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Page 1: Orthopaedics - Ningapi.ning.com/.../ORTHOPAEDICSTODAYAprJun2008.pdf · Orthopaedics April-June 2008Vol ... Symposium on Low Back Pain Dr. Vijay Kumar, Dr. Lalit Sharma, Dr. Rajesh
Page 2: Orthopaedics - Ningapi.ning.com/.../ORTHOPAEDICSTODAYAprJun2008.pdf · Orthopaedics April-June 2008Vol ... Symposium on Low Back Pain Dr. Vijay Kumar, Dr. Lalit Sharma, Dr. Rajesh

Index

53

EditorialHow Evidence-based is our Treatment of Chronic Low Back Pain?Rajesh Malhotra : 56

Symposium on Low Back PainImaging of Low Back Pain :

Surabhi Agarwal, Sarika Dua, Bhavuk Garg, Arvind Jayaswal : 59

Low Backache-Conservative Management:

Vijay Kumar, Lalit Sharma, Rajesh Malhotra : 65

Newer Surgical Modalities in the Treatment ofLumbar Disc Herniation:

Upendra BN, Arvind Jayaswal : 76

VOL X No 2 : April-June 2008

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VOL X No 2 : April-June 200854

Exercises and Precautions in the Management of Low Back Pain:

Kanchan Mittal : 83

Rheumatoid arthritisCurrent Status of Disease Modifying Anti-rheumatic Drugs (DMARDs)

in Rheumatoid Arthritis: Chaitali Sukhdeo Bajait, Mirza Shiraz Baig,

Prakashchandra Rambhau Gade, Prakash Narayan Khandelwal : 88

Pioneers in OrthopaedicsPioneers in Orthopaedics : Bhavuk Garg, Rajesh Malhotra : 95

Ortho QuizOrtho Quiz-15 : Bhavuk Garg, Rajesh Malhotra : 96

Answer and Discussion to Ortho Quiz-14 :Bhavuk Garg, Rajesh Malhotra : 97

Symposium on Low Back Pain (Contd.)

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Group Chairman & Editor in Chief : Sanjiv Malik

Managing Director : Venkatraman K

Editor : Rajesh Malhotra

Editorial Advisory Board: Abrar Ahmed, Ajoy K Sinha,Ashok N Johari, Bhavuk Garg, GS Kulkarni, HN Sinha,Jaswant Rai, Mayil Vahanan Natarajan, Mohd. Farooque, PKDave, S Bhan, S Venkat, SC Goel, SKS Marya, SM Tuli,Sushrut Babhulkar

Desk Editor : Rajiv Dhir

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The editorial opinions expressed in this publication are thoseof individual authors and not necessarily those of the publisher.Whilst every effort has been made to ensure the accuracy of theinformation in this publication, the publisher accepts no respon-sibility for errors or omissions.

For reprints (minimum order : 500) contact the ProductionDepartment. Further copies of Orthopaedics Today are avail-able from CMPMedica India Pvt Ltd, 640, 10-‘A’ Cross, West ofChord Road (2nd stage), Bangalore-560 086, Karnataka, India

Orthopaedics Today is Published and Printed by Dr. Sanjiv Malik,on behalf of CMPMedica India Pvt Ltd, 640, 10-‘A’ Cross, West ofChord Road (2nd stage), Bangalore-560 086, Karnataka, India.Editor Dr. Sanjiv Malik. Printed at Modest Print Pack (P) Ltd.,C-52, DDA Sheds, Okhla Industrial Area, Phase-I,New Delhi-110020.

ORTHOPAEDICS TODAYVol. X No. 2 April-June 2008 49-100 Rs. 100/-

ISSN 0972-1339 RNI No. DEL ENG/1999/388 www.asia.cmpmedica.com

Publisher's Information

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VOL X No 2 : April-June 200856

Dr. Rajesh MalhotraProfessor

Deptt. of OrthopaedicsAll India Institute of

Medical SciencesNew Delhi

editorial �

The management of chronic low back pain is very challenging. Low back pain has tremendoussocioeconomic burden. Choosing among available therapies can be overwhelming when youaim for clinically meaningful improvements. Uncertainty reigns about the most appropriateintervention for a particular patient. Most episodes of acute back pain resolve within four weeks.

Chronic low back pain is defined as six weeks of back pain or resulting functional limitation for 12 weeks,after which some form of operative or non operative treatment is indicated. The growing list of treatmentapproaches promoted as solution to chronic low back pain make it very difficult for the patient andphysician alike to make sense. Let us look at the evidence for various non-operative treatments forchronic low backache available in the literature.

It is expected that adequate research will support the effectiveness, safety and cost effectiveness ofa treatment before it is considered. The same, unfortunately, is not true about the treatment of low backpain where treatment options with limited scientific evidence or without being subjected to methodologi-cally sound RCTs find vocal and strong proponents. The largely commercial and competitive model ofhealth care decisions on management of chronic low back pain which has replaced scientific evidenceand expert consensus has been likened by many to shopping at a supermarket. That the market stakesare high is evident from the fact that the point prevalence of low back pain in the general adult populationis estimated at 37% whereas the 1-year prevalence is 76% and the life time prevalence is 85%. About20% of sufferers describe their pain as severe or disabling. The direct and indirect costs including medicalcosts of treatment, disability payments (in the West) and loss of productivity are high. Given the largenumber of treatment options, navigating through them without evidence-informed guide is likeshopping in a foreign super market without understanding the labels on the products. There are over60 pharmaceutical products, 32 different manual therapies, over 100 named techniques in chiropractic,physical therapy, osteopathy and massage therapy, 20 different exercise programs, 26 different passivephysical modalities, more than 9 educational and psychological therapies, over 20 different injectiontherapies, numerous minimally invasive interventions promoted as alternatives to surgery, hoards oftraditional and newer surgical approaches, extensive life-style products including braces, beds, chairs(including vibrating ones!) and ergonomic aids and, finally, a constantly changing variety of comple-mentary and alternative medical approaches. It is a challenge to anyone involved in management ofchronic low back pain, to understand the merits and drawbacks of these treatment options includingover 200 different medications, therapies, injections, products or procedures.

Moreover, look at the number of specialists who claim expertise at treating these symptoms! The list

How Evidence-based is our

Treatment of Chronic

Low Back Pain?

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57VOL X No 2 : April-June 2008

includes orthopaedic surgeons (of course!), chiropractors, neurosurgeons, physical therapists, rheumatologists,acupuncturists, neurologists, pain management specialists, osteopaths, physical medicine and rehabilitationspecialists, internists and family physicians. Naturally, the education, training, skills and experience of thisdiverse group vary considerably when it comes to treating low back pain. Thus, there exists a great deal ofvariance in expertise and opinion within each health profession and clinical subspecialty that treats chroniclow back pain. A study in US reported that 65% patients with low back pain sought care from family physiciansas compared against 22% in Australia. Interestingly, there is an eight-fold difference in the likelihood ofundergoing surgery for chronic low back pain depending on the specific region in which one resides in USA.

Continuing Medical Education, while informing clinicians of the most recent innovations which help theirpatients, rarely discuss adequately the discrepancies in the research behind the approach being presented.Generally, vague recommendations are made – usually conservative when surgery has failed and surgery whenconservative treatment has failed! That no treatment to date has managed to change the burden of chronic lowback pain is the reason for the demand for new approaches. Most of the approaches, however, find little supportfrom the available evidence. One must, however, keep in mind the fact that although evidence-based medicine(EBM) offers a framework for finding and evaluating information about specific treatments, the EBMmethodology for evaluation of treatments for chronic low back pain can result in information which is of littlevalue to clinicians or patients. Few interventions for low back pain have been studied through multiplemethodologically sound randomised controlled trials; many systematic reviews end up concluding that thereis insufficient evidence on which to base recommendations.

The American College of Physicians and American Pain Society have recently recommended Joint ClinicalPractice Guidelines for the diagnosis and treatment of low back pain as described in Table 1.

Available literature does dispel a lot of myths about treatment of chronic low back pain. Treatment modalitiesshown by EBM approach to be ineffective in treating low back pain include traction therapy (there is moreevidence against than for it!), cessation of smoking, weight reduction, bed rest, home care, topical gel, notreatment, lumbar stabilising exercises, trigger point injection and dry needling, electrotherapy modalities such

Table1: Recommendations for Diagnosis and Treatment of Low Back Pain

� Perform a focused history and physical examination and categorise the patient as

� Non specific low back pain

� Back pain potentially associated with radiculopathy or spinal stenosis, or,

� Back pain potentially associated with another specific spinal cause

History should include assessment of psychosocial risk factors which predict risk for chronicdisabling pain

� Routine imaging or other diagnostic tests are not required in patients with non specific low backpain

� Diagnostic imaging and testing should be performed when severe or progressive neurologicdeficits are present or when serious underlying conditions are suspected.

� Patients with persistent low back pain and signs or symptoms of radiculopathy or spinal stenosisshould be evaluated with MRI or CT only if they are potential candidates for surgery or epiduralsteroid injections.

� Patients should be provided evidence-based information on low back pain with regard to theirexpected course, effective self care options and should be advised to remain active

� Medication with proven benefits should be used in conjunction with back care information andself care. Potential benefits, risks and long term efficacy and safety data must be consideredbefore starting treatment. First line drugs are acetaminophen or NSAIDs.

� Patients who do not improve with self care options should receive additional non-pharmacologictherapy such as spinal manipulation for acute low back pain and interdisciplinary rehabilitation,exercises therapy, massage, spinal manipulation, yoga, cognitive behaviour therapy orprogressive relaxation for chronic pain

Roger Chou, et al. Annals of Int Med 2007;147(7):478-491.

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VOL X No 2 : April-June 200858

as TENS, IFT, diathermy and ultrasonic and, acupuncture. Bed rest is not recommended for more than two days,if necessary at all. Light activity is recommended and physical activity of any type is good enough without anydemonstrable advantage of any particular regime. Evidence-based approach has demonstrated definite effective-ness of McKenzie method, spinal manipulation therapy, spinal mobilisation, Yoga (Viniyoga), cognitive-behaviouraltherapy, interdisciplinary rehabilitation and functional restoration. Serious adverse events after spinal manipula-tion (such as worsening lumbar disc herniation or the cauda equina syndrome) have been reported to be very rare.One systematic review found no serious complications reported in more than 70 controlled clinical trials. Includingdata from observational studies, the risk for a serious adverse event was estimated as less than 1 per 1 million patientvisits.

Massage has been shown to be beneficial and possible acts through release of endorphins and relaxation. Lumbarextensor strengthening exercises have demonstrated only some short term advantage; while, in the long term, thistherapy is just like any other exercise program as the benefits are lost over prolonged duration. Prolotherapy, i.e.,intraligamentous injection of solutions aimed at promoting connective tissue repair of an incompetent structureby inducing proliferation of new cells has shown some use in cases refractory to other treatments.

Sufficient evidence exists for usefulness of analgesics such as acetaminophen, NSAIDs and muscle relaxants forchronic low back pain, at least for a short period initially. Similarly, opioids have been shown to be safe and effectivefor treating chronic low back pain.

Although evidence supporting the use of adjunctive medicines (Tricyclic antidepressants, anti-epileptics etc.) islimited, it appears reasonable to use low dose tricyclic antidepressants in mild to moderately painful radicularsyndromes after acetaminophen and NSAIDs have been tried. Anti epileptics such as gabapentin can also be used.The possible adverse effects of all drug therapies must, however, be kept in mind when they are used.

Therapeutic agents can be introduced into the lumbar epidural space through three routes namely, caudal,interlaminar and transforaminal. The instillation of therapeutic dose of corticosteroid into the anterior epiduralspace to maximally reach the targeted intervertebral disc is best accomplished by the transforaminal injectioncompared to other two techniques although the technique is more demanding technically. However, when treatingchronic low back pain with epidural steroids, it is important to ensure that cause of pain will be addressed by epiduralspace injection of corticosteroid. For example, painful lumbar facet joints would be best treated with therapeuticintra-articular injections or ablation of the joints nerve supply. Injection of corticosteroids in the epidural spacein such cases would not appropriately address the source of the symptoms. Lumbar medial nerve blocks remainthe single validated diagnostic test in confirmation of pain originating in lumbar facet joint and such diagnostictests improve the response rates to the chosen treatment.

Intradiscal therapies such as intradiscal electrothermal annuloplasty (IDET) and intradiscal radiofrequencytreatment and minimally invasive nuclear decompression using a bipolar radio frequency device are all effectivealthough functional restoration is less than pain relief. Chronic refractory cases of low back pain have shownresponse to epidural spinal cord stimulation (SCS) utilising paddle electrodes and a pulse generator stimulator(Conventional Implantable [Genesis®], Rechargeable Implantable [Eon®]), or, a Radio Frequency stimulator(ANS; St. Jude Medical Holdings BV, Netherlands) and can be reserved as an option for recalcitrant cases.

In conclusion, chronic low back pain has recently become better understood, allowing an accurate diagnosis inmost of the cases. The judicious use of fluoroscopically guided, contrast-enhanced, controlled diagnostic spinalprocedures provides better direction for the use of target-specific therapeutic interventions such as epiduralsteroid injections. The specific identification of a particular lumbosacral structure responsible for a patient’ssymptomatology aids subsequent efforts to both treat injury of this structure and help prevent symptomaggravation.

The culmination of these findings is that to best treat the different aetiologies of chronic low back pain, strategiesspecific to the implicated structure must be pursued. However, given the wide variety of non-surgical and surgicaltreatments available, physicians would still be unable to convince a large number of patients about the superiorityof their preferred treatment over others and the patients will continue to window shop in the supermarket!

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59VOL X No 2 : April-June 2008

Low back pain is extraordinarily common. Everyorthopaedic surgeon, who treats musculoskeletalproblems, sees patients with low back pain. Thenatural history of LBP is reported to be self-limitedand to have a favorable prognosis. This problem,which supposedly has a favorable natural history,can be remarkably disabling and alarming indica-tor of some underlying serious pathology. A fo-cused and detailed history and medical examina-tion coupled with appropriate imaging with properinterpretation is essential to understand the com-plex pathology of low back pain. Imaging studiesdo not determine whether a particular structure ispainful or not, rather it helps to confirm the clinicaldiagnosis made with the help of history and physi-cal examination.

WHY WE NEED IMAGING?

� To provide precise anatomical information� To confirm clinical diagnosis� To plan an effective treatment� To assess the efficacy of treatment� To plan and perform a diagnostic or therapeu-

tic intervention

Fortunately, in as many as 90 percent of patients,acute low back pain resolves within six weeksregardless of treatment methods.1, 2 More than 50percent of patients with sciatica or mild neurologicdeficits also recover, with only 5 to 10 percent of

cases requiring surgery.2, 3 Because the majority ofpatients fully or partially recover within six weeks,imaging studies are generally not recommended inthe first month of acute low back pain, however,there are several exceptions, referred to as “redflags,” that warrant further diagnostic work-upand immediate treatment. (Table 1)

The following discussion reviews specific imagingmodalities as applied to the diagnosis of low backpain.

TYPES OF IMAGING MODALITIES

� Plain X-ray films� Bone scan� Myelography� Computed tomography (CT)� Magnetic resonance imaging (MRI)� Discography

PLAIN FILMS4-7

They are usually the first imaging study to beordered as they are easy to obtain, available tomost of the physicians, inexpensive and providea lot of information. They also help to determinethe next imaging study, if needed at all. Theydemonstrate basic osseous structure, integrityand alignment of the lumbar spinal motion seg-ments. Two major drawbacks to radiography aredifficulty in interpretation and an unacceptablyhigh rate of false-positive findings. Plain filmsprovide following specific information:� Unisegmental like in tuberculosis or

multisegmental involvement as seen in lumbardegenerative disc disease

Imaging of Low Back Pain

SURABHI AGARWAL

Post Graduate

Deptt. of RadiodiagnosisAMU, Aligarh

SARIKA DUA

Post Graduate

Deptt. of RadiodiagnosisAmritsar Medical College,Punjab

BHAVUK GARG

Senior Resident

ARVIND JAYASWAL

Professor

Deptt. of Orthopaedics,AIIMS, New Delhi

SYMPOSIUM ON

LOW BACK PAIN

Keywords: Low back pain, X-ray, Bonescan, CT, MRI, Discography

Low back pain is the commonest symptom, presented to an orthopaedic surgeon.Although, most of the patients, recover regardless of treatment, imaging is frequentlyneeded to rule out or establish diagnosis. This article focuses on different modalitiesused in imaging of low back pain, regarding their indications, contraindications,application, feasibility and limitations.

“Because the majorityof patients fully or

partially recover

within six weeks,imaging studies are

generally not

recommended in thefirst month of acute

low back pain”

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VOL X No 2 : April-June 200860

� Acute or chronic process. Chronic changesinclude:� Decreased intervertebral height� Vacuum phenomenon as in disc herniation� End plate remodeling with spurs and scle-

rosis� Spinal malalignment

� Congenital or acquired pathology� Malalignment as in scoliosis or kyphosis� Destruction and erosion as seen in tumors or

infection

Plain films have high sensitivity and specificity forbony pathologies like acute fractures, spondy-lolysis or spondylolisthesis, scoliosis, kyphosis,gross degenerative changes. They have a low orno sensitivity and specificity for soft tissuepathologies like disc herniation, marrow infiltra-tion, spinal infections and tumors. Degenerativechanges are often evident on plain radiographs;however, caution must be used in making a diag-nosis based on degenerative radiographic changesbecause of the high rate of asymptomatic degen-erative changes. Radiographic evidence of de-generative change is most common in patientsolder than 40 years and is present in more than 70percent of patients older than 70 years. Degenera-tive changes have been reported to be equallypresent in asymptomatic and symptomatic per-sons. The incidence of intervertebral narrowingand irregular ossification of the vertebral endplates has also been shown to be associated withincreased age.

Commonly obtained views for plain

X-rays are

� Anteroposterior (AP) view: It helps to deter-mine the morphology, alignment and symme-try of vertebrae, spinous and transverse proc-esses, pedicles, lamina and facet joints. Thisview best shows the coronal alignment likelumbar scoliosis. Lytic and sclerotic lesions ofthe posterior elements or transverse proc-esses are best seen on AP view. Unilateralpedicle destruction as in metastatic disease

may produce ‘winking owl sign’. (Fig. 1) Apars interarticularis defect appears as an ob-lique line just inferior to the pedicles and isseen in the presence of spondylolysis. The APview of the lumbar spine should include thewhole pelvis; this allows for evaluation of theacetabulum and femoral heads and for thedetection of possible degenerative changesto the pelvis.

