evaluation and treatment of low back pain

Evaluation and Treatment of Low Back Pain: AClinically Focused Review for Primary CareSpecialistsW. Michael Hooten, MD, and Steven P. Cohen, MD

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Target Audience: The target audience for Mayo Clinic Proceedings is primar-ily internal medicine physicians and other clinicians who wish to advancetheir current knowledge of clinical medicine and who wish to stay abreastof advances in medical research.Statement of Need: General internists and primary care physicians must main-tain an extensive knowledge base on awide variety of topics covering all body sys-tems as well as common and uncommon disorders.Mayo Clinic Proceedings aimsto leverage the expertise of its authors to help physicians understandbest practicesin diagnosis and management of conditions encountered in the clinical setting.Accreditation: Mayo Clinic College of Medicine is accredited by the Accred-itation Council for Continuing Medical Education to provide continuing med-ical education for physicians.Credit Statement: Mayo Clinic College of Medicine designates this journal-based CME activity for a maximum of 1.0 AMA PRA Category 1 Credit(s).!Physicians should claim only the credit commensurate with the extent oftheir participation in the activity.Learning Objectives: On completion of this article, you should be able to:(1) distinguish the key anatomical structures implicated in the pathogenesisof low back pain; (2) identify the clinical characteristics that differentiate axialand radicular low back pain; and (3) formulate an evidence-based treatmentplan for low back pain.Disclosures: As a provider accredited by ACCME, Mayo Clinic College ofMedicine (Mayo School of Continuous Professional Development) mustensure balance, independence, objectivity, and scientific rigor in its educa-tional activities. Course Director(s), Planning Committee members, Faculty,and all others who are in a position to control the content of this educationalactivity are required to disclose all relevant financial relationships with any

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Abstract

Low back pain (LBP) is a leading cause of disability worldwide. In the absence of a classification system for painsyndromes, classification of LBP on the basis of the distribution of pain as axial (pain generally localized to thelow back) or radicular neuropathic (pain radiating to the lower extremities) is relevant to clinical practicebecause the distribution of pain is often a corollary of frequently occurring disease processes involving thelumbar spine. Common sources of axial LBP include the intervertebral disc, facet joint, sacroiliac joint, andparaspinal musculature, whereas common sources of radicular pain include a herniated intervertebral disc andspinal stenosis. The accuracy of historical and physical examination findings has been established for sacroiliacjoint pain, radiculopathy, and lumbar spinal stenosis. However, the accuracy of similar data, so-called red flags,for identifying the underlying medical sources of LBP has been overstated. Diagnostic imaging studies can beuseful, and adherence to established guidelines can protect against overuse. Multiple pharmacological trialsexist for the management of LBP; however, the long-term outcomes of commonly used drugs are mixed. Forcarefully selected patients with axial LBP, radiofrequency denervation techniques can provide sustained painrelief. In patients with radicular pain, transforaminal epidural steroid injections may provide short-term painrelief, but neurostimulation may confer more enduring benefits of refractory symptoms. Pain-related in-dications for commonly performed operations include spinal decompression for radicular symptoms as well asspinal fusion or disc prosthesis for discogenic LBP. Physical modalities and psychological treatments canimprove pain and functioning, but patient preferences may influence treatment adherence.

ª 2015 Mayo Foundation for Medical Education and Research n Mayo Clin Proc. 2015;90(12):1699-1718

From the Mayo ClinicCollege of Medicine andDepartment of Anesthesi-ology, Division of PainMedicine, Mayo Clinic,Rochester, MN (W.M.H.);Department of Anesthesi-ology and Critical CareMedicine, Department ofPhysical Medicine andRehabilitation, Johns Hop-kins School of Medicine,Baltimore, MD (S.P.C.);and Department of Anes-thesiology, Department ofPhysical Medicine andRehabilitation, UniformedServices University ofHealth Sciences, Bethesda,MD (S.P.C.).

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L ow back pain (LBP) is a leading cause ofdisability worldwide with a lifetime inci-dence of 51% to 84%.1,2 The taxonomy

of pain syndromes, including LBP, is underdevel-oped, and nowidely accepted single classificationsystem currently exists.3-5 However, classificationof LBP based on the distribution of pain as pre-dominately axial (pain localized to the low backarea) or radicular (pain radiating to the lower ex-tremities in a dermatomal distribution with orwithout accompanying LBP) is particularly rele-vant to primary care specialists because the distri-bution of pain is often a corollary of frequentlyoccurring disease processes involving the lumbarspine.6 This simple classification schemeprovidesa clinically focused framework for organizing keyhistorical and physical examination findings thatdrive the diagnostic and therapeutic decision-making processes that arise in the routine careof adults with LBP.6,7 Therefore, the purpose ofthis review was to provide a clinically focusedapproach for the evaluation and treatment ofchronic LBP for primary care specialists.

METHODSSimilar to previously published search strategies,8

databases of MEDLINE using the PubMed andOvid platforms as well as the Cochrane Databaseof Systematic Reviews were searched using thekey words low back pain, lumbar spine pain, andlumbar radiculopathy with no date restrictions.Key words pertaining to specific topics (eg, lum-bar spinal stenosis, physical examination, therapeuticspinal injections, and analgesic medication) werecross-referenced with the initial search terms us-ing the identified databases. Search terms werecross-referenced with review articles, and addi-tional articles were identified bymanually search-ing reference lists.

EPIDEMIOLOGY AND NATURAL COURSE

EpidemiologyThe estimated prevalence of LBP varies accordingto the surveillance period and specific type ofpain. For example, in a systematic review,9 thepoint prevalence of LBP was 18.3%, the1-month rate was 30.8%, and the mean annualprevalence was 38.0%. In a more recent system-atic review10 in which chronic LBP was definedas pain lasting longer than 12 weeks, the preva-lence ranged from 5.9% to 18.1%. The 1-yearincidence of an initial episode of LBP ranges

from 6.3% to 26.2%, and estimates of recurrenceat 1 year range from 24% to 80%.2,9,11

Neuropathic pain, defined as pain resultingfrom a lesion or disease affecting the somatosen-sory system, can be an important characteristicof LBP especially in individuals with a herniateddisc causing nerve root irritation and lumbar spi-nal stenosis. In individuals with predominatelychronic axial LBP, questionnaires designed todetect the distinguishing characteristics of neuro-pathic pain have found that between 17% and55% of individuals have pain that is primarilyneuropathic in nature, with a median rate of41%.12-17 This distinction is important becauseneuropathic pain may be associated with greaterlevels of physical and psychological dysfunctionas compared with other types of pain.18 The inci-dence of new-onset radicular pain ranges from1.5% to 18.5%,19,20 and the incidence of lumbarspinal stenosis has been estimated to be 5 per100,000 people.21

Natural CourseAxial LBP. Although most episodes of acuteLBP will resolve, a substantial proportion of pa-tients will develop chronic or recurrent pain. Alarge study22 that followed 973 people withacute axial LBP found that 28% had not fullyrecovered 12 months after their initial consulta-tion. Factors associated with persistence includedolder age, greater baseline pain and dysfunction,depression, fear of pain persistence, and ongoingcompensation claims.22 A systematic review23

comprising 11 studies that followed individualswith axial LBP less than3months indurationwhosought evaluation in aprimary care settingyieldedless favorable findings. Itz et al23 found that one-third of individuals recovered within 3 months,but 65% continued to experience persistent painat 1-year follow-up. This suggests that individualswho do not recover within 3 months are atincreased risk of developing chronic axial LBP.

Radicular Pain. Several studies have soughtto determine the natural course of lumbosacralradiculopathy. In one of the earliest studies exam-ining the clinical course in individuals withsciatica, Hakelius24 found that 58% of 38patients with clinical symptoms and positivecontrast myelography were symptom-free within30 days and 88% were symptom-free after 6months. A retrospective study by Saal and Saal25

reported that among 52 patients with signs and

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symptoms of lumbosacral radiculopathyconfirmed by electrodiagnostic testing whoreceived aggressive conservative care, 96% expe-rienced good (n¼35) or excellent (n¼15) out-comes at a mean follow-up period of 31 months.In both the treatment (piroxicam) and placebo-control arms of a randomized study evaluating208 patients with acute sciatica, Weber et al26

found that 64 patients (30%) continued toreport significant pain after 3 months, withfew patients experiencing resolution between3-month and 1-year follow-up. In anotherdouble-blind study27 evaluating chymopapainchemonucleolysis, 11 out of 30 patients 37% ofthe placebo-controlled group experienced a goodoutcome at 6weeks,which increased to 60%by 6months. In summary, whereas most episodes ofnew-onset radicular pain will resolve withoutaggressive treatment, 15% to 40% of individualswill experience early (<1 year) or frequent re-currences of symptoms.26,28,29 The observationthat most cases of acute radiculopathy improvewithin several months is consistent with radio-logical studies30,31 that found that approximatelytwo-thirds of herniated lumbar discs undergosignificant (>50%) resorption within 1 year.

Several instruments have been developed topredict which patients may be at risk for devel-oping chronic LBP after a back injury, with oneof the more common being the Acute Low BackPain Screening Questionnaire, which was subse-quently modified to include all musculoskeletalconditions.32 A systematic review33 found thatthe pool sensitivity of this questionnaire was0.59 and the specificity was 0.77.

Lumbar Spinal Stenosis. Lumbar spinal ste-nosis occurs when the vertebral canal is nar-rowed by surrounding bone and soft tissues,leading to compression of neural structuresincluding the spinal nerve roots. Spinal stenosisis not a singlediseaseprocess; rather, it ismultifac-torial and generally the result of a combination ofanatomical changes including intervertebral discprotrusion or herniation, facet joint hypertrophy,spondylolisthesis (forward displacement of avertebra), congenital narrowing of the vertebralcanal, or hypertrophy/buckling of the ligamen-tum flavum. Consequently, the natural historyof lumbar spinal stenosis is less auspicious,though only a minority of patients develop pro-gressively worsening symptoms. At a meanfollow-up period of 11.1 years, Minamide et al34

found that similar proportions of 34 patientswith lumbar spinal stenosis treated conservativelyexperienced improvement, no change, or wors-ening of symptoms. A cohort study35 evaluating56 patients with symptomatic mild-to-moderatelumbar spinal stenosis symptoms who weretreated conservatively found that 34 patients(60.7%) had a stable or improved clinical status ata median follow-up period of 88 months. Thesefindings are consistent with several olderstudies36,37 exhibiting that most patients withconservatively treated spinal stenosis will reporteither stable or improved symptoms at least 3years after the presentation. In a partially ran-domized study,Amundsenet al38 found that 57%of a nonrandomized cohort (n¼50) with mildsymptoms obtained a good outcome at 4-yearfollow-up whereas 44% of 18 randomized non-surgically treated patients had a good outcome at4 years.

In contrast to an acute herniateddisc thatmayresolve over time, the chronic degenerative andbony changes that characterize axial LBP and spi-nal stenosis do not generally regress. Thus, theanatomical changes that predispose to the devel-opment of axial LBP and spinal stenosis may inpart explain the discrepancies observed in theoverall prognosis of these patients.

