential mathematical equation, which other factors are involved as well; for example, endorphin includes constants; when a constant changes, everything release, total body metabolic function, but most of all there changes. Restore the constant and everything restores.” is more balanced whole body function again. “Pain”, or more correctly, the persistent nociceptive receptor activations due to accumulated tissue damage are the equation “constants”, that is, the damaged receptors Rubrefactants in the periosteum, ligaments, tendons, fascia, or muscles These stimulate the A-beta sensory inputs at the periph- are the increasing “constants” or additive damage afferents. ery and increase A-beta inputs to the dorsal horn thus These pass with the chaos of information that the brain modulating afferents and pain perception as explained has to interpret to perceive pain. Not all receptors repair above. The most potent is the commercially available after injury and, over time, the number of damaged, but Finalgon® cream. active receptors increases. By “turning off” these switches or receptors clusters, there is reduction in dorsal horn afferents and thus no amplification in the dorsal horn, and Deep tissue massage reduced afferents to the brain. This makes further sense, This activates the A-beta input, reducing increased because once the afferents to the midbrain cease, the muscle tone, and thus tension on the attachment receptors, efferent autonomic outputs (mainly sympathetic adrener- decreasing the A-delta and C fiber inputs to the dorsal gic and nor-adrenergic pathways) associated with in- horn. As the muscles relax, the accumulated metabolic creased damaged area neovascularization and other products (lactic acid, dissolved carbon dioxide, etc.) asso- tissue perfusion factors also decreases. ciated with excessive activity and reduced oxygenation Switching off the nociceptive afferents thus turns off the from squeezed tissues, which may be associated with “cascade of repair processes” in the damaged areas. brain level pain perception, gradually find their way out of Perhaps this may explain some of the local changes the muscle tissues and more oxygen and nutrients pass reported in clinical prolotherapy research. in. This results in restoration of more normal metabolic and functional activity in the muscle. At the same time, deep tissue massage sends a barrage of A-beta input to Reflexology the dorsal horns at each level, facilitating the blockade of This is a wonderful example of two extremes. As the

92 Australasian Musculoskeletal Medicine Complementary Pain Management

Chinese found many thousands of years ago, if you stand. Heat increases the blood flow, thus delivering more massage the feet very gently, you increase relaxation. substrate and removing metabolic products as well as How? Simply by increasing the A-beta inputs to the lower assisting biochemical reactions. Increased blood flow dorsal horns, thus modulating nociception all the way up may also cause more swelling when inflammation is the spinal levels up to the midbrain. After a while every- present, which may be counterproductive. The nerves can thing settles and is calm. actually work more efficiently and thus, at times, can make The opposite was also used by the Chinese. Caning of the pain appear worse, due to improved nerve conduction the feet slowly and continuously was used to torture and rates and increased afferents to the dorsal horn. kill people. How did this work? By increasing the A-delta Cold, on the other hand, reduces the blood flow and also and C fiber inputs from receptors (massive nociceptive decreases the function, physiology, and biochemistry of inputs), the opposite was achieved; death from extreme the muscles and nerves and reduces secondary swelling overload to the autonomic nervous system at midbrain in the area, as well as decreasing afferent nociceptive levels. This is one of the natural killers for prey animals in activity to the dorsal horn, thus reducing pain perception. the wild, with pressure on the throat area resulting in autonomic overload after the chase and capture, and death follows much more quickly than by simple strangu- Hypnosis lation. This rapid death occurs in captured birds, even if This involves the ability of the brain to be placed in a quickly released after capture by a predator. sleep-like dissociative state where the pain afferents can be “ignored” both by increasing efferent DLF activity as well as cerebral activity to override the areas associated TENS machines with pain perception.22 These work by fatiguing the sensory and nociceptive nerves by excessive stimulation at the receptor and primary afferent level. Once a receptor has been forced to Meditation fire many times, it runs out of neurotransmitters and the This works like hypnosis, but in this case the brain is nerve no longer feeds to the dorsal horn. This lasts only taught to ignore the nociceptive afferents by activating until the TENS is turned off and the receptors and nerves other more dominant pathways. fMRI studies have shown have time to metabolically recover their previous func- that many areas of the brain are involved in such activity tions. The dorsal horn also changes its activity, as de- and brain neuro-plasticity is the key to long term benefit of scribed by Melzack and Wall.21 such meditation.14,22

The Likon machine Aromatherapy This is a very interesting machine that came from China This is a most fascinating area of pain management that and was initially related to acupuncture methods. It has is only just starting to be understood. Olfactory inputs pass multiple settings that, when managed correctly, actually directly to the midbrain and form an important part of modulates via low wavelength electrotherapy to the auto- Pavlov’s orienting response, as the result is frequently nomic nervous system in two different ways, modulating sub-200 milliseconds in onset.8 From birth onwards, vari- the sympathetic or parasympathetic systems. The actual ous aromas are related to different environments and are settings required, and how to use the machine in the learnt as an association memory. management of muscle problems and specifically in com- Later, the presence of that same smell can help recreate plex regional pain syndromes, were deduced by simple the memory and may be calming, alerting, or even repul- trial and error over some two years by Adelaide physi- sive, but the response depends on the original environ- otherapist Aileen Jefferis. mental association. This is an underlying feature of Pav- My wife and I have extensively used this machine with lov’s original conditioned reflex development and the great benefit since 1990 and its use has allowed our ability to moderate this by environmental changes was development of the whole body functional models from well demonstrated in Stanley Kubrick’s film “A Clockwork clinical observations. Orange”. It cannot be used without careful training by those who have experience in correct Likon use, as it is very easy to incorrectly modulate the wrong part of the autonomic Stationary magnets nervous system, resulting in rapid exacerbation of symp- Despite all the claims for these, there are no blinded, toms and signs. randomized controlled trials that show any positive benefit, other than the extra warmth and support from the magnet carriers. Cold and heat Considering the physiology, these are easy to under-

November 2008 93 Complementary Pain Management

The power of mind over matter whole human body. Australas Musculoskeletal Med 2003;8:86-99. As indicated above, there are many ways in which the brain and cerebral interpretation can be fooled into ignor- 6. McKay AB. Pain and chronic low back pain: a new model? ing or downplaying the importance of the afferent nocicep- Parts 1and 2. Australas Musculoskeletal Med 2004; 9:14-25. tive information. However, if the incoming pain information 7. McKay AB. Tennis Elbow Everywhere. Australas Muscu- continues to increase or accumulate, it will eventually loskeletal Med 2005; 10: 127-30. override and redirect the brain and body’s attention to the cause as a method of protection from actual or possible 8. McKay AB. Watch the Ball- but why? Australas Musculoskel- injury. etal Med 2008; 12: 25-27. How powerful is this process? Think of the boxer getting his face and nose pummelled, or the rugby player being 9. Pavlov I. Lectures on conditioned reflexes. Vol 1. New York heavily tackled, or the person in a fight to the death with International Publishers, 1928. anything. It is then that survival and function will overrule 10. Ralston A. I cut off my right hand. www.msnbc.msn.com/id/ pain.5 However, eventually, pain perception will dominate 5956900/. because the afferents from the dorsal horns will cause overload in the midbrain autonomic control area. Either 11. Master Tyler Stephen Moon: Bravery Award, 2004. action is taken to address the pain and reduce it, or the www.governorgeneral.gov.au/res/File/PDFs/honours/br65/ whole body function will result in loss of consciousness.5,7 Media%20Notes%20-%20Commendation%20for%20 The whole body response is summarized as MOMM. Brave%20Conduct.pdf. Monitor (M) the environment; Orient (O) to the changes; 12. Hou RH, Langley RW, Szabadi E et al. Comparison of Memory (M) check for past experience of the same; and diphenhydramine and modafinil on arousal and autonomic functions in healthy volunteers. J Psychopharmacol 2007; 21: 567-78. Manage (M) by: a) Freeze/Fear initially while the situation is considered. 13. Parmenter R, Anaclet C, Guhennec C et al. The brain H3- Remember it is the excessive Freeze/Fear response receptor as a novel therapeutic target for vigilance and sleep- that may result in death via autonomic overload. wake disorders. Biochem Pharmacol 2007; 73: 1157-71. b) Flight/Fight c) Return to normal. 14. Doidge N. The brain that changes itself. Penguin, 2007. These are the steps that Pavlov first identified in 1904 to 1917,9 and now that we are starting to understand brain 15. Lin JS, Dauvilliers Y, Arnulf I et al. An inverse agonist of the neuroplasticity better,14 newer and better pain manage- histamine H(3) receptor improves wakefulness in narcolepsy: studies in orexin-l-mice and patients. Neurobiol Dis 2008: 30: 74- ment programs may be developed. 83. As I have tried to show here and in previous articles, in musculoskeletal medicine we do need to go back to the 16. Cortess S, Konofal E, Lecendreux M. Alertness and feeding basic principles of anatomical and physiological normality behaviours in ADHA: Does hypocretin/orexin system play a role? to understand what is going on. We must ensure that not Med Hypothese 2008. only do we make the right diagnosis, but that our manage- ments are also aimed at restoration of normal, rather than 17. Bogduk N. Mechanisms of musculoskeletal pain. Australas merely treating symptoms and signs after “labeling” of the Musculoskeletal Med 2006; 11: 6-18. problem instead of true diagnosis.23 18. Yang D. Reproducibility of air plethysmographic measure- ments for the evaluation of blood flow in the lower extremity. Australian Conference of Science and Medicine in Sport 2001; A References Sports medicine Odyssey – Challenges Controversies and Change. 1. Ernst E. Complimentary therapies for pain management. 19. Yelland MJ, Glasziou PP, Bogduk N et al. Prolotherapy Elsevier Mosby, 2007. injections, saline injections and exercises for chronic low back pain: a randomized trial. Spine 2004; 29: 9-16. 2. Menefee LA, Monti DA. Nonpharmacological and complimentary approaches to cancer pain management. JAOA 2005; 105: 20. Bogduk N, McKay AB. Email personal communication. 15-20. 21. Melzack R, Wall PD. Pain mechanisms; a new theory. 3. The Pathophysiology of Pain. Astra-Zeneca Pharmaceutical Science 1965; 150: 971-79. Education Booklet. J Pain and Symptom Management 2000;19: 3. 22. Grendahl JR, Rosvold, EI. Hypnosis as a treatment of chronic 4. McKay AB. Chronic low back pain and pain: simple models to widespread pain in general practice: a randomized controlled explain pain to patients. Australas Musculosketal Med 2006; 11: pilot study. 2008. www.medscape.com/viewarticle/581316 . 92-96. 23. McKay AB. Musculoskeletal Pot Pourri. Australas Muscu- 5. McKay AB, Wall D. The orienting response and the functional loskeletal Med 2006; 10: 108-110.

94 Australasian Musculoskeletal Medicine Paraspinal Nerve Injection: Its use as a presurgical diagnostic disambiguation tool and for the temporary and permanent relief of musculoskeletal pain

Dr David Roselt, Aberdovy Clinic, Bundaberg; Dr A Breck McKay, Bayside Medilink; Dr Scott Masters, Caloundra Spinal and Sports Medicine Centre

pain than those without pain.7- 9 History This evidence can free the practitioner from the need to araspinal nerve injection is an economical and image patients repeatedly with XRs, CTs, or MRIs when- minimally invasive procedure that can be used to ever they have an exacerbation of their musculoskeletal Ptreat acute spinal pain, or chronic spinal pain that pain. In the absence of red flag indicators, the yield of may be associated with radiculopathy. Radiculopathy can relevant information is very low and should not change be defined in the broadest sense as pain and dysfunction management. This can save patients needless exposure mediated by the radicles or nerve roots, the final common to ionizing radiation in the case of XR and CT, and pathway for nociception into the central nervous system expense for the patient, the insurer, and the tax payer, (CNS). depending on funding arrangements. The original work using paraspinal nerve injections was History is the best guide to diagnosis but is not com- a randomized controlled trial (RCT) by Dr Stefan Blomberg pletely reliable. Somatic referred pain and radicular pain as part of his PhD thesis in the early 1990s. Stefan runs a with or without radiculopathy can co-exist.10 pain clinic in Stockholm, Sweden.1-5 Neurogenic pain is pain evoked by the stimulation of Stefan Blomberg came to Melbourne in October 2002 peripheral axons or their cell bodies rather than peripheral as keynote speaker for the annual scientific meeting of the nerve endings as occurs with somatic pain.7 Australian Association of Musculoskeletal Medicine Radicular pain is a subset of neurogenic pain, in which (AAMM). His pragmatic approach is systematic, using his pain is evoked by stimulation of the nerve roots, dorsal root own algorithm. ganglion (DRG), or spinal nerve itself.11, 12 Because of limited sensitivity and specificity of history, In neurogenic pain the pain is perceived as arising in the examination, and imaging for diagnosing and managing peripheral area supplied by the affected nerve. As the pain musculoskeletal pain problems, Stefan believes it is hu- is perceived in a region distal to the actual pain stimulus, mane and cost-effective to offer patients a pragmatic trial neurogenic pain and radicular pain are, by definition, a of treatment when there is a chance of “cure” or significant form of referred pain.7 reduction in their pain and associated symptoms. Lumbar radicular pain (LRP) could be referred to an Musculoskeletal pain is a concept, not a well-defined area innervated by either the dorsal or the ventral rami, but entity.6 It is the brain’s unique interpretation, based on past pain in the distribution of the dorsal rami has not been learning, of chaotic afferent input to the CNS. properly defined to date. LRP can also result from irritation The history is the best guide to diagnosing musculoskel- of the ventral root or the spinal nerve itself.11-14 etal pain problems.7 LRP differs, however, from somatic and visceral re- It is vital to take a thorough history. The aim is to triage ferred pain because it does not involve the stimulation of the patient with respect to red flag conditions (such as nerve endings, and convergence onto the same second fracture, tumours benign or malignant, infection, or inflam- order neuron at the same segmental level. It is perceived mation such as ankylosing spondylitis and other seron- as arising distally because of ectopic activation of the egative spondylarthropathies), radicular pain and nerves supplying that region by irritation of the nerve radiculopathy, and somatic pain which may be associated roots, DRG or spinal nerve proximally. This manifests as with referred pain through convergence.7 referred radicular pain, that is, shooting, stabbing, lanci- The red flag checklist has been validated for acute and nating, electric shock like pain, with or without dysesthesia chronic lumbar spinal pain, and is applicable to other to that region.7 This is in contrast to somatic referred pain, areas of the body.7 which is constant in location but poorly localized and Physical examination can support historical impres- diffuse, and aching in quality.11, 12 sions and help engage the patient but lacks diagnostic Burning pain is often a feature of neurogenic pain. Deep precision without proven reliability and validity.7 It can burning pain without other features, distribution, or quali- reveal tender entheses which may be associated with ties is not necessarily neurogenic in origin. Burning sen- chronic spinal pain. sations in the skin strongly imply a neurogenic process Imaging does not show pain per se, and in the absence that may be radicular, or some other neurogenic process.7 of red flag indicators usually shows non-diagnostic age- The sensory dorsal nerve roots receive fibers from both related changes that are no more common in people with the ventral and the dorsal rami that combine briefly to form