� Lateral view: It helps to determine the mor-phology of vertebral bodies, pedicles, spinousprocesses, intervertebral disc spaces and lum-bar lordosis. This view also shows the sagittalalignment like increased or decreased lumbarlordosis. It also shows the anterior or poste-rior slippage of one vertebra over another(antero vs. retrolisthesis). Disc space is bestseen on lateral view (Fig. 2). Normally discspace increases from cranial to caudal till L4-L5 and then L5-S1 disc space is smaller. For L5-S1 interspace, coned down lateral view is moreuseful as in normal lateral view, xray beam isnot focused through this interspace and alsosacrum is at an angle to rest of the lumbarspine.

Table 1: Red flags warranting extensive diagnostic workup

Red Flags

� Progressive neurologic deficit � Cance history� Recent bowel or bladder dysfunction � Insidious onset� Saddle anaesthesia � No relief at bedtime or worsens when supine� Traumatic onset � Constitutional symptoms (e.g. fever, weight loss)� Age > 50 � Hx UTI/other infection, IV drug use, TB exposure� Male with diffuse osteoporosis of compression fracture � Immune suppression steroid use history

� Previous surgery

Fig. 1: “Winking owl sign” in a 14 year old

child with low back pain

“Caution must be used

in making a diagnosis

based on degenerativeradiographic changes

because of the high

rate of asymptomaticdegenerative changes”

“Two major drawbacksto radiography are

difficulty in

interpretation and anunacceptably high rate

of false-positive

findings”

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61VOL X No 2 : April-June 2008

� Oblique views: These views provide informa-tion regarding facet joints and parsinterarticularis. Pars interarticularis defect ap-pears like a collar on a Scotty dog, whilespondylolisthesis produces ‘decapitated’Scotty dog sign.

� Flexion & Extension views: These views helpto determine the instability. Instability is saidto present if on standing, there is >3.5 mm ofhorizontal translation or >11 of angulation atthe involved level compared with the adjacentmotion segment. Use of these views should belimited to patients who do not have otherradiographic abnormalities and patients, whoare neurologically intact, cooperative, andcapable of describing pain or early onset ofneurologic symptoms.

TOMOGRAPHY

Tomography is a technique, whereby images ofstructures in any selected plane are recordedsharply while images of structures outside theselected layer are unsharp. Through out the expo-sure, the unwanted layers are made to move rela-tive to the film and therefore make unsharp images,while the wanted layer is kept stationary to berecorded sharply. Synchronized movement of twoof the three elements, the X-ray tube, the film andthe patient is required while the third remainsstationary. This is useful if patient is not suitablefor CT or MRI or they are not available. It helps to

Fig. 2: Lateral view showing decreased disc

space between L2-3 in a case of Pott’s

spine

Fig 3: ‘Scotty dog sign’ on oblique X-ray

Fig 4: Flexion-extension views showing instability at L4-L5

“Normally disc space

increases from cranialto caudal till L4-L5 and

then L5-S1 disc spaceis smaller”

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VOL X No 2 : April-June 200862

assess the amount, extent and integrity of postop-erative spinal fusion and is significantly less costlythan CT or MRI, however, radiation dose is signifi-cantly higher than CT.

MYELOGRAPHY8-16

Myelography uses a contrast solution in conjunc-tion with plain radiography to improve visualiza-tion of the spinal cord and intrathecal nerve roots.Water-soluble contrast agents (iohexol andiopamidol) are injected into the subarachnoidspace. After injection, AP, lateral, and obliqueviews are obtained. It is a dynamic test measuringability of CSF to flow by an extradural lesion. Sincethe advent of CT and MRI, use of myelographyhas declined, but it remains a useful tool to evalu-ate the neural compression. Now-a-days, it isbeing done combined with CT and is known as CTmyelography, which has become the investiga-tion of choice to study disc herniation and/orarachadonitis in postoperative spine with metalhardware in place. It is also useful when clinicalfindings are compelling and not adequately ex-plained by CT and/or MRI. This study is howeverunable to differentiate disc herniation from bony,malignant, infectious or other extradural lesions.The most important limitation of myelography isits inability to visualize entrapment of the nerveroot lateral to the termination of the nerve rootsheath. It is thus unable to detect any far lateraldisc herniations, which reportedly account for 1 to12 percent of all lumbar disc herniations and occurmost often at the L4-L5 and L3-L4 levels. Compli-cations of this study include headache, nausea,vomiting, back pain and seizures.

BONE SCAN17-18

Bone scan assesses function and tissue metabo-lism of organs using a radionuclide (99mTc) thatemits radiation. Usually it creates abnormality ifthere is disturbance between osteoblastic andosteoclastic activity. Interruption of blood supplycreates a decrease or absence of tracer i.e. coldspot. It is excellent for detection of bony abnor-malities. It is also a useful and essential tool in themanagement of metastasis. However, in some casesof multiple myeloma or purely lytic metastasesfrom aggressive tumors, the lack of a significantosteoblastic activity can diminish sensitivity. Itsnew modification SPECT (Single Photon EmissionComputed Tomography) offers improved imagecontrast and more accurate lesion localizationthan plain bone scan but not image resolution. Itis especially useful when more accurate localiza-

tion of skeletal lesions with in large and/or ana-tomically complex bony structures is required. Itsmain clinical applications include Pars stress reac-tion, spondylolysis, spondylolisthesis stress frac-tures, acute fractures, facet osteoarthritis, facetpain syndrome, failed lumbar spine surgery syn-drome, primary and metastatic disease, infection,metabolic bone diseases, osteonecrosis and sac-roiliac joint involvement in spondyloarthropathies.An abnormal SPECT scan may help to selectpatients for intraarticular injection proceduresbecause abnormal increased facet uptake onSPECT scan has been shown to be predictive of afavorable response to facet injection.

Gallium 67 is the most effective radioactive tracerin assessing infectious spondylitis. One studycompared bone scans using gallium 67 and Tc 99mwith radiography and MRI. Gallium 67 had a sen-sitivity of 92 percent, a specificity of 100 percent,and an accuracy of 95 percent. MRI was thesecond-best method of evaluation for infection,with a sensitivity of 96 percent, a specificity of 93percent, and an accuracy of 94 percent.

COMPUTED TOMOGRAPHY (CT)6,8-10

The principal value of CT is its ability to demon-strate the osseous structures of the lumbar spineand their relationship to the neural canal in an axialplane. A CT scan is helpful in diagnosing tumors,fractures, and partial or complete dislocations. Inshowing the relative position of one bony struc-ture to another, CT scans are also helpful in diag-nosing spondylolisthesis. Soft tissue seen ingraded shadings helps to distinguish betweenligaments, nerve roots; free fat and herniated discmaterial. They are not as useful as MRI in visual-izing conditions of soft tissue structure, such asdisc infection.

The limitations of CT include less-detailed imagesand the possibility of obscuring nondisplacedfractures or simulating false ones. In addition,radiation exposure limits the amount of lumbarspine that can be scanned, and results are ad-versely affected by patient motion; spiral CT ad-dresses these weaknesses because it is moreaccurate and faster, which decreases a patient’sexposure to radiation exposure.

MAGNETIC RESONANCE IMAGING (MRI) 19-23

MRI has emerged as the procedure of choice fordiagnostic imaging of neurologic structures re-lated to low back pain. MRI is better than CT in

“The most important

limitation of

myelography is itsinability to visualize

entrapment of the

nerve root lateral tothe termination of the

nerve root sheath”

“The principal value ofCT is its ability to

demonstrate the

osseous structures ofthe lumbar spine and

their relationship to

the neural canal in anaxial plane”

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63VOL X No 2 : April-June 2008

showing the relationship of the disc to the nerve,and at locating soft tissue and non-bony struc-tures. For this reason, it is better than CT atdetecting early osteomyelitis, discitis, and epi-dural-type infections or hematomas.

MRI provides high resolution, multiaxial,multiplanar images of tissue with no known bio-hazard effects. The only contraindication to MRIis the presence of ferromagnetic implants, cardiacpacemakers, intracranial clips, or claustrophobia.As with other imaging techniques, MRI can iden-tify abnormalities in asymptomatic persons. Inone study, MRIs of 67 asymptomatic persons 20to 80 years of age were obtained. At least oneherniated disc was identified in 20 percent ofpersons younger than 60 years and in 36 percentof persons older than 60 years. Another studydiscovered that 63 percent of asymptomatic per-sons had disc protrusion, and 13 percent had discextrusion.

Many imaging centers use contrast-enhancedMRI to increase the visualization of herniateddiscs. Recent studies have concluded that con-trast enhancement in patients with previous lum-bar spine surgery added limited diagnostic valueand often resulted in more inaccurate interpreta-tions. Gadolinium is thought to enhance the ap-pearance of nerve roots in viral or inflammatoryconditions and can help distinguish recurrent discherniation from scar tissue in the postoperativespine.

DISCOGRAPHY24

Discography is used in conjunction with CT orMRI to localize disc herniation or fissure in theannulus fibrosis. A volume of contrast media isinjected into the disc space to determine the integ-rity of the intervertebral disc. In the normal disc,the annulus fibrosis solidly encloses the nucleuspulposus and is only capable of accepting 1 to 1.5mL of contrast media. If 2 mL or more of contrastmedia can be injected, there is likely to be adegenerative change in the disc.

In addition to determining the available volume ofthe disc, discography is used to reproduce thesymptoms associated with a possible herniateddisc. The patient’s response to pain can helpconfirm the source of the symptoms. When salineor dye is injected, it pressurizes the disc, and thepatient is able to confirm that this pain is the sameas the pain he or she has been having.

Discography should be used cautiously becauseof the possibility of false-positive results. Discog-raphy is an invasive test that has an inherent risk

Fig 5: Axial CT scan showing lumbar canal

stenosis

Fig. 6: MRI showing clearer picture of sacral chordoma than plain X-rays in a patient presenting with low back pain

“MRI has emerged asthe procedure of

choice for diagnostic

imaging of neurologicstructures related to

low back pain”

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VOL X No 2 : April-June 200864

of infection and neural injury. It should be usedonly to confirm an initial diagnosis, not as theprimary diagnostic tool.

Although, a great advancement has been madein the field of imaging, they should not beapplied blindly to all patients. We must notforget that images are just shadows and a properinterpretation in the light of clinical history andfindings is essential to bring out true figures outof them.

REFERENCES1. Kelsey JL, White AA 3d. Epidemiology and impact

of low-back pain. Spine 1980;5:133-42.2. Von Korff M, Saunders K. The course of back

pain in primary care. Spine 1996;21:2833-7.3. Andersson GB, Svensson HO, Oden A. The

intensity of work recovery in low back pain. Spine1983;8:880-4.

4. Freeborn DK, Shye D, Mullooly JP, Eraker S,Romeo J. Primary care physicians’ use of lumbarspine imaging tests: effects of guidelines andpractice pattern feedback. J Gen Intern Med1997;12:619-25.

5. Bigos SJ. Acute low back problems in adults.Rockville, Md: US Department of Health andHuman Services, Public Health Service, Agencyfor Health Care Policy and Research, 1994;AHCPR publication no. 95-0642.

6. Bell GR, Ross JS. Diagnosis of nerve rootcompression. Myelography, computed tomogra-phy, and MRI. Orthop Clin North Am 1992;23:405-19.

7. Inaoka M, Yamazaki Y, Hosono N, Tada K,Yonenobu K. Radiographic analysis of lumbarspine for low-back pain in the general population.Arch Orthop Trauma Surg 2000;120:380-5.

8. Dublin AB, McGahan, Reid MH. The value ofcomputed tomographic metrizamide myelographyin the neuroradiological evaluation of the spine.Radiology 1983;146:79-86.

9. Bosacco SJ, Berman AT, Garbarino JL, TeplickJG, Peyster R. A comparison of CT scanning andmyelography in the diagnosis of lumbar discherniation. Clin Orthop 1984;190:124-8.

10. Haughton VM, Eldevik OP, Magnaes B, AmundsenP. A prospective comparison of computed tomog-raphy and myelography in the diagnosis ofherniated lumbar disks. Radiology 1982;142:103-10.

11. Maroon JC, Kopitnik TA, Schulhof LA, Abla A,Wilberger JE. Diagnosis and microsurgical ap-proach to far-lateral disc herniation in the lumbarspine. J Neurosurg 1990;72:378-82.

12. Siebner HR, Faulhauer K. Frequency and specificsurgical management of far lateral disc herniations.Acta Neurochir (Wien) 1990;105:124-31.

13. Mokri B, Piepgras DG, Miller GM. Syndrome oforthostatic headaches and diffuse pachymeningealgadolinium enhancement. Mayo Clin Proc1997;72:400-13.

14. Schievink WI, Meyer FB, Atkinson JL, Mokri B.Spontaneous spinal cerebrospinal fluid leaks andintracranial hypotension. J Neurosurg 1996;84:598-605.

15. Raskin NH. Lumbar puncture headache: a review.Headache 1990;30:197-200.

16. Patel MR, Louie W, Rachlin J. Postoperativecerebrospinal fluid leaks of the lumbosacral spine:management with percutaneous fibrin glue. AJNRAm J Neuroradiol 1996;17:495-500.

17. Reinartz P, Schaffeldt J, Sabri O, Zimny M, NowakB, Ostwald E, et al. Benign versus malignantosseous lesions in the lumbar vertebrae: differen-tiation by means of bone SPET. Eur J Nucl Med2000;27:721-6.

18. Savelli G, Chiti A, Grasselli G, Maccauro M, RodariM, Bombardieri E. The role of bone SPET studyin diagnosis of single vertebral metastases.Anticancer Res 2000;20:1115-20.

19. Boden SD, Davis DO, Dina TS, Patronas NJ,Wiesel SW. Abnormal magnetic-resonance scansof the lumbar spine in asymptomatic subjects. Aprospective investigation. J Bone Joint Surg Am1990;72:403-8.

20. Boos N, Reider R, Schade V, Spratt KF, SemmerN, Aebi M. The diagnostic accuracy of magneticresonance imaging, work perception, and psycho-social factors in identifying symptomatic discherniations. Spine 1995;20:2613-25.

21. Mullin WJ, Heithoff KB, Gilbert TJ Jr, Renfrew DL.Magnetic resonance evaluation of recurrent discherniation: is gadolinium necessary? Spine2000;25:1493-9.

22. Bradley WG. Use of contrast in MR imaging of thelumbar spine. Magn Reson Imaging. Clin N Am1999;7:439-57.

23. Modic MT, Feiglin DH, Piraino DW, Boumphrey F,Weinstein MA, Duchesneau PM, et al. Vertebralosteomyelitis: assessment using MR. Radiology1985;157:157-66.

24. Carragee EJ, Tanner CM, Khurana S, Hayward C,Welsh J, Date E, et al. The rates of false-positivelumbar discography in select patients without lowback symptoms. Spine 2000;25:1373-81.

“Discography should

be used cautiously

because of thepossibility of

false-positive results.

Discography is aninvasive test that has

an inherent risk of

infection and neuralinjury. It should be

used only to confirm

an initial diagnosis,not as the primary

diagnostic tool”

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65VOL X No 2 : April-June 2008

Low back pain is a common and costly medicalcondition. Although, low back pain rarely indi-cates a serious disorder, it is a major cause of pain,disability, and social cost. The annual prevalenceof low back pain in the United States is estimatedat 15% to 20%,1 and the lifetime prevalence is over60%.2,3 Low back pain is the second most commonsymptomatic reason for all physician visits (upperrespiratory symptoms are first).4 Low back painconstitutes the most common reason for visits toorthopaedists and neurosurgeons.5

The annual incidence of low back ache in UnitedStates has been projected to be 5% per year, withan associated prevalence of 60% to 90%.6 Theone-month prevalence of low back pain is esti-mated to be 43% of the population.7

CLASSIFICATION

Back pain is classified into three categories basedon the duration of symptoms.� Acute back pain - Pain that has been present

for six weeks or less.

� Subacute back pain- Pain that has a six- to 12-week duration

� Chronic back pain- Pain that lasts longer than12 weeks.8

Around 60 percent of patients with acute low backpain return to work within one month, and 90percent return within three months.9

AETIOLOGY

Low back pain has many different causes.Frymoyer suggested that nearly 85% of low backconditions cannot be diagnosed on the basis ofthe history, findings of the physical examination,or diagnostic testing.10 The rapid resolution ofmost back pain often prevents a diagnosis fromever being made. Confounding the problems withdiagnosis is the difficulty in understanding themotive of the patient seeking help. Psychologicaland emotional factors, particularly depression,can play a role.11

The various causes of backache can also bedivided into mechanical and non-mechanical con-ditions.

Mechanical conditions

Mechanical causes of acute low back pain include

Low Backache-ConservativeManagement

VIJAY KUMAR

Assistant Professor

LALIT SHARMA

Senior Resident

RAJESH MALHOTRA

Professor

Deptt. of Orthopaedics

AIIMS, New Delhi

SYMPOSIUM ON

LOW BACK PAIN

Low back pain constitutes the most common reason for visits to orthopaedists andneurosurgeons. The diagnosis for low back pain requires a careful history andphysical examination to determine whether the causes are mechanical or secondaryand more threatening. Components of a conservative management program for lowback pain patients include patient education, controlled physical activity, bed rest, useof lumbosacral orthotic devices and traction, physical modalities such as heat or coldpacks, exercise, drug therapy in the form of NSAIDs and muscle relaxants andselective spinal injections.

Keywords: Low back pain, Lumbago,Spondylosis, Scintigraphy, Heat, Diathermy,Acupuncture

“Low back pain is thesecond most common

symptomatic reason

for all physician visits(upper respiratory

symptoms are first)”

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VOL X No 2 : April-June 200866

dysfunction of the musculoskeletal andligamentous structures. Pain can originate fromthe disc, annulus, facet joints and muscle fibres.These include low back pain/strain/sprain, lum-bago, facet joint syndrome, sacroiliac syndromes,segmental dysfunction, somatic dysfunction,ligamentous strain, and myofascial syndrome.They involve processes in the muscles and/orligaments which are difficult to reliably identify byphysical examination or diagnostic testing. Occa-sionally, the source may be the hip joint andmusculature.