CLINICALLY ORIENTED ANATOMY OF THELUMBAR SPINEAlthough the anatomy of the lumbar spine iscomplex, several key anatomical structurescontribute to commonly encountered clinicalproblems including the vertebral body, inter-vertebral disc, facet joint, paraspinal muscles,and ligamentum flavum. The lumbar spine iscomposed of 5 vertebrae; however, estimatesof the prevalence of lumbosacral transitionalvertebrae (LSTVs) range from 7% to 30%.39

The transverse processes of the fifth lumbar(L5) vertebral body may be broad and elon-gated, which can lead to complete sacralfusion. The assimilation of the L5 vertebrainto the sacrum is termed sacralization of L5.Conversely, the first sacral (S1) vertebra mayform articulations with the S2 vertebral bodyand even have well-formed lumbar-type facetjoints and a lumbar-sized intervertebral disc.The term lumbarization refers to an S1 vertebrathat has features of a lumbar vertebra. The cor-rect identification of LSTVs is important toavoid surgical and procedural errors attributed

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to inaccurate vertebral body enumeration andto ensure accurate correlation of clinical symp-toms. One approach to enumerating the lumbarvertebrae involves identifying the most caudalrib (12th rib) that articulates with the 12ththoracic vertebral body (T12). The vertebralbody immediately caudal to T12 is designatedL1, and the remainder of lumbar vertebrae areenumerated sequentially in the caudal direction.Although anLSTVhas been associatedwith radic-ular pain because of compression of spinal nerveroots,40,41 studies that have sought to establish anassociation between LSTVs and the occurrence ofaxial LBP have been mixed, with only certaintypes of LSTVs (eg, pseudarthrosis) being linkedto LBP.42,43

The intervertebral disc is an avascular fibro-cartilaginous structure that allows movement be-tween adjacent vertebral bodies (Figure 1). Eachlumbar intervertebral disc is approximately 4 cmin diameter and 7 to 10mm in thickness,44 and itis composed of an outer annulus fibrosus and aninner nucleus pulposus. The annulus is a denseconcentric ring of layered collagen fibers that sur-rounds the nucleus and resists tensile forces. Thenucleus pulposus contains collagen and elastinfibers embedded within a hydrated proteoglycangel. Disc degeneration is associated with annulartears and dehydration of the nucleus pulposus,which can lead to decreased disc height, impairedmechanical function, rupture, and compressionof spinal nerve roots (Figure 2). In addition,nerve and vascular ingrowth into the disc andexposure of these nerves to inflammatory media-tors have been associated with axial LBP.45,46

Lumbar facet joints, also referred to as thezygapophysial joints, are true synovial jointsformed by the superior and inferior articulatingprocesses of 2 adjacent vertebrae (Figure 3). The

inferior aspect of each lumbar facet joint isinnervated by themedial branch of the posteriorprimary rami at the same level of the facet joint,and the superior aspect is innervated by themedial branch from 1 level above. This dualinnervation is important when considering tar-geted diagnostic and interventional therapiesfor lumbar facet pain. From a biomechanicalperspective, the 2 facet joints and the interverte-bral disc at each spinal level are interdependentand form what is referred to as a motionsegment, otherwise termed the three-joint com-plex.47 In this manner, the lumbar spine canbe conceptualized as a stacked series of motionsegments. Whereas the intervertebral disc is theprincipal weight- or load-bearing structure ofeach motion segment, the role of the facet jointsis to limit torsion and resist forward displace-ment of the vertebral segment. However, inthe setting of degenerative disc disease and asso-ciated disc space narrowing, the total load trans-mitted to the facet joint increases and cansometimes exceed 50% of the total load placedon the vertebral segment.48,49 Pathophysiologi-cally, osteoarthritic changes involving the lum-bar facet joints are common and include jointspace narrowing due to degenerative thinningof the cartilage, presence of inflammatory cellsand mediators, increased vascularization, sub-chondral bone remodeling, and osteophyteformation, which can contribute to axial LBPand spinal stenosis.50,51 These osteoarthriticchanges, particularly osteophyte formation,can contribute to neural foraminal stenosisand compression of the exiting nerve root,which can lead to the development of radicularpain.

The ligamentum flavum extends along theposterior aspect of the vertebral columnand con-nects the laminae of the adjacent vertebrae(Figure 4). The ligamentum flavum is 2- to3-mm thick and is composed of elastin andcollagen fibers in a 2:1 ratio; the elastin fibersprovide elasticity, and the collagenfibers providetensile strength and stability. Hypertrophy of theligamentum flavum is multifactorial and hasbeen associated with older age, mechanicalstress, increased body mass index (calculated asthe weight in kilograms divided by the heightin meters squared), and alterations in cytokineand proteinase inhibitor concentrations.52,53

Ligamentum flavum hypertrophy can be animportant contributor to the development of

FIGURE 1. Intervertebral disc structure.





spinal stenosis, especially when it occurs inconjunction with other disease processes thatnarrow the spinal canal, including facet jointarthropathy and disc protrusions.54

Multiplemuscles affect lumbar spine functionand can be categorized into 3 major anatomicalgroups relative to the torso: the posterior, ante-rior, and lateral groups (Figure 5).55 Together,these 3 muscle groups control movement of thespine, contribute to the stabilization of the verte-bral column, and provide proprioceptive feed-back.56 The posterior group, composed ofsuperficial (ie, erector spinae and serratus poste-rior inferior), intermediate (ie, longissimus thora-cis), and deep (ie, multifidus and quadratuslumborum) layers, arise from the transverse andspinous processes of the vertebrae and insert onthe iliac crests and sacrum. The deeper musclesspan fewer vertebrae comparedwith themore su-perficial muscles, and the muscles more adjacenttomidline are of greater diameter. Themuscles ofthe posterior group are responsible for extending,lateral bending, and torsionof the spine. The ante-rior group is chiefly composed of the abdominalwall (ie, rectus abdominis, external oblique, andinternal oblique) and is primarily responsible forflexion of the spine, but these muscles alsocontribute to lateral bending and torsional move-ment. The lateral group includes the psoas andiliacus muscles. The psoas muscle arises fromthe lateral aspects of the lumbar vertebrae, andthe iliacus muscles arise from the anterior iliumand lateral sacrum. These 2 muscles join as theymove laterally to insert on the lesser trochanterof the femur and are often referred to as the iliop-soas muscle. The iliopsoas is a powerful flexor ofthe thigh and works to maintain an upright anderect posture. Current evidence suggests thatthe cross-sectional area and density of paraspinalmuscles are reduced in patients with LBP,57,58

and alterations in muscle activation and fat infil-tration of the paraspinal muscles have beenobserved in these patients.59,60 In addition,reduced paraspinal muscle density has been asso-ciated with facet joint osteoarthritis, spondylolis-thesis, and disc space narrowing.58

HISTORY AND PHYSICAL EXAMINATION

Significance of “Red Flag” SymptomsA critical aspect in the evaluation of axial orradicular pain is to identify nonmusculoskeletaldiseases that may be responsible for the patients’

symptoms. Although the differential diagnosisof LBP is broad, most nonmusculoskeletal dis-ease states can be categorized as neoplastic, in-flammatory, visceral (which includes pelvicand retroperitoneal structures), infectious,vascular, endocrine, and traumatic (Table 1).61

The risk factors, historical features, and physicalexamination findings associated with nonmus-culoskeletal diseases are widely referred to asred flags, but the accuracy, or risk-benefit ratio,of many previously recognized red flag signsand symptoms has been called into ques-tion.62,63 In a prospective study64 that involved1172 consecutive patients receiving primarycare for acute LBP, 11 patients (0.9%) wereidentified as having “serious spinal pathology”including 8 with vertebral compression frac-tures, 2 with inflammatory arthritides, and 1with cauda equina syndrome. Although theprevalence of serious pathology was low, 4 clin-ical factors were statistically significantly associ-ated with vertebral compression fractures,

FIGURE 2. A, Lateral view of the potential effects of disc bulging anddegenerative changes on spinal nerve roots. B, Axial view of a rupturedlumbar intervertebral disc.

FIGURE 3. Anatomy and innervation of thelumbar facet joint. Also depicted are bilateralfractures of the pars interarticularis (pars defect)and an osteoarthritic facet joint.

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including female sex, age greater than 70 years,trauma, and prolonged use of corticosteroids.64

A set of similar red flag indicators were iden-tified in 2 systematic reviews65,66 that investi-gated the accuracy of various clinical factorsused to screen for vertebral compression frac-tures and spinal malignant neoplasm(Table 1). In clinical practice, the use of redflag indicators should supplement but notsupplant clinical judgment on the evaluationof nonmusculoskeletal disease processes.

Axial LBPThe differential diagnosis of axial LBP is broad butcommonly involves lumbar spine structures thatinclude the intervertebral discs, facet joints, sacro-iliac joints, andparaspinalmusculature. Althoughnonspecific,67 some historical features and char-acteristic signs and symptoms associated withaxial LBP may be helpful in determining thesource of pain. The intervertebral disc can be asource of pain in up to 40% of patients with axial

LBP. These patients tend to be younger (age<45years), and though the onset tends to be insidiousin most cases, in some instances an inciting eventmay be described (ie, lifting, bending, andtwisting).6,45,68 Discogenic LBP is oftenworsenedby activities that load the spine, and a history ofsitting intolerance and improvement of painwith recumbency are often reported. Patientswill often localize pain to the midline of thespine,69 but pain can be referred to the upperthigh and up to 20% will experience pain distalto the knee.46,70 Although no physical examina-tion findings can accurately discriminate patientswith discogenic pain,68 greater midline tender-ness may be an indicator in some patients.69

Axial LBP attributed to the lumbar facet jointsis estimated to affect approximately 15% to 30%of patients.6,71,72 Although numerous studieshave attempted to identify thehistorical andphys-ical examination findings associated with lumbarfacet pain, no discrete set of clinical markers hasbeen delineated.47 However, the onset of lumbarfacet pain is generally insidious and it occursmorefrequently in older adults (age>65 years).6 Lum-bar facet pain is generally worsened by prolongedstanding and relievedwith sitting or recumbency,which decreases the load on the joints.73 In somepatients, pain may be localized to the paraspinalregion with or without radiation to the groin,thigh, or occasionally distal to the knee.47,69 Onphysical examination, no test is considered to besensitive for identifying a painful facet joint.Although small and methodologically flawedstudies suggested that pain with extension andaxial rotation was indicative of facet arthropathy,diagnostic studies using double local anestheticand placebo-controlled facet blocks, cada-veric studies using infrared markers, andcorrelative studies evaluating lumbar facetradiofrequency denervation outcomes haveall refuted this assertion.72,74-76

Sacroiliac joint pain occurs in 15% and30% of individuals with axial LBP69,77 and isassociated with a specific inciting event in40% and 50% of occurrences; motor vehiclecollisions and falls are 2 of the most commoncauses.78 Patients will often report pain in thegluteal or paraspinal (below the fifth lumbarvertebra) regions with or without radiation tothe thigh, but up to 28% of patients mayhave referral of pain distal to the knee.78,79

Although discogenic pain is often character-ized by sitting intolerance, sacroiliac joint

FIGURE 4. Cross-sectional view of the lumbar spine, depicting ligamentousstructures.





pain may be worsened during transitionalmovements, such as rising from a sitting posi-tion.80 On physical examination, previousstudies81-83 suggest that a combination ofphysical maneuvers rather than a single testcan accurately identify patients with sacroiliacjoint pain (Table 2). In the differential diag-nosis of sacroiliac joint pain, it is importantto rule out piriformis muscle syndrome.84

The piriformis muscle originates from the in-ner surface of the sacrum and attaches to thegreater trochanter of the femur. Unilateral orbilateral buttock pain with radiation in an L5 orS1 dermatomal distribution (when impingementon the sciatic nerve is present) is characteristic,and pain intensity typically fluctuates throughoutthe day.84 On physical examination, transglutealbuttock tenderness can often be elicited, paincan sometimes be provoked by maneuversthat stretch the muscle (eg, adduction and in-ternal rotation of the hip), and the straight legraising test result is typically negative, whichhelp distinguish piriformis muscle syndromefrom radicular pain. A digital rectal examina-tion, which may be significant for tenderness,can aid in the diagnosis.