November 2008 95 Paraspinal Nerve Injection

the spinal nerve just distal to the intervertebral foramen. pain be defined and delineated where possible, as they The sinuvertebral nerves (SVNs) are recurrent branches arise from different anatomical structures and are caused of the ventral rami that re-enter the intervertebral foramina by different pathological mechanisms.10 to be distributed within the vertebral canal, formed by a Radiculopathy may be more rigorously defined as ob- somatic root from a ventral ramus and an autonomic root jective loss of sensory and/or motor function as a result of from a grey ramus communicans. In the intervertebral conduction block.11 It might include numbness, motor foramina, the lumbar SVNs run across the back of the loss, wasting, weakness, and loss of reflexes. Paresthesia vertebral body just below the upper pedicle supplying the and or numbness can occur with nerve root compression periosteum and also the outer third to half of the interver- or nerve root inflammation and signify conduction block.12 tebral disc, and the posterior longitudinal ligament (PLL) at Ill-defined paresthesia can also occur as a manifestation that level and also the level above. The SVNs also supply of somatic referred but raises the possibility of associated the blood vessels of the vertebral canal, the ventral aspect radiculopathy. of the dura mater, the dural sleeves enclosing the nerve Any lesion that affects the integrity of the lumbosacral roots, and the spinal nerves as far as the intervertebral nerve root can cause LRP, radiculopathy, or both.10 foramina, where the dura merges with and becomes the Lumbar radicular pain is caused by more than a mass epineurium of the spinal nerve. Ascending and descend- effect. CT and MRI studies have shown that patients ing meningeal branches travel one segment rostrally and whose symptoms of “sciatica” (radicular pain with or two segments caudally respectively. All the nerve roots without radiculopathy) have resolved often still show the and the roots of the cauda equina are covered with their same mass effects on follow-up imaging.24, 25 own sleeve of pia mater and bathed in cerebrospinal fluid Disc herniations or protrusions evident on CT or MRI (CSF) which percolates through the subarachnoid space may not even be associated with low back pain or LRP, of the dural sac. The pia mater of each nerve root extends and may be totally asymptomatic.8, 9 as far as the spinal nerve, as does an extension of the Ectopic impulses, and hence perception of pain, may be subarachnoid space.12 generated as a result of: Therefore, somatic pain could be expected as part of • mechanical deformation of the DRG any nerve root irritation or compression syndrome via • mechanical stimulation of previously damaged nerve effects on the dural sleeve enclosing the nerve root. This roots produces nociception from stimulation of nerve endings in • inflammation of the roots or DRG, related to chemical the dural sleeve supplied by the SVNs, which is relayed via radiculitis and/or the ventral rami to the spinal nerve and then the dorsal root • possible ischemic damage to the DRG.10, 15, 16, 17, 20, 21 before entering the dorsal horn of the spinal cord.12 It is conceivable that radicular pain from ectopic stimu- Compression of nerve roots evokes a brief discharge at lation of the dorsal root or DRG could be referred to the the time of application but then the root becomes silent. region supplied by the dorsal ramus. This could produce DRG compression can produce sustained activity in noci- radicular pain in the distribution of the dorsal ramus which ceptive axons and interestingly also Aβ fibers.12 supplies the zygapophysial joints, the paraspinal mus- Clinical experiments have shown compressing normal cles, and the skin in the paraspinal areas.12 Similarly. it nerve roots with urinary catheters evokes paresthesia and could refer to the regions supplied by the sinuvertebral numbness but not pain.12 nerves, that is, the vertebral body, intervertebral disc, PLL, Prolapsed nucleus pulposis produces chemical radicu- and meningeal blood vessels.12 litis via phospholipase A2, producing hyperemia, increased Radiculopathy and radicular pain involving referral to permeability, and edema of the nerve roots, which causes areas supplied by fibers from the dorsal ramus could be conduction block.16-18 The hyperemia produces venous subtle in terms of clinical presentation and is possible from engorgement, producing DRG ischemia,19 and thrombo- a basic science perspective. It could conceivably be sis of radicular veins may occur.16 related to a chemical radiculitis due to the release of Persistence of the inflammation produces fibrosis of the demyelinating enzymes from an anular fissure with or nerve roots and the perineural tissue.22 This explains without an obvious prolapsed intervertebral disc,15- 21 but conduction block in affected nerve roots, but the mecha- also from foraminal stenosis, or other less common causes nism of radicular pain is obscure. Ectopic discharges from affecting the ventral ramus. DRG ischemia is the most likely cause.19 This defines Perineural fibrosis is another possible cause of radicular radicular pain as neurogenic. 12 pain that could be present in the absence of gross mor- However, the pain of radiculitis may also involve the phology on imaging.22, 23 It most commonly occurs after dural sleeve of the affected nerve roots. This is innervated disc herniation or after disc surgery, and seems to re- by the SVN; pain may arise from irritation of nerve endings spond better to local anesthetic and steroid injections if in the dura, which produces somatic pain. Pain from tried before any surgery is attempted.23 radiculitis may have been misinterpreted, and may not be In patients presenting with features of somatic spinal intrinsically radicular, but may in fact be referred somatic pain and LRP together on history, it is important that each pain from the inflamed dura of the nerve root sleeve.12

96 Australasian Musculoskeletal Medicine Paraspinal Nerve Injection

Radicular pain and somatic referred pain are not mutu- ring to regions supplied by fibers from the dorsal ramus. ally exclusive. They can co-exist. Radicular pain may be Given the favorable natural history of LRP, authorities superimposed on a background of somatic referred pain. recommend that in the absence of other indications such Although not absolute, certain features may assist in as cauda equina syndrome, progressive motor loss, or distinguishing between somatic pain and radicular pain.10 other red flag features, imaging is not required unless See table below. there is failure to improve 4-6 weeks after the onset of Clinical examination does not diagnose the cause of LRP.27 LRP if present, but may help establish the presence or Imaging is best reserved for patients not responding to absence of radiculopathy.10 conservative treatment, and for whom surgery is being Although lumbar disc herniation is the commonest cause considered. In patients with a history of “sciatica” or in of LRP, there are no distinctive features either in the whom a red flag condition seems likely, appropriate imaging history or physical examination that would implicate the is indicated. MRI is the investigation of choice. It detects intervertebral disc as the cause of pain.10 all significant red flag and surgical causes, and is radiation Definitive diagnosis can be made only by imaging stud- free. ies that support the clinical diagnosis of LRP based on Electrophysiological studies in patients presenting with history, and based primarily on the quality of the pain. The acute LRP are generally not indicated unless peripheral straight leg raise clinical test has the best sensitivity, but neuropathy instead is suspected clinically. These tests a low specificity with an average likelihood ratio of 1.5 cannot determine the precise spinal nerve level associ- which is meagre.10 Other tests such as dorsiflexion of the ated with disc herniation and radicular pain. Electromyo- foot, impaired ankle reflex, sensory deficit and muscle gram studies correlate poorly with the anatomical level of atrophy have modest to poor sensitivities and specificities.10 a disc herniation. 27 In younger and middle-aged patients the pretest prob- Electrophysiological studies may also be indicated to ability of disc herniation is high, whereas in the elderly, exclude more distal nerve damage, verify suspected foraminal stenosis or spinal stenosis are more likely muscle weakness by needle electromyogram, or to as- causes of LRP,10 with or without associated radiculopathy. sess pre-operative baseline muscle status before surgery The natural history of LRP is that patients can expect a for radiculopathy related to recurrent disc herniation.27 dramatic reduction in the severity of pain, with treatment The efficacy of steroid injection for the treatment of LRP limited to simple analgesics, and patients should be en- may be due to its anti-inflammatory effects on inflamed couraged to maintain or resume daily activities. For se- nerve roots, 28 inherent local anesthetic properties, 29 or as vere pain, opioids can be used judiciously.10 a membrane stabiliser suppressing ectopic impulses.30 Bed rest is no more effective than watchful waiting. Steroids injected transforaminally under fluoroscopy Depending on the severity of the LRP and the response to may offer significant pain relief for an extended period of medication, the early resumption of daily activities should time.31, 32 The results are less impressive if given by the be actively encouraged. interlaminar route, but caudal epidural injection may be At 12 months, at least 50% of patients can expect to be tried in the rooms if lumbar radicular pain and or free of leg pain, but at least 60–70% will continue to radiculopathy is suggested clinically, or the patient has experience low back pain.26 failed to respond to paraspinal nerve injection in a mixed This low back pain has been attributed to somatic pain presentation with elements of somatic and radicular pain.33 via stimulation of nociceptive nerve endings in the disc or A transforaminal epidural injection of long acting local related structures, but it often arises at the same time as anesthetic and corticosteroid should be considered in this the radicular symptoms or signs. It could conceivably be setting, given the potential for significant and lasting relief a manifestation of radiculopathy and radicular pain refer- of pain.10

Distinguishing features of LRP and somatic referred pain

Feature Radicular pain Somatic referred pain Depth Deep as well as superficial Deep only, lacks any cutaneous quality Quality Shooting, lancinating, like an electric shock Dull, aching, like an expanding pressure Pattern Narrow band Wide area Travelling Relatively fixed in location Quasi-segmental, but not dermatomal Quasi-segmental, but not dermatomal Not distinguishable by segment Not distinguishable by segment Boundaries difficult to define Distribution Entire length of lower limb Anywhere in lower limb BUT BUT below knee > above knee proximal > distal

November 2008 97 Paraspinal Nerve Injection

A recent systematic review concluded that there is moderate evidence for interlaminar epidurals in the cervi- Indications cal spine and limited evidence in the lumbar spine for long- Primary indications: somatic with or without referred term relief of radicular pain. spinal pain, acute, or chronic, possibly associated with The evidence for cervical and lumbar transforaminal radiculopathy. This may be diagnosed prospectively or epidural steroid injections is moderate for long-term im- retrospectively when revealed after overlying somatic provement in managing radicular pain. The evidence for pain that has been clouding the clinical picture has re- caudal epidural steroid injections is moderate for long- solved with paraspinal nerve injection. term relief in managing radicular pain and chronic low Secondary indications: after failed epidural injection, back pain.33 when undiagnosed or coexistent somatic spinal with or For somatic spinal pain, paraspinal nerve injection should without referred pain is diagnosed or suspected. be considered. It blocks nociception into the dorsal horn of the spinal cord via the dorsal nerve root, and can relieve somatic pain while the patient is on the table, allowing a resumption of usual activities of daily living with stretching and walking that can stimulate Aβ fibers which detect Contraindications gross spinal movements. This input rises to the midbrain, Absolute contraindications: red flag conditions; un- and can help to block incoming nociception by increasing corrected or suspected coagulopathy; known allergy to descending pain control mechanisms. local anesthetic/corticosteroid, for example, lignocaine, Components of radicular pain and or radiculopathy may Celestone Chronodose, etc.; local infection. be also present but clinical examination lacks sensitivity Relative contraindications: anticoagulation therapy - and specificity.10 injection is still possible, with careful technique and fine Imaging with MRI does not always resolve the dilemma 25G needles if the INR is within recommended reference as there is an increasing prevalence of false positive MRI ranges; frail elderly patients; those prone to vasovagal findings with age.8, 9 episodes. Patients with previous spinal surgery and metal A trial of treatment may relieve distressing symptoms, internal fixation can be injected, carefully avoiding infiltra- and avoid expensive and unnecessary imaging. Red flag tion close to the metal using a no-touch or sterile tech- features are uncommon, accounting for less than 1% of nique, aiming to bathe the dorsal ramus and or other causes of low back pain in a primary care setting.34, 35 paraspinal nerves with local anesthetic with or without In the original trials by Blomberg on subacute low back corticosteroid. pain (pain for 6-12 weeks), including patients with radicular leg pain, the average number of parasacrococcygeal paraspinal nerve injections needed for lasting pain relief was 1-2. In Australia, musculoskeletal pain medicine doctors using this approach have found that people with chronic Equipment spinal pain of many years’ duration can benefit from on Paraspinal nerve injections can be done with minimal average 1-4 injections given at weekly or greater intervals, equipment after marking relevant land marks using a no- with a cumulative effect that seems not diminished by touch technique in the rooms. Equipment for treating greater intervals between injections. allergic reactions and vasovagal reactions should be The importance of diagnosis, education, and assurance readily to hand. cannot be underestimated, with recommendations for light activity, stretching,36 manual therapy if applicable and a graded home exercise program utilizing walking of great benefit in maintaining improvement. Procedure The parasacrococcygeal paraspinal nerve injections for lumbar spinal pain are usually done with the patient lying prone or in the lateral position if this is problematic, and the Level of evidence injections are given paraspinally to block the nerves There is Level II evidence from Stefan Blomberg’s RCT entering the neuraxis adjacent to the edges of the sacrum in the early 1990s, using parasacrococcygeal paraspinal and coccyx bilaterally. injection.1-5 One of the papers was published in Spine in The injection site can be at C1-2 (coccygeal) as in 1994.5 Blomberg’s original work and involves infiltration up and In Australia, there is level IV evidence from some case down beside the sacrum and coccyx, usually bilaterally to series.37-41 A pilot study in Queensland has also been block multiple nerve roots and spinal nerves. Entry site of conducted. Data collection has been completed, with injection can be at other sites parasacrally, such as at S4 results currently being analysed. or S2, and infiltration performed up and down the