Nonmechanical conditions

The non-mechanical conditions include neopla-sia, infection, and inflammatory arthritis such asankylosing spondylitis. Most conditions associ-ated with other visceral organs involve abdomi-nal, pelvic, or retroperitoneal processes adjacentto the spine. Most of these conditions cause othersymptoms too, in addition to low back pain.

HISTORY

The diagnosis of low back pain requires a

careful history to determine whether the causesare mechanical or secondary and more threat-ening.

History should include patient’s age, constitu-tional symptoms and presence of night pain, bonepain or morning stiffness. The patient should beasked about the occurrence of visceral pain, symp-toms of claudication and neurologic symptomssuch as numbness, weakness, radiating pain, andbowel and bladder dysfunction.

It is also important to inquire about the specificcharacteristics and severity of pain, a history oftrauma, previous therapy and its efficacy, and thefunctional impact of the pain on the patient’s workand activities of daily living. An assessment ofsocial and psychological factors (e.g., depres-sion) may yield information that affects the treat-ment plan.

Systemic or visceral disease

A history of cancer, unexplained weight loss, ageabove 50 years, or failure of conservative therapyare risk factors for low back pain due to cancer.12

Most cancers involving the spine are metastaticfrom the breast, lung, or prostate. Factors asso-ciated with spinal infections include a history ofrecent or ongoing urinary or skin infections,indwelling catheter, or injection drug use. Feveris not a common symptom or finding (low sensi-tivity), but when present, it increases the chanceof an infectious aetiology. Compression frac-tures of the spine are associated with significanttrauma, age over 50 years (though age over 70years is more specific), corticosteroid use, orosteoporosis. Ankylosing spondylitis is sug-gested by morning stiffness, improvement withexercise, onset at age less than 40 years, slowonset, and pain for at least 3 months.13,14 Otherfactors such as symptoms unrelated to activity,pain that is worse when lying down, presence ofatherosclerosis risk factors, and gastrointestinalor genitourinary symptoms can be helpful insuggesting other underlying visceral or sys-temic aetiologies.

PHYSICAL EXAMINATION (TABLE 1)

Patients should be assessed when standing andunclothed for spine symmetry, posture, and flex-ibility. Palpation can assess spinal (bone) versusparaspinal (soft tissue) pain and its severity. Anabdominal and/or pelvic exam may be indicated ifthe history is suggestive of pathology in these

Table 1: Red flags for acute low back pain

History

� Cancer

� Unexplained weight loss

� Immunosuppression

� Prolonged use of steroids

� Intravenous drug use

� Urinary tract infection

� Pain that is increased or unrelieved by rest

� Fever

� Age >50 years or <20 years

� Significant trauma related to age (e.g., fall from a height or motorvehicle accident in a young patient, minor fall or heavy lifting in apotentially osteoporotic or older patient or a person with possibleosteoporosis)

� Bladder or bowel incontinence

� Urinary retention (with overflow incontinence)

Physical examination

� Saddle anaesthesia

� Loss of anal sphincter tone

� Major motor weakness in lower extremities

� Fever

� Vertebral tenderness

� Limited spinal range of motion

� Neurologic findings persisting beyond one month

� Structural spinal deformity

“Pain can originatefrom the disc,

annulus, facet joints

and muscle fibres”

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67VOL X No 2 : April-June 2008

areas. For back pain associated with buttock orgroin symptoms, the hip should be assessed forpain and range of motion. The examination shouldinclude:

Gait and posture

All patients with low back pain should be ob-served for walk and overall posture. Scoliosis maybe functional and may indicate underlying musclespasm or neurogenic involvement.

Range of motion

The examiner should record the patient’s forwardflexion, extension, lateral flexion and lateral rota-tion of the upper torso. Pain with forward flexionis the most common response and usually reflectsmechanical causes. If pain is induced by backextension, spinal stenosis should be considered.The evaluation of spinal range of motion haslimited diagnostic use,15 although it may be helpfulin planning and monitoring treatment.

Heel-toe walk and squat and rise

A patient unable to walk heel to toe, and squat andrise may have neurologic compromise.

Palpation of the sciatic notch

Tenderness over the sciatic notch with radiationto the leg often indicates irritation of the sciaticnerve or nerve roots.

Straight leg raising test

With the patient in the supine position, each leg israised separately until pain occurs. The anglebetween the bed and the leg should be recorded.Pain that occurs when the angle is between 30 and60 degrees is a provocative sign of nerve rootirritation. Bending the knee while maintaining hipflexion should relieve the pain, and pressure in thepopliteal region should worsen it (popliteal com-pression test).16 If placing the knee back in fullextension during straight leg raising anddorsiflexing the ankle also increase the pain(Lasègue’s sign), nerve root and sciatic nerveirritation is likely.

The result of straight leg raising is positive in 95percent of patients with a proven herniated disc atsurgery, but it is also positive in 80 to 90 percentof patients without any form of disc protrusion atsurgery.17 In contrast, crossed straight leg raisingis less sensitive but much more specific for discherniation. In the crossed straight leg raising test,the contralateral, uninvolved leg is raised. The testresult is positive when pain is produced.

Reflexes and motor and sensory testing

This abbreviated neurologic examination of thelower extremities allows the detection of mostclinically important radiculopathy related to lum-bar disc herniation. If patients with abnormalfindings on these tests do not show improve-ment by one month, further diagnostic work-upis necessary.18 Those with progressive symp-toms should undergo further evaluation withoutdelay (Table 2).

“Nonorganic” signs

Functional overlay, or signs of excessive painbehaviour, should be assessed. “Nonorganic”signs of physical impairment have been described.19

The presence of three or more of these signs isthought to suggest a nonphysiologic element ofthe patient’s presentation. In this situation, fur-ther psychologic testing and/or behavioural inter-vention may be warranted (Table 3).

Table 2: Physical Examination Findings Associated with Specific

Nerve Root Impingement

Nerve Strength Sensation Reflex

Root

L2

Iliopsoas Anterior thigh, Nonegroin

L3

Quadriceps Anterior/lateral thigh Patellar

L4

Quadriceps, ankle Medial Patellardorsiflexion (heel walking) ankle/foot

L5

First toe dorsiflexion Dorsum of foot None

S1

Ankle plantar flexion Lateral plantar Achilles(toe walking) foot

Table 3: Waddell’s Tests for Nonorganic Physical Signs

Test Inappropriate response

Tenderness Superficial, nonanatomic tenderness to light touchSimulation

Axial loading Vertical loading on a standing patient’s skull produces lowback pain

Rotation Passive rotation of shoulders and pelvis in same planecauses low back pain

Distraction Discrepancy between findings on sitting and supinestraight leg raising tests

Regional disturbances

Weakness ”Cogwheel” (give-way) weakness

Sensory Nondermatomal sensory loss

Overreaction Disproportionate facial expression, verbalisation or tremorduring examination

*Three or more inappropriate responses suggest complicating psychoso-

cial issues in patients with low back pain.

“For back pain

associated withbuttock or groin

symptoms, the hip

should be assessed forpain and range of

motion”

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VOL X No 2 : April-June 200868

RADIOGRAPHIC EVALUATION

There is no evidence that routine plain radiogra-phy in patients with nonspecific low back pain isassociated with a greater improvement in patientoutcomes than selective imaging.20-22 In addition,exposure to unnecessary ionising radiation shouldbe avoided. This issue is of particular concern inyoung women because the amount of gonadalradiation from obtaining a single plain radiograph(2 views) of the lumbar spine is equivalent to beingexposed to a daily chest radiograph for more than1 year.23 Routine advanced imaging (computedtomography [CT] or magnetic resonance imaging[MRI]) is not associated with improved patientoutcomes24 and identifies many radiographic ab-normalities that are poorly correlated with symp-toms25 but could also lead to additional, possiblyunnecessary interventions.26-27

Findings from both plain radiographs andadvanced imaging studies are poorly associatedwith low back pain symptoms.28-32 The prevalenceof lumbar disk degeneration increases with agebeginning in the fourth decade and is common inpatients without low back pain. One-third of pa-tients below 30 years of age have disc degenera-tion, as do 60% between 40 and 60 years andalmost all patients over 60 years.31 Similar findingsare found for patients with spondylosis and facetjoint arthritis. Spondylolysis (defect involving thepars interarticularis) is equally prevalent in normaland symptomatic subjects. Other findings includ-ing congenital anomalies, disc calcification,Schmorl nodes (disk material within a vertebralbody), and mild-moderate scoliosis are also foundin both asymptomatic and symptomatic persons.32

Lumbar disc herniation or spinal stenosis areradiographically detected only with advancedimaging such as CT or MRI. These findings havebeen observed in asymptomatic patients. Mag-netic resonance imaging (MRI) and computed

tomographic (CT) scanning have been found todemonstrate abnormalities in “normal” asympto-matic people.28,29,33,34 In one study, MRI scansrevealed herniated discs in approximately 25 per-cent of asymptomatic persons less than 60 yearsof age and in 33 percent of those more than 60 yearsof age.29

Advanced radiographic studies

Studies such as CT or MRI should be obtained inpatients with a history, examination, or prior teststhat strongly suggest a serious cause for backpain, such as cauda equina syndrome, infection,or tumour. For patients with sciatica likely due toa herniated disk or spinal stenosis, unless majorneurologic abnormalities are identified, earlyimaging is unnecessary because many patientswill improve with conservative treatment.35,36 Ifsuch patients do not improve with a course ofconservative care, imaging studies are appropri-ate.

Bone scintigraphy

Bone scanning with SPECT (single-photon-emis-sion computed tomography) allows physiologicassessment of bone by identifying increasedosteoblastic activity. It is a highly sensitive studywith a low specificity, making it a good screeningtest for degenerative changes or metastatic dis-ease. It may be useful for localising a pain genera-tor when multiple radiographic abnormalities areidentified. 37

Physiologic assessment

Electrodiagnostic assessments such as needleelectromyography and nerve conduction studiesare useful in differentiating peripheral neuropathyfrom radiculopathy or myopathy. If timed appro-priately, these studies are helpful in confirming theworking diagnosis and identifying the presence orabsence of previous injury. They are also useful inlocalising a lesion, determining the extent of injury,predicting the course of recovery and determiningwhether structural abnormalities (as seen on ra-diographic studies) are of functional significance.The timing of the studies is important, aselectromyographic findings may not be presentuntil two to four weeks after the onset of symp-toms. Hence, electrodiagnostic studies have onlya limited role in the evaluation of acute low backpain.38

LABORATORY TESTS

Laboratory tests generally are not necessary in

Table 4: Selective indications for radiography in acute low back pain

� Age >50 years� Significant trauma� Neuromotor deficits� Unexplained weight loss (10 lb in six months)� Suspicion of ankylosing spondylitis� Drug or alcohol abuse� History of cancer� Use of corticosteroids� Temperature >37.8°C (100.0°F)� Recent visit (within 1 month) for same problem and no improvement� Patient seeking compensation for back pain

“The result of straight

leg raising is positive

in 95 percent ofpatients with a proven

herniated disc at

surgery, but it is alsopositive in 80 to 90

percent of patientswithout any form of

disc protrusion at

surgery. In contrast,crossed straight leg

raising is less

sensitive but muchmore specific for disc

herniation”

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69VOL X No 2 : April-June 2008

the initial evaluation of acute low back pain. Iftumour or infection is suspected, a complete bloodcell count and erythrocyte sedimentation rateshould be obtained. Other blood studies, such astesting for HLA-B27 antigen (present in ankylosingspondylitis) and serum protein electrophoresis(abnormal results in multiple myeloma), are notrecommended unless clinically warranted. Addi-tional laboratory tests, such as urinalysis, shouldbe tailored to the possible diagnoses suggestedby the history and physical findings.39

Conservative management

Components of a conservative management pro-gram for low back pain patients include patienteducation, controlled physical activity, bed rest,exercise and drug therapy in the form of NSAIDsand muscle relaxants.

Bed rest

Bed rest is a common treatment for low back pain.While some authors have shown that bed rest canprovide a benefit with regard to alleviating overallpain, others have shown a quicker return to workwith little or no bed rest.40-42 One randomisedclinical trial found that patients with two days ofbed rest had clinical outcomes similar to those inpatients with seven days of bed rest.42 The currentrecommendation is two to three days of bed restin a supine position for patients with acuteradiculopathy.40-45 The biomechanical rationale forbed rest is that intradiscal pressures are lower inthe supine position. However, rolling over in bedmay result in increased intradiscal pressure. Sit-ting, even in a reclined position, actually raisesintradiscal pressures43 and can theoreticallyworsen disc herniation and pain. Bed rest is notbenign if it is continued for too long a duration asmuscles become deconditioned, cardiovascularfunction-diminishes, individuals lose time fromwork and, with continuing bed rest, start to viewthemselves as ill.88 Activity modification is nowthe preferred recommendation for patients withnon neurogenic pain.

Medications

Although no analgesic should be promoted as acure for pain or a replacement for non-pharmaco-logical interventions, medications are frequentlyused in the non-operative care of low back pain.

Medications in several classes have been shown tohave moderate, primarily short-term benefits forpatients with low back pain. Acetaminophen is a

first-line option for treatment of acute or chronic lowback pain because of a more favourable safetyprofile and low cost.46-49 Nonselective NSAIDs aremore effective for pain relief than is acetaminophen,50

but they are associated with well-knowngastrointestinal and renovascular risks .48 There isan association between exposure tocyclooxygenase-2–selective or most nonselectiveNSAIDs and increased risk for myocardial infarc-tion.51 Cardiovascular and gastrointestinal risk fac-tors should be assessed before prescribing NSAIDsand one should recommend the lowest effectivedoses for the shortest periods necessary.

Opioid analgesics or tramadol can be used judi-ciously in patients with acute or chronic low backpain who have severe, disabling pain that is notcontrolled (or is unlikely to be controlled) withacetaminophen and NSAIDs. The potential ben-efits and harms of opioid analgesics includingdrug abuse and addiction should be carefullyweighed before starting therapy.52-54

Muscle relaxants have a role in acute back pain andare more effective than a placebo alone.Paraspinous muscle spasm associated with acuteback injuries of various aetiologies responds wellto these medications. Muscle relaxants work foronly a limited period and are often associated withhepatotoxicity that is generally reversible andusually not serious.55-56

Depression is common in patients with chroniclow back pain and should be assessed and treatedappropriately.57 Antidepressants also have a rolein the management of low back pain, especiallywhen there is a comorbid mood disorder. Theirconcomitant effects as analgesics and antidepres-sants are particularly useful for individuals inwhom back pain would otherwise be increased bydepression. Likewise, when anxiety predominates,the threshold for pain perception is lowered.58

While antidepressants may be effective when usedalone, they may be extremely effective, comparedwith a placebo, when they are part of combinationtherapy. Tricyclic antidepressants are an optionfor pain relief in patients with chronic low backpain.59-60 Gabapentin is associated with small, short-term benefits in patients with radiculopathy.61-62

For acute or chronic low back pain,benzodiazepines appear to be similarly effectiveas skeletal muscle relaxants for short-term painrelief,55 but are also associated with risks for abuse,addiction, and tolerance.

“The currentrecommendation is

two to three days of

bed rest in a supineposition for patients

with acute

radiculopathy”

“Magnetic resonance

imaging (MRI) andcomputed tomographic

(CT) scanning have

been found todemonstrate

abnormalities

in “normal”asymptomatic

people”

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VOL X No 2 : April-June 200870

Systemic corticosteroids are not recommendedfor treatment of low back pain with or withoutsciatica, because they have not been shown to bemore effective than placebo.63-66

Physical modalities

Physical modalities may be used to diminish symp-toms for short periods of time. These counterirri-tant forms of therapy include ice massage, hotpacks, diathermy, ultrasound and transcutaneouselectrical stimulation (TENS).

Ice massage/cold packs

Patients with acute low back pain may experienceanalgesia with ice massage or cold packs whichdecrease swelling, pain, and muscle spasm duringthe acute phase of an injury as it reduces metabolicactivity locally, decreases muscle spindle activity,and slows nerve conduction. Cold pack relievespain and spasm for longer than superficial heat.Patients who experience increased alpha motorneuron discharges with cold application haveincreased muscle spasm and do not tolerate thisform of therapy. Patients may have at least 33%reduction in pain following ice massage.67

Heat

Heat is another form of counterirritant therapy thathas utility in the treatment of low back pain. Heatshould not be used in patients with back painsecondary to trauma as it causes vasodilatationand increased blood flow, thereby resulting inincreased damage to a recently traumatised area.However, heat increases the elastic properties ofconnective tissues and is useful in patients whocomplain of stiffness associated with their backpain. Heat also decreases gamma fibre activity,muscle spindle excitability and resting muscletension. There are two modalities of heat applica-tion–superficial and deep heat. Superficial heatpenetrates to the subcutaneous tissues.Hydrocollator packs, heating pads, infrared heatand whirlpools generate superficial heat. Themaximal safe exposure for these forms of therapyis 30 minutes applied directly to the skin at 45°C.Deep heat generated by diathermy or ultrasoundpenetrates to structures below the subcutaneoustissues. Deep heat is given in 20 minute sessions.Heat has been shown to be helpful for reducingpain in hospitalised patients with low back dis-comfort.68

Although physiologically cold therapy should beused in patients with acute pain, and heat in

patients with chronic pain, these modalities mayhave the opposite effect. The recommendationshould be cold for acute pain and heat for chronicpain initially. If the patient does not respond, orhas an exacerbation of symptoms, the oppositetemperature modality should be tried.

Injection therapy

Selective spinal injections produce focused andcontrolled anaesthesia of particular anatomic struc-tures to help define loci of pain. In addition to thisdiagnostic benefit, the addition of the potent anti-inflammatory effects of glucocorticoids to thelocal anaesthetic also offers a therapeutic poten-tial.