Axial LBP related to the paraspinal muscle orligament strain is oftenprecipitatedbyboth stren-uous andnonstrenuous activities includingheavylifting, repetitive movements, spinal torsion, ortrauma. The onset of pain is generally delayedby 1 to 2 days and is often localized to thelumbosacral region. On physical examination,

hypomobility due to muscle spasm or guardingmay be evident, and pain may be reproducedwith palpation of the paraspinal musculature.Although anymuscle or ligament can potentiallybe affected, frequently involved structuresinclude the multifidus, quadratus lumborum,erector spinae, and psoas muscles, as well asinterspinous and supraspinous ligaments.85

Myofascial pain may be an important contrib-uting factor to other sources of LBP or a pri-mary cause by itself and is characterized bythe presence of trigger points that are hyperir-ritable tense bands of skeletal muscles.86 Pa-tients will typically present with a history oflocalized or regional pain, and the range of mo-tion may be reduced in the affected muscles.On physical examination, palpation of a triggerpoint will typically provoke sharp localizedpain that may be referred to a contiguousbody region, although this can be difficult, ifnot impossible to discern, in nonsuperficialmuscles.86

A source of axial LBP often seen in children,adolescents, and young adults is bilateral stressfractures of the pars interarticularis (Figure 3),otherwise termed spondylolysis or a pars defect,which can lead to the development of spondy-lolisthesis. The incidence of lumbar spondylol-ysis ranges from 6% to 8%, and 95% of theoccurrences involve the L5 vertebra.87 Patientswill typically present with axial LBP, with orwithout a radicular component, that isworsened by activities involving repetitive

FIGURE 5. Muscle groups that contribute to lumbar spine function.

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flexion-extension movements of the lumbarspine. Although conservative treatment is gener-ally sufficient, surgerymay be required to preventthe progression of spondylolisthesis.87

Radicular PainHerniated Intervertebral Disc. Similar toaxial LBP, the differential diagnosis of radicularpain is broad, but approximately 90% of casesin the nonelderly are caused by a herniated inter-vertebral disc at the L4-L5 or L5-S1 level.55,88

Another important source of radicular pain in-cludes foraminal stenosis, which is commonbecause of far lateral disc herniation or facet jointhypertrophy.An inciting eventmayormaynot beidentified, but some patients report experiencinga “pop” in the region of the lumbar spine followedby the gradual onset of pain over the next 1 to 2days. However, the single most important his-torical factor is the distribution of pain, which

should follow a dermatomal pattern,89 thoughapproximately one-third of people have multipleaffected dermatomes (Table 3).90 In contrast tonociceptive pain, neuropathic LBP is oftendescribed as a sharp, lancinating, or burningsensation. Patients may report that pain isworsened by forward bending, coughing,sneezing, or prolonged sitting and improvedwith recumbency. When localizing theaffected nerve root on the basis of the derma-tomal distribution of pain, it is important torecognize that each nerve root exits the spinalcolumnbeneath the pedicle of the vertebral bodywith the same number as the nerve. For instance,the L4 nerve root exits beneath the pedicle of theL4 vertebral body, which is situated above theinterspinal disc at this level. Therefore, disrup-tion of the disc situated between the L4 and L5vertebrae will typically impinge the traversing L5nerve root (unless it is a far lateral herniation that

TABLE 1. Medical (Nonmusculoskeletal) Causes of Low Back Pain and Posttest Probability (PTP) of Red Flag Signs to Detect Fracture andMalignancy

Medical (nonmusculoskeletal) causes of low back pain

Neoplastica Inflammatorya Viscerala Infectiousa Vasculara Endocrinea Traumatica

Metastaticcarcinoma

Ankylosing spondylitis Endometriosis Osteomyelitis Aortic aneurysm Osteoporoticfractures

Vertebralfracture

Multiple myeloma Psoriatic spondylitis Prostatitis Epiduralabscess

Aortic dissection Paget disease Rib fracture

Lymphoma Rheumatoid arthritis Nephrolithiasis Discitis Spinal hemangioma Pelvic fractureLeukemia Reiter syndrome Aortic

aneurysmHerpes zoster Inferior vena cava

obstructionHip fracture

Spinal cord tumors Enteropathicspondylitis

Pancreatitis Pyelonephritis Sickle cell crisis

PTP of red flag signs to detect vertebral compression fracture

Red flag sign PTP (95% CI)b

Contusion or abrasion 62% (49%-74%)Prolonged corticosteroid use 33% (10%-67%)Severe trauma 11% (8%-16%)Older age 9% (3%-25%)Multiple signs present

Combination of any 3Female 90% (34%-99%)Age >70 ySevere traumaProlonged corticosteroid use

PTP of red flag signs to detect spinal malignancy

Red flag sign PTP (95% CI)b

History of malignancy 33% (22%-46%)

aData from N Engl J Med.61bData from BMJ65 and Cochrane Database Syst Rev.66





accounts for <10% of cases), but not the L4nerve root. On physical examination, the speci-ficities of various physical tests and neurologicalfindings for detecting lumbar radiculopathy aregood, but the sensitivities are generally low(Table 2).90,91

One potentially devastating source of LBPis cauda equina syndrome, which is causedby severe compression of the cauda equina dueto massive midline disk herniation, tumor, orepidural abscess.92 Cauda equina syndrome is asurgical emergency characterized by the suddenonset of axial or radicular pain, leg weakness,bowel and/or bladder dysfunction, and loss ofperineal sensation, which is also referred to assaddle anesthesia.

Lumbar Spinal Stenosis. Lumbar spinal ste-nosis can be associated with both axial andradicular pain, but the hallmark symptom isneurogenic claudication, which has a sensitivityand specificity of 88% (95% CI, 78%-98%) and34% (95% CI, 18%-50%), respectively.93

Patients with neurogenic claudication will typi-cally report the onset or worsening of radicularpain when standing and walking (sensitivity,71%; specificity, 30%), and rapid improvementin pain with sitting (sensitivity, 52%; specificity,83%).93,94 Pain will often radiate into the but-tocks, thighs, and/or legs in the distribution of 1or more dermatomes. Although the mechanismof neurogenic claudication has not been fullyelucidated, the prevailing evidence suggests thatactivities associatedwith lumbar extension,whichreduces the cross-sectional area of the spinalcanal, leads to mechanical compression andsubsequent impairment of the nerve.95 Thisproposed mechanism partly explains the revers-ibility of symptoms with lumbar flexion, whichincreases the cross-sectional area of the spinalcanal and neural foramina.96 Other importanthistorical factors associated with a diagnosis oflumbar spinal stenosis include age greater than 65years (sensitivity, 77%; specificity, 69%) and thepresence of bilateral buttock or leg pain (sensi-tivity, 88%; specificity, 34%).93,94 On physical

TABLE 2. Accuracy of Physical Examination Tests for Sacroiliac JointeRelated Pain, Lumbar Radiculopathy, and Lumbar Spinal Stenosis

Pain problem Test Description Sensitivity (95% CI) Specificity (95% CI)

Sacroiliac jointpaina

Compression Compression of the iliac crest in the lateral position If 3 or more tests reproduce pain:

Distraction Downward pressure on the anterior superior iliac crest Sensitivity range, 78%-79%Patrick (FABER test) Flexion abduction external rotation of the thigh and hip Specificity range, 85%-94%Gaenslen Hyperextension of the leg on the affected sideThigh trust Adduction of the flexed hip on the affected sideFortin finger Pain localized 1 fingerbreadth of the posterior iliac crestGillet Flexion of the leg toward the chest while standing

Lumbarradiculopathyb

Straight leg raising Patient supine and hip flexed with knee extended 64% (56%-71%) 57% (47%-66%)

Cross straight leg raising Pain with passive extension of the contralateral leg 28% (22%-35%) 90% (85%-94%)Muscle weakness During ankle dorsiflexion or extension of the great toe 27% (20%-37%) 93% (88%-97%)Impaired reflexes Achilles tendon (S1 radiculopathy) 15% (9%-21%) 93% (88%-97%)

Patellar tendon (L4 radiculopathy) 15% (9%-21%) 75% (55%-89%)Sensory deficits Reduced tactile sensation, tingling, and numbness 28% (21%-36%) 66% (56%-74%)Forward flexion Pain with bending forward in the standing position 45% (37%-53%) 74% (65%-81%)

Lumbar spinalstenosisc

Romberg Imbalance when standing with feet together and eyesclosed

39% (24%-54%) 91% (81%-100%)

Gait abnormality Wide-based gait 43% (28%-58%) 97% (91%-100%)Spinal flexion No pain with lumbar flexion 79% (67%-91%) 44% (27%-61%)Spinal extension Thigh pain with 30-s lumbar extension 51% (36%-66%) 69% (53%-85%)Vibration deficit Reduced vibratory sense (128-Hz tuning fork) 53% (38%-68%) 81% (67%-95%)Pinprick deficit Reduced pinprick sense (medial/lateral foot or calf) 47% (32%-62%) 81% (67%-95%)Impaired reflex Absent Achilles tendon reflex 46% (31%-61%) 78% (64%-92%)

aData from Man Ther,81 Arch Phys Med Rehabil,82 and J Pain.83bData from J Neurol90 and Cochrane Database Syst Rev.91cData from Arthritis Rheum.92

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examination, the accuracy of motor or sensoryfindings is generally reliable, and most likelyreflect the involvement of the proprioceptive fi-bers in the posterior columns of the spinal cord(Table 2).93,96 Other important considerations inthe differential diagnosis of lumbar spinal stenosisinclude hip osteoarthritis, trochanteric bursitis,and vascular claudication. Vascular claudicationcan be distinguished from neurogenic claudi-cation by signs of poor perfusion, includingdiminished pedal pulses, pallor, and decreasedtemperature in the feet. One study97 foundthat a positive “shopping cart sign” (relief ofpain when leaning forward as if pushing ashopping cart) and pain that was triggered bystanding alone and relieved by sitting were themost reliablemeans to differentiate neurogenicfrom vascular claudication.

DIAGNOSTIC TESTING

Diagnostic ImagingDespite the availability of practice guidelinesfor more than 20 years,98 overuse of imagingpersists. This is important because imaginghas long been recognized as a key contributorto the overall costs of LBP,99 and early imaginghas not been shown to improve outcomes ofpatients with axial or radicular pain.100-102 In

addition, imaging abnormalities not directlyrelated to the patients’ symptoms may leadto extraneous testing, contribute to moreaggressive treatments, and diminish patients’health perception.103,104 Best practice guide-lines for diagnostic imaging for LBP havebeen published by the American College ofPhysicians (Table 4).105 The timing and indi-cations for obtaining imaging studies in theseguidelines are risk-stratified and center aroundthe temporal course of the patients’ symptoms,which allow these recommendations to bereadily implemented in daily clinical practice.

ElectrodiagnosticsElectromyography and nerve conduction studiesare the principal electrodiagnostic tests used inthe evaluation of patients with radicular painand lumbar spinal stenosis. In general, the pri-mary objectives of electrodiagnostics for radicularpain are 2-fold.106 First, if indicated, electrodiag-nostic tests are useful to confirm the existence ofradiculopathy and to exclude the presence ofother peripheral nerve disorders (eg, mononeur-opathy multiplex and plexopathy).106 Second,electrodiagnostic testing can help clarify whichnerve root levels are involved, determine thetypeofnerve rootdysfunction (eg, demyelination,axonal loss, and presence of conduction block),

TABLE 3. Sensory, Motor, and Reflex Abnormalities Associated With Lumbar Spine Radiculopathy

Root Region of painDermatomal sensory

distribution Motor Reflex

L1 Inguinal Inguinal None CremastericL2 Inguinal

Anterior thighProximal anterior and medial

thighHip flexionHip adductionSome knee extension

CremastericThigh adductor

L3 Anterior thigh and knee Anterior and medial thigh Knee extensionHip flexionHip adduction

Patellar (knee)Thigh adductor

L4 Anterior thigh andanteromedial leg

Anterior knee and medial leg Hip extensionHip flexionHip adduction

Patellar

L5 Posterolateral thighLateral legMedial foot

Anterolateral legDorsal aspect footGreat toe

Foot dorsiflexionKnee flexionHip abductionToe extension/flexion

Possibly internalHamstring

S1 Posterior thigh/legHeelLateral foot

Posterolateral legHeelLateral Foot

Plantar flexionToe flexionKnee flexionHip extension

Achilles (ankle)

Adapted from Bartleson et al55 with permission.





andprovide informationon the severity and chro-nicity of nerve root abnormalities.106 Electrodiag-nostics can complement thefindings ofdiagnosticimaging studies107,108 and are particularly usefulin the following 2 clinical scenarios: (1) physicalexamination does not correlate with imagingstudies and (2) to clarify the functional signifi-cance of an imaging abnormality.106 Previousstudies109,110 have found a sensitivity ranging be-tween 40% and 85% in detecting lumbosacralradiculopathy, depending on the reference stan-dard. However, electrodiagnostic tests are time-sensitive because nerve root abnormalities maynot be reliably detectable until 3 weeks after theonset of symptoms.106,111

Diagnostic InjectionsDiagnostic injections are often used to confirma putative diagnosis and to identify patientswho may be candidates for further interven-tional treatments. For example, blocks target-ing nerves innervating the lumbar facet joints(eg, medial branch blocks) and sacroiliacjoints (eg, both intra- and extra-articularblocks) help distinguish patients with axialLBP who may be candidates for percutaneousradiofrequency denervation procedures.112,113

Provocative discography is often touted as theonly means to establish a relationship betweendisc pathology and symptoms but is character-ized by a high false-positive rate in some pa-tients (eg, those with psychopathology andprevious surgery).114 Furthermore, the evi-dence that discography may improve surgicaloutcomes is limited to a recent subgroup anal-ysis of a randomized study115 comparingfusion outcomes in those patients who under-went presurgical discography screening andthose who did not. In patients with radicularpain, selective nerve root blocks can beconsidered when imaging, physical examina-tion, or electrodiagnostic studies are inconsis-tent or noncorroborative.116 Patients shouldbe referred to a pain medicine specialist withexpertise in performing and interpreting theoutcomes of diagnostic injections.