98 Australasian Musculoskeletal Medicine Paraspinal Nerve Injection

parasacrococcygeal region with 15 ml of 0.5% plain ligno- thoracic radicular pain still occurs, and can be subtle in its caine with Celestone Chronodose or comparable steroid clinical presentation.44, 45 solution typically using 2 ampoules, that is, 2 ml in and The cervical transverse process tips can be infiltrated around the dorsal nerve rami to block nociception entering using lignocaine 0.5% with or without dexamethasone, a the dorsal roots and hence dorsal horn segmentally. non-particulate corticosteroid, using 0.4 ml for each spinal A 22 or 23 G 50-60 mm needle or longer spinal needle nerve from C3-7 especially if tender unilaterally or bilater- is used using a no-touch technique. This has the effect of ally . reversing the wind-up and central sensitization that is the Non-particulate steroids are safer in case of intravascu- usual cause for persistent spinal pain, acutely, or chroni- lar injection.46 cally when it can be associated with radiculopathy. A study published in Spine in 2007 on cervical If patients are needle phobic or in significant pain or transforaminal epidurals steroid injections (TFEIs) looked markedly tender, consider infiltrating first with 5 ml of at 30 cases of brain or spinal cord infarction (16 brain, 12 lignocaine 0.5% either side at the entry site and infiltrating cervical spinal cord, and 2 combined brain/spinal cord up and down in the usual directions using a 38 mm 25 G infarcts), over three times greater than the sum of all needle. This can be done routinely or in selected patients. published infarcts previously (n = 8 published case re- There may be variable lumbosacral tenderness, and ports). diagnosis is best made on the basis of history and or pain Of all the cases reported, four involved only corticoster- diagram. oid with no local anesthetic. All four cases involved meth- There may be tenderness paraspinally on digital rectal ylprednisolone and resulted in brain infarction, three of examination and Stefan Blomberg teaches the injection which were fatal. This is the strongest association to date with a per rectal (PR) guiding digit in the anus to assess for between particulate corticosteroids and brain or spinal tenderness, to guide the depth of injection, and to stretch cord infarctions. the parasacrococcygeal ligaments after paraspinal nerve The authors point out that although co-occurrence of injection has blocked the nociception and relieved the alternative mechanisms of injury (for example, vertebral pain. This was used in the published trials so is the artery dissection or needle-induced vasospasm) is possi- preferred method, though omitting this aspect of the ble, it supports an embolic mechanism of action. injection may still produce an effective outcome if patients This was the first study to propose a “top of the basilar” are uncomfortable with the idea after informing them of the artery mechanism, whereby the steroid embolus travels to trial details and evidence. The use of the PR guide could the confluence of the distal basilar artery, its thalamo- be reserved as an option for later inclusion or considera- perforate branches, the superior cerebellar artery, and the tion if there is failure to respond to an unguided injection posterior cerebral artery. Occlusion of these arteries gives without the associated stretching. rise to midbrain, pons, cerebellum, thalamus, and or Needling of any tender entheses after blocking the temporal and occipital lobe infarctions. dorsal rami may have additional reflex effects to reset the In order to minimize the risk of complications, the au- dorsal horn and reverse the wind-up and central thors suggest : 1) using real-time fluoroscopy with non- sensitization and persistent pain. ionic contrast and digital subtraction to maximize detec- Additional paraspinal nerves may be blocked from L1-5 tion of vascular uptake during cervical TFEIs; 2) using a if needed with lignocaine 0.5% using 1.5-2 ml with or test dose of local anesthetic prior to injecting corticoster- without corticosteroid each side for each involved seg- oid to prevent irreversible neurologic sequelae; 3) using ment, aiming for the inferior aspect of the attachment of microbore extension tubing to minimize needle move- the transverse process to the vertebral arch in order to ment while changing syringes; 4) using minimal if any block the dorsal rami. The history, pain diagram, and sedation to allow for clinical neurologic monitoring; 5) spinal tenderness and persistence of pain are the best using a shorter-acting local anesthetic such as lignocaine, guide to choosing additional spinal nerves to block. It is preferably at the lowest possible concentration and dose, important to update and review the anatomy regularly.42, 43 to minimize high spinal anesthesia occurrence or severity; Similarly, thoracic spinal pain may be treated by inject- 6) using blunt needles; 7) screening for arterial dissection ing the dorsal rami at the inferior aspect of the attachment risk factors; and 8) using a non-particulate corticosteroid of the transverse process to the vertebral arch with ligno- such as dexamethasone.46 caine 0.5% using 1.5-2 ml with or without corticosteroid A recent experimental animal study using a rat model each side at each involved segmental level. The history, suggested that corticosteroids may add no extra efficacy pain diagram, and spinal tenderness and persistence of to local anesthetic injection in treating radiculopathy, pain are the best guide to choosing additional spinal suggesting that corticosteroid may be unnecessary for nerves to block. nerve root infiltration (NRI).47 Thoracic radicular pain due to disc prolapse is less The paraspinal injection is meant to be extradural but common than in the lumbar and cervical regions but other these points are certainly worth bearing in mind. Cervical mechanisms could be involved. Chronic thoracic spinal injections should be attempted only by experienced doc- pain is more commonly of zygapophysial joint origin, but tors with a sound knowledge of the anatomy and the

November 2008 99 Paraspinal Nerve Injection

techniques involved. a small dose of dilute 0.5% lignocaine with or without Cervical paraspinal nerve injection may succeed in dexamethasone reduces any substantial risk. blocking nociception arriving in both the dorsal rami sup- Paralysis is possible with injections in the cervical re- plying the posterior elements of the spine, and ventral rami gion, into a vertebral or smaller vessel usually with which transmit nociception from the intervertebral discs particulate corticosteroid solution via steroid embolus and dural sleeves and dura to the dorsal root via the spinal producing thrombosis, cord or brain stem infarction and or nerve. It may, therefore, help with discogenic pain. death. Injection directly into the spinal cord itself can The patient is placed in the lateral position and the tips produce similar, possibly more localized effects. of the cervical lateral masses or transverse processes are Alternatives to paraspinal injection include other con- carefully marked, and then a no-touch technique is used. servative management; epidural injection may be consid- It is important to be aware of the course of the vertebral ered if there is a poor response to paraspinal nerve artery which is exposed between lateral masses. It is injection, as radicular pain or even radiculopathy involving prudent to be very gentle and withdraw if the tip is not fibers related to the dorsal ramus may be present. How- contacted at the appropriate depth or if there is uncertainty ever, cervical transforaminal epidural steroid injection per about needle position. se remains out of favour in view of safety concerns. Utilizing a low dose of local anesthetic such as 0.4 ml of Referral for formal cervical or lumbar medial branch blocks, 0.5% lignocaine alone with or without non-particulate with or without radiofrequency neurotomy if positive with steroid such as dexamethasone enhances the safety of controlled blocks, is supported strongly by the evidence the procedure. base and is the ideal and only proven treatment for Z joint Alternatively, a posterior approach can be used to block pain but unfortunately is not always available or done to the dorsal rami or at least the medial branches from ISIS standards. behind. The injection is approximately on the same level as the spinous process, the articular pillar, and the tips of the cervical lateral masses or transverse processes. The needle can be inserted slightly inferiorly and 2.5 cm lateral to the spinous process and aimed at the posterior aspect Results of the articular pillar to be blocked. After bony contact is The results have been very good empirically and when made, the depth of contact is noted and the needle followed up in clinical practice, but more formal study is repositioned aiming towards the most lateral aspect of the strongly indicated, with case series the best way to pro- articular pillar. The 25 G or larger needle is advanced, but, ceed in private musculoskeletal or general medical prac- if it walks off laterally, is withdrawn and redirected slightly tice. medially and advanced to the depth of the previous bony contact. After the needle is felt to be the optimum position, the hub is observed for blood or cerebrospinal fluid. If neither is evident, gentle aspiration can be attempted. If the Conclusions aspiration test is negative, 1.5 ml of solution of local Paraspinal nerve injection offers a valuable way of anesthetic such as lignocaine 0.5% with or without dex- managing acute pain or chronic pain that may be associ- amethasone can be injected to block the medial branch of ated with radiculopathy. This may be fully revealed only the dorsal ramus at that level. after a trial of treatment. It seems to work best for somatic The patient is usually shown some gentle stretching with or without referred spinal pain but this can coexist with exercises to use as part of a home-based rehabilitation or be associated with radicular pain and/or radiculopathy.50 program 2-3 times daily and also if there is a flare of pain. The paraspinal nerve injections can also clarify a mixed It is useful to utilize post-isometric relaxation with deep somatic and radicular presentation and relieve somatic breathing in accordance with Sherrington’s second law to pain which may mask associated radicular pain and/or achieve a painless stretch.48, 49 radiculopathy. This may allow a more precise diagnosis of specific level nerve root impingement syndromes, which may then be more amenable to surgery with microdiscectomy, etc. Persistent musculoskeletal pain is likely to have a large Complications neuropathic component. Some 20 years ago Professor These include bleeding, infection, pain, scarring, inad- Bogduk delivered a lecture at an AAMM or APS meeting vertent epidural or subarachnoid injection producing a in which he threatened a nightmare. The proposition was high spinal anesthetic if sufficient volume and concentra- that there was no such entity as musculoskeletal pain: that tion of local anesthetic is injected too close to the neuraxis. it was all neuropathic. A subdural injection can give similar results to a subarach- Even osteoarthritis is neuropathic (at the micro level). noid injection but with a prolonged onset time. However, Radiofrequency neurotomy may work not because it

100 Australasian Musculoskeletal Medicine Paraspinal Nerve Injection

denervates a painful joint but because the articular nerves Care 1993; 11: 83-90. are neuropathic, in that some of the afferents are injured. The pain arises not from the joint but because of afferent 3. Blomberg S, Tibblin G. A controlled, multicentre trial of manual imbalance. Denaturing the nerves resets the balance. therapy with steroid injections in low-back pain: functional variables, side-effects and complications during four months follow- Could the result of the Bone and Joint Decade be: it’s all up. Clinical Rehabil 1993; 7: 49-62. neural? All treatments work by resetting the dorsal horn? This is certainly not an argument for more surgery, etc., 4. Blomberg S, Svardudd K, Tibblin G. A randomized study of as surgery is effective only for intractable radicular pain or manual therapy with steroid injections in low-back pain: tel- for other rare red flag conditions such as cauda equina ephone interview follow-up of pain, disability, recovery and drug syndrome, unstable fracture, tumour, or infection. consumption. Eur Spine J 1994; 3:246-254. Paraspinal nerve injections may reduce the volume of back surgery and increase the precision of that 5. Blomberg S, Hallin G, Grann K, et al. Manual therapy with which is done once pain treatable by injection is steroid injections – a new approach to treatment of low back pain: a controlled multicentre trial with an evaluation by orthopedic removed and the masking is uncovered. surgeons. Spine 1994; 19: 569-77. Public pain clinics in Australia are difficult to access, with extremely long waiting lists for persistent non-malignant 6. Bogduk N. Mechanisms of musculoskeletal pain. Australas pain. They usually have a multi-disciplinary approach Musculoskeletal Med 2006;1: 7-19. which may assist function in the short-term but the Austral- ian experience reveals very small and temporary effects, 7. Bogduk N, McGuirk B. Pain Research and Clinical Manage- as revealed at the recent AAMM annual scientific meeting ment, Vol 13. Medical Management of Acute and Chronic Low in Melbourne. A recent audit in the Newcastle pain clinic Back Pain. An Evidence-Based Approach. Elsevier, 2002. showed no change in median pain, no increase in return 8. Boden SD, Davis DO, Dina TS et al. Abnormal magnetic- to work. Similar results from Stephen J Gibson with the resonance scans of the lumbar spine in asymptomatic subjects. Victorian experience with CBT showed that one-third of A prospective investigation. J Bone Joint Surg Am 1990; chronic pain patients ended up worse. These patients 72(3):403-8. commonly represent to primary care doctors for further assistance. 9. Jensen MC, Brant-Zawadzki MN, Obuchowski N et al. Mag- We believe that a trial of paraspinal nerve injections is netic resonance imaging of the lumbar spine in people without definitely indicated for acute pain not responding to oral back pain. N Engl J Med 1994; 331(2): 69-73. analgesia and simple physical measures, for example, stretching, or chronic spinal pain that is commonly asso- 10. Govind J. Lumbar radicular pain. Aust Family Physician 2004; 33(6): 409-41. ciated with radiculopathy, before referral for a surgical opinion. Surgery is not indicated in the absence of red flag 11. Merskey H, Bogduk N (eds.) Classification of chronic pain. conditions as outlined above. Surgery may still have a role Descriptions of chronic pain syndromes and definitions of pain for intractable radicular pain after a trial of epidural injec- terms. 2nd ed. Seattle; IASP Press, 1994. tion of local anesthetic with or without steroid, either transforaminally or via the caudal route. Paraspinal nerve 12. Bogduk N. Clinical Anatomy of the Lumbar Spine and injection can help clarify the diagnosis and can offer very Sacrum. 3rd ed. Edinburgh; Churchill Livingstone, 1997. effective treatment for somatic spinal pain components. It may also work like a selective nerve block if well placed, 13. Howe JF. A neurophysiological basis for the radicular pain of nerve root compression. In Bonica JJ, Liebeskind JC, Albe- avoiding the dangers of a transforaminal epidural injection Fessard DG, eds. Advances in pain research and therapy. Vol 3. if the injection is lateral to the intervertebral foramina and New York; Raven Press, 1979, pp. 647-57. epidural space. Surgery is indicated for cauda equina syndrome or progressive motor impairment related to 14. Howe JF, Loeser JD, Calvin WH. Mechanosensitivity of radiculopathy. dorsal root ganglion and chronically injured axons: a physiological basis for the radicular pain of nerve root compression. Pain 1977; 3: 25-41.

15. McCarron RF, Wimpee MW, Hudkins PG, Laros GS. The References inflammatory effect of nucleus pulposus. A possible element in the pathogenesis of low-back pain. Spine 1987; 12(8): 760-64. 1. Blomberg S, Svardsudd K, Mildenberger F. A controlled, multicentre trial of manual therapy in low back pain; initial status, 16. Olmarker K, Blomquist J, Strömberg J et al. Inflammatogenic sick-leave and pain score during follow-up. Scand J Prim Health properties of nucleus pulposus. Spine 1995 Mar 15; 20(6): 665- Care 1992; 10: 170-78. 69. 2. Blomberg S, Svardudd K, Tiblin G. Manual therapy with steroid 17. Saal JS, Franson RC, Dobrow R et al. High levels of injections in low-back pain: improvement of quality of life in a inflammatory phospholipase A2 activity in lumbar disc herniations. controlled trial with four months’ follow-up. Scand J Prim Health

November 2008 101 Paraspinal Nerve Injection

Spine 1990; 15: 674-78. 33. Abdi S, Datta S, Trescot AM et al. Epidural steroids in the management of chronic spinal pain: a systematic review. Pain 18. Franson RC, Saal JS, Saal JA. Human disc phospholipase Physician 2007;10(1): 185-212. A2 is inflammatory. Spine 1992; 17: S129-S132. 34. Wilk V. Acute low back pain - assessment and management. 19. Rydevik BL, Myers R, Powell HC. Pressure increase in the Aust Family Physician 2004; 33(6): 385-480. dorsal root ganglion following mechanical compression. Spine 1989; 14: 574-76. 35. Deyo RA, Rainville J, Kent DL. What can the history and physical examination tell us about low back pain? JAMA 1992; 20. Ozaktay AC, Kallakuri S, Cavanaugh JM. Phospholipase A2 26(6): 760-65. sensitivity of the dorsal root and dorsal root ganglion. Spine 1998; 23(12): 1297-306. 36. Bogduk N, McGuirk B. The “Indahl” Exercises for Low Back Pain. Australas Musculoskeletal Med 2008; (1): 8-14. 21. Chen C, Cavanaugh JM, Ozaktay AC et al. Effects of phospholipase A2 on lumbar nerve root structure and function. 37. McKay AB, Wall D. The Orienting Response and the Func- Spine 1997; 22(10): 1057-64. tional Whole Human Body. Australas Musculoskeletal Med 2003; 8(2): 86-99. 22.. Cooper RG, Freemont AJ, Hoyland JA et al. Herniated intervertebral disc-associated periradicular fibrosis and vascular 38. McKay AB. Pain and Chronic Low Back Pain: A New Model? abnormalities occur without inflammatory cell infiltration. Spine Part 1.The Hypothesis and Model. Australas Musculoskeletal 1995; 20(5): 591-98. Med 2004; 9(1): 14-19.