The epidural space is the most common locationfor selective injections. With fluoroscopic guid-ance, an interlaminar, caudal, or transforaminalapproach can be used.69 Epidural steroid injec-tions are most useful in the treatment of nerve rootirritation and are also used in patients with nerveroot compression who do not respond to con-servative management. Corticosteroids areinjected directly into the epidural space to in-crease the anti-inflammatory effect in comparisonto oral corticosteroids. The treatment course in-cludes three injections given at variable intervals(days to weeks). Epidural injections have beenfound to be effective in some patients.70 Epiduralcorticosteroids may be considered in patientswho have radiculopathy secondary to compres-sion and are poor candidates for surgical interven-tion.

Patients who have localised areas of muscle orligamentous tenderness are also candidates forlocal anaesthetic therapy. The area injected maybe an area of local trauma or a myofascial triggerpoint.71

Facet or zygapophyseal joints can be generatorsof low back pain with referred buttock and lower-limb pain. Use of a controlled injection techniquehas shown that facet joints can produce low backpain.72 In this circumstance, patients have re-ceived injections of anaesthetic and corticoster-oid to decrease pain.73 The injections are done-under fluoroscopic control and facets both at andabove the level of the involved joint must beblocked in order to obtain adequate analgesiasince each facet joint receives sensory innerva-tion from two spinal levels. Injections are givenevery 2-4 weeks for three sessions. Even in studies

“Activity modification

is now the preferred

recommendation forpatients with non

neurogenic pain”

“The recommendationshould be cold for

acute pain and heat for

chronic pain initially.If the patient does not

respond, or has an

exacerbation ofsymptoms, the

opposite temperature

modality shouldbe tried”

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71VOL X No 2 : April-June 2008

reporting a good response, the mean pain relief isonly 30%.74

Radiofrequency dorsal rhizotomy is a techniquethat denervates the facet joint by the localisedinsertion of a probe that destroys the afferentfibres with a radiofrequency current.75 The resultsof dorsal rhizotomy have been variable. Modestsuccess has been shown with single-level rhizo-tomy. Multilevel rhizotomy have better outcomes.76

Exercise

It includes stretching and strength training, backschool for the education of patients, and othermodalities to address low back pain. They offerbenefit by decreasing local muscle spasm andstabilising the spine. Physical therapy, particu-larly in the form of therapeutic exercises, is particu-larly helpful in controlling mechanical low backpain.77-82 A number of different exercise programmesare available for patients with low back pain. Theseinclude flexion exercises, extension exercises,stretching regimens, progressive-resistance exer-cises, and dynamic stabilisation training and aero-bic conditioning. Stand-alone strengthening pro-grammes have also shown benefit.83 Currently,however, it is unclear whether one form of exercisetherapy is more effective than another, but all seemto provide benefit.84 As a generalisation, patientwith mechanical disorders of the discs prefersextension exercises, while those with posteriorcomponent disease prefer flexion exercises. Inmost circumstances patients eventually receive acombination of both forms of exercise.

Exercises may also play a significant role in pre-venting back pain in asymptomatic individuals. Ina comparison with educational strategies, me-chanical supports and risk modification, exercisesthat strengthened back and abdominal muscleswere the only intervention associated with de-creased frequency and duration of low back pain.85

Massage has also shown to decrease symptomsand improve function in patients with nonspecificlow back pain, especially when the massage wascoupled with exercise and education.86

For acute low back pain (duration <4 weeks),spinal manipulation administered by providerswith appropriate training is associated with smallto moderate short-term benefits.87 Supervisedexercise therapy and home exercise regimens arenot effective for acute low back pain,88 and the

optimal time to start exercise therapy after theonset of symptoms is after 2 to 6 weeks.89

For subacute (duration >4 to 8 weeks) low backpain, intensive interdisciplinary rehabilitation(defined as an intervention that includes a physi-cian consultation coordinated with a psychologi-cal, physical therapy, social, or vocational inter-vention) is moderately effective.90

For chronic low back pain, the moderately effectivenonpharmacologic therapies include acupunc-ture,91,92 exercise therapy,88 massage therapy,93 cog-nitive-behavioural therapy or progressive relaxa-tion,94,95 intensive interdisciplinary rehabilitation,96

Viniyoga-style yoga,97 and spinal manipulation,87

Exercise programmes that incorporate individualtailoring, supervision, stretching, and strengthen-ing are associated with the best outcomes.88

TRACTION

Traction is another modality used during therapy.The goal of lumbar traction is to distract the lumbarvertebrae. There are many potential effects, suchas enlargement of the intervertebral foramen, crea-tion of a vacuum to reduce herniated discs, place-ment of the posterior longitudinal ligament undertension to aid in reduction of herniated discs,relaxation of muscle spasm, and freeing of adher-ent nerve roots.98 Intradiscal pressure can bedecreased by 20% to 30%.99 Prospective studieshave shown, however, that traction is not a meanswith which to definitively manage low back painand that it does change its natural history.78

LUMBOSACRAL ORTHOTIC DEVICES

The purpose of a lumbosacral orthosis is to stabi-lize or immobilise. The indications for prescribingan orthosis are vertebral body fracture, spondy-lolysis with spondylolisthesis and the need forpostoperative support. There is no evidence inliterature to support long term use of orthotics forthe treatment of low back pain. The reasons for notprescribing orthoses include concerns about alack of compliance on the part of the patient,creating psychological dependence, and validat-ing the disability. Although weakening of posturalback and abdominal muscles has also been aconcern, it has been shown not to occur to anysubstantial extent.99 The ability of orthoses to limitmotion is in doubt, with conflicting reports in theliterature. Axelsson et al100 found no limitation ofsagittal translation in patients who wore athoracolumbosacral orthosis.101 Corset-type

“As a generalisation,

patient withmechanical disorders

of the discs prefers

extension exercises,while those with

posterior component

disease prefer flexionexercises”

“Exercise programmesthat incorporate

individual tailoring,

supervision,stretching, and

strengthening are

associated with thebest outcomes”

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VOL X No 2 : April-June 200872

orthoses have been shown to decrease interseg-mental motion at all levels by 30%.102 Orthoses donot appear to change the natural history of lowback pain.

DOCTOR-PATIENT RELATIONSHIP

The importance of the interaction of the physicianand patient education in the therapy of low backpain patients cannot be overlooked. Educationalprogrammes such as back school, where a numberof individuals with back pain gather together todiscuss ways of improving their situation, havebeen shown to be an effective way of controllingpatients symptoms. Some schools are directed atgroups. Some are organised for individuals withacute or chronic back pain.103 Back school hasbeen shown to decrease pain and time missed fromwork compared to placebo interventions.104

It is important to provide the patient with clear,concise information that emphasises treatment asbeing time to heal and reassurance that the painwill improve. Education should include informa-tion on causes of back pain, pain resolution, whytesting is rarely needed, usual activity/work andother treatment recommendations, when to con-tact the clinician, when surgery is indicated, andprevention. Written material can reinforce verbalinformation.

Indications for surgical evaluation

Select groups of patients with acute low back painshould undergo immediate surgical evaluation.Patients with suspected cauda equina lesions(characterised by saddle anaesthesia, sensorimo-tor changes in the legs and urinary retention)require immediate surgical investigation. Surgicalevaluation is also indicated in patients with wors-ening neurologic deficits or intractable pain that isresistant to conservative treatment.

It is appropriate to consider a patient for surgeryif he/she has a severe or progressive neurologicdeficit, or meets all four of the following criteria:� Leg pain is equal to or worse than back pain� Positive straight leg raise test� No response to conservative therapy for 4 to

6 weeks for patients with a herniated lumbardisk or 8 to 12 weeks for those with spinalstenosis

� Imaging shows lesion corresponding to symp-toms35

Following are the clinical practice guidelines

issued by the American College of Physicians andthe American Pain Society for the diagnosis andtreatment of low backache:78

� Recommendation 1: Clinicians should con-duct a focused history and physical examina-tion to help place patients with low back paininto any one of the three broad categories:nonspecific low back pain, back pain poten-tially associated with radiculopathy or spinalstenosis, or back pain potentially associatedwith another specific spinal cause. Historyshould include assessment of psychosocialrisk factors, which predict risk for chronicdisabling back pain .

� Recommendation 2: Clinicians should not rou-tinely obtain imaging or other diagnostic testsin patients with nonspecific low back pain.

� Recommendation 3: Clinicians should per-form diagnostic imaging and testing for pa-tients with low back pain when severe orprogressive neurologic deficits are present orwhen serious underlying conditions are sus-pected on the basis of history and physicalexamination.

� Recommendation 4: Clinicians should evalu-ate patients with persistent low back pain andsigns or symptoms of radiculopathy or spinalstenosis with magnetic resonance imaging(preferred) or computed tomography only ifthey are potential candidates for surgery orepidural steroid injection (for suspectedradiculopathy).

� Recommendation 5: Clinicians shouldprovide patients with evidence-based infor-mation on low back pain with regard to theirexpected course, advise patients to remainactive, and provide information about effec-tive self-care options.

� Recommendation 6: For patients with lowback pain, clinicians should consider the useof medications with proven benefits in con-junction with back care information and self-care. Clinicians should assess severity of base-line pain and functional deficits, potential ben-efits, risks, and relative lack of long-term effi-cacy and safety data before initiating therapy.For most patients, first-line medication op-tions are acetaminophen or non steroidal anti-inflammatory drugs.

� Recommendation 7: For patients who do notimprove with self-care options, cliniciansshould consider the addition of nonpharmacologic therapy with proven benefits–for acute low back pain, spinal manipulation;

“It is important toprovide the patient

with clear, concise

information thatemphasises treatment

as being time to heal

and reassurance thatthe pain will improve”

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73VOL X No 2 : April-June 2008

for chronic or subacute low back pain, inten-sive interdisciplinary rehabilitation, exercisetherapy, acupuncture, massage therapy,spinal manipulation, yoga, cognitive-behav-ioural therapy, or progressive relaxation.

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95. Ostelo RW, van Tulder MW, Vlaeyen JW, LintonSJ, Morley SJ, Assendelft WJ. Behaviouraltreatment for chronic low-back pain. CochraneDatabase Syst Rev 2005;(1):CD002014.

96. Guzmán J, Esmail R, Karjalainen K, MalmivaaraA, Irvin E, Bombardier C. Multidisciplinaryrehabilitation for chronic low back pain: system-atic review. BMJ 2001;322(7301):1511-6.

97. Sherman KJ, Cherkin DC, Erro J, Miglioretti DL,Deyo RA. Comparing yoga, exercise, and a self-care book for chronic low back pain: arandomized, controlled trial. Ann Intern Med2005;143(12):849-56.

98. White AA III, Panjabi MM (Eds). In: ClinicalBiomechanics of the spine. 2nd Edn. LippincottWilliams & Wilkins 1990.

99. Scientific approach to the assessment andmanagement of activity- related spinal disor-ders. A monograph for clinicians. Report of theQuebec Task Force on Spinal Disorders. Spine1987;12(7 Suppl):S1-59.

100. Axelsson P, Johnsson R, Strömqvist B. Effect oflumbar orthosis on intervertebral mobility. Aroentgen stereophotogrammetric analysis. Spine1992;17(6):678-81.

101. Walsh NE, Schwartz RK. The influence ofprophylactic orthoses on abdominal strengthand low back injury in the work place. Am JPhys Med Rehabil 1990;69(5):245-50.

102. Fidler MW, Plasmans CM. The effect of fourtypes of support on the segmental mobility ofthe lumbosacral spine. J Bone Joint Surg Am1983;65(7):943-7.

103. White AH. Back school and other conservativeapproaches to low back pain. St Louis: Mosby;1983.

104. Mooney V. Symposium on the lumbar spine:Alternative approaches for the patient beyondthe help of surgery. Orthop Clin North Am1975;6(1):331-34.

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VOL X No 2 : April-June 200876

Newer Surgical Modalitiesin the Treatment ofLumbar Disc HerniationUPENDRA BN

Senior Research Associate

ARVIND JAYASWAL

Professor

Dept. of Orthopaedics,

AIIMS, New Delhi

SYMPOSIUM ON

LOW BACK PAIN

It is essential to know the natural history of lumbardisc prolapse, before discussion of surgicalmodalities available for herniated lumbar disc.Lumbar disc herniation has a favourable naturalhistory (i.e., the clinical course of the diseasewithout therapeutic intervention). Hakelius1

reported on patients with lumbar disc herniationwho were treated with only bed rest and a corsetfor two months. He observed a marked reductionin pain and improvement in function over time:80% of the patients had major improvements aftersix weeks; 90%, after twelve weeks; and 93%, aftertwenty-four weeks. Other studies have revealedless favourable results in that, although mostpatients without surgical treatment had improve-ment, 30% had persistent pain and restrictions atwork and leisure activities after one year.2 It hasalso been observed that majority of disc herniationsdiminish in size over time, with 80% decreasing by>50%.3 Larger disc herniations tend to regressmore, most likely because of their higher watercontent. A positive correlation has been notedbetween regression of lumbar disc herniations

Lumbar disc herniations managed nonoperatively, resolve in more than 80% of cases.For the rest, conventional disc surgery has proved to be effective, but entails the risksof general anaesthesia and neural complications. This has led to a constant search forless invasive and safe procedures to treat this benign condition, paving way for anumber of percutaneous day care procedures done without anaesthesia. This articleexplores the various newer surgical options available for surgical treatment of lumbardisc herniation and attempts to provide a rationale for appropriate use of each of theseprocedures.

Keywords: Lumbar disc, Disc herniation,Microendoscopic discectomy, Arthroscopic

and resolution of symptoms,3,4 and regression isthought to occur as the herniated tissue dehy-drates and immunological responses help to resorbthe disc material. It is rare for an extruded orsequestrated disc herniation of four months ormore duration to require surgery, after the onset ofsymptoms.5 It has been suggested thatnoncontained lumbar disc herniation can be treatedwithout surgery, if these patients can tolerate thesymptoms for the first two months.5 Hence, indi-cation for surgery cannot be based on MRI find-ings of a large prolapsed disc. The currently ac-cepted indications for nonoperative treatment oflumbar disc herniation include the absence of aprogressive neurological deficit or cauda equinasyndrome.6 Thus, nonoperative treatment is theinitial “default” pathway for the majority of pa-tients with lumbar radiculopathy due to disc her-niation.

It follows that only a small fraction of patients,about 10-20%, would require surgical interventionfor persistent radicular pain despite good non-operative treatment for 4-6 weeks consisting oflimited bed rest (1-2 days), nonsteroidal anti-in-flammatory drugs (NSAIDs) exercise regimens,epidural steroids, and patient education.

“The currently

accepted indicationsfor nonoperative

treatment of lumbar

disc herniation includethe absence of a

progressive

neurological deficit orcauda equina

syndrome. Thus,

nonoperative treatmentis the initial “default”

pathway for the

majority of patientswith lumbar

radiculopathy due to

disc herniation”

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77VOL X No 2 : April-June 2008

There are a number of surgical options for tacklingsymptomatic herniated disc which can broadly begrouped as follows:� Interlaminar approach

� Conventional open discectomy: Fenes-tration/Laminotomy

� Microscopic Discectomy: Using opera-tive microscope

� Micro-Endoscopic Discectomy (MED):Using video-assisted endoscope

� Intradiscal Procedures or Percutaneous Discdecompressions (C-arm guided; “blind pro-cedure”)� Chemonucleosis: Chemopapain� Percutaneous Manual Disc Decompres-

sion� Automated Percutaneous Disc Decom-

pression (APDD)� Percutaneous Laser Disc Decompression

(PLDD)� Disc nucleoplasty-radiofrequency

Coblation� Intradiscal ozone therapy� Intradiscal electrothermal annuloplasty

(IDET)� Posterolateral foraminal approach (with en-

doscopic visualisation)� Arthroscopic Microdiscectomy (AMD -

Parviz Kambin).� Selective Endoscopic Discectomy™

(SED™) using Yeung’s Endoscopic SpineSurgery system (YESS)

Interlaminar surgery, involving open fenestration/laminotomy, microendoscopic discectomy (MED)and microscopic discectomy, has been shown to

have excellent clinical outcomes in patients withsymptomatic disc extrusion or sequestration notresponding to conservative management. Thebest results of 99.5% complete or partial pain reliefwere obtained when the disc was free in the canalor sequestered. Incomplete herniation or extru-sion of disc material into the canal resulted incomplete relief for 82% of patients. Excision of thebulging or protruding disc that had not rupturedthrough the annulus resulted in complete relief in63%, and removal of the normal or minimally bulg-ing disc resulted in complete relief in 38%, whichis near the stated level for the placebo response.7,8

Hence, patient selection with radiological correla-tion is crucial to good surgical results. Micro-scopic discectomy has long been considered the“gold standard” surgical treatment for herniatedlumbar disc. Many studies have reported consist-ently favourable results. A successful outcome at6 months in a long term follow-up study wasachieved in 91% of the cases which declinedslightly to 83% at 10-year follow-up.9 In principle,the microscope provides better illumination, bet-ter resolution for visualisation of intracanal struc-tures like epidural vessels and facilitates teaching.Microendoscopic discectomy (MED) combinesthe advantage of good illumination as in micro-scopic discectomy and avoids stripping of mus-cles from the midline. The interlaminar space isapproached with serial dilatation of the paraspinalmuscles with dilators and docking of the endo-scope at desired site (Fig.1). Results of MED haveshown to have equal efficacy as of open or micro-scopic discectomy10 with the advantage of spar-ing midline stripping of lumbar musculature, theclinical significance of which is still not known.

However, conventional open disc surgery and theless invasive interlaminar approaches (MED andmicroscopic discectomy) entails risks of generalanaesthesia, dural tears (2-7%), epidural fibrosis,and chronic postoperative low back pain.11,12 Thishas led to a constant search for less invasive andsafe procedures to treat this benign condition.Percutaneous disc decompression proceduremeets the criteria of being less invasive and pro-vides better safety as an alternative to conven-tional inter-laminar discectomy. These procedurescan be done on an outpatient basis with an awakepatient under local anaesthesia. All the intradiscaldecompression procedures use a common poste-rolateral image-guided percutaneous guidewireinserted into the corresponding disc followed by,either removal of the nucleus or ablating it withFig.1: (A) Microdiscectomy (B) Micro-Endoscopic Discectomy (MED)

A B

“The best results of

99.5% complete or

partial pain relief wereobtained when the disc

was free in the canal

or sequestered”

“In principle, the

microscope providesbetter illumination,

better resolution for

visualisation ofintracanal structures

like epidural vessels

and facilitatesteaching.