TREATMENT OF LBP

Pharmacological TreatmentThere are multiple trials evaluating a plethoraof medication classes for LBP, but asidefrom studies conducted in patients with

radiculopathy, most have been performed inpatients with axial LBP. There is strong evidencein support of nonsteroidal anti-inflammatorydrugs for chronic LBP compared with placebofor up to 3 months, but long-term outcomestudies are lacking.117 Muscle relaxants aremore effective than placebo for nonspecific LBP,with stronger evidence supporting their use foracute rather than chronic pain. However, cautionshould be exercised when prescribing drugs suchas carisoprodol andbenzodiazepines,which carrygreater risks (eg, physical dependence) but nogreater efficacy thandoothermuscle relaxants.118

For antidepressants, the results of systematic re-views are mixed. One narrative review119 foundthat 3 of 5 systematic reviews evaluating 14 ran-domized trials found some evidence of benefit.In general, tricyclic antidepressants have beenfound to have superior efficacy than serotonin-norepinephrine reuptake inhibitors, which, inturn, are more efficacious than serotonin-specific reuptake inhibitors.120 Opioids,including tramadol and tapentadol, have beenshown to be effective for episodes of acute LBP,as well as for chronic LBP unresponsive to moreconservative treatment.121,122 However, thelong-term benefits of opioids, or superiorityover nonopioid analgesic medications, remainunproven. For instance, in a systemic review,

TABLE 4. American College of Physicians Guideline for Imaging in Patients WithLow Back Paina,b

Clinical action Imaging modality Indications for initial imaging

Immediate imaging Radiograph andESR

Major risk factors for cancer

MRI Suspect spinal infectionSigns of cauda equina syndromeSevere neurological deficits

Defer imaging until afterinitial treatment

Radiograph and/orESR

Weaker risk factors for cancer

Risk factors for inflammatoryarthritides

Risk factors for vertebralcompression fracture

MRI Signs of radiculopathySigns of spinal stenosis

No imaging Improved/resolved pain 1 mo aftertreatment

Previous imaging with no change inclinical status

aESR ¼ erythrocyte sedimentation rate; MRI ¼ magnetic resonance imaging.bData from Ann Intern Med.105

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Chaparro et al123 found low- to moderate-qualityevidence for the short-term benefits of opioids ascompared with placebo. For pain relief and func-tional improvement, no evidence was found tosuggest that opioidswere superior to nonsteroidalanti-inflammatory drugs or antidepressants.123

Few well-designed clinical trials exist foradjuvant medication treatment of radicularpain. Gabapentinoids have shown mixed resultsin randomized controlled trials as stand-aloneand add-on analgesic medications, with a large,placebo-controlled, industry-sponsored study124

failing to show efficacy for pregabalin. An un-published industry-sponsored study125 foundno efficacy for oxcarbazepine in 145 patientswith lumbosacral radiculopathy. However,2 placebo-controlled crossover studies126,127

found efficacy for topiramate, a medicationnot classified as a first- or second-line treatmentof neuropathic pain. In a double-blind, placebo-controlled, crossover study128 comparingnortriptyline, sustained-release morphine,and the combination of nortriptyline andmorphine to an active placebo, small reductionsin pain for all treatment groups were observed,andmore thanhalf of patients reported adverse ef-fects. A more recent meta-analysis found that theefficacy for duloxetine in patients with chronicLBP was similar to other medications includingnonsteroidal anti-inflammatory drugs, opioids,selective serotonin reuptake inhibitors, andglucosamine.129

Recently, evidence has emerged in support ofa possible infectious etiology for some cases ofLBP.130 A double-blind placebo-controlledstudy131 performed in 162 patients with chronicLBP and endplate signal changes indicative ofedema (Modic type 1) after a recent (<24months) disc herniation found significant reduc-tions in both back and leg pain in those treatedwith oral antibiotics for 100 days. The rationalebehind antibiotic treatment is that tears in theouterfibers of annulusfibrosusmay enable anaer-obic bacteria to enter the disc, resulting in a low-grade inflammatory process132; however, thesefindings are yet to be replicated.

Therapeutic Injections and FluoroscopicallyGuided ProceduresThe use of injections and other minimally inva-sive interventions for LBP has risen dramaticallyover the past decade, but increased use has notbeen accompanied by a concomitant reduction

in disability rates or surgical procedures.133,134

If therapeutic injections are considered to be atreatment option, the patient should be referredto a pain medicine specialist with expertise inperforming image-guided injections. Fluoro-scopically guided corticosteroid injections tar-geting the facet joints have not been shown toprovide significant benefits in controlled trials,whereas intra- and extra-articular sacroiliacjoint injections have been shown to provideonly short-term benefits.47,135 However,after the appropriate diagnostic blocks,various radiofrequency denervation (ie,nerve ablation) procedures have been associ-ated with sustained pain relief in carefullyselected patients with facet and sacroiliacjoint pain.47,78,135

Interventional treatments of discogenic axialLBP have been largely disappointing. Placebo-controlled studies evaluating intradiscal ste-roids136,137 and cytokine inhibitors138 haveyielded negative results. Although an initialplacebo-controlled study139 evaluating intradiscalmethylene blue injection foundmore than a 90%success rate at 2-year follow-up, the lack of sup-porting preclinical evidence and the failure toreplicate these results in subsequent uncontrolledstudies140,141 has led to the virtual abandonmentof this treatment. Several techniques have beendeveloped to treat discogenic LBP by heatingintradiscal elements. Although an early controlledstudy142 suggested that somepatientsmaybenefitfrom intradiscal electrothermal therapy, a treat-ment that purportedly acts by coagulatingpain re-ceptors, altering collagen architecture in the disc,and sealing annular tears, subsequent studieseither failed to replicate these results143,144 orfound that anybenefit tended tobe short-lived.145

More recently, a similar procedure known as bia-cuplasty has emerged that circumvents some ofthe technical problems associated with perform-ing intradiscal electrothermal therapy. A singlerandomized trial146 found that patients who un-derwent biacuplasty obtained better pain reliefand functional improvement than did a controlgroup who underwent sham lesioning, with theresults persisting through1-year follow-up.How-ever, concerns about long-term effectiveness andthe propensity for disc injury after annulus punc-ture limit the use of this treatment.

The effects of local anesthetic, steroid, orbotulinum toxin injections for muscle-related axial LBP are mixed, and the findings





of 2 systematic reviews suggest that thesetreatments provide only limited short-termpain relief.147,148

Epidural steroid injections (ESIs) are themostfrequently performed pain management proce-dures for radicular pain. In well-selected patients,ESIs appear to provide significant benefit ascompared with sham injections and conservativetreatment for approximately 6 weeks, thoughsome patients may obtain longer benefit.17

Similar to other treatments, patients with greaterdisease burden, receiving opioid therapy, andwith coexisting psychosocial dysfunction areless likely to respond to ESIs.149-151 A recent sys-tematic review152 found that ESIs may possiblyreduce the need for surgery in the short-term,but the evidence for long-term surgerypreventionis mostly anecdotal and based on indirect evi-dence or small clinical trials.153 Technical factorsthat may improve ESI treatment results includethe use of transforaminal rather than interlaminarinjections and the use of depo-steroids.17 How-ever, the administration of transforaminaldepo-steroids may be associated with rare butcatastrophic consequences including spinal cordinfarction.154 This has led researchers to investi-gate alternatives to ESI. One such alternativethat has garnered intense interest is the use of in-flammatory cytokine inhibitors such as the tumornecrosis factor antagonist etanercept. Yet, to date,clinical trials155-157 evaluating epidural etanercepthave yielded conflicting results.

Physical Modalities and PsychologicalTreatmentsAn extensive array of physical modalities andbehavioral treatments are used for axial and radic-ular pain. Some of the more widely used physicalmodalities associated with improvements in painand functioning include exercise,158 specificallywalking,159 yoga,160 and Pilates.161 When exer-cise is recommended, patientsmay bemore likelyto participate in programs that reflect their indi-vidual preferences, previous exercise experiences,and fitness level.162 Other forms of treatmentassociated with favorable outcomes includemassage,163 acupuncture,164 therapeuticultrasound,165 and manipulative spinaltherapies,166,167 and there is some evidencethat supports the integration of these treatmentsinto conventional medical therapy for LBP.168

Although these treatments appear to provideshort-term benefit compared with no treatment,

the evidence supporting the superiority oversham therapy, other treatments, or long-termbenefit is at best mixed.169 Transcutaneous elec-trical nerve stimulation is widely used in clinicalpractice, but current evidence does not supportits use for LBP.170,171

Chronic LBP can have devastating effectson emotional functioning and sense of well-being.172 One of the most widely used psycho-logical treatments of chronic LBP is cognitivebehavioral therapy, which focuses on exam-ining the relationships between thoughts, feel-ings, and behaviors. This form of therapy isassociated with improvements in overallemotional functioning and can be deliveredin individual or group sessions or as partof a more comprehensive multidisciplinarybiopsychosocial rehabilitation program.173,174

Mindfulness-based stress reduction is a pro-gram that incorporates a combination ofmeditation, bodily awareness, and yoga-likemovements. Recent evidence suggests thatthis form of treatment may lead to improve-ments in pain acceptance, but evidence sup-porting its effectiveness in improving painintensity and physical functioning remainsinconclusive.175

Lumbar Spine Surgery, Neurostimulation,and Intrathecal Drug DeliveryA broad range of operative techniques are used totreat LBP, including spinal decompression, dis-cectomy, foraminotomies, disc prosthesis (artifi-cial disc replacement), minimally invasive andmicrosurgeries, and various approaches for spinalfusionwith orwithout instrumentation. The indi-cations for performing the various lumbar spineoperations are complex and depend, in part, onindividual patient factors, but geographic varia-tions in surgical rates suggest that other factors,including access to health care resources, mayinfluence the surgical decision-making pro-cess.176,177 The general indications for commonlyperformed lumbar spine operations include spi-nal decompression for radicular symptomsincluding lumbar spinal stenosis as well as spinalfusion or disc prosthesis for discogenic LBPwithout nerve root involvement.