23. Lutze M, Stendel R, Vesper J, Brock M. Periradicular therapy 39. McKay AB. Pain and Chronic Low Back Pain: A New Model? in lumbar radicular syndromes: methodology and results. Acta Part 2. Observations and clinical material. Australas Muscu- Neurochir (Wien) 1997; 139(8): 719-24. loskeletal Med 2004 9(1): 20-25.

24. Maigne JY, Rime B, Delinge B. Computed tomographic 40. McKay AB. Tennis Elbow Everywhere. Australas Muscu- follow up study of forty-eight cases of nonoperatively treated loskeletal Med 2005; 10(2): 127-30. lumbar intervertebral disc herniation. Spine 1992; 17: 1071-74. 41. McKay AB. Chronic Low Back Pain and Pain: Simple Models 25. Delauce-Cavallier MC, Budet C, Lardeo JD et al. Lumbar disc to Explain Pain to Patients. Australas Musculoskeletal Med herniation: computed tomography scan changes after conserva- 2006: (2) 92-96. tive treatment of nerve root compression. Spine 1992; 17: 927- 33. 42. Agur AM, Dalley AF. Grant’s atlas of anatomy. 12th ed. Baltimore; Lippincott, Williams & Wilkins, 2008. 26. Weber H, Holme I, Amlie E. The natural course of acute sciatica with nerve root symptoms in a double blind placebo 43. Waldman SD. Atlas of Interventional Pain Management. 2nd controlled trial evaluating the effect of piroxicam. Spine 1993; 18: ed. Philadelphia; Saunders, 2004. 1433-38. 44. Malanga GA, McLean JP. Thoracic Discogenic Pain Syn- 27. Anderson GBJ, Brown MD, Dvorak J et al. Consensus drome. http://emedicine.medscape.com/article/96284-overview summary on the diagnosis and treatment of lumbar disc herniation. Spine 1996; 21(Suppl 24S): 75S-78S. 45. Manchikanti L, Boswell MV, Singh V et al. Prevalence of facet joint pain in chronic spinal pain of cervical, thoracic, and lumbar 28. Olmarker K, Byrod G, Cornefjord M et al. Effects of regions. BMC Musculoskelet Disord 2004; 5: 15. methyprednisolone on nucleus pulposis-induced nerve root injury. Spine 1994; 19: 1803-08. 46. Scanlon GC, Moeller-Bertram T, Romanowsky SM, Wallace MS. Cervical Transforaminal Epidural Steroid Injections: More 29. Johanson A, Hao J, Sjolund B. Local corticosteroid applica- Dangerous Than We Think? Spine 2007; 32(11): 1249-56. tion blocks transmission in normal nociceptive fibres. Acta Anaesthesiol Scand 1990; 34: 335-38. 47. Tachihara H, Sekiguchi M, Kikuchi S, Konno S. Do corticosteroids produce additional benefit in nerve root infiltra- 30. Devor M, Govrin-Lippmann R, Raper P. Corticosteroids tion for lumbar disc herniation? Spine 2008; 33(7): 743-47. suppress ectopic neural discharge originating in experimental neuromas. Pain 1985; 22: 127-37. 48. http://nobelprize.org/nobel_prizes/medicine/laureates/1932/ sherrington-bio.html 31. Thelander U, Fagerlund M, Friberg S, Larsson S. Straight leg raising test versus radiological size, shape and position of 49. http://www.worldscibooks.com/medsci/etextbook/p210/ lumbar disc hernias. Spine 1992; 17: 395-99. p210_chap1.pdf

32. Lutz E, Vad VB, Wisneski RJ. Fluoroscopic transforaminal 50. Can pain be more or less neuropathic? Editorial. Pain 2004; lumbar epidural steroids: an outcome study. Arch Phys Rehabil 110: 510-11. 1998; 79:1362-66.

102 Australasian Musculoskeletal Medicine Journal Abstracts

This section aims to update the reader with some of the more significant musculoskeletal research published in the last year which is listed on the Medline and CINAHL databases.

BACK PAIN rior to normal care at three and 12 months and to massage at 12 months. It resulted in moderate improvements in Little P, Lewith G, Webley F et al. Randomised control- disability and pain-free days. Twenty-four lessons were led trial of Alexander technique lessons, exercise, only marginally better than six lessons combined with the and massage (ATEAM) for chronic and recurrent back exercise program. Interestingly the exercise program pain. Br Med J 2008; 337: a884. doi:10.1136/bmj.a884. provided modest but useful benefits from a relatively brief Objective. To determine the effectiveness of lessons in GP/nurse intervention. the Alexander technique, massage therapy, and advice The results suggest that the Alexander technique is a from a doctor to take exercise (exercise prescription) reasonable choice for the treatment of chronic low back along with nurse-delivered behavioural counselling for pain. It stands alongside other self-management options patients with chronic or recurrent back pain. with some evidence for effectiveness such as supervised Design. Factorial randomised trial. tailored exercise programs. When recommending self- Setting. 64 general practices in England. management options, patient preferences and expecta- Participants. 579 patients with chronic or recurrent low tions should be considered. back pain; 144 were randomised to normal care, 147 to The results also offer a weak endorsement for home- massage, 144 to six Alexander technique lessons, and based exercise prescribed by a GP with follow-up by a 144 to 24 Alexander technique lessons; half of each of nurse. Massage therapy may offer short term benefits. – these groups were randomised to exercise prescription. Dr Michael Yelland Interventions. Normal care (control), six sessions of massage, six or 24 lessons on the Alexander technique, and prescription for exercise from a doctor with nurse Friedman BW, Esses D, Solorzano C et al. A randomized delivered behavioural counselling. placebo-controlled trial of single-dose im corticoster- Main outcome measures. Roland Morris disability score oid for radicular low back pain. Spine 2008;33(18): (number of activities impaired by pain) and number of E624-29. Department of Emergency Medicine, Albert days in pain. Einstein College of Medicine, Bronx, NY 10467, USA. Results. Exercise and lessons in the Alexander tech- [email protected]. nique, but not massage, remained effective at one year Study Design. A randomized, double-blind, placebo- (compared with control Roland disability score 8.1: mas- controlled trial of patients with radicular low back pain who sage -0.58, 95% confidence interval -1.94 to 0.77, six present to an emergency department (ED) within 1 week lessons -1.40, -2.77 to -0.03, 24 lessons -3.4, -4.76 to - of pain onset. 2.03, and exercise -1.29, -2.25 to -0.34). Exercise after six Objective. We hypothesized that a single intramuscular lessons achieved 72% of the effect of 24 lessons alone 160 mg dose of methylprednisolone acetate would im- (Roland disability score -2.98 and -4.14, respectively). prove pain and functional outcomes 1 month after ED Number of days with back pain in the past four weeks was discharge if the corticosteroid were administered early in lower after lessons (compared with control median 21 disease symptomatology. days: 24 lessons -18, six lessons -10, massage -7) and Summary of background data. Parenteral corticosteroids quality of life improved significantly. No significant harms are not recommended for acute, radicular low back pain, were reported. though their role in this disease process is ill-defined. To Conclusions. One to one lessons in the Alexander date, this medication class has only been studied in a technique from registered teachers have long-term ben- highly selected group of patients requiring hospitalization. efits for patients with chronic back pain. Six lessons Methods. Adults between the ages of 21 and 50 who followed by exercise prescription were nearly as effective presented to an ED with low back pain and a positive as 24 lessons. Trial registration: National Research Reg- straight leg raise test were enrolled. The primary outcome ister N0028108728. was change in pain intensity on an 11 point numerical rating scale 1 month after ED visit. Secondary outcomes Comment. The study was a large, well-conducted 1 month after ED discharge included analgesic use, randomized controlled trial comparing the short-term and functional disability, and adverse medication effects. long-term effects of the Alexander technique with mas- Results. Six hundred thirty-seven patients were ap- sage and normal care and also the effects of an unsuper- proached for participation, 133 were eligible, and 82 were vised home-based aerobic exercise program (prescribed randomized. Baseline characteristics were comparable by a general practitioner with follow-up behavioural coun- between the groups. The primary outcome, a comparison selling from a nurse). The Alexander technique was supe- of the mean improvement in pain intensity, favored meth-

November 2008 103 Journal Abstracts

ylprednisolone by 1.3 (P = 0.10). Some secondary out- led Trials up to and including June 2007 if reported in comes favored methylprednisolone, such as use of anal- English, Dutch, or German. We also screened references gesic medication within the previous 24 hours (22% vs. given in relevant reviews and identified trials. Randomized 43%, 95% CI for difference of 20%: 0%-40%) and func- trials and double-blind controlled trials of NSAIDs in non- tional disability (19% vs. 49%, 95% CI for difference of specific low back pain with or without sciatica were in- 29%: 9%-49%). Adverse medication effects 1 week after cluded. ED discharge were reported by 32% of methylprednisolone Results. In total, 65 trials (total number of patients = and 24% of placebo patients (95% CI for difference of 9%: 11,237) were included in this review. Twenty-eight trials -12% to 30%). (42%) were considered high quality. Statistically signifi- Conclusion. This study was a negative study, though cant effects were found in favor of NSAIDs compared with there was a suggestion of benefit of methylprednisolone placebo, but at the cost of statistically significant more side acetate in a population of young adults with acute radicu- effects. There is moderate evidence that NSAIDs are not lar low back pain. Further work with a larger sample of more effective than paracetamol for acute low back pain, patients is needed. but paracetamol had fewer side effects. There is moderate evidence that NSAIDs are not more effective than Comment. This study, though negative, exhibited a other drugs for acute low back pain. There is strong trend towards the positive or analgesic effects, and was evidence that various types of NSAIDs, including COX-2 significant for medication use and functional disability. It NSAIDs, are equally effective for acute low back pain. was probably underpowered. It is not clear whether these COX-2 NSAIDs had statistically significantly fewer side patients had true radicular pain or somatic referred pain or effects than traditional NSAIDs. a combination in individual cases. They were assumed to Conclusion. The evidence from the 65 trials included in have an acute disc prolapse based on having low back this review suggests that NSAIDs are effective for short- pain and a positive straight leg raise test, without it being term symptomatic relief in patients with acute and chronic clear whether this produced true radicular leg pain as low back pain without sciatica. However, effect sizes are should be the case, or just aggravated the low back pain. small. Furthermore, there does not seem to be a specific Methylprednisolone (Depo-Medrol) 160 mg was used, type of NSAID, which is clearly more effective than others. that is, 40 mg x 4 amps – IM, without any problems, and The selective COX-2 inhibitors showed fewer side effects the authors said that they would use this dose in further compared with traditional NSAIDs in the randomized trials. controlled trials included in this review. However, recent It could be considered for additional pain relief if oral studies have shown that COX-2 inhibitors are associated analgesia is not enough in this somewhat ill-defined with increased cardiovascular risks in specific patient setting, especially if there is no access to a caudal or populations. transforaminal epidural injection. Alternatively, one could try a paraspinal nerve injection if there is a possible Comment. Here is the latest review on NSAIDs for low somatic component with or without radicular/neuropathic back pain for the Cochrane Collaboration http:// component to the pain presentation. – Dr David Roselt www.cochrane.org/. It is consistent with previous reviews, showing short- term symptomatic relief in patients with acute and chronic Roelofs PD, Deyo RA, Koes BW at al. Nonsteroidal low back pain without sciatica. Effect sizes are small, and anti-inflammatory drugs for low back pain: an up- there is no long-term effect on the natural history of chronic dated Cochrane review. Spine 2008;33(16): 1766-74. spinal pain. Side-effects continue to be an issue and Department of General Practice, Erasmus MC, University these agents must be used cautiously if at all. Analgesics Medical Center, Rotterdam, the Netherlands. are often preferable and safer from both GI and cardiovas- [email protected]. cular perspectives. – Dr David Roselt Study Design. A systematic review of randomized controlled trials. Objectives. To assess the effects of nonsteroidal anti- Nath S, Nath CA, Pettersson K. Percutaneous lumbar inflammatory drugs (NSAIDs) and COX-2 inhibitors in the zygapophysial (Facet) joint neurotomy using treatment of nonspecific low back pain and to assess radiofrequency current, in the management of chronic which type of NSAID is most effective. low back pain: a randomized double-blind trial. Spine Summary of Background Data. NSAIDs are the most 2008;33(12): 1291-97; discussion 1298. Smärtkliniken frequently prescribed medications worldwide and are (The Pain Clinic), Umeå, Sweden. [email protected]. widely used for patients with low back pain. Selective Study Design. A randomized controlled study of percu- COX-2 inhibitors are currently available and used for taneous radiofrequency neurotomy was conducted in 40 patients with low back pain. patients with chronic low back pain (20 active and 20 Methods. We searched the MEDLINE and EMBASE controls). databases and the Cochrane Central Register of Control- Objective. The aim of the study was to evaluate the