Microendoscopic

discectomy (MED)combines the

advantage of good

illumination as inmicroscopic

discectomy and avoids

stripping of musclesfrom the midline”

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VOL X No 2 : April-June 200878

chemicals (ozone, chemopapain), laser orradiofrequency. They all work with the basic con-cept of ‘jelly dough-nut theory’as depicted inFig.2 i.e., a negative intradiscal pressure producedby nucleus removal or ablation creates a suctioneffect and pulls back the protruded nucleus frag-ment.13,14 The procedure works best in containeddisc herniations, however proponents of theseprocedures claim that it works well even in discextrusions which have not yet sequestrated.

The concept of decompression of the nucleus,rather than direct visualisation and excision of theprotruded part of the disc, is not new. In 1951,Hult15 reported relief of both low-back and sciaticpain in 30 patients following fenestration of theannulus through an open retroperitoneal ap-proach, stating, “If an anterolateral incision ismade in the disc, it should be possible to divert thepressure in that direction and thereby prevent itfrom being transmitted posteriorly.” The advan-tages of percutaneous discectomy include avoid-ance of epidural bleeding and perineural fibrosis,elimination of reherniation in the spinal canalthrough the surgically induced annular fenestra-tion, preservation of spinal stability, and estab-lishment of a portal away from the neural elementsfor future herniation.’

CHEMONUCLEOLYSIS

Chymopapain chemonucleosis was the first per-cutaneous intradiscal therapy and involvesenzymatic dissolution of nucleus pulposus byhydrolysis of the charged proteoglycan compo-nent in the nucleus pulposus.16 Chemonucleolysisbecame popular in the 1970s after its introductionas a therapy for a contained lumbar disc prolapse,i.e., without fragment sequestration into the spinalcanal. However, complications began to be re-ported. Intense back pain and stiffness were ob-served in 20%-40% of cases. Though rare, fatalcomplications such as anaphylaxis, transversemyelitis, cartilaginous endplate damage, and haem-orrhage were reported.17 It was suggested that an

anaphylactic immunologic reaction induced byantigens of the chymopapain protein and neuro-toxicity were the main causes of adverse affects.18,19

Concerns about its safety and controversy aboutits effectiveness have led to it being used veryrarely today.

PERCUTANEOUS MANUAL NUCLEOTOMY

This involves removal of disc nucleus through acannula placed percutaneously on the posterola-teral aspect of the annulus. It was first introducedby Hijikata et al20 in 1975 with satisfactory out-come in 75% of his patients who underwentnuclear resection. Technical difficulty in perform-ing in the L

5-S

1 interspace and on obese patients,

and large cannula size were the main disadvan-tages.21

APLD (AUTOMATED PERCUTANEOUS LUMBAR

DISCECTOMY)

Onik et al22 redesigned and reengineered the per-cutaneous discectomy technique and introducedthe automated technique for disc removal in 1984.An 8-inch–long probe is inserted through a 2.5-mm cannula positioned against the annulus fibro-sus and used both as a cutting instrument and foraspiration of disc material. Patient selection crite-ria are critical for good results. If disc herniation is>50% of the anteroposterior diameter of the spinalcanal or extruded disc fragments are observed onCT/MRI, the outcome will be poor.23

Newer devices include a thin, blunt-tipped suc-tion and cutting probe such as the StrykerDekompressor® Percutaneous Discectomy Probe,or the Endius® MDS MicroDebrider System, in-serted percutaneously and the terminal portion ofthe probe is placed into the herniated disc usingfluoroscopic guidance. The device is used tosuction out some or all of the degenerated centraldisc tissue. Clinical efficacy studies have reportedvarious success rates ranging from 29%–60%,24

much inferior to the consistent results ofInterlaminar Discectomy procedures.

LASER DISCECTOMY

Intradiscal laser discectomy uses laser energy tovaporise part of the nucleus volume to debulk thedisc space and decrease discal pressure for re-gression of disc protrusion. Use of the laser inintradiscal procedures began in the 1980s. Themost common lasers for disc decompression arepotassium titanyl-phosphate (KTP), neodymium:yttrium-aluminum-garnet (Nd:YAG) and

Fig. 2: Percutaneous Intradiscal disc decompression and Jelly Dough-nut

theory

“Percutaneous disc

decompression

procedure meets thecriteria of being less

invasive and provides

better safety as analternative to

conventional

inter-laminardiscectomy”

“The procedure works

best in contained disc

herniations”

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79VOL X No 2 : April-June 2008

holmium:YAG (Ho:YAG). Percutaneous lasernucleolysis is more expensive than APLD and hasbeen shown to have inadequate temperature con-trol, causing damage in nerve root tissue, thevertebral body, and endplates.14,25 As a result,laser discectomy has a limited role in the manage-ment of patients with LBP and sciatica. Laserdiscectomy yields variable success rates depend-ing on the type of laser energy used26,27 andis significantly less effective thanchemonucleolysis.28

INTRADISCAL ELECTROTHERMAL

ANNULOPLASTY (IDET)

Intradiscal electrothermal annuloplasty (IDET)does not decrease intradiscal pressure, thereforethis procedure cannot be used as a percutaneousdisc decompression procedure, but rather to re-lieve pain by way of thermal ablation of nerveendings.29 Discogenic pain is believed to arisefrom annular fissures extending from the nucleusto the outer annulus preceding actual disc hernia-tion.30 IDET is a minimally invasive procedure fordiscogenic pain in patients failing conservativetreatment regimens and who otherwise may be acandidate for spinal fusion.31 Typical IDET proce-dures can generate sufficient heat to producenerve ablation. Placement of the heating elementwithin 5-10 mm in the middle or outer annulusachieves the desired temperatures more readily.The IDET procedure relieves discogenic painthrough thermal nociceptive fibre destruction,biochemical mediation of inflammation, stimula-tion of an outer annular healing response, cauteri-sation of vascular ingrowth, and induced healingof annular tears.32

NUCLEOPLASTY

Nucleoplasty is a non-heat–driven process thatuses Coblation technology, using bipolarradiofrequency technology applied to a conduc-tive medium (e.g., saline) to achieve tissue removalwith minimal thermal damage to collateral tissues.33

Temperature is kept below 70°C to minimise ther-mal penetration and adjacent tissue damage. TheCoblation technique causes a localised, low tem-perature molecular disintegration. This processcreates a plasma field of highly ionised particlessurrounding the electrode that have adequateenergy to disintegrate molecular bonds within thenucleus material. The result is volumetric nucleustissue removal by way of creation of multipleintradiscal channels by the wand, with minimalcollateral tissue necrosis. A cadaveric study dem-

onstrated that nucleoplasty was highly effectiveat reducing intradiscal pressure in nondegeneratedcontained discs, but had minimal effect in reduc-ing intradiscal pressure in severely degenerativediscs34 in which most nucleus material already hasdesiccated. Nucleoplasty thus is not effective intreating severely degenerated discs. Results arecomparable to APLD.

OZONE THERAPY

This is another chemonucleolysis technique thatinjects the combination of oxygen and ozone intothe disc and around the nerve root. Oxygen-ozonetherapy exploits the chemical properties of ozone,an unstable allotropic form of oxygen. Many bio-logic effects have been attributed to ozone:bactericidal, fungicide, and virustatic;immunomodulating action;35 and analgesic andanti-inflammatory effects.36 Oxygen–ozonetherapy causes dehydration of the fibrillary matrixof the nucleus pulposus, revealing collagen fibresand regression (vacuole formation and fragmenta-tion)–a sort of disc “mummification”.37 Successrates are similar to those of enzymaticchemonucleolysis with no anaphylactic reactionsor serious side effects reported.

ENDOSCOPIC PERCUTANEOUS DISC

DECOMPRESSION

The evolution from blind manual posterolateraldiscectomy to endoscopic or arthroscopic extrac-tion of disc fragments in the late 1980s becamefeasible because of technological advances andthe availability of small-calibre, high-resolutionglass fibre-optics that enabled the operating sur-geon to visually differentiate anatomically normal

Fig. 3: Arthroscopic Microdiscectomy

(AMD)

“Clinical efficacy

studies have reportedvarious success rates

ranging from

29%-60%, muchinferior to the

consistent results of

InterlaminarDiscectomy

procedures”

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VOL X No 2 : April-June 200880

from abnormal periannular and intracanalicularstructures (Fig 3). Subsequent studies in cadaversnot only made it possible to identify a safe zone onthe dorsolateral corner of the annulus where theinstruments could be positioned but also permit-ted a description of the zone’s radiographic land-marks.38 Labeled “arthroscopic discectomy” orthe Arthroscopic Microdiscectomy (AMD) byKambin, endoscopic techniques have sinceevolved through several generations of technol-ogy. The results from endoscopic discectomychallenge efficacy of open discectomy with stud-ies showing a success rate of above 80%. How-ever, sequestered and migrated fragments cannotbe decompressed via an arthroscopic technique,where an interlaminar procedure is recommended.

Selective Endoscopic Discectomy™ is a mini-mally invasive spine surgery technique that uti-lises an endoscope39 via the transforaminal routeto treat herniated, protruded, extruded, or degen-erative discs that are a contributing factor to legand back pain. The excellent visualisation via theendoscope permits the surgeon to selectivelyremove a portion of the herniated nucleus pulpo-sus that is contributing to the patients’ leg andback pain.

Thermal annuloplasty is an adjunctive procedurethat uses bipolar electro-thermal energy(radiofrequency and/or laser) to ablate the sensi-tised pain nociceptors in the annulus, and toshrink and tighten the stretched collagen fibers ofthe annulus. Thus, the weakened annulus ordefect left by the disc herniation is contracted andpossibly sealed from within the disc. This combi-nation procedure and the endoscopic system usedto perform the unique procedure was pioneeredand developed by Dr Anthony Yeung,40 with in-struments developed with the Richard Wolf In-strument Company (YESS–Yeung EndoscopicSpine Surgery system).

As we have seen, there are a large number ofsurgical procedures for tackling a symptomaticlumbar disc herniation; however, on close scru-tiny one can appreciate that only a few procedureshave given time-tested results. The Interlaminarapproach has given the best results with over 80%good outcome.40 Percutaneous suction discectomy(a success rate of 27% to 44%) and percutaneouslaser discectomy (a success rate of 29% to 69%)have not proved as successful as traditional ap-proaches.41 In individuals with a disc protrusion

with an intact annulus, these methods are used todebulk the central aspect of theintervertebral disc. In contrast, arthroscopicmicrodiscectomy, a procedure that is aimed atextraction of herniated disc fragments by usingtechniques that enable visualisation of the herni-ated fragment from the disc interior, has beenreported to have a success rate of about 80-90%,which is comparable with that of traditional lami-notomy and disc excision but with lower surgicalmorbidity.42 Although the technique is appealing,recent studies have shown that the ultimate out-come, rate of recurrent herniation of a disc, or rateof reoperation are not significantly different fromthose after traditional discectomy.43 It is techni-cally demanding, requires specialized equipmentand expertise, and is limited to specific types ofherniations.43

With so many surgical options, the treating sur-geon is always confronted with the problem ofselecting a particular procedure in a given patient.It is important to consider the type of herniation(contained disc, extruded or sequestrated disc)and location of disc herniation (L

3-L

4, L

4-L

5 or

L5-S

1) as a guide to choose a procedure best suited

for a particular patient. Also, the location of hernia-tion at a given level i.e foraminal, extraforaminal orcentral/paracentral have important implication inselection of the surgical procedure.

Patients with central or paracentral herniations,especially with extruded or sequestrated at L

4-L

5

or L5-S

1 are best suited for conventional

interlaminar discectomy. Studies have shown that,for lumbar microdiscectomy, patients with discherniations at the L

5-S

1 level had significantly

better outcomes than did those at the L4–L

5 level.

Patients with sequestered or extruded lumbar discherniations had significantly better outcomes thandid those contained herniations. It has been sug-gested that patients with contained discherniations, a predominance of back pain, onrestricted duty and smoking should be counselledbefore surgery of the potential for less satisfac-tion, poorer outcomes scores, and decreasedreturn to duty rates.44 In contrast a patient with aforaminal or extra-foraminal disc herniation atL

3-L

4 or L

4-L

5 is best suited for postero lateral

(Transforaminal) Arthroscopic discectomy or theYeung’s procedure.

In general, an interlaminar approach is optimal forL

5-S

1 level as it has a wide interlaminar space and

“The results from

endoscopic

discectomy challengeefficacy of open

discectomy with

studies showing asuccess rate of above

80%. However,

sequestered andmigrated fragments

cannot be

decompressed via anarthroscopic

technique, where an

interlaminar procedureis recommended”

“The Interlaminar

approach has given the

best results with over80% good outcome.40

Percutaneous suction

discectomy (a successrate of 27% to 44%)

and percutaneous laserdiscectomy (a success

rate of 29% to 69%)

have not proved assuccessful as

traditional

approaches”

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81VOL X No 2 : April-June 2008

a very narrow foraminal space, with iliac crestoverhanging, making the transforaminal route verycumbersome. On the contrary, the interlaminarspace is very narrow at L

3-L

4 and the foraminal

space is wider with good access for thetransforaminal procedures (AMD/ YESS). TheL

4-L

5 level can be approached both via the

interlaminar as well as the transforaminal routeequally well. The location of herniation will furthergive the appropriate route of approach. Theforaminal and extra-foraminal herniations obvi-ously favour the transforaminal route where as thecentral and the paracentral herniations are moreamenable to be tackled via the interlaminar route.Hence, the interlaminar and the transforaminalapproaches are not to be used as mutually exclu-sive blanket procedures for all types and levels ofherniations, but should be used appropriatelywith judicious assessment according to the leveland the location of herniation.

Currently the intradiscal procedures are used forcontained disc protrusions not responding toconservative management. Although there hasnot yet been a percutaneous intradiscal proceduredeveloped with the superior therapeutic efficacyof open surgery, these procedures are less inva-sive and avoid the complications of open surgery.All of these procedures have limitations, but theirtherapeutic effect increases substantially withcareful patient selection and proper technique.New appliances and techniques to treat LBP orsciatica continue to evolve, and numerouscontrolled studies are underway. With tremen-dous technologic advances, use of minimally in-vasive techniques to treat chronic back pain andsciatica continues to expand.

REFERENCES

1. Hakelius A. Prognosis in sciatica. A clinical follow-up of surgical and non-surgical treatment. ActaOrthop Scand Suppl 1970;129:1-76.

2. Weber H. The natural history of disc herniationand the influence of intervention. Spine1994;19(19):2234-38; discussion 2233.

3. Saal JA, Saal JS, Herzog RJ. The natural historyof lumbar intervertebral disc extrusions treatednonoperatively. Spine 1990;15(7):683-6.

4. Bush K, Cowan N, Katz DE, Gishen P. Thenatural history of sciatica associated with discpathology. A prospective study with clinical andindependent radiologic follow-up. Spine1992;17(10):1205-12.

5. Ito T, Takano Y, Yuasa N. Types of lumbarherniated disc and clinical course. Spine2001;26(6):648-51.

6. Rhee JM, Schaufele M, Abdu WA. Radiculopathyand the herniated lumbar disc. Controversiesregarding pathophysiology and management. JBone Joint Surg Am 2006;88(9):2070-80.

7. Spangfort EV. The lumbar disc herniation. Acomputer-aided analysis of 2,504 operations.Acta Orthop Scand Suppl 1972;142:1-95.

8. Carragee EJ, Kim DH. A prospective analysis ofmagnetic resonance imaging findings in patientswith sciatica and lumbar disc herniation. Correla-tion of outcomes with disc fragment and canalmorphology. Spine 1997;22(14):1650-60.

9. Findlay GF, Hall BI, Musa BS, Oliveira MD, FearSC. A 10-year follow-up of the outcome of lumbarmicrodiscectomy. Spine 1998;23(10):1168-71.

10. Wu X, Zhuang S, Mao Z, Chen H. Microendoscopicdiscectomy for lumbar disc herniation: surgicaltechnique and outcome in 873 consecutivecases. Spine 2006;31(23):2689-94.

11. Onik G, Mooney V, Maroon JC, Wiltse L, Helms C,Schweigel J, et al. Automated percutaneousdiscectomy: a prospective multi-institutional study.Neurosurgery 1990;26(2):228-32; discussion 232-3.

12. Maroon JC, Quigley MR, Gleason PL. Is there afuture for percutaneous intradiscal therapy? ClinNeurosurg 1996;43:239-51.

13. Mayers HM. Spine update. Percutaneous lumbardisc surgery. Spine 1994;19(23):2719-23.

14. Nerubay J, Caspi I, Levinkopf M, Tadmor A, BubisJJ. Percutaneous laser nucleolysis of the interver-tebral lumbar disc. An experimental study. ClinOrthop Relat Res 1997;(337):42-4.

15. Hult L. Retroperitoneal disc fenestration in low-back pain and sciatica; a preliminary report. ActaOrthop Scand 1951;20(4):342-8.

16. Brown MD. Update on chemonucleolysis. Spine1996;21(24 Suppl):62S-8S.

17. Nordby EJ, Wright PH, Schofield SR. Safety ofchemonucleolysis. Adverse effects reported in theUnited States, 1982-1991. Clin Orthop Relat Res1993;(293):122-34.

18. Agre K, Wilson RR, Brim M, McDermott DJ.Chymodiactin postmarketing surveillance. Demo-graphic and adverse experience data in 29,075patients. Spine 1984;9(5):479-85.

19. Hall BB, McCulloch JA. Anaphylactic reactionsfollowing the intradiscal injection of chymopapainunder local anesthesia. J Bone Joint Surg Am1983;65(9):1215-9.

20. Hijikata S, Nakayama T, Yamagishi M, et al.Percutaneous nucleotomy: a new treatment methodfor lumbar disc herniation. J Toden Hosp1975;5:39-44. Hijikata S, Yamgishi M, MakayamaT, Oomori K. Percutaneous discectomy. A newtreatment method for lumbar disc herniation. JToden Hosp 1975;5:5-13

21. Maroon JC. Current concepts in minimally invasivediscectomy. Neurosurgery 2002;51(5 Suppl):S137-

45.22. Onik G, Helms CA, Ginsburg L, Hoaglund FT,

Morris J. Percutaneous lumbar diskectomy using anew aspiration probe. AJR Am J Roentgenol1985;144(6):1137-40.