In a systematic review178 that investigatedthe effects of spinal decompression comparedwith nonoperative management of radicularpain, early surgery within 12 weeks of the onsetof radicular pain was associated with faster pain

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relief compared with prolonged conservativetreatment. However, there was no significantgroup difference in pain or functionality at 1-and 2-year follow-up.178 In patients with lumbarspinal stenosis with or without spondylolisthe-sis, decompressive laminectomy was associatedwith improved pain, disability, and quality oflife than was conservative treatment.179,180 Thefavorable benefits of surgical decompressionemerged at 3 to 6 months and were still evident2 to 4 years after surgery.179 However, a recentsystematic review181 found that decompressionwith fusion was not superior to decompressionalone for lumbar spinal stenosis and concludedthat the efficacy of various surgical treatmentsremains uncertain. For discogenic LBP, disabilityscores at 2- to 4-year follow-up were similarin patients randomized to undergo spinalfusion or cognitive behavioral-based painrehabilitation.182,183 Although disc prosthesisis associated with more preserved range ofmotion than is spinal fusion and, in somecontexts, may be superior to spinal fusion

for improvements in pain and disability,184

the outcomes compared to pain rehabilitationare mixed.185 For example, in a randomizedcomparative trial,185 patients allocated to un-dergo disc prosthesis experienced a statisti-cally significant but not a clinically meaningfulreduction in disability scores at 2-year follow-up as compared with patients allocated toreceive pain rehabilitation.

Neurostimulation, which includes spinalcord, dorsal root ganglion, motor cortex, anddeep brain stimulation, provides pain reliefthrough modulation of the nervous system. Spi-nal cord stimulation, themostwidely used neuro-stimulation technique, involves placement ofelectrodes in the epidural space. This techniqueexerts its analgesic effects by stimulating large,fast-conducting sensory fibers, thereby inhibitingthe slower-conducting A-delta and C nociceptivefibers responsible for pain transmission. Inessence, conventional spinal cord stimulationacts by creating an area of paresthesia withinthe anatomical distribution of pain, though

Muscle/ligament• Delayed onset• Lumbosacral region• Muscle spasm• Hypomobility• Possible myofascial

component

Sacroiliac joint• Gluteal pain/

off-midline below L5• Worse with transitional

movements (risingfrom the sitting position)

• EBM physical examination tests

Facet joint• Age >65 years• Pain worse with standing• Paraspinal distribution

Intervertebral disc• Age <45 years• Sitting intolerance• Pain worse with spine loading• Midline distribution

Spinal stenosis• Age >65 years• Neurogenic claudication• Improved with forward flexion• Radicular pain buttocks/leg• Multiple dermatomes• EBM physical examination tests

Herniated disc• Gradual onset, 1-2 days• Pain worse with cough/sneeze• Sharp/burning pain• Improved with recumbency• Single or multiple dermatomes• EBM physical examination tests

• Insidious onset• Improves with

recumbency• Pain referral to

thigh

Axial LBP Radicular pain

• Incitingevent common

FIGURE 6. Summary of clinical and anatomical characteristics of axial LBP and radicular pain. EBM ¼ evidence-based medicine; LBP ¼low back pain.





high-frequency and burst stimulation have beenfound to be more effective than traditional stimu-lation for alleviating pain without the accompa-nying paresthesias.55,186 One of the most widelyrecognized indications for neurostimulation is re-fractory radicular pain in association with failedback surgery syndrome.187 Although the evi-dence supporting neurostimulation for axialLBP is limited, recent randomized studies187,188

found high-frequency spinal cord stimulation tobe more effective than conventional stimulation.Referral to a pain medicine specialist for a neuro-stimulation evaluation is typically reserved for pa-tients who have failed other pain therapiesincluding medications, injections, and physicalmodalities.

Intrathecal drug delivery systems, alsoreferred to as pain pumps or morphine pumps,administer medications directly to the intrathecalspace.189 A small caliber catheter is placed percu-taneously in the intrathecal space and tunneledsubcutaneously to a programmable reservoirpump that is typically implanted in the subcu-taneous tissues of the lower abdominal region.Medications that are typically used as solo therapyor in combination include opioids (eg,morphine,hydromorphone, and fentanyl), local anestheticmedications (eg, bupivacaine), clonidine, andziconotide, which is a novel N-type voltage-gated calcium channel blocker approved onlyfor intrathecal use.190 Although the primary indi-cation for intrathecal drug delivery is intractablecancer-related pain, patients with refractory andpossibly inoperableLBPdue to failedback surgerysyndrome or, less frequently, spinal stenosis mayoccasionally be considered for intrathecal drugdelivery.187,189

CONCLUSIONIn the absence of a widely recognized classifica-tion system for pain syndromes, classifying LBPasmechanical or neuropathic provides a cohesivemodel for organizing the large body of knowl-edge surrounding the evaluation and treatmentof LBP in daily clinical practice (Figure 6). Thesensitivity and specificity of some historical andphysical examination findings have been estab-lished for commonly occurring sources of LBP,including sacroiliac joint pain, radiculopathy,and lumbar spinal stenosis. However, red flag in-dicators of serious underlying pathology are ac-curate only for vertebral compression fractureand spinal malignancy. Diagnostic testing,

including electrodiagnostics and injections, canbe useful in identifying the source of LBP, andadherence to established guidelines governingdiagnostic imaging can potentially diminish therisk of unnecessary resource utilization. Multiplepharmacological trials exist for both axial andradicular pain; however, the long-term outcomesof commonly used drugs remainmixed. For care-fully selected patients with sacroiliac joint andfacet-related LBP, radiofrequency denervationtechniques can provide sustained pain relief.For patients with radicular pain, transforaminalESIs and neurostimulation may provide short-and longer-term pain relief, respectively. The in-dications for performing the various lumbarspine operations are complex and depend, inpart, on individual patient factors. However, thegeneral indications for commonly performed op-erations include spinal decompression for radic-ular symptoms and spinal fusion or discprosthesis for discogenic LBP. A broad array ofphysical modalities and psychological treatmentscan improve pain and functioning, but individualpatient preferences may influence treatmentadherence.

Abbreviations and Acronyms: ESI = epidural steroidinjection; LBP = low back pain; LSTV = lumbosacral tran-sitional vertebra

Correspondence: Address to W. Michael Hooten, MD,Department of Anesthesiology, Mayo Clinic, Charlton 145,200 First St SW, Rochester, MN 55902 ([email protected]). Individual reprints of this article and a boundreprint of the entire Symposium on Pain Medicine willbe available for purchase from our website www.mayoclinicproceedings.org.

The Symposium on Pain Medicine will continue in anupcoming issue.

REFERENCES1. Murray CJ, Atkinson C, Bhalla K, et al; US Burden of Dis-

ease Collaborators. The state of US health, 1990-2010:burden of diseases, injuries, and risk factors. JAMA. 2013;310(6):591-608.

2. Henschke N, Kamper SJ, Maher CG. The epidemiology andeconomic consequences of pain. Mayo Clin Proc. 2015;90(1):139-147.

3. Fillingim RB, Bruehl S, Dworkin RH, et al. The ACTTION-American Pain Society Pain Taxonomy (AAPT): anevidence-based and multidimensional approach to classifyingchronic pain conditions. J Pain. 2014;15(3):241-249.

4. Geurts JW. Classification and management of low back pain: Isthis the right direction? Eur J Pain. 2015;19(3):293-294.

5. Henriques AA, Dussán-Sarria JA, Botelho LM, Caumo W.Multidimensional approach to classifying chronic pain condi-tionsdless is more. J Pain. 2014;15(11):1199-1200.

LOW BACK PAIN


1713







6. DePalma MJ, Ketchum JM, Saullo T. What is the source ofchronic low back pain and does age play a role? Pain Med.2011;12(2):224-233.

7. DePalma MJ, Ketchum JM, Saullo TR. Multivariable analyses ofthe relationships between age, gender, and body mass indexand the source of chronic low back pain. Pain Med. 2012;13(4):498-506.

8. Cohen SP. Epidemiology, diagnosis, and treatment of neckpain. Mayo Clin Proc. 2015;90(2):284-299.

9. Hoy D, Brooks P, Blyth F, Buchbinder R. The epidemiologyof low back pain. Best Pract Res Clin Rheumatol. 2010;24(6):769-781.

10. Hoy D, Bain C, Williams G, et al. A systematic review of theglobal prevalence of low back pain. Arthritis Rheum. 2012;64(6):2028-2037.

11. Taylor JB, Goode AP, George SZ, Cook CE. Incidence and riskfactors for first-time incident low back pain: a systematic re-view and meta-analysis. Spine J. 2014;14(10):2299-2319.

12. Freynhagen R, Baron R, Gockel U, Tölle TR. painDETECT: anew screening questionnaire to identify neuropathic compo-nents in patients with back pain. Curr Med Res Opin. 2006;22(10):1911-1920.

13. El Sissi W, Arnaout A, Chaarani MW, et al. Prevalence ofneuropathic pain among patients with chronic low-back painin the Arabian Gulf Region assessed using the leeds assess-ment of neuropathic symptoms and signs pain scale. J IntMed Res. 2010;38(6):2135-2145.

14. Beith ID, Kemp A, Kenyon J, Prout M, Chestnut TJ. Identifyingneuropathic back and leg pain: a cross-sectional study. Pain.2011;152(7):1511-1516.

15. Kaki AM, El-Yaski AZ, Youseif E. Identifying neuropathic painamong patients with chronic low-back pain: use of the LeedsAssessment of Neuropathic Symptoms and Signs pain scale.Reg Anesth Pain Med. 2005;30(5):422-428.

16. Hassan AE, Saleh HA, Baroudy YM, et al. Prevalence of neuro-pathic pain among patients suffering from chronic low backpain in Saudi Arabia. Saudi Med J. 2004;25(12):1986-1990.

17. Cohen SP, Bicket MC, Jamison D, Wilkinson I, Rathmell JP.Epidural steroids: a comprehensive, evidence-based review.Reg Anesth Pain Med. 2013;38(3):175-200.

18. Smith BH, Torrance N, Bennett MI, Lee AJ. Health and qualityof life associated with chronic pain of predominantly neuro-pathic origin in the community. Clin J Pain. 2007;23(2):143-149.

19. Younes M, Béjia I, Aguir Z, et al. Prevalence and risk factors ofdisk-related sciatica in an urban population in Tunisia. JointBone Spine. 2006;73(5):538-542.

20. Matsudaira K, Kawaguchi M, Isomura T, et al. Identification ofrisk factors for new-onset sciatica in Japanese workers: findingsfrom the Japan epidemiological research of Occupation-related Back pain study. Spine (Phila Pa 1976). 2013;38(26):E1691-E1700.

21. Melancia JL, Francisco AF, Antunes JL. Spinal stenosis. HandbClin Neurol. 2014;119:541-549.

22. Henschke N, Maher CG, Refshauge KM, et al. Prognosis in pa-tients with recent onset low back pain in Australian primarycare: inception cohort study. BMJ. 2008;337:a171.

23. Itz CJ, Geurts JW, van Kleef M, Nelemans P. Clinical course ofnon-specific low back pain: a systematic review of prospectivecohort studies set in primary care. Eur J Pain. 2013;17(1):5-15.

24. Hakelius A. Prognosis in sciatica: a clinical follow-up of surgicaland non-surgical treatment. Acta Orthop Scand Suppl. 1970;129:1-76.

25. Saal JA, Saal JS. Nonoperative treatment of herniated lumbarintervertebral disc with radiculopathy: an outcome study.Spine (Phila Pa 1976). 1989;14(4):431-437.

26. Weber H, Holme I, Amlie E. The natural course of acutesciatica with nerve root symptoms in a double-blind pla-cebo-controlled trial evaluating the effect of piroxicam. Spine(Phila Pa 1976). 1993;18(11):1433-1438.

27. Fraser RD. Chymopapain for the treatment of intervertebraldisc herniation: the final report of a double-blind study. Spine(Phila Pa 1976). 1984;9(8):815-818.

28. Suri P, Rainville J, Hunter DJ, Li L, Katz JN. Recurrence of radic-ular pain or back pain after nonsurgical treatment of symp-tomatic lumbar disk herniation. Arch Phys Med Rehabil. 2012;93(4):690-695.