104 Australasian Musculoskeletal Medicine Journal Abstracts

possible beneficial effect of percutaneous radiofrequency component of their pain that was completely relieved by zygapophysial joint neurotomy in reducing pain and physi- controlled medial branch blocks. It was this pain that was cal impairment in patients with pain from the lumbar treated in a placebo-controlled trial of lumbar medial zygapophysial joints, selected after repeated diagnostic branch neurotomy. blocks. The results clearly show that the effects of lumbar Summary of Background Data. Facet or zygapophysial medial branch neurotomy cannot be attributed to placebo joint pain may be one of the causes of chronic low back effects. The effects are real. pain and may be treated by a percutaneous radiofrequency This treatment did not as expected relieve every pain denervation. Patients may possibly be identified by a the patients had, that were not the target of the interven- positive diagnostic block. These blocks need to be re- tion. The index pain was relieved as postulated, and peated as false positive responses to single blocks occur. corroborated by improvements in function. In all previous studies patients treated with radiofrequency Lumbar medial branch neurotomy as a monotherapy is denervation have been selected after single diagnostic not indicated for all patients with back pain. However, the blocks resulting in a varying degree of relief. study showed that medial branch neurotomy could be a Methods. All patients were examined by an orthopedic complementary therapy in patients typical of a pain clinic surgeon before and 6 months after the treatment (sham or population. It also dispelled accusations that lumbar me- active). Inclusion criteria were 3 separate positive facet dial branch neurotomy is a placebo. blocks. Denervation was achieved by multiple lesions at Professor Bogduk wonders whether critics will next each level in an effort to provide effective denervation. complain that Dr Nath should have recruited highly se- Results. The active treatment group showed statistically lected, ideal patients, with pure zygapophysial joint pain, significant improvement not only in back and leg pain but with no comorbidity, and who would be atypical of patients also back and hip movement as well as the sacro-iliac joint seen in conventional practice. test. Pre operative sensory deficit and weak or absent 1.Dreyfuss P, Halbrook B, Pauza K et al. Efficacy and validity of ankle reflex normalized (P < 0.01) and (P < 0.05), respec- radiofrequency neurotomy for chronic lumbar zygapophysial tively. There was significant improvement in quality of life joint pain. Spine 2000;25: 1270-77. variables, global perception of improvement, and gener- 2.Hooten WM, Martin DP, Huntoon MA. Radiofrequency neu- alized pain. The improvement seen in the active group rotomy for low back pain: evidence-based procedural guidelines. was significantly greater than that seen in the placebo Pain Med 2005;6:129-38. group with regard to all the above-mentioned variables. None of our patients had any complication other than 3.Bogduk N. Evidence-informed management of chronic back transient postoperative pain that was easily managed. pain with facet injections and radiofrequency neurotomy. Spine Conclusion. Our study indicates that radiofrequency J 2008;8: 56-64. facet denervation is not a placebo and could be used in the treatment of carefully selected patients with chronic low 4.International Spine Intervention Society. Lumbar medial branch back pain. blocks. In: Bogduk N, ed. Practice Guidelines for Spinal Diagnos- tic and Treatment Procedures. San Francisco; International Spinal Intervention Society, 2004, pp. 47-65. Comment. In a point of view, Professor Nik Bogduk in the same copy of Spine points out that a previous outcome 5.International Spine Intervention Society. Lumbar medial neu- study by Dreyfuss et al.1 showed excellent results could rotomy. In: Bogduk N, ed. Practice Guidelines for Spinal Diag- be achieved with lumbar medial branch neurotomy. How- nostic and Treatment Procedures. San Francisco; International ever, that study was criticized for having no controls, for Spinal Intervention Society, 2004, pp. 188-218. being highly selective in its recruitment criteria, for enroll- – Dr David Roselt ing only a small proportion of potential patients, and for being too small a study. Later systematic reviews of lumbar medial branch neurotomy demanded randomized Bogduk N. Evidence-informed management of chronic controlled trials, but none of the controlled trials that low back pain with facet injections and radiofrequency followed used correct surgical technique for this proce- neurotomy. Spine J 2008;8(1): 56-64. Pain Medicine dure, and none selected patients on the basis of controlled Department, University of Newcastle, Newcastle, Aus- diagnostic blocks.2,3 tralia. [email protected]. This is first study since Dreyfuss et al. to use controlled The management of chronic low back pain (CLBP) has diagnostic blocks to select patients,4 and the first to use proven to be very challenging in North America, as evi- approved ISIS techniques.5 denced by its mounting socioeconomic burden. Choosing Professor Nik Bogduk points out also that Dr Nath did amongst available nonsurgical therapies can be over- not select ideal patients, free of comorbidity, with good whelming for many stakeholders, including patients, health function, and no depression. His patients were enrolled providers, policy makers, and third-party payers. Although from a pain clinic population, and they had other co- all parties share a common goal and wish to use limited morbidities. Nevertheless, they were able to identify a healthcare resources to support interventions most likely

November 2008 105 Journal Abstracts

to result in clinically meaningful improvements, there is joint interventions in the management of sacroiliac joint often uncertainty about the most appropriate intervention pain. for a particular patient. To help understand and evaluate Study Design. A systematic review using the criteria as the various commonly used nonsurgical approaches to outlined by the Agency for Healthcare Research and CLBP, the North American Spine Society has sponsored Quality (AHRQ), Cochrane Review Group Criteria for this special focus issue of Spine Journal, titled “Evidence- therapeutic interventions and AHRQ, and Quality Assess- Informed Management of Chronic Low Back Pain Without ment for Diagnostic Accuracy Studies (QUADAS) for Surgery”. Articles in this special focus issue were contrib- diagnostic studies. uted by leading spine practitioners and researchers, who Methods. The databases of EMBASE and MEDLINE were invited to summarize the best available evidence for (1966 to December 2006), and Cochrane Reviews were a particular intervention and encouraged to make this searched. The searches included systematic reviews, information accessible to nonexperts. Each of the articles narrative reviews, prospective and retrospective studies, contains five sections (description, theory, evidence of and cross-references from articles reviewed. The search efficacy, harms, and summary) with common subhead- strategy included sacroiliac joint pain and dysfunction, ings to facilitate comparison across the 24 different inter- sacroiliac joint injections, interventions, and ventions profiled in this special focus issue, blending radiofrequency. narrative and systematic review methodology as deemed Results. The results of this systematic evaluation re- appropriate by the authors. It is hoped that articles in this vealed that for diagnostic purposes, there is moderate special focus issue will be informative and aid in decision evidence showing the accuracy of comparative, control- making for the many stakeholders evaluating nonsurgical led local anesthetic blocks. Prevalence of sacroiliac joint interventions for CLBP. pain is estimated to range between 10% and 27% using a double block paradigm. The false-positive rate of single, Comment. This common abstract applies to this and a uncontrolled, sacroiliac joint injections is around 20%. The series of reviews of these topics in Spine Journal in the evidence for provocative testing to diagnose sacroiliac first edition this year. This edition looks at evidence- joint pain is limited. For therapeutic purposes, intraarticular informed management of chronic low back pain with 24 sacroiliac joint injections with steroid and radiofrequency interventions including epidural steroid injections, mas- neurotomy were evaluated. Based on this review, there is sage, trigger point injections, functional restoration, and limited evidence for short-term and long-term relief with many others. – Dr David Roselt intraarticular sacroiliac joint injections and radiofrequency thermoneurolysis. Conclusions. The evidence for the specificity and valid- Hansen HC, McKenzie-Brown AM, Cohen SP, ity of diagnostic sacroiliac joint injections is moderate. The Swicegood JR, Colson JD, Manchikanti L. Sacroiliac evidence for accuracy of provocative maneuvers in diag- joint interventions: a systematic review. Pain Physi- nosis of sacroiliac joint pain is limited. The evidence for cian 2007;10(1): 165-84. The Pain Relief Center, Conover, therapeutic intraarticular sacroiliac joint injections is lim- NC 28613, USA. hans.hippocrates.org. ited. The evidence for radiofrequency neurotomy in man- Background. The sacroiliac joint is a diarthrodial syno- aging chronic sacroiliac joint pain is limited. vial joint with abundant innervation and capability of being a source of low back pain and referred pain in the lower Comment. There is no doubt that sacroiliac joints are extremity. There are no definite historical, physical, or innervated and are capable of producing low back and radiological features to provide definite diagnosis of sac- referred pain in the lower extremity.1 The authors point out roiliac joint pain, although many authors have advocated that the literature on diagnostic sacroiliac joint injections provocational maneuvers to suggest sacroiliac joint as a and non-invasive diagnostic techniques is superior to the pain generator. An accurate diagnosis is made by control- literature on therapeutic interventions. Due to the lack of led sacroiliac joint diagnostic blocks. The sacroiliac joint significant literature, the level of evidence was low for has been shown to be a source of pain in 10% to 27% of therapeutic interventions. It is important that previous suspected cases with chronic low back pain utilizing studies are replicated and high quality evidence pro- controlled comparative local anesthetic blocks. duced. The full text article is available free at Intraarticular injections, and radiofrequency neurotomy www.painphysicianjournal.com. have been described as therapeutic measures. This sys- 1. Bogduk N. The sacroiliac joint. Clinical Anatomy of Lumbar tematic review was performed to assess diagnostic test- Spine and Sacrum. 4th ed. New York; Churchill Livingstone, ing (non-invasive versus interventional diagnostic tech- 2005, pp. 173-81. niques) and to evaluate the clinical usefulness of interventional techniques in the management of chronic sacroiliac joint pain. NECK PAIN Objective. To evaluate and update the available evidence regarding diagnostic and therapeutic sacroiliac Buitenhuis J, de Jong PJ, Jaspers JP, Groothoff JW.

106 Australasian Musculoskeletal Medicine Journal Abstracts

Catastrophizing and causal beliefs in whiplash. Spine Atluri S, Datta S, Falco FJ, Lee M. Systematic review of 2008;33(22): 2427-33; discussion 2434. Medical De- diagnostic utility and therapeutic effectiveness of partment, Univé Insurance and Department of Social thoracic facet joint interventions. Pain Physician Medicine, University Medical Center Groningen, Univer- 2008;11(5): 611-29. Tri-State Spine Care Institute, sity of Groningen, the Netherlands. [email protected]. Cincinnati, OH 45230, USA. [email protected]. Study Design. Prospective cohort study. Background. Chronic mid back and upper back pain Objective. This study investigates the role of pain caused by thoracic facet joints has been reported in 34% catastrophizing and causal beliefs with regard to severity to 48% of the patients based on the responses to control- and persistence of neck complaints after motor vehicle led diagnostic blocks. Systematic reviews have estab- accidents. lished moderate evidence for controlled comparative local Summary of Background Data. In previous research on anesthetic blocks of thoracic facet joints in the diagnosis low back pain, somatoform disorders and chronic fatigue of mid back and upper back pain, moderate evidence for syndrome, pain catastrophizing and causal beliefs were therapeutic thoracic medial branch blocks, and limited found to be related to perceived disability and prognosis. evidence for radiofrequency neurotomy of therapeutic Furthermore, it has been argued with respect to whiplash facet joint nerves. that culturally dependent symptom expectations are re- Objectives. To determine the clinical utility of diagnostic sponsible for a chronic course. and therapeutic thoracic facet joint interventions in diag- Methods. Individuals involved in traffic accidents who nosing and managing chronic upper back and mid back initiated compensation claim procedures with a Dutch pain. insurance company were sent questionnaires (Q1) con- Study Design. Systematic review of diagnostic and taining the Neck Disability Index, the Pain Catastrophizing therapeutic thoracic facet joint interventions. Scale, and the Causal Beliefs Questionnaire-Whiplash. Methods. Review of the literature for utility of facet joint Of 1252 questionnaires dispatched, 747 (59.7%) were interventions in diagnosing and managing facet joint pain returned. Only car occupants with neck complaints were was performed according to the Agency for Healthcare included in this study (n = 140). Complaints were moni- Research and Quality (AHRQ) criteria for diagnostic stud- tored using additional questionnaires administered 6 (Q2) ies and observational studies and the Cochrane Muscu- and 12 months (Q3) after the accident. RESULTS: Pain loskeletal Review Group criteria as utilized for interven- catastrophizing and causal beliefs were related to the tional techniques for randomized trials. The level of evi- severity of concurrent whiplash disability. The severity of dence was classified as Level I, II, or III based on the initial complaints was related to the severity and persist- quality of evidence developed by United States Preven- ence of whiplash complaints. Attributing initial neck com- tive Services Task Force (USPSTF) for therapeutic inter- plaints to whiplash was found to predict the persistence of ventions. Recommendations were based on the criteria disability at 6 and 12 months follow-up, over and above the developed by Guyatt et al. Data sources included relevant severity of the initial complaints. literature of the English language identified through Conclusion. The results suggest that causal beliefs may searches of Medline and EMBASE from 1966 to July 2008 play a major role in the perceived disability and course of and manual searches of bibliographies of known primary neck complaints after motor vehicle accidents, whereas and review articles. Results of the analysis were per- pain catastrophizing is predominantly related to concur- formed for diagnostic and therapeutic interventions sepa- rent disability. The current findings are consistent with the rately. view that an early conviction that neck complaints are Outcome Measures. For diagnostic interventions, stud- caused by the medico-cultural entity whiplash has a ies must have been performed utilizing controlled local detrimental effect on the course of symptoms. anesthetic blocks. For therapeutic interventions, the primary outcome measure was pain relief (short-term relief Comment: This study confirms what musculoskeletal = up to 6 months and long-term relief > 6 months) with pain medicine practitioners have suspected about the secondary outcome measures of improvement in func- importance of patients’ beliefs and catastrophizing in tional status, psychological status, return to work, and determining outcomes. The importance of early interven- reduction in opioid intake. tion in assessment, with history and examination, educa- Results. Based on the controlled comparative local tion, assurance, maintenance of usual activities of daily anesthetic blocks, the evidence for the diagnosis of tho- living (ADLs), and light activity as much as possible, is racic facet joint pain is Level I or II-1. The evidence for apparent. The use of local heat to relax the muscles, and therapeutic thoracic medial branch blocks is Level I or II- gentle range of movement exercises, using deep breath- 1. The recommendation is IA or 1B/strong for diagnostic ing in the form of post-isometric relaxation home exer- and therapeutic medial branch blocks. cises, along with simple analgesics and/or opioids briefly Conclusion. The evidence for the diagnosis of thoracic if necessary, seem to go a long way to manage pain and facet joint pain with controlled comparative local anesthetic prevent disability before the lawyers become involved or blocks is Level I or II-1. The evidence for therapeutic facet non-evidence-based input occurs. – Dr David Roselt joint interventions is Level I or II-1 for medial branch