23. Fries JW, Abodeely DA, Vijungco JG, Yeager VL,Gaffey WR. Computed tomography of herniatedand extruded nucleus pulposus. J Comput AssistTomogr 1982;6(5):874-87.

24. Chatterjee S, Foy PM, Findlay GF. Report of acontrolled clinical trial comparing automated per-cutaneous lumbar discectomy and microdiscectomyin the treatment of contained lumbar disc hernia-tion. Spine 1995;20(6):734-8.

25. Cvitanic OA, Schimandle J, Casper GD, TirmanPF. Subchondral marrow changes after laserdiskectomy in the lumbar spine: MR imaging

“In general, an

interlaminar approach

is optimal for L5-S

1

level as it has a wide

interlaminar space and

a very narrowforaminal space, with

iliac crest

overhanging, makingthe transforaminal

route very

cumbersome. On thecontrary, the

interlaminar space is

very narrow at L3-L

4

and the foraminal

space is wider with

good access for thetransforaminal

procedures (AMD/

YESS). TheL

4-L

5 level can be

approached both via

the interlaminar aswell as the

transforaminal routeequally well”

“The foraminal andextra-foraminal

herniations obviously

favour thetransforaminal route

where as the central

and the paracentralherniations are more

amenable to be tackled

via the interlaminarroute”

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VOL X No 2 : April-June 200882

findings and clinical correlation. AJR Am JRoentgenol 2000;174(5):1363-9.

26. Choy DS. Percutaneous laser disc decompression(PLDD): twelve years’ experience with 752 proce-dures in 518 patients. J Clin Laser Med Surg1998;16(6):325-31.

27. Choy DS, Ascher PW, Ranu HS, Saddekni S,Alkaitis D, Liebler W, et al. Percutaneous laserdisc decompression. A new therapeutic modality.Spine 1992;17(8):949-56.

28. Reinhard S, Wittenberg R, Kraemer J.Chemonucleolysis versus laser disc decompres-sion: a prospective randomized trial. J Bone JointSurg [Br] 1997;79(2):S247.

29. Derby R, Eek B, Chen Y, et al. IntradiscalElectrothermal Annuloplasty (IDET): a novel ap-proach for treating chronic discogenic back pain.Neuromodulation 2000;3:5-9.

30. Coppes MH, Marani E, Thomeer RT, Groen GJ.Innervation of “painful” lumbar discs. Spine1997;22(20):2342-49; discussion 2349-50.

31. Heary RF. Intradiscal electrothermal annuloplasty:the IDET procedure. J Spinal Disord2001;14(4):353-60.

32. Saal JS, Saal JA. Management of chronicdiscogenic low back pain with a thermal intradiscalcatheter. A preliminary report. Spine2000;25(3):382-8.

33. Sharps LS, Isaac Z. Percutaneous disc decom-pression using nucleoplasty. Pain Physician2002;5(2):121-6.

34. Chen YC, Lee SH, Chen D. Intradiscal pressurestudy of percutaneous disc decompression withnucleoplasty in human cadavers. Spine2003;28(7):661-5.

35. Wenzel DG, Morgan DL. Interactions of ozoneand antineoplastic drugs on rat lung fibroblastsand Walker rat carcinoma cells. Res CommunChem Pathol Pharmacol 1983;40(2):279-87.

36. Bocci V, Luzzi E, Corradeschi F, Paulesu L, Di

Stefano A. Studies on the biological effects ofozone: 3. An attempt to define conditions foroptimal induction of cytokines. LymphokineCytokine Res 1993;12(2):121-6.

37. Andreula CF, Simonetti L, De Santis F, Agati R,Ricci R, Leonardi M. Minimally invasive oxygen-ozone therapy for lumbar disk herniation. AJNRAm J Neuroradiol 2003;24(5):996-1000.

38. Kambin P, O’Brien E, Zhou L, Schaffer JL.Arthroscopic microdiscectomy and selectivefragmentectomy. Clin Orthop Relat Res1998;(347):150-67.

39. Yeung AT, Tsou PM. Posterolateral endoscopicexcision for lumbar disc herniation: Surgicaltechnique, outcome, and complications in 307consecutive cases. Spine 2002;27(7):722-31.

40. Asch HL, Lewis PJ, Moreland DB, Egnatchik JG,Yu YJ, Clabeaux DE, et al. Prospective multipleoutcomes study of outpatient lumbarmicrodiscectomy: should 75 to 80% success ratesbe the norm? J Neurosurg 2002;96(1 Suppl):34-44.

41. Hanley EN Jr, Delamarter RB, McCulloch JA,Takahashi K. Surgical indications and techniques.

In: Wiesel SW, Weinstein JN, Dvorak J, Bell G,eds. The lumbar spine. 2nd ed. Philadelphia: WBSaunders, 1996:492-524.

42. McCulloch JA. Focus issue on lumbar discherniation: macro- and microdiscectomy. Spine1996;21(24 Suppl):45S-56S.

43. Hermantin FU, Peters T, Quartararo L, Kambin P.A prospective, randomized study comparing theresults of open discectomy with those of video-assisted arthroscopic microdiscectomy. J BoneJoint Surg Am 1999;81(7):958-65.

44. Dewing CB, Provencher MT, Riffenburgh RH, KerrS, Manos RE. The outcomes of lumbarmicrodiscectomy in a young, active population:correlation by herniation type and level. Spine2008;33(1):33-8.

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Exercises and Precautionsin the Management ofLow Back Pain

KANCHAN MITTAL

Suptd. Physiotherapist

AIIMS, New Delhi

SYMPOSIUM ON

LOW BACK PAIN

Regular exercise and proper lifting techniqueshelp prevent low back problems from developing.Proper lifting involves keeping an object close tothe body and avoiding bending forwarding, reach-ing, and twisting while lifting. Low back pain anddisc degeneration are both more likely to developamong sedentary people than those who are physi-cally active. However, long-term participation insome competitive sports may contribute to spinaldisc degeneration.

While heavy lifting and other strenuous labourmay contribute to low back pain, one trial foundthat people with sedentary jobs gained more ben-efit from an exercise programme than those whohave physically hard or moderate occupations.Motivational programmes may also improve exer-cise consistency, which in turn decreases pain anddisability. People with low back pain who wish toembark on an exercise programme should firstconsult with a physical therapist or other practi-tioner who is skilled in this field.

Regular supervised exercises have therapeutic effect and help prevent low backproblems. Strengthening exercises of spinal core muscles long with the strengtheningof leg muscles and stretching exercises can really reduce the occurrence of backpain. Stress management techniques help in reducing the activity of sympatheticnervous system leading to relaxation of the muscles of the body and hence allow thespine to return to its normal alignment. Work station adjustments can help in keepingbackaches at bay.

Keywords: Back pain, Exercises,Stretching exercises, Stress managementrecommendations

One study reported that the therapeutic exercisessignificantly improved chronic low back pain com-pared to exercise performed at home without pro-fessional guidance. Another trial reported thatwomen with chronic low back pain who begansupervised back strengthening exercises at a fit-ness centre were more consistent exercisers thanthose who started and continued therapeutic ex-ercises at home

Both groups experienced significant improvementin pain. However, the supervised group experi-enced better long-term improvement.

STRENGTH TRAINING

The term “spineless” is usually applied to a personwho lacks courage or confidence and lives inconstant fear. Just as the mind affects the body, sothe body affects the mind. By strengthening yourback you can overcome fear and rebuild confi-dence in your back.

Having strong core muscles can also make adifference in the prevention of low back pain.Many research studies show that the strong ab-dominal and stabilising back muscles can aid in theappropriate rigidity of the lower back. These

“Having strong coremuscles can also

make a difference in

the prevention of lowback pain”

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VOL X No 2 : April-June 200884

specific muscles, if strong and well trained, canincrease core stability and decrease movement inthe lower back. Increased movement in the lowerback due to weak core muscles and obesity canlead to early wear and tear in the joints causingpain and disability.

Pelvic floor exercises

Pelvic floor exercises and lower abdominal exer-cises can help to reduce the strain of back inpregnancy. To perform a safe and easy lowerabdominal exercise, get down onto your handsand knees and level your back so that it is roughlyflat. Breathe in and then as you breathe out,perform a pelvic floor exercise and at the same timepull your belly button in and up. Hold this contrac-tion for 5-10 seconds without holding your breathand without moving your back. Relax the musclesslowly at the end of the exercise. Leg raising in thesame kneeling position helps in improving backmuscles of the leg as well as spinal extensors

without putting any strain on abdomen especiallyin pregnancy (Fig 1).

Strengthening of legs

The muscles in the calves and the quadricepsmuscles in the thighs are critical to back support.When calves and thighs are strong, they reducethe amount of work required by the back to sup-port the weight of the body as well as when liftingheavy loads. This is noticeable when standing,climbing stairs, getting out of the bed in themorning, or getting up after sitting in a chair. TheGluteal Squeezes can be helpful to increasestrength of gluteal muscles to make standing andwalking easier.

Stretching exercises

People who stretch regularly have far fewer backproblems than those who do not stretch at all.When done properly, stretching is one of the mostpleasant and beneficial experiences possible. Asyour back improves, progress from easier stretchesto difficult stretches.

When you stretch, notice how stretching andlengthening the muscle affects the pain. If the painbecomes worse, the muscle is already over-stretched. So you need to back off the stretch tothe point before the pain starts and then hold thestretch there for as long as one is comfortable.� Simple stretch : As up as possible with or

without heel off the ground. This helps tostretch spinal muscles and strengthen calves,quadriceps, and gluteal muscles (Fig. 2).

� Back extension exercise : Lie down on thestomach, keeping palms in line with chest,slowly extend chin as head is raised with neck,and chest off the floor, breath normally (Fig. 3).This is an excellent stretch to improve thecurvature of the spine. It stretches and elon-gates all the back muscles, without the spinehaving to bear any weight. It opens up thespaces between the vertebrae and decom-presses the nerve root. One can come back toFig. 2 : Stretching exercise - Simple stretch

Fig. 1: Pelvic floor exercises

“It has been reported

that people with

chronic low back painwho began supervised

back strengthening

exercises at a fitnesscentre were more

consistent exercisers

than those who startedand continued

therapeutic exercises

at home”

“Leg raising in

kneeling position helpsin improving spinal

extensors even in

pregnancy withoutcausing any strain on

the abdomen”

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85VOL X No 2 : April-June 2008

� Arching exercise : This strengthens and tonesthe muscles of entire back. It stretches theshoulder and neck while opening spaces inback; also improves posture (Fig. 4).

� Knee raises : Knee raises stretch the musclein the hips, knees, and lower spine whilekeeping the spine in a protected position asshown in Fig.5.

� Bent exercise knee supine twist : The bentknee supine twist loosen the spine via a gentletwisting motion. It is a very effective and safetwisting stretch for the entire spine and hips,required for overall spine flexibility (Fig. 6).

� Lateral bending to the right and left, like twist-ing, is an excellent stretch for the muscles inthe lateral part of the spine. It helps to improvethe range of motion and flexibility of the back.Same can be done in lying position also (Fig.7).

� Kneel in a comfortable position on the floor.Stretch arms in front of you and slide handsalong the floor, walking with fingers along theground, extending and lengthening upper backas you stretch. This gives traction feel to thespine and helps in decompression also asdescribed in Fig. 8.

Fig. 3 : Stretching exercise - Back extension

exercise

Fig. 4: Stretching exercise - Arching exercise

Fig. 7 : Stretching exercise - Lateral bendingFig. 8 : Stretching exercise - Kneel down

and stretch arms in front

Fig. 6 : Stretching exercise - Bent knee

suspine twist

Fig. 5: Stretching exercise - Knee raises

original position after holding in same posi-tion for 5 sec. Repeat for 10 times. Repeatedexercises help to strengthen the whole ofspine.

“After prolonged

sitting or bending

position of spine, tryto avoid immediate

lifting without doing

some extensionmovement is a good

preventive measure”

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VOL X No 2 : April-June 200886

workstation without impediment? (i.e. desk-top thin, chair arms aren’t in the way and thereis clear leg room)

� Is the seat height adjusted with the users’thighs parallel or slightly inclined downwardsto the floor?

� Is the backrest height adjusted to fit the smallof the users’ back and adequately support thespine?

� Is the backrest angle adjusted for the user tosit upright whilst keying?

Desk

� Are the user’s forearms parallel to the floor orangled slightly downward?

� Is the desk height adjustable? If YES, is thedesk easily adjustable? If NO, has the userbeen provided with a footrest?

� Is the footrest wide enough for both feet?

Sitting

� Use a chair with arms to help you stand up andsit down more easily.

� Get up regularly and have a short walk aboutto prevent stiffness and promote circulation.

� Sit in chairs with good lower back support, usework surfaces that are a comfortable height,and rest one foot on a low stool (Fig. 11) .

Fig. 9 : Interdependence of abilities

Flexibility, strength, muscular endurance, co-ordination all are interdependent (Fig.9).

Some instructions for your work station

(Fig. 10)

Chair

� Is the chair easily adjusted from a seatedposition? Can the user get close to the

Fig. 10 : Instructions for workstation

Fig. 11 : Sit in chairs with good support to

the lower back

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87VOL X No 2 : April-June 2008

� General recommendations for people recuper-ating from low back pain include wearing low-heeled comfortable shoes if standing for longperiods, and supporting the low back duringlong periods of driving

Lifting

Do not lift heavy objects.

Riding in a car

To get in, sit onto the seat by putting your bottomin first, and then move your legs in afterwards byputting weight on your hands.

GENERAL TENDENCIES

We tend to do things. Several routine daily lifeactivities involve prolonged bending and thenlifting as described below. Be aware of them and tryto avoid back strain by taking extra time before youlift.� Lifting a heavy suitcase after a long flight.� Repetitive bending in the garden after a lei-

surely read of the morning paper.� Lifting something heavy during home renova-

tions after bending repeatedly.� Bending forward to pick up something from

the floor (as light as a piece of paper) aftersitting in front of your computer or watchingTV.

RECOMMENDATIONS

� After being in a prolonged bent position,stand upright and bend backwards with yourhands at the waist to support your backwardbend. This movement will compensate for theelongation of the back tissues.

� Repeat five to ten times. If you experienceback pain, you may be extending too far back-wards or this exercise is not appropriate foryou due to some other back ailment.

� If you can remember and are able to, try toavoid immediate lifting after prolonged for-ward flexion.

� Use your judgment. Lag times between ex-tended forward flexion and lifting depend onan individual’s physical fitness.

� Try a support pillow in bed. Sleeping on yourside with a wedge-shaped pillow placed underyour tummy has been shown to reduce backpain.

� If you have pain over your tailbone (coccyx),make sure that you avoid slumping whensitting and arch your back as much as iscomfortable. Try sitting on a soft cushion ora cushioned ring.

Emotional distress has been associated with ag-gravated low back pain, including that caused bya herniated disc. The effects of counselling aimedat reducing emotional stress on back pain remainunknown, though this approach has been used insome clinics employing multidisciplinary ap-proaches to treat chronic lower back pain. Themind and body connection will help us to under-stand how stress works, how it affects our back,and how to help our back heal through stressmanagement and relaxation techniques. This helpsto reduce the activity of the sympathetic nervoussystem while strengthening the influence of theparasympathetic system. Stress managementcauses all the muscles in body to relax, includingthe muscles in back, allowing the spine to returnto its normal alignment.

“People who dostretching exercises

regularly have fewerback problems than

those who do not

stretch at all”

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VOL X No 2 : April-June 200888

Current Status of DiseaseModifying Anti-rheumaticDrugs (DMARDs) inRheumatoid Arthritis

CHAITALI SUKHDEO BAJAIT

Resident

MIRZA SHIRAZ BAIG

Lecturer

PRAKASHCHANDRA

RAMBHAU GADE

Professor and Head

PRAKASH NARAYAN

KHANDELWAL

Associate Professor

Deptt. of PharmacologyGovt. Medical CollegeAurangabad

RHEUMATOID ARTHRITIS

INTRODUCTION

Rheumatoid arthritis (RA) is a chronic, inflamma-tory, autoimmune disorder. It is characterised byintense joint pain due to inflammation, irreversiblebony destruction, systemic complications due toextra articular tissue involvement and ultimatelyprogressive functional decline. Table 11 enumer-ates the revised ACR criteria for classification ofRA.2

PATHOPHYSIOLOGY

RA is characterised by development of hyperplas-tic synovial membrane (i.e., pannus) that has beeninfiltrated by B-cell and macrophages, which leads

The management of RA has come a long way from the ‘pyramidal’ approach of the1970s. Modern treatment emphasises early use of disease modifying antirheumaticdrugs (DMARDs). According to new guidelines, along with non-steroidal anti-inflamma-tory drugs (NSAIDs) and steroids, DMARDs should be started within three months ofdiagnosis for most patients. An algorithmic approach to the use of DMARDs,suggested by the American College of Rheumatology, provides a general guidelineand consideration when starting, changing or adding DMARDs to the treatment ofpatient with active disease. This article reviews the current status of disease modifyinganti-rheumatic drugs (DMARDs) in rheumatoid arthritis.

Keywords: Antirheumatics, Diseasemodifying antirheumatics, Antimalarials,Tumour necrosis factor, Etanercept,Methotrexate

Table 1: Revised ACR criteria for classifi-

cation of RA2

1 Morning stiffness greater than 1hr greater than 6 weeks’ duration

2 Swelling in 3 or more joints forgreater than 6 weeks’ duration

3 Swelling in wrist, MCP or PIPgreater than 6 weeks’ duration

4 Symmetrical joint swelling

5 Rheumatoid nodules

6 Serum rheumatoid factor

7 Hand X-ray changes – erosionsor decalcification

Require 4 or more for classification

to the production and release of proinflammatorycytokines i.e. IL-1b, IL-6, IL-15, and tumour necro-sis factor (TNF -α). This leads to further localisedand systemic inflammation, leading to

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89VOL X No 2 : April-June 2008

synoviocyte, chondrocyte and osteoclast activa-tion and cartilage and bone destruction.1

DISEASE MODIFICATION THERAPY

The management of RA has come a long way fromthe ‘pyramidal’ approach of the 1970s. Moderntreatment emphasises early use of disease modi-fying antirheumatic drugs (DMARDs).3 Accord-ing to new guidelines, along with non-steroidalanti-inflammatory drugs (NSAIDs) and steroids,DMARDs should be started within three monthsof diagnosis for most patients. List of DMARDsavailable to treat RA is given in Table 2.