29. Casey E. Natural history of radiculopathy. Phys Med RehabilClin N Am. 2011;22(1):1-5.

30. Saal JA. Natural history and nonoperative treatment of lumbardisc herniation. Spine (Phila Pa 1976). 1996;21(24 suppl):2S-9S.

31. Benoist M. The natural history of lumbar disc herniation andradiculopathy. Joint Bone Spine. 2002;69(2):155-160.

32. Linton SJ, Boersma K. Early identification of patients at risk ofdeveloping a persistent back problem: the predictive validity ofthe Orebro Musculoskeletal Pain Questionnaire. Clin J Pain.2003;19(2):80-86.

33. Sattelmayer M, Lorenz T, Röder C, Hilfiker R. Predictive valueof the Acute Low Back Pain Screening Questionnaire and theÖrebro Musculoskeletal Pain Screening Questionnaire forpersisting problems. Eur Spine J. 2012;21(suppl 6):S773-S784.

34. Minamide A, Yoshida M, Maio K. The natural clinical course oflumbar spinal stenosis: a longitudinal cohort study over a min-imum of 10 years. J Orthop Sci. 2013;18(5):693-698.

35. Micankova Adamova B, Vohanka S, Dusek L, Jarkovsky J,Bednarik J. Prediction of long-term clinical outcome in patientswith lumbar spinal stenosis. Eur Spine J. 2012;21(12):2611-2619.

36. Johnsson KE, Udén A, Rosén I. The effect of decompressionon the natural course of spinal stenosis: a comparison of sur-gically treated and untreated patients. Spine (Phila Pa 1976).1991;16(6):615-619.

37. Johnsson KE, Rosén I, Udén A. The natural course of lumbarspinal stenosis. Clin Orthop Relat Res. 1992;279:82-86.

38. Amundsen T, Weber H, Nordal HJ, Magnaes B, Abdelnoor M,Lilleâs F. Lumbar spinal stenosis: conservative or surgical man-agement? A prospective 10-year study. Spine (Phila Pa 1976).2000;25(11):1424-1435; discussion 1435-1426.

39. Konin GP, Walz DM. Lumbosacral transitional vertebrae: clas-sification, imaging findings, and clinical relevance. AJNR Am JNeuroradiol. 2010;31(10):1778-1786.

40. Taskaynatan MA, Izci Y, Ozgul A, Hazneci B, Dursun H,Kalyon TA. Clinical significance of congenital lumbosacral mal-formations in young male population with prolonged lowback pain. Spine (Phila Pa 1976). 2005;30(8):E210-E213.

41. Otani K, Konno S, Kikuchi S. Lumbosacral transitional verte-brae and nerve-root symptoms. J Bone Joint Surg Br. 2001;83(8):1137-1140.

42. Tang M, Yang XF, Yang SW, et al. Lumbosacral transitionalvertebra in a population-based study of 5860 individuals: prev-alence and relationship to low back pain. Eur J Radiol. 2014;83(9):1679-1682.

43. Nardo L, Alizai H, Virayavanich W, et al. Lumbosacral transi-tional vertebrae: association with low back pain. Radiology.2012;265(2):497-503.

44. Roberts S, Menage J, Urban JP. Biochemical and structuralproperties of the cartilage end-plate and its relation to theintervertebral disc. Spine (Phila Pa 1976). 1989;14(2):166-174.

45. Simon J, McAuliffe M, Shamim F, Vuong N, Tahaei A. Disco-genic low back pain. Phys Med Rehabil Clin N Am. 2014;25(2):305-317.

46. Kallewaard JW, Terheggen MA, Groen GJ, et al. 15. Disco-genic low back pain. Pain Pract. 2010;10(6):560-579.

47. Cohen SP, Raja SN. Pathogenesis, diagnosis, and treatment oflumbar zygapophysial (facet) joint pain. Anesthesiology. 2007;106(3):591-614.

48. Yang KH, King AI. Mechanism of facet load transmission as ahypothesis for low-back pain. Spine (Phila Pa 1976). 1984;9(6):557-565.

49. Adams MA, Hutton WC. The mechanical function of the lum-bar apophyseal joints. Spine (Phila Pa 1976). 1983;8(3):327-330.





50. Izzo R, Guarnieri G, Guglielmi G, Muto M. Biomechanics ofthe spine. Part I: spinal stability. Eur J Radiol. 2013;82(1):118-126.

51. Gellhorn AC, Katz JN, Suri P. Osteoarthritis of the spine: thefacet joints. Nat Rev Rheumatol. 2013;9(4):216-224.

52. Kosaka H, Sairyo K, Biyani A, et al. Pathomechanism of loss ofelasticity and hypertrophy of lumbar ligamentum flavum inelderly patients with lumbar spinal canal stenosis. Spine (PhilaPa 1976). 2007;32(25):2805-2811.

53. Sairyo K, Biyani A, Goel V, et al. Pathomechanism of ligamen-tum flavum hypertrophy: a multidisciplinary investigationbased on clinical, biomechanical, histologic, and biologic as-sessments. Spine (Phila Pa 1976). 2005;30(23):2649-2656.

54. Szpalski M, Gunzburg R. Lumbar spinal stenosis in the elderly:an overview. Eur Spine J. 2003;12(suppl 2):S170-S175.

55. Bartleson J, Deen GH. Spine Disorders: Medical and SurgicalManagement. Cambridge: Cambridge University Press; 2009.

56. Leinonen V, Kankaanpää M, Luukkonen M, et al. Lumbar para-spinal muscle function, perception of lumbar position, andpostural control in disc herniation-related back pain. Spine(Phila Pa 1976). 2003;28(8):842-848.

57. Chan ST, Fung PK, Ng NY, et al. Dynamic changes of elasticity,cross-sectional area, and fat infiltration of multifidus atdifferent postures in men with chronic low back pain. SpineJ. 2012;12(5):381-388.

58. Kalichman L, Hodges P, Li L, Guermazi A, Hunter DJ. Changesin paraspinal muscles and their association with low back painand spinal degeneration: CT study. Eur Spine J. 2010;19(7):1136-1144.

59. Silfies SP, Squillante D, Maurer P, Westcott S, Karduna AR. Trunkmuscle recruitment patterns in specific chronic low back painpopulations. Clin Biomech (Bristol, Avon). 2005;20(5):465-473.

60. Teichtahl AJ, Urquhart DM, Wang Y, et al. Physical inactivity isassociated with narrower lumbar intervertebral discs, high fatcontent of paraspinal muscles and low back pain and disability.Arthritis Res Ther. 2015;17:114.

61. Deyo RA, Weinstein JN. Low back pain. N Engl J Med. 2001;344(5):363-370.

62. Chou R, Qaseem A, Snow V, et al; Clinical Efficacy Assess-ment Subcommittee of the American College of Physicians;American College of Physicians; American Pain Society LowBack Pain Guidelines Panel. Diagnosis and treatment of lowback pain: a joint clinical practice guideline from the AmericanCollege of Physicians and the American Pain Society [pub-lished correction appears in Ann Intern Med. 2008 (Correction:Diagnosis and treatment of low back pain.)]. Ann Intern Med.2007;147(7):478-491.

63. Underwood M, Buchbinder R. Red flags for back pain. BMJ.2013;347:f7432.

64. Henschke N, Maher CG, Refshauge KM, et al. Prevalence ofand screening for serious spinal pathology in patients present-ing to primary care settings with acute low back pain. ArthritisRheum. 2009;60(10):3072-3080.

65. Downie A, Williams CM, Henschke N, et al. Red flags toscreen for malignancy and fracture in patients with low backpain: systematic review [published correction appears inBMJ. 2014;348:g7]. BMJ. 2013;347:f7095.

66. Williams CM, Henschke N, Maher CG, et al. Red flags toscreen for vertebral fracture in patients presenting with low-back pain. Cochrane Database Syst Rev. 2013;(1):CD008643.

67. Malik KM, Cohen SP, Walega DR, Benzon HT. Diagnosticcriteria and treatment of discogenic pain: a systematic reviewof recent clinical literature. Spine J. 2013;13(11):1675-1689.

68. Schwarzer AC, Aprill CN, Derby R, Fortin J, Kine G,Bogduk N. The prevalence and clinical features of internaldisc disruption in patients with chronic low back pain. Spine(Phila Pa 1976). 1995;20(17):1878-1883.

69. Depalma MJ, Ketchum JM, Trussell BS, Saullo TR,Slipman CW. Does the location of low back pain predict itssource? PM R. 2011;3(1):33-39.

70. Ohnmeiss DD, Vanharanta H, Ekholm J. Relation betweenpain location and disc pathology: a study of pain drawingsand CT/discography. Clin J Pain. 1999;15(3):210-217.

71. Schwarzer AC, Wang SC, Bogduk N, McNaught PJ, Laurent R.Prevalence and clinical features of lumbar zygapophysial jointpain: a study in an Australian population with chronic lowback pain. Ann Rheum Dis. 1995;54(2):100-106.

72. Schwarzer AC, Aprill CN, Derby R, Fortin J, Kine G,Bogduk N. Clinical features of patients with pain stemmingfrom the lumbar zygapophysial joints: is the lumbar facet syn-drome a clinical entity? Spine (Phila Pa 1976). 1994;19(10):1132-1137.

73. Laslett M, McDonald B, Aprill CN, Tropp H, Oberg B. Clinicalpredictors of screening lumbar zygapophyseal joint blocks:development of clinical prediction rules. Spine J. 2006;6(4):370-379.

74. Ianuzzi A, Little JS, Chiu JB, Baitner A, Kawchuk G, Khalsa PS.Human lumbar facet joint capsule strains: I. During physiolog-ical motions. Spine J. 2004;4(2):141-152.

75. Revel M, Poiraudeau S, Auleley GR, et al. Capacity of the clin-ical picture to characterize low back pain relieved by facetjoint anesthesia: proposed criteria to identify patients withpainful facet joints. Spine (Phila Pa 1976). 1998;23(18):1972-1976; discussion 1977.

76. Cohen SP, Hurley RW, Christo PJ, Winkley J, Mohiuddin MM,Stojanovic MP. Clinical predictors of success and failure forlumbar facet radiofrequency denervation. Clin J Pain. 2007;23(1):45-52.

77. Maigne JY, Aivaliklis A, Pfefer F. Results of sacroiliac joint dou-ble block and value of sacroiliac pain provocation tests in 54patients with low back pain. Spine (Phila Pa 1976). 1996;21(16):1889-1892.

78. Cohen SP, Chen Y, Neufeld NJ. Sacroiliac joint pain: acomprehensive review of epidemiology, diagnosis and treat-ment. Expert Rev Neurother. 2013;13(1):99-116.

79. Slipman CW, Jackson HB, Lipetz JS, Chan KT, Lenrow D,Vresilovic EJ. Sacroiliac joint pain referral zones. Arch PhysMed Rehabil. 2000;81(3):334-338.

80. Young S, Aprill C, Laslett M. Correlation of clinical examina-tion characteristics with three sources of chronic low backpain. Spine J. 2003;3(6):460-465.

81. Laslett M, Aprill CN, McDonald B, Young SB. Diagnosis ofsacroiliac joint pain: validity of individual provocation testsand composites of tests. Man Ther. 2005;10(3):207-218.

82. van der Wurff P, Buijs EJ, Groen GJ. A multitest regimen ofpain provocation tests as an aid to reduce unnecessary mini-mally invasive sacroiliac joint procedures. Arch Phys Med Reha-bil. 2006;87(1):10-14.

83. Szadek KM, van der Wurff P, van Tulder MW,Zuurmond WW, Perez RS. Diagnostic validity of criteria forsacroiliac joint pain: a systematic review. J Pain. 2009;10(4):354-368.

84. Michel F, Decavel P, Toussirot E, et al. Piriformis musclesyndrome: diagnostic criteria and treatment of a monocen-tric series of 250 patients. Ann Phys Rehabil Med. 2013;56(5):371-383.