November 2008 107 Journal Abstracts

blocks. Recommendation is 1A or 1B/strong for diagnostic Conclusion. Therapeutic cervical medial branch nerve and therapeutic medial branch blocks. blocks, with or without steroids, may provide effective management for chronic neck pain of facet joint origin. Comment. This is good evidence for this common condition and supports the use of medial branch blocks Comment. This study shows therapeutic efficacy from (MBBs) for diagnosis and treatment of thoracic repeated cervical medial branch blocks that could repre- zygapophysial joint pain. sent another option for treating chronic somatic cervical No evidence is available for thoracic intraarticular injec- spinal pain. Paraspinal cervical nerve injections performed tions and radiofrequency neurotomy. Intraarticular blocks in the rooms that seem to have a very beneficial clinical with local anesthetic with or without steroid are not sup- effect may be working along similar lines in a less targeted ported by the same level of evidence as MBBs, and non-specific fashion. Both treatments may be worthy of certainly seem to give disappointing results in clinical further study. – Dr David Roselt practice, and appear to be of very limited value. The full text article is available free at www. painphysicianjournal.com or more simply via the top right hand corner of the Pubmed abstract available at http:// SPINE www.ncbi.nlm.nih.gov/pubmed/. – Dr David Roselt Byun WM, Ahn SH, Ahn MW.Significance of perianular enhancement associated with anular tears on mag- Manchikanti L, Singh V, Falco FJ, Cash KM, Fellows B. netic resonance imagings in diagnosis of Cervical medial branch blocks for chronic cervical radiculopathy. Spine 2008;33(22): 2440-43. Depart- facet joint pain: a randomized, double-blind, control- ment of Diagnostic Radiology, College of Medicine, led trial with one-year follow-up. Spine 2008;33(17): Yeungnam University, Daemyungdong, Namku, Daegu, 1813-20. Pain Management Center of Paducah, Paducah, Korea. [email protected]. KY, USA. [email protected]. Study Design. Retrospective analysis of magnetic reso- Study Design. A double-blind, randomized, controlled nance imaging (MRI) and clinical findings about chemical trial. radiculitis-associated anular tear in patients with Objective. To determine the clinical effectiveness of radiculopathy. therapeutic local anesthetic cervical medial branch blocks Objective. To investigate MRI findings of the chemical with or without steroid in managing chronic neck pain of radiculitis caused by anular tears and to determine whether facet joint origin. chemical radiculitis detected by MRI is the cause of Summary of Background Data. The prevalence of per- radiculopathy. sistent neck pain, secondary to involvement of cervical Summary of Background Data. Many studies document facet or zygapophysial joints, has been described in that irritation of adjacent nerve roots by a chemical media- controlled studies as varying from 39% to 67%. Intra- tor of inflammation from the nucleus pulposus may result articular injections, medial branch nerve blocks, and neu- in radiculopathy. Computed tomography (CT) discogra- rolysis of medial branch nerves have been described in phy may be the best examination for diagnosing discogenic managing chronic neck pain of facet joint origin. chemical radiculitis but is too invasive. A reliable imaging Methods. A total of 120 patients were included, with 60 method for replacing invasive provocative CT discogra- patients in each of the local anesthetic and steroid groups. phy and diagnosing chemical radiculitis is required. All the patients met the diagnostic criteria of cervical facet Methods. The study population consisted of 12 patients joint pain by means of comparative, controlled diagnostic with pain referred to leg(s) with or without low back pain blocks, and the inclusion criteria. Group I consisted of who underwent lumbar spine MRI. All cases of our study medial branch blocks with bupivacaine. Group II con- demonstrated perianular enhancement caused by chemi- sisted of cervical medial branch blocks with bupivacaine cal radiculitis associated with anular tears. Patterns and and steroid. Numerical pain scores, Neck Disability Index, locations of perianular enhancement adjacent to anular opioid intake, and work status were evaluated at baseline, tears on MRI were assessed. MRI findings were com- 3 months, 6 months, and 12 months. pared with clinical symptoms and/or provocative Results. Significant pain relief (>or=50%) and functional transforaminal epidural injection (n = 6). For documenta- status improvement was observed at 3 months, 6 months, tion of the relationship between perianular enhancement and 12 months in over 83% of patients. The average and radiculopathy, provocative CT discography was per- number of treatments for 1 year was 3.5 +/- 1.0 in the formed in 2 cases. nonsteroid group and 3.4 +/- 0.9 in the steroid group. Results. Perianular enhancement associated with anular Duration of average pain relief with each procedure was 14 tears revealed thick linear patterns (2.5-7 mm thickness) +/- 6.9 weeks in the nonsteroid group, and it was 16 +/- 7.9 along margins of anular tears on contrast enhanced axial weeks in the steroid group. Significant relief and functional T1-weighted images with fat suppression. Locations of improvement was reported for 46 to 48 weeks in a year. perianular enhancement adjacent to anular tears were at

108 Australasian Musculoskeletal Medicine Journal Abstracts

foraminal (n = 6) and extraforaminal portions (n = 6). CT interbody fusion. They suggested that the zone of granula- discography showed a leak of contrast from anular tear to tion tissue with extensive innervations along the tears in the the perianular regions. Pain reproduction at contrast leak posterior part of the painful disc may be responsible for level during discography showed concordant pain. There causing the pain of discography and of discogenic low was an apparent correlation between perianular enhance- back pain. Also, they described the adjacent tissues ment on MRI and clinical symptoms or provocative epi- surrounding the anular tears replaced by disorganized dural nerve root injection in all cases. and vascularized granulation and scar tissue.8 Conclusion. The perianular enhancement adjacent to Crock in 1986 raised the concept of internal disc disrup- anular tears on MRI may be relevant in the diagnosis of tion, suggesting that trauma to the intervertebral disc symptomatic chemical radiculitis. resulted in the production of inflammatory substances within the nucleus pulposus that could have local Comment. Many studies document that irritation of autoimmune effects causing back pain, and chemical adjacent nerve roots by a chemical mediator of inflamma- effects on the adjacent nerve roots result in leg pain, but tion from the nucleus pulposus may result in radiculopathy. typically no neurologic deficit.9 Common recognized causes of sciatica include disc There were several studies for chemical radiculitis, but herniation and spinal stenosis, central or foraminal, but noninvasive diagnostic imaging studies are rare. In the some patients presenting with radiculopathy can show no current study, contrast-enhanced axial T1-weighted im- evidence of nerve root compression on magnetic reso- ages showed enhancement at regions of all perianular nance imaging (MRI). inflammations and anular tears. The authors suggest Patients with anular tears may experience low back pain enhancement at perianular regions and anular tears is and radiation into the lower limb. The posterior aspects of caused by break-down of the normal vessel wall barrier to the disc and posterior longitudinal ligament are innervated the diffusion of gadolinium out of the vessels around by the sinuvertebral nerves. The posterolateral aspects of vascularized granulation. the discs receive branches from adjacent ventral primary Detection of perianular inflammation on noncontrast T1- rami and from rami communicantes near their junction and T2-weighted images is difficult because there is with ventral primary rami. The lateral aspects of the discs similar signal intensity at the site of inflammation com- receive other branches from the rami communicantes. pared to adjacent normal structures, such as nerve roots Marshall et al1 proposed the concept of chemical radicu- and epidural fat. This is why contrast enhanced axial T1- litis because of the rupture of the anulus fibrosus and weighted images with fat suppression are important for dissemination of disc fluid along nerve roots. detection and diagnosis of perianular inflammation. If anular tears occur, these nerve endings may be Nonspecific HIZs on T2-weighted images seems to be irritated by the acid metabolites, that is, phospholipase a reliable marker of painful anular disruption. The authors (PL) A22 and prostaglandin (PG) E23 contained in the suggest that perianular enhancement associated with material from the herniating disc. anular tears on MRI could be considered as the reliable The pain associated with anular tears has been termed new marker of symptomatic anular tears in diagnosis of discogenic, and it has been shown to radiate to the legs in radiculopathy. Limitations of the study included the small the absence of nerve compression.4 number of patients. Also provocative CT discography was Kayama et al. suggest, based on data from dog models, not performed in all cases. It is possible that no perianular that leakage of nucleus pulposus material from anular enhancement on MRI can be detected in some cases with tears, with injury to adjacent nerve roots, might be one chemical radiculitis. Further study may be required to pathophysiologic mechanism in patients with low back assess the sensitivity of this test. The use of gadolinium pain and sciatica without radiologic evidence of disc adds extra cost and additional time due to extra se- herniation.5 quences so gadolinium-enhanced MRI generally is not a Peng et al. reported that there was a significant positive routine examination of patients with radiculopathy. How- correlation between the site of anular tear and the side of ever, the authors suggest gadolinium-enhanced study radiating pain.6 with fat suppression is helpful for detecting perianular Anular tears manifest on MRI as a high-intensity zone enhancement by the inflammatory cytokines if patients (HIZ). The presence of HIZs within the posterior anulus presenting with radiculopathy reveal no evidence of nerve seen on T2-weighted MRI has aroused great interest and root compression or spinal stenosis on noncontrast MRI. even controversy regarding whether the HIZs was closely Provocative CT discography is the best examination for associated with a concordant pain response on awake diagnosing discogenic chemical radiculitis but is too inva- discography.7, 8 sive. Contrast MRI is an excellent modality for replacing However, MRI studies about chemical radiculitis asso- invasive provocative CT discography and diagnosing ciated with anular tears are rare. chemical radiculitis. The authors suggest that perianular Peng et al. investigated the histologic features of 19 enhancement adjacent to anular tears on MRI may be specimens of lumbar intervertebral discs from 17 patients relevant in the diagnosis of symptomatic chemical radicu- with discogenic low back pain during posterior lumbar litis.

November 2008 109 Journal Abstracts

1. Marshall LL, Trethewie ER, Curtain CC. Chemical radiculitis. treated conservatively. A clinical, physiological and immunological study. Clin Orthop Results. The survival rate for all RA patients was signifi- Relat Res 1977;61-67. cantly reduced when compared with average survival in Norway (P < 0.001). The operated group had a signifi- 2. Ozaktay AC, Kallakuri S, Cavanaugh JM. Phospholipase A2 cantly lower survival rate than the nonoperated group. In sensitivity of the dorsal root and dorsal root ganglion. Spine 1998;23(12): 1297-306. patients with severe instability of the cervical spine, the defined selection criteria for surgical intervention were 3. Muramoto T, Atsuta Y, Iwahara T et al. The action of prostag- specific. By comparison of calculated propensity scores, landin E2 and triamcinolone acetonide on the firing activity of the operated and nonoperated groups were too different lumbar nerve roots. Int Orthop 1997;21: 172-75. to be directly comparable. After surgery only 11 patients (5%) experienced residual pain in the neck or neurologic 4. Moneta GB, Videman T, Kaivanto K et al. Reported pain during symptoms. None of these patients were alive at the end of lumbar discography as a function of anular ruptures and disc the study, signifying that residual pain or neurologic symp- degeneration. A re-analysis of 833 discograms. Spine 1994;19: toms are poor prognostic signs (P = 0.015). In the oper- 1968-74. ated group, anterior subluxation and vertical settling greater 5. Kayama S, Konno S, Olmarker K et al. Incision of the anulus than the lower indication limits did not have a significant fibrosus induces nerve root morphologic, vascular, and func- influence on the survival rate, but there was a reduced tional changes. An experimental study. Spine 1996;21: 2539-43. survival for patients with subaxial subluxations. A clear association was found between increased vertical settling 6. Peng B, Wu W, Li Z et al. Chemical radiculitis. Pain 2007;127:11- and sudden death. 16. Conclusion. RA with neck involvement is a progressive and serious condition with reduced lifetime expectancy. 7. Lim CH, Jee WH, Son BC et al. Discogenic lumbar pain: Hence, our interpretation is that operative intervention association with MR imaging and CT discography. Eur J Radiol 2005;54: 431-37. improves local symptoms and most likely changes the condition from worse to better by increasing lifetime ex- 8. Peng B, Hou S, Wu W et al. The pathogenesis and clinical pectancy in high risk patients. Since the per- and postop- significance of a high-intensity zone (HIZ) of lumbar interverte- erative complications are few, a changed attitude toward bral disc on MR imaging in the patient with discogenic low back more liberal indications for earlier surgery may reduce the pain. Eur Spine J 2006;15: 583-87. symptoms and the mortality rate even more.

9. Crock HV. Internal disc disruption. A challenge to disc pro- Comment. It is important to be mindful of possible lapse fifty years on. Spine 1986;11: 650-53. cervical spine involvement in rheumatoid arthrtitis (RA) – Dr David Roselt and to consider early referral for surgical assessment or review in these patients if symptomatic or if clinically significant disease is detected incidentally, such as during Paus AC, Steen H, Røislien J et al. High mortality rate pre-operative assessment for other surgery. – Dr David in rheumatoid arthritis with subluxation of the cervi- Roselt cal spine: a cohort study of operated and nonoperated patients. Spine 2008;33(21): 2278-83. Orthopaedic De- partment, Rikshospitalet University Hospital, Oslo, Nor- Kim HJ, Lee HM, Kim HS et al. Life expectancy after way. [email protected]. lumbar spine surgery: one- to eleven-year follow-up Study Design. In a prospective cohort study 532 pa- of 1015 patients. Spine 2008;33(19): 2116-21; discus- tients with rheumatoid arthritis (RA) and subluxations of sion 2122-23. Department of Orthopaedic Surgery, Yonsei the cervical spine were consecutively collected during University College of Medicine, Seoul, Korea. 1974-1999. OBJECTIVE: The aims of the study were to Study Design. Retrospective study. assess important factors affecting the mortality rate and Objectives. To investigate the 10-year survival of a large the timing of surgical intervention. number of elderly patients who underwent spine surgery Summary of Background Data. The average follow-up for lumbar spinal stenosis, and to identify significant risk time from the first visit to death or to the end of the study factors and compare them with age- and gender-matched was 8.5 (SD, 5.7) years. Of the 217 operated patients 144 controls from the general population. (66%) died, and of the 315 nonoperated patients 137 Summary of Background Data. There have been many (43%) died. studies on treatment options and surgical outcomes for Methods. Patients were selected for operative interven- lumbar spinal stenosis. However, survival outcomes after tion based on anterior, vertical and subaxial subluxations, lumbar spinal stenosis surgery have not previously been pain, and/or cervical neurology. Survival analyses were studied. Because these operations are usually performed used for comparisons between patients with RA and the for elderly patients, we consider patient survival or life normal population, and between the operated and those expectancy to be a significant outcome measure.