However, the decision of which DMARD to startis less clear. In any given patient, any of theDMARDs can be efficacious and well tolerated.However, no one DMARDs is efficacious and safein every patient. In fact, few patients experienceremission on any DMARDs, and most experience

some sort of side effect from the medication pre-scribed to treat the disease.4 An algorithmic ap-proach to the use of DMARDs has been putforward by the American College of Rheumatol-ogy (Fig. 1). This provides a general guideline andconsideration when starting, changing or addingDMARDs to the treatment of patient with activedisease.

METHOTREXATE (MTX)

Over the past 10-25 years, methotrexate (MTX) hasbecome the most popular DMARD in the treatmentof RA. MTX inhibits dihydrofolate reductase en-zyme and thus prevents proliferation of immunecells. There are two biochemical mechanisms bywhich MTX may modulate inflammation. Theycause promotion of adenosine release and inhibi-tion of pathologic transmethylation reaction. Ad-enosine has potent anti-inflammatory actions. Italso directly inhibits the cellular response of IL-1.

Efficacy

� Rapid dose escalation is possible for MTXfrom 7.5 mg/week to more than 25 mg per weekwithout parallel increase in toxicity.

� MTX is relatively inexpensive and the moni-toring necessary for toxicity is less expensivethan for gold, D-penicillamine, other immuno-suppressive agents or cytotoxic drugs.

� MTX can suppress disease activity in asignificant proportion of patients with longstanding RA in whom other therapies havefailed.5

Fig. 1: Guidelines for management of Rheumatoid arthritis published by

American College of Rheumatology (Arthritis Rheum. 2002;46: 328-46)

Table 2: List of Disease Modifying Anti-

rheumatoid Drugs

Traditional small molecular mass drugs

� Methotrexate (MTX)

� Sulphasalazine (SSZ)

� Antimalarials: Chloroquine,

Hydroxychloroquine (HCQ)

� D-penicillamine

� Cyclosporine-A

� Azathioprine

� Leflunomide

� Gold salts: Sodium aurothiomalate,

Auranofin

� Minocycline

Biological agents

Anti-tumour necrosis Etanercept

factor-alpha (TNF-α) Infliximab

Adalimumab

Interleukin 1 (IL-1) blocker Anakinra

Anti-B cell (CD 20) antibody Rituximab

Blockers of T cell activation Abatacept

“Modern treatment of

rheumatoid arthritis

emphasises early useof disease modifying

antirheumatic drugs

(DMARDs)”

“DMARDs should be

started within threemonths of diagnosis

for most patients”

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VOL X No 2 : April-June 200890

� In patients with early RA, MTX is effective atslowing progression and can also reduce theradiographic evidence of joint destruction.

� Using MTX as a building block or the corner-stone of combination therapy has resulted inenhanced efficacy over MTX alone, withoutadded increase in side effects.6-8

� MTX is as effective as etanercept andleflunomide in head to head study.

SULPHASALAZINE (SSZ)

Sulphasalazine consists of two agents, sulphur(sulphapyridine) and a salicylate component,5-amino salicylic acid. Sulphapyridine is the activecomponent in treating RA. It decreases rheuma-toid factor levels and suppresses generation ofsuperoxide free radicals and cytokine release byinflammatory cells.

Efficacy

Several studies have established the efficacy ofSSZ in RA. In a double-blind, randomised trial of60 patients with RA who had not previously beentreated with DMARDs, investigators demon-strated that patient randomised to receive SSZhad significantly less evidence of radiographicprogression than did patients treated withhydroxychloroquine.9 A more recent study com-paring SSZ to leflunomide demonstrated the clearutility of SSZ in the treatment of RA.10 SSZ alsoappears to be efficacious and well tolerated incombination with MTX and hydroxy chloro-quine.7

ANTIMALARIALS (CHLOROQUINE /

HYDROXYCHLOROQUINE)

Antimalarials (chloroquine/hydroxychloroquine)are seen as milder drugs. They act by stabilisingthe lysosomal membrane and inhibiting the me-tabolism of deoxyribonucleotides.

Efficacy

Strong evidences supporting utility of HCQ inearly and mild disease comes from the HERA trialin which patients were randomised to receiveeither HCQ or placebo over a period of 36 weeks.11

HCQ has been found to have equal efficacy toSSZ. However, to date, there are no convincingdata on the ability of hydroxychloroquine to slowradiographic progression and for thosepatients with active, progressing disease,hydroxychloroquine will be inadequate asmonotherapy. In general, the mild benefits and therelative lack of toxicity make this a reasonable

agent in early or mild disease or as an adjunct tocombination therapy.4

LEFLUNOMIDELeflunomide is an isoxazole derivative with dis-ease modifying and immunomodulatory proper-ties. It acts by inhibiting the dihydroorotate dehy-drogenase (DHODH) enzyme in the pyrimidinesynthesis resulting in the blockade of the prolif-eration of T cells which needs high concentrationof pyrimidines.12

EfficacyThe role of leflunomide in the treatment of RA isevolving over time. It appears to be very effectiveas a monotherapy as an alternative to MTX and issafe and effective as an addition to MTX in com-bination therapy. In a ‘pivotal’ trial of leflunomideversus MTX versus placebo, the ACR ‘Responderindex’ over the 52 week study was 52% withleflunomide, 46% with MTX and 26% with pla-cebo. Clearly, leflunomide is effective asmonotherapy and has the ability to slow the radio-graphic progression in RA. However, it is appro-priate to consider using leflunomide as an add-onto MTX for patients who have only partial re-sponse with MTX. 4

GOLD SALTSGold salts are sodium aurothiomalate and auranofin.They suppress cell-mediated immunity.Aurothiomalate also reduces lysosomal enzymeactivity and histamine release from mast cells andsuppresses phagocytic activity of neutrophils.Auranofin inhibits release of PGE

2, LTB

4, IL-1 and

TNF-α.

Although early use of gold salt injections mayretard progression of joint erosions, it is mainlyused as a second line of drug in resistant cases dueto the need for meticulous monitoring for serioustoxicity (e.g. cytopenia, proteinuria) and the costsof administration and monitoring. Auranofin isless efficacious than MTX, injectable gold,D- penicillamine or SSZ. However, it can be com-bined with HCQ, SSZ or MTX in treating earlystages of active synovitis.

D-PENICILLAMINED-penicillamine causes a selective decrease inCD4+ helper / inducer T cells. Though it is effec-tive in treating RA, it has been is categorised as a‘second line agent’ because of high incidence ofadverse effects, making the withdrawal of the drugnecessary in 30% of the patients.

“The MIRA studygroup showed an

improvement in

moderately severe RA”

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MINOCYCLINE

The use of minocycline has been based on thetheory that, rheumatoid arthritis may have aninfective aetiology. Trials have been contradic-tory, but the balance of early trials showed benefit.Response included clinical as well as improve-ment in acute phase response. The MIRA studygroup (Minocycline in Rheumatoid Arthritis)showed an improvement in moderately severeRA. O’Dell has published recent data on the earlyuse of minocycline in rheumatoid arthritis andreported a greater remission rate in patients treatedearly within the first year with minocycline.13,14

Radiological progression has not been slowed byuse of the drug.

CYCLOSPORINE

Cyclosporine is an immunosuppressant and hasbeen used by transplantation immunologists toreduce solid organ allograft rejection, for severalyears. It inhibits the activation of CD4+ helper-Tlymphocytes by blocking IL-2 and other T-helpertype 1 (Th1) cytokine production and by inhibit-ing CD40 ligand expression in T-lymphocytes.The latter effect prevents T cells from deliveringCD40 dependent signals to B-cells.4

In one clinical trial, when combined with MTX,48% patients in cyclosporine/MTX groupachieved 20% improvement according to ACRcriteria as compared to 16% in MTX alone group.15

There is little to be gained by using this drug asmonotherapy early in disease, but in patients withRA who cannot tolerate hydroxychloroquine andNSAID and therefore, need a second line drug tocombine with these, cyclosporine is a reasonablealternative.

AZATHIOPRINE

Azathioprine is a chemotherapeutic agent, alsoused as an immunosuppressant in RA. It inhibitspurine synthesis necessary for proliferation oflymphocytes.

Azathioprine can be used alone or in combina-tion in RA, often as a “steroid-sparing agent’.One factor that leads to early toxicity fromazathioprine is heterozygosity for mutantthiopurine methyltransferase alleles. Patientswith this defect metabolise the drug poorly andare forced to discontinue therapy within 1 monthbecause of haematologic side effects. Hence,this drug is reserved as a second line drug inresistant cases.16

BIOLOGICAL AGENTS

TNF antagonists

The pivotal role of tumour necrosis factor-α(TNF-α) in initiation and perpetuation of the in-flammatory and proliferative processes of rheu-matoid synovitis has been already mentionedpreviously. As a class, the TNF inhibitors appearto be the most effective means of improving symp-toms and sign of disease, increasing function andreducing radiographic evidence of progression ofRA.4

Etanercept

Etanercept is a genetically engineered dimer of P75TNF receptor linked to FC portion of human IgG.It binds to circulating or cell-bound TNF-α mol-ecules and prevents them from binding to thecellular TNF-receptor.

In a comparative trial, etanercept in combinationwith MTX was evaluated versus MTX alone.Seventy one percent patients in the combinationgroup met ACR 20 criteria as compared to 27% ofthose receiving MTX alone. More important werethe data that 39% of those receiving the combina-tion and only 3% of those receiving MTX alonemet the ACR-50 percent improvement criteria.17

The most interesting results of all studies, hasbeen the ability of etanercept to slow radiographicprogression more than MTX.18

Infliximab

Infliximab is a chimeric anti-TNF monoclonal anti-body. It cross-links with soluble as well as mem-brane-bound TNF-α receptors and thus neutral-ises the action of circulating TNF-α.

In the ATTRACT trial, a phase III study involving428 patients, infliximab demonstrated significantbenefit in patients with long standing and refrac-tory RA. Patients failing to respond to MTX wererandomised to receive placebo, infliximab (3mgper kg every 4 weeks or every 8 weeks), orinfliximab (10 mg /kg every 4 weeks or every 8weeks). After 34 weeks, The ACR-20 responserate seen with placebo / MTX was 17% comparedto 42%, 48%, 59% and 59% respectively. In theinfliximab 3 mg per kg every 8 weeks groups,radiographic progression was also significantlyreduced.8

Adalimumab

Adalimumab, a recombinant human IgGmonoclonal antibody specific for human TNF-α,

“In patients with RA

who cannot toleratehydroxy-chloroquine

and NSAID and

therefore, need asecond line drug to

combine with these,

cyclosporine is areasonable

alternative”

“Azathioprine can be

used alone or in

combination in RA,often as a “steroid-

sparing agent’ ”

“The MIRA studygroup showed an

improvement in

moderately severe RA”

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VOL X No 2 : April-June 200892

inhibits binding of TNF-α to both of its receptorsand lyses cells that bear TNF-α on their surfaces.

A 52-week, double blind, placebo controlled studywas carried out involving patients with active RAwho were receiving stable dose of MTX. Patientswere randomly assigned to receive adalimumab 20mg S.C. weekly or adalimumab 40 mg every otherweek (EOW) with placebo on the alternate week orplacebo weekly (QW). Substantial inhibition ofradiographic progression was observed for bothjoint space narrowing and erosions, particularlyfor the 40 mg EOW treatment group. The investi-gators concluded that adalimumab given subcu-taneously QW (20mg) or EOW (40mg) with con-comitant MTX significantly inhibited progressionof structural joint damage and improved signs andsymptoms of RA in patients who previously wereincomplete responders to MTX.19

Current status of anti-TNF drugs

The TNF-inhibiting agents have demonstrated asuperior ability to reduce signs and symptoms ofRA, inhibit progression of structural damage andimprove physical function in patients with thisdisease. Despite this, their role in armamentariumremains debated. The debate focuses on severalfactors including costs, lack of long-term safetydata and the ability of traditional approaches toeffectively treat a large number of patients. It issuggested that, patients should be treated withMTX prior to advancing to a TNF-inhibitor. With-out head to head studies, the question as to whichagent affords the greatest efficacy cannot beanswered. However, there is evidence that somepatients may respond better to one TNF inhibitorthan another.

Anakinra

Anakinra is a recombinant interleukin –1 receptorantagonist which inhibit the biological actions ofthe pro-inflammatory cytokine IL-1.

It is indicated for use in patients with moderate tosevere RA, who have not had an adequateresponse to conventional DMARD therapy. Theseagents can be used in conjuction with methotexateor other DMARDs (other than TNF blockingagents). Currently, it is most often used in patientswho have tried and failed a TNF inhibitor.

Abatacept

Abatacept, a T-cell inhibitor, is a soluble fusionprotein. It works as a selective co-stimulation

modulator that inhibits T-cell activation and ac-cordingly prevents the co-stimulation of a signalthat is necessary for a full activation ofT-lymphocytes. It has been approved by the Foodand Drug Administration (FDA) in December 2005.

Efficacy

Controlled clinical trials have shown that optimaldosing of abatacept significantly reduced struc-tural damage progression (including decreasederosions and joint space narrowing) and improvedthe total joint score. Studies have also shownsignificant improvements in the quality of lifemeasures, ACR 20, 50 and 70 scores, and DAS28scores. Abatacept is indicated for patients whohave had an inadequate response to TNF antago-nists at any stage of the disease.

Rituximab

Rituximab is a chimeric IgG monoclonal antibodythat binds to and destroys mature B-cells, but notstem or plasma cells. Controlled clinical trials haveprovided evidence that rituximab has a favourablerisk-benefit ratio in patients with RA in whom TNF-α therapy was inadequate. Studies have alsoshown clinically meaningful improvements in pa-tient reported outcomes. Researchers have alsoshown improvements in ACR 20, 50 and 70 re-sponses as well as improved DAS 28. At this time,no data is available on the effects of rituximabwhen it comes to slowing radiographic progres-sion of the disease. Rituximab is indicated forpatients who have not improved with TNF antago-nist therapy.18

Since DMARDs are immunomodulaters, periodicmonitoring for early detection of toxicity is neces-sary. During therapy, following investigationsshould be done:� Complete blood count� Liver function tests� Hepatitis B and C serology� Chest radiograph� Serum creatinine� Urine analysis

Table 3 describes the specific adverse effects ofindividual DMARDs. Table 4 describes the dos-ing schedule of DMARDs.

STATUS OF COMBINATION THERAPY WITH

DMARDs IN RA

Although the concept of using combination ofDMARDs to treat RA is not new, the general

“Adalimumab, a

recombinant humanIgG monoclonal

antibody specific for

human TNF-a, inhibitsbinding of TNF-a to

both of its receptors

and lyses cells thatbear TNF-a on their

surfaces”

“Abatacept, a T-cell

inhibitor, is a soluble

fusion protein. Itworks as a selective

co-stimulation

modulator that inhibitsT-cell activation and

accordingly prevents

the co-stimulation of asignal that is

necessary for a full

activation ofT-lymphocytes”

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93VOL X No 2 : April-June 2008

acceptance of this therapeutic approach has comeabout only recently. Patients who are resistant tomonotherapy, are candidates for combinationtherapy. Multiple drugs act synergistically atmultiple points in the cascade of inflammation.

Strategies for combining DMARDs

DMARDs can be combined in four ways.� In the step up approach, treatment is started

with one DMARD and a second DMARD isadded if the optimal response has not beenachieved.

� In the step down approach, therapy is startedwith combination of DMARDs and gradually,one of the agents is withdrawn.

� In the parallel strategy, two DMARDs areadministered concurrently throughout.

� In the saw tooth strategy, as the therapeuticeffect of one of the DMARDs wanes off, a newagent is substituted or combined with thedrug, which has lost its efficacy.

Most commonly used combinations of DMARDs

� MTX and Antimalarials: Most commonlyused combination. In a randomised controlledtrial of 6 months duration, MTX and HCQ werefound to be statistically superior to HCQalone in improving various outcome meas-ures like articular index, morning stiffness,joint pain, ESR and radiographic progression.

� MTX and SSZ: There were initial concernsthat this combination is antifolate but later, itwas shown that, it was well tolerated.

� MTX and leflunomide: Leflunomide can beeffective as monotherapy or in combination ofMTX. But due to incidences of hepatotoxic-ity, there is a controversy regarding the safetyof leflunomide and MTX combination.

� MTX, SSZ and HCQ: When there is unsatisfac-tory response to combination of two DMARDs,one can use triple therapy. This is the mostcommonly used combination in triple therapy.

� Combination with biological agents: It isrecommended that, biological agents shouldbe reserved for patients with active RA whosesymptoms are resistant to conventionalDMARDs. In such case, one can add a bio-logical agent to ongoing treatment with MTXor other DMARDs.

Alternative combinations which can be

used in resistant cases

� Methotrexate and cyclosporine� Methotrexate and gold salt

Table 4: Dosing schedule of DMARDs

Name of DMARD Dose

Methotrexate 7.5 – 25 mg wkly orally or parenterally (S.C or IM)along with folic acid (1 mg /day or 5 mg/wk)

Sulphasalazine Starting 0.5 g/day x1 wk followed by 1g / day x 1 wkthen 1.5 g/day x 1 wk. Maintenance dose is 2 g /day. Maximum dose is 3 g/ day

Chloroquine 250 mg daily orally

Hydroxychloroquine 200-400 mg daily

Leflunomide Loading dose is 100 mg daily for 3 days then 20mg/daily orally

Gold salt Aurothiomalate ® 50 mg weekly IM to a total of 1 gor 6 months therapy; thereafter a maintenance doseof 50 mg monthly. Auranofin ® 6 mg/day orally.