85. Vora AJ, Doerr KD, Wolfer LR. Functional anatomy and path-ophysiology of axial low back pain: disc, posterior elements,sacroiliac joint, and associated pain generators. Phys MedRehabil Clin N Am. 2010;21(4):679-709.

86. Malanga GA, Cruz Colon EJ. Myofascial low back pain: a re-view. Phys Med Rehabil Clin N Am. 2010;21(4):711-724.

87. Leone A, Cianfoni A, Cerase A, Magarelli N, Bonomo L. Lum-bar spondylolysis: a review. Skeletal Radiol. 2011;40(6):683-700.

88. Koes BW, van Tulder MW, Peul WC. Diagnosis and treat-ment of sciatica. BMJ. 2007;334(7607):1313-1317.

89. Czyrny JJ, Lawrence J. The importance of paraspinal muscleEMG in cervical and lumbosacral radiculopathy: review of100 cases. Electromyogr Clin Neurophysiol. 1996;36(8):503-508.

LOW BACK PAIN


1715



90. Vroomen PC, de Krom MC, Knottnerus JA. Diagnostic valueof history and physical examination in patients suspected ofsciatica due to disc herniation: a systematic review. J Neurol.1999;246(10):899-906.

91. van der Windt DA, Simons E, Riphagen II, et al. Physical ex-amination for lumbar radiculopathy due to disc herniation inpatients with low-back pain. Cochrane Database Syst Rev.2010;(2):CD007431.

92. Gardner A, Gardner E, Morley T. Cauda equina syndrome: areview of the current clinical and medico-legal position. EurSpine J. 2011;20(5):690-697.

93. Katz JN, Dalgas M, Stucki G, et al. Degenerative lumbar spinalstenosis. Diagnostic value of the history and physical examina-tion. Arthritis Rheum. 1995;38(9):1236-1241.

94. Suri P, Rainville J, Kalichman L, Katz JN. Does this older adultwith lower extremity pain have the clinical syndrome of lum-bar spinal stenosis? JAMA. 2010;304(23):2628-2636.

95. Kobayashi S. Pathophysiology, diagnosis and treatment ofintermittent claudication in patients with lumbar canal steno-sis. World J Orthop. 2014;5(2):134-145.

96. Katz JN, Harris MB. Clinical practice: lumbar spinal stenosis.N Engl J Med. 2008;358(8):818-825.

97. Nadeau M, Rosas-Arellano MP, Gurr KR, et al. The reliabilityof differentiating neurogenic claudication from vascular claudi-cation based on symptomatic presentation. Can J Surg. 2013;56(6):372-377.

98. Bigos S, Bowyer O, Braen G, et al. Acute Low Back Problems inAdults. Rockville, MD: Agency for Health Care Policy andResearch, Public Health Service, US Dept of Health and Hu-man Services; December 1994. Clinical Practie Guidline No.14. AHCPR Publication No. 95-0642.

99. Deyo RA. Cascade effects of medical technology. Annu RevPublic Health. 2002;23:23-44.

100. Chou R, Fu R, Carrino JA, Deyo RA. Imaging strategies forlow-back pain: systematic review and meta-analysis. Lancet.2009;373(9662):463-472.

101. Jarvik JG, Gold LS, Comstock BA, et al. Association of earlyimaging for back pain with clinical outcomes in older adults[published corrections appear in JAMA. 2015 (Incorrect align-ment and omitted data in tables)]. JAMA. 2015;313(11):1143-1153.

102. Cohen SP, Gupta A, Strassels SA, et al. Effect of MRI on treat-ment results or decision making in patients with lumbosacralradiculopathy referred for epidural steroid injections: a multi-center, randomized controlled trial [published correction ap-pears in Arch Intern Med. 2012;172(8):673]. Arch Intern Med.2012;172(2):134-142.

103. Graves JM, Fulton-Kehoe D, Jarvik JG, Franklin GM. Healthcare utilization and costs associated with adherence to clinicalpractice guidelines for early magnetic resonance imagingamong workers with acute occupational low back pain. HealthServ Res. 2014;49(2):645-665.

104. Ash LM, Modic MT, Obuchowski NA, Ross JS, Brant-Zawadzki MN, Grooff PN. Effects of diagnostic information,per se, on patient outcomes in acute radiculopathy and lowback pain. AJNR Am J Neuroradiol. 2008;29(6):1098-1103.

105. Chou R, Qaseem A, Owens DK, Shekelle P; Clinical Guide-lines Committee of the American College of Physicians. Diag-nostic imaging for low back pain: advice for high-value healthcare from the American College of Physicians [publishedcorrection appears in Ann Intern Med. 2012;156(1, pt 1):71].Ann Intern Med. 2011;154(3):181-189.

106. Sandoval AE. Electrodiagnostics for low back pain. Phys MedRehabil Clin N Am. 2010;21(4):767-776.

107. Haig AJ, Geisser ME, Tong HC, et al. Electromyographic andmagnetic resonance imaging to predict lumbar stenosis, low-back pain, and no back symptoms. J Bone Joint Surg Am.2007;89(2):358-366.

108. Reza Soltani Z, Sajadi S, Tavana B. A comparison of magneticresonance imaging with electrodiagnostic findings in the

evaluation of clinical radiculopathy: a cross-sectional study.Eur Spine J. 2014;23(4):916-921.

109. Plastaras CT, Joshi AB. The electrodiagnostic evaluation ofradiculopathy. Phys Med Rehabil Clin N Am. 2011;22(1):59-74.

110. Mondelli M, Aretini A, Arrigucci U, Ginanneschi F,Greco G, Sicurelli F. Clinical findings and electrodiagnostictesting in 108 consecutive cases of lumbosacral radiculop-athy due to herniated disc. Neurophysiol Clin. 2013;43(4):205-215.

111. Plastaras CT. Electrodiagnostic challenges in the evaluation oflumbar spinal stenosis. Phys Med Rehabil Clin N Am. 2003;14(1):57-69.

112. Cohen SP, Hurley RW, Buckenmaier CC III, Kurihara C,Morlando B, Dragovich A. Randomized placebo-controlledstudy evaluating lateral branch radiofrequency denervationfor sacroiliac joint pain. Anesthesiology. 2008;109(2):279-288.

113. Cohen SP, Williams KA, Kurihara C, et al. Multicenter, ran-domized, comparative cost-effectiveness study comparing 0,1, and 2 diagnostic medial branch (facet joint nerve) blocktreatment paradigms before lumbar facet radiofrequencydenervation. Anesthesiology. 2010;113(2):395-405.

114. Provenzano DA. Diagnostic discography: what is the clinicalutility? Curr Pain Headache Rep. 2012;16(1):26-34.

115. Margetic P, Pavic R, Stancic MF. Provocative discographyscreening improves surgical outcome. Wien Klin Wochenschr.2013;125(19-20):600-610.

116. Yeom JS, Lee JW, Park KW, et al. Value of diagnostic lumbarselective nerve root block: a prospective controlled study.AJNR Am J Neuroradiol. 2008;29(5):1017-1023.

117. Kuijpers T, van Middelkoop M, Rubinstein SM, et al. A systematicreview on the effectiveness of pharmacological interventions forchronic non-specific low-back pain. Eur Spine J. 2011;20(1):40-50.

118. van Tulder MW, Touray T, Furlan AD, Solway S, Bouter LM;Cochrane Back Review Group. Muscle relaxants for nonspe-cific low back pain: a systematic review within the frameworkof the Cochrane collaboration. Spine (Phila Pa 1976). 2003;28(17):1978-1992.

119. Williamson OD, Sagman D, Bruins RH, Boulay LJ, Schacht A.Antidepressants in the treatment for chronic low back pain:questioning the validity of meta-analyses. Pain Pract. 2014;14(2):E33-E41.

120. Finnerup NB, Sindrup SH, Jensen TS. The evidence for phar-macological treatment of neuropathic pain. Pain. 2010;150(3):573-581.

121. Lasko B, Levitt RJ, Rainsford KD, Bouchard S, Rozova A,Robertson S. Extended-release tramadol/paracetamol inmoderate-to-severe pain: a randomized, placebo-controlledstudy in patients with acute low back pain. Curr Med ResOpin. 2012;28(5):847-857.

122. Biondi D, Xiang J, Benson C, Etropolski M, Moskovitz B,Rauschkolb C. Tapentadol immediate release versus oxyco-done immediate release for treatment of acute low backpain. Pain Physician. 2013;16(3):E237-E246.

123. Chaparro LE, Furlan AD, Deshpande A, Mailis-Gagnon A,Atlas S, Turk DC. Opioids compared to placebo or othertreatments for chronic low-back pain. Cochrane DatabaseSyst Rev. 2013;(8):CD004959.

124. Baron R, Freynhagen R, Tölle TR, et al; A0081007 Investiga-tors. The efficacy and safety of pregabalin in the treatmentof neuropathic pain associated with chronic lumbosacral rad-iculopathy. Pain. 2010;150(3):420-427.

125. Zhou M, Chen N, He L, Yang M, Zhu C, Wu F. Oxcarbaze-pine for neuropathic pain. Cochrane Database Syst Rev. 2013;(3):CD007963.

126. Khoromi S, Patsalides A, Parada S, Salehi V, Meegan JM,Max MB. Topiramate in chronic lumbar radicular pain. J Pain.2005;6(12):829-836.

127. O’Connor AB, Dworkin RH. Treatment of neuropathic pain:an overview of recent guidelines. Am J Med. 2009;122(10suppl):S22-S32.





128. Khoromi S, Cui L, Nackers L, Max MB. Morphine, nortriptylineand their combination vs. placebo in patients with chroniclumbar root pain. Pain. 2007;130(1-2):66-75.

129. Cawston H, Davie A, Paget MA, Skljarevski V, Happich M.Efficacy of duloxetine versus alternative oral therapies: an indi-rect comparison of randomised clinical trials in chronic lowback pain. Eur Spine J. 2013;22(9):1996-2009.

130. Urquhart DM, Zheng Y, Cheng AC, et al. Could low gradebacterial infection contribute to low back pain? A systematicreview. BMC Med. 2015;13:13.

131. Albert HB, Sorensen JS, Christensen BS, Manniche C. Antibi-otic treatment in patients with chronic low back pain andvertebral bone edema (Modic type 1 changes): a double-blind randomized clinical controlled trial of efficacy. Eur SpineJ. 2013;22(4):697-707.

132. Albert HB, Kjaer P, Jensen TS, Sorensen JS, Bendix T,Manniche C. Modic changes, possible causes and relation tolow back pain. Med Hypotheses. 2008;70(2):361-368.

133. Manchikanti L, Falco FJ, Singh V, et al. Utilization of interven-tional techniques in managing chronic pain in the Medicarepopulation: analysis of growth patterns from 2000 to 2011.Pain Physician. 2012;15(6):E969-E982.

134. Deyo RA, Mirza SK, Turner JA, Martin BI. Overtreating chronicback pain: time to back off? J Am Board Fam Med. 2009;22(1):62-68.

135. Hansen H, Manchikanti L, Simopoulos TT, et al. A systematicevaluation of the therapeutic effectiveness of sacroiliac jointinterventions. Pain Physician. 2012;15(3):E247-E278.

136. Khot A, Bowditch M, Powell J, Sharp D. The use of intradiscalsteroid therapy for lumbar spinal discogenic pain: a random-ized controlled trial. Spine (Phila Pa 1976). 2004;29(8):833-836; discussion 837.

137. Simmons JW, McMillin JN, Emery SF, Kimmich SJ. Intradiscalsteroids: a prospective double-blind clinical trial. Spine (PhilaPa 1976). 1992;17(6 suppl):S172-S175.

138. Cohen SP, Wenzell D, Hurley RW, et al. A double-blind,placebo-controlled, dose-response pilot study evaluating intra-discal etanercept in patients with chronic discogenic low backpain or lumbosacral radiculopathy. Anesthesiology. 2007;107(1):99-105.