110 Australasian Musculoskeletal Medicine Journal Abstracts

Methods. Between January 1997 and June 2006, patients etal Review Group for randomized trials were used. underwent spine surgery for lumbar spinal stenosis. The Methods. Data sources included relevant English litera- date of death was verified using records from the National ture performed by a librarian experienced in Evidence Health Insurance Corporation. Cumulative 10-year survival Based Medicine (EBM), as well as manual searches of was calculated using the Kaplan-Meier method, and the bibliographies of known primary and review articles and survival of patients who had undergone spine surgery was abstracts from scientific meetings within the last 2 years. compared to that of age- and sex-matched members of the Three reviewers independently assessed the trials for the general population. A Cox multivariate regression analysis quality of their methods. Subgroup analyses were per- was used in order to compare the survival rates for different formed among trials with different control groups, with covariates. different techniques of epidural injections (interlaminar, Results. Using Kaplan-Meier curves, the overall 10- transforaminal, and caudal), with different injection sites year survival was 87.8% in patients 60 to 70 years old at (cervical/thoracic, lumbar/sacral), and with timing of out- surgery, and 83.8% in patients 70 to 85 years old at come measurement (short- and long-term). surgery. The 10-year survival rate of female patients and Outcome Measures. The primary outcome measure is patients who underwent fusion surgery were higher than pain relief. Other outcome measures were functional those of male patients and patients with nonfusion sur- improvement, improvement of psychological status, and gery. Compared to the adjusted corresponding portion in return to work. Short-term improvement is defined as 6 general population, the standardized mortality ratios were weeks or less, and long-term relief is defined as 6 weeks 0.21, 0.53, and 0.45 in patients aged 50 to 59, 60 to 69, and or longer. 70 to 85, respectively. Results. In managing lumbar radicular pain with Conclusion. Elderly patients who underwent spine sur- interlaminar lumbar epidural steroid injections, the evi- gery for spinal stenosis had reduced mortality compared dence is strong for short-term relief and limited for long- to the corresponding portion of the general population. term relief. In managing cervical radiculopathy with cervi- Therefore, surgery for spinal stenosis is a justifiable pro- cal interlaminar epidural steroid injections, the evidence is cedure even in elderly patients. moderate. The evidence for lumbar transforaminal epidural steroid injections in managing lumbar radicular pain Comment. This study looks at the 10-year survival of is strong for short-term and moderate for long-term relief. 1015 elderly patients who underwent spine surgery for The evidence for cervical transforaminal epidural steroid lumbar spinal stenosis and shows pretty favorable out- injections in managing cervical nerve root pain is moder- comes ,with substantially reduced mortality compared to ate. The evidence is moderate in managing lumbar radicular that of the general population. It seems quite reasonable pain in post lumbar laminectomy syndrome. The evidence to consider referring for a surgical opinion even elderly for caudal epidural steroid injections is strong for short- patients with significantly limiting spinal claudication. – Dr term relief and moderate for long-term relief, in managing David Roselt chronic pain of lumbar radiculopathy and postlumbar laminectomy syndrome. Conclusion. There is moderate evidence for interlaminar Abdi S, Datta S, Trescot AM, Schultz DM, Adlaka R, epidurals in the cervical spine and limited evidence in the Atluri SL, Smith HS, Manchikanti L. Epidural steroids lumbar spine for long-term relief. The evidence for cervical in the management of chronic spinal pain: a system- and lumbar transforaminal epidural steroid injections is atic review. Pain Physician 2007 Jan;10(1): 185-212. moderate for long-term improvement in managing nerve University of Miami, Miller School of Medicine, Miami, FL root pain. The evidence for caudal epidural steroid injec- 33136, USA. [email protected]. tions is moderate for long-term relief in managing nerve Background. Epidural injection of corticosteroids is one root pain and chronic low back pain. of the most commonly used interventions in managing chronic spinal pain. However, there has been a lack of Comment. This paper from 2007 provides supportive well-designed randomized, controlled studies to deter- evidence for the use of epidural injection of corticosteroids mine the effectiveness of epidural injections. Conse- in managing chronic spinal pain. The authors conclude quently, debate continues as to the value of epidural that there is moderate evidence for lumbar transforaminal steroid injections in managing spinal pain. epidural steroid injections for long-term improvement in Objective. To evaluate the effect of various types of managing nerve root pain. The evidence for caudal epi- epidural steroid injections (interlaminar, transforaminal, dural steroid injections is moderate for long-term relief in and caudal), in managing various types of chronic spinal managing nerve root pain and chronic low back pain. pain (axial and radicular) in the neck and low back regions. The full text article is available free at www. Study design. A systematic review utilizing the criteria painphysicianjournal.com or more simply via the top right established by the Agency for Healthcare Research and hand corner of the Pubmed abstract available at http:// Quality (AHRQ) for evaluation of randomized and non- www.ncbi.nlm.nih.gov/pubmed/. – Dr David Roselt randomized trials, and criteria of Cochrane Musculoskel-

November 2008 111 Journal Abstracts

Tachihara H, Sekiguchi M, Kikuchi S, Konno S. Do effect at this level on somatic components of radiculopathy, corticosteroids produce additional benefit in nerve and represent in part a non-target-specific ESI that is root infiltration for lumbar disc herniation? Spine possible in the rooms. 2008; 33(7): 743-47. Department of Orthopaedic Sur- Various studies have shown that NRI using local gery, Fukushima Medical University School of Medicine, anesthetic or a combination of local anesthetic and corti- Fukushima, Japan. [email protected]. costeroid can provide both short- and long-term pain Study Design. Experimental animal study. relief.1–6 Objective. To determine whether corticosteroids pro- Recent studies have reported that, not only mechanical duce additional benefit to nerve root infiltration (NRI) for compression due to intervertebral disc protrusion, but also experimental lumbar disc herniation. nociceptive and inflammatory mediators originating from Summary of Background Data. NRI is used for nonsur- the nucleus pulposus (NP) play important roles in the gical treatment of radicular symptoms caused by lumbar onset of sciatic pain in LDH.7–13 disc herniation or lumbar spinal canal stenosis. Various Local injection of corticosteroid to provide anti-inflam- studies have shown that NRI using local anesthetic or matory effects to the affected nerve root appears to be a combinations of local anesthetic and corticosteroid can promising approach. Interestingly, whether corticosteroids provide both short- and long-term pain relief. However, produce additional benefit in NRI is still controversial. whether corticosteroids produce additional benefit to NRI A randomized, double-blinded, controlled trial described remains controversial. the effectiveness of corticosteroids, with 67% of patients Methods. A total of 174 adult female Sprague-Dawley in the group receiving both local anesthetic and steroid rats were used in this study. The left L5 nerve root and avoiding the need for operative intervention, compared dorsal root ganglion (DRG) were exposed. For the with 28% in the group receiving local anesthetic alone.5 nontreatment group, autologous nucleus pulposus was However, another randomized, double-blinded, control- harvested from the tail and applied to the DRG. For led trial found that corticosteroids produced no additional treatment groups, 1% lidocaine (Lido group), 0.4% dex- benefit to NRI using local anesthetic agents for the treat- amethasone (Dexa group), 1% lidocaine + 0.4% dexam- ment of chronic radicular pain.4 ethasone (Lido + Dexa group), or saline (Saline group) Another randomized, double-blinded trial showed that was injected into the underlayer of epineurium just distal the combination of corticosteroids and bupivacaine had to the nucleus pulposus. At 2, 7, 14, and 21 days after short-term effects, but the steroid group experienced a surgery, withdrawal threshold was determined using the “rebound” phenomenon at three and six months.2 von Frey test for mechanical allodynia. Expression of The present results indicate that NRI prevented me- tumor necrosis factor (TNF)-alpha in the DRG was exam- chanical allodynia and decreased expression of TNF- ined by immunohistochemical analyses and alpha in the DRG for experimental LDH. However, no immunoblotting. additional benefit from using corticosteroid in NRI was Results. Withdrawal threshold decreased in the demonstrated. nontreatment group from day 2 to day 14. Conversely, The therapeutic mechanisms of NRI using local Lido, Dexa, and Lido + Dexa groups showed no de- anesthetic have been investigated. Application of NP to creases in withdrawal thresholds, and no significant differ- the nerve root induces an increase in endoneurial fluid ences were observed among these 3 groups. Immunohis- pressure (EFP) and a decrease of blood flow in the DRG.14 tochemical analyses showed that TNF-alpha was local- Increased pressure is caused by interference with cap- ized in DRG neurons in all groups. Immunoblotting showed illary flow and intraneurial edema, followed by breakdown that expression of TNF-alpha in the DRG was lower in of the myelin sheath and other cytoplasmic components of Lido, Dexa, and Lido + Dexa groups than in the Schwann cells and the axon.15,16 These changes are nontreatment group. No significant differences were ob- thought to represent an important pathogenic mechanism served among these 3 groups. associated with sciatica caused by disc herniation. Conclusion. NRI prevented mechanical allodynia. How- Lidocaine reportedly reduces the increase in EFP and ever, no additional benefit from using corticosteroid was pathophysiological changes in the DRG induced by NP.17 identified, suggesting that corticosteroid may be unneces- Increased intraradicular blood flow has also been ob- sary for NRI. served in compressed spinal nerve roots after NRI with lidocaine.18 Comment. This rat model suggests that corticosteroids NRI with lidocaine may thus exert therapeutic effects by may add no extra efficacy to local anesthetic injection in improving EFP and blood flow in the DRG. treating radiculopathy. Furthermore, a relationship between lidocaine and acid- Nerve root infiltration (NRI), also known as transforaminal sensing ion channel 3 (ASIC3) has recently been re- epidural steroid injection (TFESI), is used for nonsurgical ported.19 treatment of radicular symptoms caused by lumbar disc ASIC3 is a sodium channel associated with acidosis and herniation (LDH) or lumbar spinal canal stenosis. increased inflammatory pain. ASIC3 is up-regulated in Paraspinal nerve injections may also have a beneficial DRG neurons following the disc herniation model. Lido-

112 Australasian Musculoskeletal Medicine Journal Abstracts

caine decreases ASIC3 expression in DRG neurons and the unnecessary for NRI. pain associated with the disc herniation model. These findings suggest the possibility that lidocaine decreases 1. Abdi S, Datta S, Lucas LF. Role of epidural steroids in the acidosis by increasing blood flow. management of chronic spinal pain: a systemic review of effectiveness and complications. Pain Physician 2005;8: 127-43. In addition, Hasue suggested that lidocaine breaks up the vicious circle of pain, desensitizing the central and 2. Karppinen J, Malmivaara A, Kurunlahti M et al. Peri-radicular peripheral nervous systems by blocking abnormal im- infiltration for sciatica: a randomized controlled trial. Spine pulses from and to the involved nerve root and DRG.20 2001;13: 1056-67. Corticosteroids have shown anti-inflammatory properties related to inhibition of prostaglandin synthesis and 3. Lutz GE, Vad VB, Wisneski RJ. Fluoroscopic transforaminal decreases in regional levels of inflammatory mediators lumbar epidural steroids: an outcome study. Arch Phys Med such as interleukin-1, TNF and phospholipase A2.21-23 Rehabil 1998;79:1362-66. In patients with LDH, elevated levels of phospholipase 4. Ng L, Chaudhary N, Sell P. The efficacy of corticosteroids in A2, prostaglandin E2 production, and inflammatory periradicular infiltration for chronic radicular pain: a randomized, cytokines may directly or indirectly stimulate the nerve double-blind, controlled trial. Spine 2005;30:857-62. root, and inflammatory reactions may play an important pathogenic role in causing sciatica after disc herniation.24, 25 5. Riew KD, Yin Y, Gilula L et al. The effect of nerve root injections Recent studies have shown the pro-inflammatory on the need for operative treatment of lumbar radicular pain. J cytokine TNF-alpha in NP plays a vital role in the develop- Bone Joint Surg Am 2000;82A: 1589-93. ment of NP-induced inflammatory changes in the nerve root.9, 26 6. Vad VB, Bhat AL, Luts GE et al. Transforaminal epidural Corticosteroids thus have therapeutic effects on radicu- steroid injections in lumbarsacral radiculopathy: a prospective randomized study. Spine 2002;27: 11-16. lar symptoms caused by LDH due to their anti-inflammatory function. 7. Aoki Y, Rydevik B, Kikuchi S. Local application of disc-related Corticosteroids also reduce increases in early vascular cytokines on spinal nerve roots. Spine 2002;27: 1614-17. permeability in spinal nerve roots and inhibit reductions in nerve conduction velocity induced by epidural application 8. Hou SX, Tang JG, Chen HS et al. Chronic inflammation and of NP.27 compression of the dorsal root contribute to sciatica induced by Corticosteroids exert anesthetic-like actions on nocic- the intervertebral disc herniation in rats. Pain 2003;105: 255-64. eptive C-fiber conduction independent of their anti-inflammatory properties.28 9. Igarashi T, Kikuchi S, Myers RR. Exogenous tumor necrosis factor-alpha mimics nucleus pulposus-induced neuropathology. Conversely corticosteroids have been shown to pos- 29 Molecular, histologic, and behavioral comparisons in rats. Spine sess direct neurotoxic effects on peripheral nerve tissue. 2000;25: 2975-80. Dexamethasone causes reduced blood flow in normal nerves and DRG.30 10. McCarron RF, Wimpee MW, Hudkins PG. The inflammatory Corticosteroids have some detrimental effects on the effect of nucleus pulposus: a possible element in the pathogenesis function of macrophages, which are thought to play a role of low-back pain. Spine 1987;12: 760-64. in the resorption of herniated intervertebral discs.31 Methylprednisolone contains 40% polyethylene glycol 11. Olmarker K, Rydevik B, Nordberg C. Autologous nucleus as a buffer, while hydrocortisone contains benzyl alcohol, pulposus induces neurophysiologic and histologic changes in porcine cauda equina nerve roots. Spine 1993;18: 1425-32. both buffering agents known to be neurotoxic.32, 33 Corticosteroids may thus have both beneficial and harm- 12. Olmarker K, Blomquist J, Strömberg J. Inflammatogenic ful effects on nerve tissue. properties of nucleus pulposus. Spine 1995;20: 665-69. The present study focused on TNF-alpha, which plays a very important role in the development of NP-induced 13. Olmarker K, Myers RR. Pathogenesis of sciatic pain: role of inflammatory changes in the nerve root. NRI decreased herniated nucleus pulposus and deformation of spinal nerve root expression of TNF-alpha in the DRG for experimental and dorsal ganglion. Pain 1998;78: 99-105. LDH. But other factors may contribute to sciatica caused by disc herniation. 14. Yabuki S, Kikuchi S, Olmarker K et al. Acute effects of nucleus pulposus on blood flow and endoneurial fluid pressure The authors feel that further studies focussing on other in rat dorsal root ganglia. Spine 1998;23: 2517-23. factors may reveal different findings and provide further information on the pathomechanisms of NRI. 15. Myers RR, Mizisin AP, Powell HC et al. Reduced nerve blood Nonsurgical treatments for radicular symptoms using NRI flow in hexachlorophen neuropathy. J Neuropath Exp Neurol in clinical situations seem likely to continue to develop. 1982;41: 391-99. In this study, combinations of local anesthetic and corticosteroid did not result in multiplicative or synergistic 16. Myers RR, Powell HC, Costello ML et al. Endoneurial fluid actions in this study, suggesting corticosteroid may be pressure: Direct measurement with micropipettes. Brain Res

November 2008 113 Journal Abstracts

1978;148: 510-15. 1996;21: 218-24.