D-Penicillamine 150 mg/day for 3 months, increasing gradually to amaximum dose of 750 mg/day orally

Minocycline 100 mg BD orally

Cyclosporine 3-5 mg/kg/day orally

Azathioprine 1.5 – 3 mg/kg/day orally

TNF-antagonist Etanercept: 50 mg once weekly or 25 mg twice perweek by subcutaneous injection. Infliximab: 3 mg/kgwith infusions at weeks 0, 2 & 6 & every 8 weeksthereafter. Adalimumab: 40 mg every two weeksubcutaneously.

Anakinra 100 mg daily subcutaneously.

Table 3: Specific adverse effects of individual DMARDs

DMARD Specific adverse effects

Methotrexate Bone marrow suppression, hepatotoxicity, alopecia, andhypersensitivity pneumonitis

Sulphasalazine G6PD deficiency-related anaemia with haemolysis,reversible reduction in sperm count, nephrotoxicity,mood alteration, hepatotoxicity

Chloroquine Retinopathy, photosensitivity

Leflunamide Bone marrow suppression, hepatotoxicity, alopecia

Gold salt Conjunctivitis, proteinuria, thrombocytopenia

D-penicillamine Stomatitis, metallic taste, myasthenia gravis, polymyosi-tis, thyroiditis

Minocycline Tooth discolouration, hypersensitivity pneumonitis, pho-tosensitivity, hyperpigmentation

Cyclosporine Nephrotoxicity, hypertension, hyperkalaemia, hepato-toxicity, hirsutism

Azathioprine Bone marrow suppression, hypersensitivity hepatitiswith cholestasis, infections,

TNF-antagonist Mycobacterial and bacterial infection, drug inducedlupus, multiple sclerosis, optic neuritis, Guillian Barresyndrome, pancytopenia, aplastic anaemia

Anakinra Injection site reaction

Abatacept Headache, hypertension, upper respiratory tract infec-tion

Rituximab Infusion-related hypersensitivity, late-onset neutropenia

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VOL X No 2 : April-June 200894

� Methotrexate and azathioprine� Cyclosporine and chloroquine/

hydroxychloroquine� Gold salt and cyclosporine� Cyclosporine and sulphasalazine� Hydroxychloroquine, azathioprine and cyclo-

phosphamide� Hydroxychloroquine, gold salt and methotrex-

ateTable 5 is a summary of recommendations forusing DMARDs in RA.20

REFERENCES1. Mochan E, DiRosa L. Emerging Agents For RA:

Can They Have An Impact? Arthritis Practitioner2006;2(5):22-27.

2. Arnett FC, Edworthy SM, Bloch DA, McShane DJ,Fries JF, Cooper NS, et al. The AmericanRheumatism Association 1987 revised criteria forthe classification of rheumatoid arthritis. ArthritisRheum 1988;31(3):315-24.

3. Kakar A, Kumar A. Current status of combinationtherapy with disease modifying antirheumaticdrugs in rheumatoid arthritis. J Indian RheumatolAssoc 2002:10:36-44.

4. Genovese. Treatment of Rheumatoid Arthritis. InHarris ED, Budd RC, Firestein GS, Genovese MC,Sergent JS, Ruddy S, et al. editors. Kelley’sTextbook of Rheumatology. Vol II.7th Ed. ElsevierSaunders2005.p.1088-1100.

5. Rau R, Schleusser B, Herborn G, Karger T. Long-term treatment of destructive rheumatoid arthritiswith methotrexate. J Rheumatol 1997;24(10):1881-89.

6. Rau R, Herborn G, Karger T, Werdier D. Retarda-tion of radiologic progression in rheumatoidarthritis with methotrexate therapy. A controlledstudy. Arthritis Rheum 1991;34(10):1236-44.

7. O’Dell JR, Haire CE, Erikson N, Drymalski W,Palmer W, Eckhoff PJ, et al. Treatment ofrheumatoid arthritis with methotrexate alone,sulfasalazine and hydroxychloroquine, or a com-bination of all three medications. N Engl J Med1996;334(20):1287-91.

8. Lipsky PE, van der Heijde DM, St Clair EW, FurstDE, Breedveld FC, Kalden JR, et al. Infliximaband methotrexate in the treatment of rheumatoidarthritis. Anti-Tumor Necrosis Factor Trial in Rheu-matoid Arthritis with Concomitant Therapy StudyGroup. N Engl J Med 2000;343(22):1594-602.

9. Weinblatt ME, Kremer JM, Bankhurst AD, BulpittKJ, Fleischmann RM, Fox RI, et al. A trial of

etanercept, a recombinant tumor necrosis factorreceptor: Fc fusion protein, in patients withrheumatoid arthritis receiving methotrexate. NEngl J Med 1999;340(4):253-59.

10. Hannonen P, Mottonen T, Hakola M, Oka M.Sulfasalazine in early rheumatoid arthritis. A 48-week double-blind, prospective, placebo-control-led study. Arthritis Rheum 1993;36(11):1501-09.

11. Smolen JS, Kalden JR, Scott DL, Rozman B,Kvien TK, Larsen A, et al. Efficacy and safety ofleflunomide compared with placebo andsulphasalazine in active rheumatoid arthritis: adouble-blind, randomised, multicentre trial. Euro-pean Leflunomide Study Group. Lancet1999;353(9149):259-66.

12. A randomized trial of hydroxychloroquine in earlyrheumatoid arthritis: the HERA Study. Am J Med1995;98(2):156-68.

13. Krensky AM, Vincenti F, Bennet WM.Immunosuppressants, Tolerogens andimmunostimulants. In Brunton LL, Lazo JS, ParkerKL, editors. Goodman and gilman’s The pharma-cological basis of therapeutics. 11th Ed.McGraw-Hill 2005;p1405-32.

14. Stein CM, Pincus T, Yocum D, Tugwell P, Wells G,Gluck O, et al. Combination treatment of severerheumatoid arthritis with cyclosporine and meth-otrexate for forty-eight weeks: an open-labelextension study. The Methotrexate-CyclosporineCombination Study Group. Arthritis Rheum1997;40(10):1843-51.

15. Black AJ, McLeod HL, Capell HA, Powrie RH,Matowe LK, Pritchard SC, et al. Thiopurinemethyltransferase genotype predicts therapy-limit-ing severe toxicity from azathioprine. Ann InternMed 1998;129(9):716-18.

16. O’Dell JR, Paulsen G, Haire CE, Blakely K, PalmerW, Wees S, et al. Treatment of early seropositiverheumatoid arthritis with minocycline: four-yearfollow-up of a double-blind, placebo-controlledtrial. Arthritis Rheum 1999;42(8):1691-95.

17. Bluhm GB, Sharp JT, Tilley BC, Alarcon GS,Cooper SM, Pillemer SR, et al. Radiographicresults from the Minocycline in Rheumatoid Arthri-tis (MIRA) Trial. J Rheumatol 1997;24(7):1295-302.

18. Firestein GS, Zvaifler NJ. Anticytokine therapy inrheumatoid arthritis. N Engl J Med 1997;337(3):195-97.

19. Bathon JM, Martin RW, Fleischmann RM, TesserJR, Schiff MH, Keystone EC, et al. A comparisonof etanercept and methotrexate in patients withearly rheumatoid arthritis. N Engl J Med2000;343(22):1586-93.

20. Kremer JM. Rational use of new and existingdisease-modifying agents in rheumatoid arthritis.Ann Intern Med 2001;134(8):695-706.

Table 5: Recommendations for using DMARDs in RA20

Condition Recommendation

Persistent synovitis and radiographic erosion Initiate therapy with oral methotrexate along with folic acid

Inadequate response to oral methotrexate Switch to parenteral methotrexate

Inadequate response to parenteral methotrexate Add sulphasalazine and hydroxychloroquine

Inadequate response to MTX, SSZ and HCQ Discontinue SSZ and HCQ. Add leflunomide

If patient has toxicity or inadequate response Discontinue leflunomide, add etanercept

If patient has toxicity or inadequate response Discontinue etanercept, add infliximab or try alternative combinations

“In the saw tooth

strategy, as thetherapeutic effect of

one of the DMARDs

wanes off, a newagent is substituted or

combined with the

drug, which has lostits efficacy”

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95VOL X No 2 : April-June 2008

Pioneers in OrthopaedicsPIONEERS IN ORTHOPAEDICS

BHAVUK GARG

Senior Resident

RAJESH MALHOTRA

Professor

Deptt. of Orthopaedics

AIIMS, New Delhi

Sir Benjamin Collins Brodie (June 9, 1783-October21, 1862) was an English physiologist and surgeonwho pioneered research into bone and joint dis-ease. He must be considered as one of the found-ers of modern orthopaedic surgery.

Brodie was born in Winterslow, Wiltshire. He re-ceived his early education from his father; thenchoosing medicine as his profession he went toLondon in 1801 and attended the lectures of JohnAbernethy. Two years later he became a pupil of SirEverard Home at St George’s Hospital, and in 1808was appointed assistant surgeon at that institution,on the staff of which he served for over thirty years.Brodie presented a paper to the Royal Society in1810 on ‘Dissection of a foetus with no heart’.Although he described this work as having ‘little orno value’ it gave him entry into the Society. Thesame year he delivered the Croonian Lecture on ‘theinfluence of the brain on the action of the heart andthe generation of animal heat’. He was awarded theCopley Medal in 1811 for his physiological re-searches, and in 1816 he married Ann Sellon, thedaughter of a barrister. In 1820 he was elected afellow of the Royal Society, to which in the next fouror five years he contributed several papers describ-ing original investigations in physiology.

The next 30 years were his most productive, withmajor contributions coming in two areas. The firstwas his study of joint disease, and the second wasthe re-organisation of surgical training. At this periodhe also rapidly obtained a large and lucrative practiceand from time to time wrote on surgical questions,contributing numerous papers to the Medical andChirurgical Society and to the medical journals. Hismost important work is widely acknowledged to bethe 1818 treatise Pathological and Surgical Obser-vations on the Diseases of the Joints, in which heattempted to trace the beginnings of disease in thedifferent tissues that form a joint and to give an exactvalue to the symptom of pain as evidence of organicdisease. This volume led to the adoption by sur-geons of more conservative measures in the treat-ment of diseases of the joints, with consequent

reduction in the numberof amputations and thesaving of many limbsand lives. He also wroteon diseases of the uri-nary organs and on lo-cal nervous affectionsof a surgical character.On 19 November 1845 atSt George’s, Brodie de-livered a lecture on thetopic for which he is bestremembered - chronicosteomyelitis; later to become known as Brodie’sabscess. The account of this condition precededradiography but is so accurate that one can at onceimage the X-ray appearance.

In 1854 he published anonymously a volume ofPsychological Inquiries-eight years later, the ex-panded, revised and updated 1862 volume ap-peared under his name. He received many honoursduring his career and attended to the health of theRoyal Family, starting with George IV. He was alsosergeant-surgeon to William IV and Queen Victo-ria and was made a baronet in 1834. He became acorresponding member of the French Institute in1844, DCL of Oxford in 1855, president of the RoyalSociety in 1858 and subsequently, the first presi-dent of the General Medical Council.

Sir Benjamin Collins Brodie died in Broome Park,Surrey at the age of 79. His collected works, withautobiography, were published in 1865 under theeditorship of Charles Hawkins. Brodie was with-out doubt a great man. He was one of the first tospeak out against smoking, and his description ofthe death of Sir Robert Peel from a fracturedclavicle is fascinating.

Brodie’s eldest son, also known as Sir BenjaminCollins Brodie, was appointed professor of chem-istry at Oxford in 1865, and is chiefly known for hisinvestigations on the allotropic states of carbonand for his discovery of graphitic acid.

Sir Benjamin Collins Brodie(1783-1862)

“Brodie was without

doubt a great man. He

was one of the first to

speak out against

smoking, and his

description of the

death of Sir Robert

Peel from a fractured

clavicle is

fascinating”

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VOL X No 2 : April-June 200896

ORTHO QUIZ-15

ORTHO QUIZ

Question: Discuss the most probable diagnosis.

BHAVUK GARG

Senior Resident

RAJESH MALHOTRA

Professor

Deptt. of Orthopaedics

AIIMS, New Delhi

Response ForResponse ForResponse ForResponse ForResponse Formmmmm✄✄✄✄✄

Send your answers to:

ORTHOPAEDICS TODAY

QUIZ

A-9/3, DLF City, Phase-I,

Gurgaon-122002 (Haryana)

ORTHO QUIZ 2008 NO. 15

Name: _____________________________________________

Address: ___________________________________________

__________________________________________________

My Diagnosis is: _____________________________________

First Ten correct entries would receive one year complimentary subscription of any of our publications

IDR Triple I CIMS Obs. & Gynae Today Paediatrics Today

Cardiology Today Ophthalmology Today Gastroenterology Today Orthopaedics Today

CASE HISTORY

A 22-year-old male presented to us in casualty with history of road traffic accident with injury to leftknee. Patient was having severe pain in left knee and was unable to move the knee. The pain was notassociated with any radiation or neurovascular deficit. He had no other injuries.

On examination, significant findings included tenderness and swelling over left knee joint. Attempt tomove knee joint was very painful. AP & lateral radiographs of his knee joint are shown below. Discussthe most probable diagnosis.

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97VOL X No 2 : April-June 2008

Answer and Discussion toOrtho Quiz 14

ORTHO QUIZ

BHAVUK GARG

Senior Resident

RAJESH MALHOTRA

Professor

Deptt. of Orthopaedics

AIIMS, New Delhi

Answer to Ortho Quiz 2008 No. 14

Bertolotti’s Syndrome

Since we have not received any correct entry thereare no winners this time

DISCUSSION

Bertolotti’s syndrome refers to the association ofback pain with lumbosacral transitional vertebrae.This syndrome is characterised by anomalousenlargement of the transverse process of the mostcaudal lumbar vertebra which may articulate orfuse with the sacrum or ilium.

This syndrome was first described by Bertolotti in1917.1 He associated these changes with low backpain which he subsequently attributed to arthriticchange on the basis of clinical and radiologicalexamination. The syndrome is said to affect 4% to8% of the population.2

AETIOLOGY5,6

The exact cause of Bertolotti’s syndrome is un-known. MRI-based studies have described de-generative changes of the intervertebral disc inrelation to lumbosacral transitional vertebrae. Ithas been observed that disc above a transitionalvertebra appears at risk of increased degenerativechange while the disc below appears protected.Some authors have suggested that this phenom-enon is due to hypermobility and abnormal torqueof the intervertebral space above the transitionalvertebra and that there was less degenerativechange at the level below because the anomalousarticulations allow less movement between the L5and S1 vertebrae. There is a possible role of the

iliolumbar ligament in this phenomenon but itsexact role is unclear.

CLINICAL FEATURES

This is a congenital condition and is usually notsymptomatic until one’s later twenties or earlythirties, yet there are cases found where Bertolotti’sis symptomatic at a much earlier age. Low backpain is the most common symptom. Of importanceis that this syndrome will result in a pain generat-ing from the disc above resulting in a “sciatic” typeof a pain correlating to the 5th lumbar nerve rootusually.

RADIOGRAPHIC FINDINGS6,7

The x-ray picture is characteristic. Usually thetransitional vertebra will have a “spatulated” trans-verse process on one side resulting in articulationor partial articulation with the sacrum or at time theilium and in some cases with both. MRI is theinvestigation of choice. The overall incidence ofstructural pathology (e.g., spinal stenosis anddisc protrusion) detected by MRI is not appar-ently higher in patients with transitional verte-brae, but the distribution of these lesions is signifi-cantly different. Disc bulge or herniation, when itoccurs, is nearly nine times more common at theinterspace immediately above the transitionalvertebra than at any other level. Spinal stenosisand nerve root canal stenosis are more common at

“This syndrome is

characterised by

anomalousenlargement of the

transverse process of

the most caudallumbar vertebra which

may articulate or fuse

with the sacrum orilium”

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VOL X No 2 : April-June 200898

or near the interspace above the transitional ver-tebra than at any other level. Degenerative changeat the articulation between the transverse processof the transitional vertebra and the pelvis is anuncommon occurrence; when seen there is nosignificant correlation with the reported side ofpain.

TREATMENT7-9

To date, there is no agreement as to how to treatthese patients. Some studies have reported goodpain relief after a steroid and local anaestheticinfiltration in anomalous lumbosacral articulations.Some authors have described posterolateral fu-sion or resection of accessory process for recalci-trant cases.

REFERENCES

1. Bertolotti M. Contributo alla conoscenze dei vizi didifferenzazione regionale del rachide con specialeriguardo alla assimilazione sacrale della V. lombare.Radiologique Medica (Torino) 1917;4:113-44 (inItalian).

2. Elster AD. Bertolotti’s syndrome revisited: transi-tional vertebrae of the lumbar spine. Spine1989;14:1373-7.

3. Luoma K, Vehmas T, Raininko R, Luukkonen R,Riihimaki H. Lumbosacral transitional vertebra:relation to disc degeneration and low back pain.Spine 2004;29:200-5.

4. Aihara T, Takahashi K, Ogasawara A, et al.Intervertebral disc degeneration associated withlumbosacral transitional vertebrae: a clinical andanatomical study. J Bone Joint Surg [Br] 2005;87-B:687-91.

5. Brown MF, Rockall AG, Hallam P, Hall-Craggs MA,Edgar MA. Transitional lumbo-sacral vertebrae:incidence of disc degeneration above and below[abstract]. J Bone Joint Surg [Br] 2000;82-B(Suppl II):180.

6. Beattie PF, Meyers SP. Magnetic resonanceimaging in low back pain: general principles andclinical issues. Phys Ther 1998;78:738-53.

7. Tehranzadeh J, Andrews C, Wong E. Lumbarspine imaging: normal variants, imaging pitfallsand artifacts. Radiol Clin North Am 2000;38:1207-53.

7. Marks RC, Thulbourne T. Infiltration of anomalousarticulations: steroid and anesthetic injections in10 back-pain patients. Acta Orthop Scand1991;62:139-41.

8. Jonsson B, Stromqvist B, Egund N. Anomalouslumbosacral articulations and low back-pain: evalu-ation and treatment. Spine 1989;14:831-4.

9. Santavirta S, Tallroth K, Ylinen P, Suotanta H.Surgical treatment of Bertolotti’s syndrome: follow-up of 16 patients. Arch Orthop Trauma Surg1993;112:82-7.

“Some studies havereported good pain

relief after a steroid

and local anaestheticinfiltration in

anomalous

lumbosacralarticulations”

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