139. Peng B, Pang X, Wu Y, Zhao C, Song X. A randomizedplacebo-controlled trial of intradiscal methylene blue injectionfor the treatment of chronic discogenic low back pain. Pain.2010;149(1):124-129.

140. Gupta G, Radhakrishna M, Chankowsky J, Asenjo JF. Methy-lene blue in the treatment of discogenic low back pain. PainPhysician. 2012;15(4):333-338.

141. Kim SH, Ahn SH, Cho YW, Lee DG. Effect of intradiscalmethylene blue injection for the chronic discogenic lowback pain: one year prospective follow-up study. Ann RehabilMed. 2012;36(5):657-664.

142. Pauza KJ, Howell S, Dreyfuss P, Peloza JH, Dawson K,Bogduk N. A randomized, placebo-controlled trial of intradis-cal electrothermal therapy for the treatment of discogenic lowback pain. Spine J. 2004;4(1):27-35.

143. Freeman BJ, Fraser RD, Cain CM, Hall DJ, Chapple DC.A randomized, double-blind, controlled trial: intradiscal elec-trothermal therapy versus placebo for the treatment ofchronic discogenic low back pain. Spine (Phila Pa 1976).2005;30(21):2369-2377; discussion 2378.

144. Kvarstein G, Måwe L, Indahl A, et al. A randomized double-blindcontrolled trial of intra-annular radiofrequency thermal disctherapyda 12-month follow-up. Pain. 2009;145(3):279-286.

145. Freedman BA, Cohen SP, Kuklo TR, Lehman RA, Larkin P,Giuliani JR. Intradiscal electrothermal therapy (IDET) forchronic low back pain in active-duty soldiers: 2-year follow-up. Spine J. 2003;3(6):502-509.

146. Kapural L, Vrooman B, Sarwar S, et al. Radiofrequency intradis-cal biacuplasty for treatment of discogenic lower back pain: a12-month follow-up. Pain Med. 2015;16(3):425-431.

147. Waseem Z, Boulias C, Gordon A, Ismail F, Sheean G,Furlan AD. Botulinum toxin injections for low-back painand sciatica. Cochrane Database Syst Rev. 2011;(1):CD008257.

148. Staal JB, de Bie RA, de Vet HC, Hildebrandt J, Nelemans P. In-jection therapy for subacute and chronic low back pain: anupdated Cochrane review. Spine (Phila Pa 1976). 2009;34(1):49-59.

149. Jamison RN, VadeBoncouer T, Ferrante FM. Low back painpatients unresponsive to an epidural steroid injection: identi-fying predictive factors. Clin J Pain. 1991;7(4):311-317.

150. Hopwood MB, Abram SE. Factors associated with failure oflumbar epidural steroids. Reg Anesth. 1993;18(4):238-243.

151. Kirpalani D, Mitra R. Is chronic opioid use a negative predictivefactor for response to cervical epidural steroid injections?J Back Musculoskelet Rehabil. 2011;24(3):123-127.

152. Bicket MC, Horowitz JM, Benzon HT, Cohen SP. Epidural in-jections in prevention of surgery for spinal pain: systematic re-view and meta-analysis of randomized controlled trials. Spine J.2015;15(2):348-362.

153. Riew KD, Park JB, Cho YS, et al. Nerve root blocks in thetreatment of lumbar radicular pain: a minimum five-yearfollow-up. J Bone Joint Surg Am. 2006;88(8):1722-1725.

154. Atluri S, Glaser SE, Shah RV, Sudarshan G. Needle positionanalysis in cases of paralysis from transforaminal epidurals:consider alternative approaches to traditional technique. PainPhysician. 2013;16(4):321-334.

155. Cohen SP, White RL, Kurihara C, et al. Epidural steroids, eta-nercept, or saline in subacute sciatica: a multicenter, random-ized trial. Ann Intern Med. 2012;156(8):551-559.

156. Ohtori S, Miyagi M, Eguchi Y, et al. Epidural administration ofspinal nerves with the tumor necrosis factor-alpha inhibitor,etanercept, compared with dexamethasone for treatmentof sciatica in patients with lumbar spinal stenosis: a prospec-tive randomized study. Spine (Phila Pa 1976). 2012;37(6):439-444.

157. Freeman BJ, LudbrookGL, Hall S, et al. Randomized, double-blind,placebo-controlled, trial of transforaminal epidural etanercept forthe treatment of symptomatic lumbar disc herniation. Spine (PhilaPa 1976). 2013;38(23):1986-1994.

158. Searle A, Spink M, Ho A, Chuter V. Exercise interventions forthe treatment of chronic low back pain: a systematic reviewand meta-analysis of randomised controlled trials [publishedonline ahead of print February 13, 2015]. Clin Rehabil. doi:10.1177/0269215515570379.

159. Lawford BJ, Walters J, Ferrar K. Does walking improve disabilitystatus, function, or quality of life in adults with chronic lowback pain? A systematic review [published online ahead of printJune 18, 2015]. Clin Rehabil. doi:10.1177/0269215515590487.

160. Cramer H, Lauche R, Haller H, Dobos G. A systematic reviewand meta-analysis of yoga for low back pain. Clin J Pain. 2013;29(5):450-460.

161. Wells C, Kolt GS, Marshall P, Hill B, Bialocerkowski A. Theeffectiveness of Pilates exercise in people with chroniclow back pain: a systematic review. PLoS One. 2014;9(7):e100402.

162. Slade SC, Patel S, Underwood M, Keating JL. What are patientbeliefs and perceptions about exercise for nonspecific chroniclow back pain? A systematic review of qualitative studies. Clin JPain. 2014;30(11):995-1005.

163. Furlan AD, Imamura M, Dryden T, Irvin E. Massage for lowback pain: an updated systematic review within the frameworkof the Cochrane Back Review Group. Spine (Phila Pa 1976).2009;34(16):1669-1684.

164. Lam M, Galvin R, Curry P. Effectiveness of acupuncture fornonspecific chronic low back pain: a systematic review andmeta-analysis. Spine (Phila Pa 1976). 2013;38(24):2124-2138.

165. Ebadi S, Henschke N, Nakhostin Ansari N, Fallah E, vanTulder MW. Therapeutic ultrasound for chronic low-backpain. Cochrane Database Syst Rev. 2014;(3):CD009169.

LOW BACK PAIN


1717

http://10.1177/0269215515570379

http://10.1177/0269215515590487



166. Franke H, Franke JD, Fryer G. Osteopathic manipulative treat-ment for nonspecific low back pain: a systematic review andmeta-analysis. BMC Musculoskelet Disord. 2014;15:286.

167. Franke H, Fryer G, Ostelo RW, Kamper SJ. Muscle energytechnique for non-specific low-back pain. Cochrane DatabaseSyst Rev. 2015;(2):CD009852.

168. Kizhakkeveettil A, Rose K, Kadar GE. Integrative therapies for lowback pain that include complementary and alternative medicinecare: a systematic review. Glob Adv Health Med. 2014;3(5):49-64.

169. Rubinstein SM, van Middelkoop M, Kuijpers T, et al.A systematic review on the effectiveness of complementaryand alternative medicine for chronic non-specific low-backpain. Eur Spine J. 2010;19(8):1213-1228.

170. Khadilkar A, Odebiyi DO, Brosseau L, Wells GA. Transcuta-neous electrical nerve stimulation (TENS) versus placebo forchronic low-back pain. Cochrane Database Syst Rev. 2008;(4):CD003008.

171. Dubinsky RM, Miyasaki J. Assessment: efficacy of transcutaneouselectric nerve stimulation in the treatment of pain in neurologicdisorders (an evidence-based review): report of the Therapeu-tics and Technology Assessment Subcommittee of the Amer-ican Academy of Neurology. Neurology. 2010;74(2):173-176.

172. Snelgrove S, Liossi C. Living with chronic low back pain: ametasynthesis of qualitative research. Chronic Illn. 2013;9(4):283-301.

173. Kamper SJ, Apeldoorn AT, Chiarotto A, et al. Multidisciplinarybiopsychosocial rehabilitation for chronic low back pain.Cochrane Database Syst Rev. 2014;(9):CD000963.

174. Henschke N, Ostelo RW, van Tulder MW, et al. Behaviouraltreatment for chronic low-back pain. Cochrane Database SystRev. 2010;(7):CD002014.

175. Cramer H, Haller H, Lauche R, Dobos G. Mindfulness-basedstress reduction for low back pain: a systematic review. BMCComplement Altern Med. 2012;12:162.

176. Pannell WC, Savin DD, Scott TP, Wang JC, Daubs MD.Trends in the surgical treatment of lumbar spine disease inthe United States. Spine J. 2015;15(8):1719-1727.

177. Mroz TE, Lubelski D, Williams SK, et al. Differences in the sur-gical treatment of recurrent lumbar disc herniation amongspine surgeons in the United States. Spine J. 2014;14(10):2334-2343.

178. Jacobs WC, van Tulder M, Arts M, et al. Surgery versus con-servative management of sciatica due to a lumbar herniateddisc: a systematic review. Eur Spine J. 2011;20(4):513-522.

179. Kovacs FM, Urrútia G, Alarcón JD. Surgery versus conservativetreatment for symptomatic lumbar spinal stenosis: a systematicreview of randomized controlled trials. Spine (Phila Pa 1976).2011;36(20):E1335-E1351.

180. Chou R, Baisden J, Carragee EJ, Resnick DK, Shaffer WO,Loeser JD. Surgery for low back pain: a review of the evidencefor an American Pain Society Clinical Practice Guideline. Spine(Phila Pa 1976). 2009;34(10):1094-1109.

181. Machado GC, Ferreira PH, Harris IA, et al. Effectiveness of sur-gery for lumbar spinal stenosis: a systematic review and meta-analysis. PLoS One. 2015;10(3):e0122800.

182. Ibrahim T, Tleyjeh IM, Gabbar O. Surgical versus non-surgical treatment of chronic low back pain: a meta-analysis of randomised trials [published correction appearsin Int Orthop. 2009;33(2):589-590]. Int Orthop. 2008;32(1):107-113.

183. Mirza SK, Deyo RA. Systematic review of randomized trialscomparing lumbar fusion surgery to nonoperative care fortreatment of chronic back pain. Spine (Phila Pa 1976). 2007;32(7):816-823.

184. Wei J, Song Y, Sun L, Lv C. Comparison of artificial total discreplacement versus fusion for lumbar degenerative disc dis-ease: a meta-analysis of randomized controlled trials. IntOrthop. 2013;37(7):1315-1325.

185. Hellum C, Johnsen LG, Storheim K, et al. Surgery with discprosthesis versus rehabilitation in patients with low backpain and degenerative disc: two year follow-up of randomisedstudy. BMJ. 2011;342:d2786.

186. Pope JE, Falowski S, Deer TR. Advanced waveforms and fre-quency with spinal cord stimulation: burst and high-frequency energy delivery. Expert Rev Med Devices. 2015;12(4):431-437.

187. Deer TR, Mekhail N, Provenzano D, et al; NeuromodulationAppropriateness Consensus Committee. The appropriate useof neurostimulation of the spinal cord and peripheral nervoussystem for the treatment of chronic pain and ischemic dis-eases: the Neuromodulation Appropriateness ConsensusCommittee. Neuromodulation. 2014;17(6):515-550; discussion550.

188. Kapural L, Yu C, Doust MW, et al. Novel 10-kHz high-frequency therapy (HF10 Therapy) Is Superior to traditionallow-frequency spinal cord stimulation for the treatment ofchronic back and leg pain: The SENZA-RCT randomizedcontrolled trial. Anesthesiology. 2015;123(4):851-860.

189. Prager J, Deer T, Levy R, et al. Best practices for intrathecaldrug delivery for pain. Neuromodulation. 2014;17(4):354-372;discussion 372.

190. Deer TR, Prager J, Levy R, et al. Polyanalgesic Consensus Con-ference 2012: recommendations for the management of painby intrathecal (intraspinal) drug delivery: report of an interdis-ciplinary expert panel. Neuromodulation. 2012;15(5):436-464;discussion 464-466.





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