17. Onda A, Yabuki S, Kikuchi S et al. Effects of lidocaine on 26.. Olmarker K, Larsson K. Tumor necrosis factor [alpha] and blood flow and endoneurial fluid pressure in a rat model of nucleus pulposus-induced nerve root injury. Spine 1998;23: herniated nucleus pulposus. Spine 2001;26: 2186-91. 2538-44.

18. Yabuki S, Kikuchi S. Nerve root infiltration and sympathetic 27. Byrod G, Otani K, Brisby H et al. Methylprednisolone reduces block: an experimental study of intraradicular blood flow. Spine the early vascular permeability increases in spinal nerve roots 1995;20: 901-6. induced by epidural nucleus application. J Orthop Res 2000;18: 983-87. 19. Ohtori S, Inoue G, Koshi T et al. Up-regulation of acid- sensing ion channel 3 in dorsal root ganglion neurons following 28. Johansson A, Hao J, Sjolund B. Local corticosteroid applica- application of nucleus pulposus on nerve root in rats. Spine tion blocks transmission in normal nociceptor C-fibres. Acta 2006;31: 2048-52. Anaesthesiol Scand 1990;34: 335-38.

20. Hasue M. Pain and the nerve root. Spine 1993;18: 2053-58. 29. Mackinnon SE, Hudson MB, Gentile F et al. Peripheral nerve injection injury with steroid agents. Plast Reconstr Surg 1982;69: 21. Bendrups A, Hilton A, Meagear A et al. Reduction of tumor 482-89. necrosis factor alpha and interleukin-1 beta levels in human synovial tissue by interleukin-4 and glucocorticoid. Rheumatol 30. Shishido H, Kikuchi S, Heckman H et al. Dexamethasone Int 1993;12: 217-20. decreases blood flow in normal nerves and dorsal root ganglia. Spine 2002;27: 581-86. 22. Kantrowitz F, Robinson DR, McGuire MDB. Corticosteroids inhibit prostaglandin production by rheumatoid synovia. Nature 31. Minamide A, Tamaki T, Hashizume H et al. Effects of steroid 1975;258: 737. and lipopolysaccharide on spontaneous resorption of herniated intervertebral discs: an experimental study in the rabbit. Spine 23. Lee HM, Weinstein JN, Meller ST et al. The role of steroids 1998;23: 870-6. and their effects on phospholipase A2. An animal model of radiculopathy. Spine 1998;23: 1191-96. 32. Chino N, Awad EA, Kottke FJ. Pathology of propylene glycol administered by perineural and intramuscular injection in rats. 24. Saal JS, Franson RC, Dobrow R et al. High levels of Arch Phys Med Rehabil 1974;55: 33-38. inflammatory phospholipase A2 activity in lumbar disc herniations. Spine 1990;15: 674-78. 33. Sun CN, White JH. Destruction and remyelinization of peripheral nerve after alcohol injury. Exp Pathol 1974;9: 169-74. 25. Takahashi H, Suguro T, Okazima Y et al. Inflammatory – Dr David Roselt cytokines in the herniated disc of the lumbar spine. Spine

114 Australasian Musculoskeletal Medicine The 12th IASP World Congress on Pain Glasgow, Scotland, 18-22 August 2008

Dr A Breck Mackay

nd so with the farm sold, cashed up on 30 June but …. 2008, we went to Scotland and the 12th Intern- Sunday had seen the usual rash of pre-conference Aational Association for the Study of Pain (IASP) refresher courses, all summarized in the available book World Congress on Pain in Glasgow. published by IASP. Monday had the obligatory official Yes, we made a few mistakes, like arriving in the United opening and then it got underway. The plenaries were Kingdom during the coldest and wettest summer for 60 excellent and covered many divergent topics from sodium years. A coupe of days in London to burn off the jet-lag, channels and pain, joint pain neuronal mechanisms, stress then to Aberdeen for the pre-conference meeting on and chronic pain and fibromyalgia, clinical pain in genetic Primary Care Management of Back Pain, which did not disorders, neurochemistry of pain, pain and suffering even get under way (not enough registrants), but next day following torture (it missed the torture of patients by the visit to Royal Lochnagar Whisky Distillery at Crathie doctors not actually listening and jumping to the wrong near Balmoral made up in part, especially the bottles of 50- conclusions without any examination), pain in the devel- year-old Special Reserve Whisky. (Enough was sent oping world (India), understanding pain mechanisms, home to last a few years or until the next visit!) external validity of randomized trials and to whom they A drive around Scotland to all the scenic bits, such as apply (this confirmed that randomized trials apply only to Pitlochry, Inverness, down past Loch Ness to Glencoe those conforming to the trial patient types … that is, to (very eerie), to Loch Lomond and the Robbie Burns almost no one else), the neurobiology of itch and pain, memorials, to Thornhill, and back to Glasgow was well inhibition in pain amplification and generation, cytokines worth it. Getting in to the Quality Hotel in Glasgow was an in pain, pediatric pain and palliative management quality, exercise in itself. We drove around in the rain, four times pain memory extinction, neuronal spinal cord pain process- (a long way when you add all the one-way street diver- ing, the ubiquitous catastrophizing, neuropathic pain at sions) and found only one door and no parking anywhere, the spinal level, and traumatic nerve injury. because it is beside and, in fact, part of the main railway Now if you were not mind boggled by all those, then station! We gave up, took the car to the hire place and said there were 90 workshops held between 10.00-11.30 and fill it up … no petrol stations anywhere near Glasgow (only 15.30 to 17.00 each day, with the special interest groups on the M8 or main roads outside the city) and asked them meeting on the Wednesday afternoon …. or you could join to take us to the hotel. the various tours. Only tragedy was that the organizers Amazingly, as we drove past the side of the railway had not managed to get it sorted out and, unlike Sydney station the driver suddenly turned sharp right, dived into where every workshop and plenary was recorded and an obscured street and up into the station to park where available on CD, only the plenaries were video recorded. you would least expect … beside the railway platform! The What a stuff up! Miss a workshop or 2-5 that you wanted main entrance to the hotel is inside the Central Station. to go to, and there is no way of finding out what was Into our Quality Hotel which had the forlorn appearance of discussed until the abstracts are published in 2009. Surely Grizabella the Glamour Cat from “Cats”… seen much they should have improved the recording output after the better days but now very old, tattered, and torn. high Sydney standard in 2005. Perhaps 2010 in Montreal And so to the conference. Canada might be better. Held in the Glasgow Conference and Convention Cen- Of the workshops I attended, the one on fibromyalgia, tre (looking like an armadillo perched outside a bloody big trigger points, and myofascial pain rehashed all that has square barn) but with a holding capacity way above the gone before and not one new item came up. “The manag- 6,500 delegates. So they shut off half of each of the five ing low back pain: where do we go from here?” was done biggest barn areas and had the presentations in the front by three epidemiologists who waffled on about the statis- half of each as well as the many lesser rooms in the tics and added not one useful or relevant new option. This complex. The armadillo held the main auditorium with a was a total waste of time compared to our work in Australia maze of steps and passages to get into it and you often and they did not even consider anything other than ended up nowhere near where you wanted to sit. Oh well, randomized controlled trials, and they really are a non- it was only for the plenary sessions. entity when one realizes that pain is a unique personal The facilities were good as long as you liked the coffee experience and successful management is achieved only and junk food styles available and the nearest other in each patient, thus only N=1 trials can give you compa- outlets were in Glasgow a six-minute walk and 10-minute rable and useful results. Sorry, the statistical boys and tube train ride to central station. It was not at all near the girls presenting could not cope with that idea. They like big standard of the Sydney Convention Centre where the 11th numbers per trial. IASP World Congress on Pain was held in 2005. Bigger Functional pain syndrome was going somewhere. I

November 2008 115 The 12th IASP World Congress on Pain

never found out just where, and CRPS: nerve, immune anywhere else in the string … and missing the whole pain and endothelial cell interactions was fascinating and mind concept of one unique experience to each patient, involv- boggling, with a new laboratory model in the rat by Dr ing sensory and emotional fear of, or actual damage. Terrence Coderre from Canada. (I am biased because he And yes, we did go to the Edinburgh Military Tattoo. Be agreed our Australian whole body function models were sensible, stop at home, be comfortable and warm, have a good and need to be followed up.) Pain in older persons nice drink and eats beside you, hear it all clearly. Do not was old material and missed the effects of accumulated get soaked by the very heavy mists (I would hate to see enthesis damage as one gets older. Preventing chronic their rain). Do not feel that sardines are very loosely pain in primary care was not very useful at all. And packed in comparison and actually hear the music and performance of the performance measures was analysis performance, for sure as hell we could not as we got of the analysis. I lost their plot. Longitudinal perspective on uncomfortably jammed into our seats, knees in the person musculoskeletal pain in the population was very drawn out in front, knees behind in our back, looking from left and and then I was done! right like on the side of a king-sized tennis court, elbows Overall? Scotland is very lovely, but I would have hooked each side and the rain saturating everything preferred to see it without the rain. Aberdeen, Edinburgh, below the waist. What a waste of money! and Glasgow confirmed in my mind why so many Scottish Will I go in 2010 to the 13th IASP World Congress on Pain persons emigrate. If that is what it is like in summer, who in Montreal Canada from August 29 – September 2, 2010? in their right mind would stick around for very short days Yes, but only because I can add it to a Greek Island and long cold dark nights for the rest of the year? cruise and conference, a visit to Bulgaria (to a family The whole Pain Congress reminded me that pain is like physician who is doing what we do and getting the same a new long sausage that has not been twisted into bundles results), a London visit, time in Montreal, and a visit to of three. Then it is twisted up and each “expert in pain friends in Ottawa as well. Must make a wholesome trip out research and management” is busily beavering away on of it to enjoy it fully! their own sausage, oblivious to those on either side or

116 Australasian Musculoskeletal Medicine Educational Activities

MASTERS, DIPLOMA, AND CERTIFICATE COURSES IN MUSCULOSKELETAL MEDICINE

FLINDERS UNIVERSITY DIPLOMA/CERTIFICATE IN MUSCULOSKELETAL MEDICINE DATE TITLE/KEY VENUE PROVIDER CONTACT CME POINTS RESOURCE PERSON 23 - 27 July Due to Norm Flinders Medical Flinders University Mr Michael McKay TBA Broadhurst’s Centre School of Health McKay, Ph: +61 8 8201 3913; retirement, this Sciences, Bedford [email protected] course will not be Park SA 5042 presented until his replacement is appointed.

UNIVERSITY OF OTAGO DIPLOMA/CERTIFICATE IN MUSCULOSKELETAL MEDICINE DATE TITLE/KEY VENUE PROVIDER CONTACT DETAILS FOR CME POINTS RESOURCE ALL PAPERS PERSON On campus papers 7-14 March MSMX701 On-campus course University of Otago Enrolments: Veronica Mixture of points Clinical University of Otago, McGroggan including small Diagnosis Pt 1 Christchurch Tel. +64 3 364 1086 group points 17-21 August MSMX701 Pt 2 Fax +64 3 364 0909 University of Otago Email: veronica.mcgroggan 23-29 May MSMX709 On-campus course @otago.ac.nz Clinical Christchurch or Therapeutics Geoff Harding Ph: +61 7 3269 5522 Distance taught Fax +61 7 3269 6407 papers Email: [email protected] March-June MSMX704 Pain Distance taught website: www.uoc.otago.ac/ papers - fortnightly departments/msm MSMX711Pain audioconferences Assessment (new ex University of paper) Otago, Christchurch

July-October MSMX708 Pain Management

March 2009 MSMX702 Tissues

MSMX703 MSM Disorders

UNIVERSITY OF NEWCASTLE MASTERS IN PAIN MEDICINE

DATE TITLE VENUE PROVIDER CONTACT CME POINTS 2008 Masters in Internet Grad school at Laura.Miller@newcastle. N/A Pain University of edu.au - administrative Medicine Newcastle, NSW liaison at Uni of Newcastle or Phillipa.Powis@newcastle. edu.au for information about the course

November 2008 117 Educational Activities

AUSTRALIAN COLLEGE OF PHYSICAL MEDICINE DIPLOMA OF PHYSICAL MEDICINE

DATE TITLE VENUE PROVIDER CONTACT CME POINTS On hold in Diploma of Sydney Australian College Shane Maloney, ph (02) 9438 tba 2008/2009 Physical Medicine of Physical Medicine 5088, Fax (02) 9438 5755 Manual admin@ Techniques for northsidephysicalmedicine. the treatment of com.au or visit the website musculoskeletal www.physicalmedicineaustralia. dysfunction com.au

OTHER MUSCULOSKELETAL MEDICINE EDUCATIONAL ACTIVITIES

DATE TITLE VENUE PROVIDER CONTACT CME POINTS 28-30 Nov Injection Adelaide Margaret Taylor Ph (08) 8378 1254 RACGP 40 points 08 and 2009 Techniques for [email protected] category 1 date TBA Pain (incl. Prolo- therapy)

5-6 Dec 08 AAOM workshop Denver, USA American Association Ph 888 867 1920 Lumbar sacral of Orthopedic email [email protected] spine and lower Medicine extremities

28 Dec - 7 Med. Challenges Antarctica cruise World Travel Ros or Stephanie, World Travel For physiotherap- Jan Series: Conferen- from Argentina 2/142 Bundall Rd, Bundall 4217 ists only ces in Antarctica: Ph 1800 249 804 The Mackenzie Email [email protected] approach to musculoskeletal pain

28-31 Jan The American Honolulu, USA American Academy of www.painmed.org/annual_mtg/ NA Academy of Pain Pain Medicine overview.html Medicine’s 25th annual meeting

5-8 April The Pain Sydney Australian Pain DC Conferences Continuum: Society Ph (02) 9954 4400 Making pain www.apsoc.org.au history

3 evenings Prolotherapy in Adelaide Margaret Taylor Ph (08) 8378 1254 RACGP 40 points in 2009 Sports Med: [email protected] Category 1 3 x 2.5 hrs

August Australian Sunshine Coast AAMM, ACPM, AFMM, www.dcconferences.com.au/ Musculoskeletal NZAMM aamm2009 Medicine DC Conferences Conference PO Box 637 North Sydney NSW 2059, Ph (02) 9954 4400 Fax (02) 9954 0666 aamm2009@dcconferences. com.au

26-30 March International Conf.Rendezvous Hotel NZAMSM www.musculoskeletal.co.nz 2010 on Low Back Pain Auckland Spine in Action - Can 118 Australasian Musculoskeletal Medicine