Volume 1996, Article 5

December 1996

The MIT Press

Journal of

ContemporaryNeurology

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2 Contemporary Neurology Volume 1996, Number 5

IntroductionLow back pain is extremely common and has major economic signifi-cance in industrial societies. It is reported to occur in 26% of the work-ing population each year and occurs to a disabling degree in 2 to 8%.Eighty percent of the population have at least one episode of low backpain in their lifetimes. It is the fifth leading reason for medical office vis-its in the United States. Low-back injury compensation accounts for33% of all workers compensation costs (1/3 for medical treatment, 2/3for indemnity). Seventy-five percent of compensation payments go toback patients, although they constitute only 3% of total compensationpatients (Klein et al, 1984; Hart et al, 1995).

Low back pain occurs most frequently between the ages of twentyand forty and is more severe in older patients. There is no strong asso-ciation based on sex, height, body weight, or physical fitness. High-riskoccupations include miscellaneous labor, garbage collection, warehousework, and nursing, all of which are usually associated with lifting,twisting, bending, and reaching.

PrognosisThe typical attack involves 35 days (median) of pain and 9 to 21 daysout of work. Those who are out of work longer than 6 months haveonly a 50% likelihood of returning. This drops to 25% after more than1 year out and to nil after 2 years. After an initial episode, the probabil-ity of recurrence is increased fourfold. Treatment tends to be less suc-cessful in workers compensation cases. The average cost for care is 4.5times greater if the patient is represented by an attorney.

ClassificationLow back pain is an important part of neurologic and general medicalpractice. Of all office visits for back pain, 56% are to family practitionersand internists, 25% are to orthopedic surgeons, 7% are to neuro-surgeons, and 4% are to neurologists. These patients make up 10% ofthe average neurologists caseload (Hart et al, 1995). The neurologist isusually called upon to evaluate and treat the patient with acute or sub-acute pain and symptoms and signs of nerve-root irritationradiatingpain, weakness, numbness, and bladder or bowel symptoms. Such pa-tients make up a small minority of those with low back pain. In many ofthese cases, the neurologist is also asked to assess the presence and de-gree of impairment (physical defect) and disability (what the patient canor cant do as a result of this defect) (AMA, 1993).

There are a multitude of causes of low back pain. Even when there isevidence of nerve-root involvement (radiculopathy), not every patienthas a herniated lumbar disc. The classifications outlined in Table 1 maybe helpful in the differential diagnosis.

N E U R O L O G Y I N P R A C T I C E

Neurologic Approachto Diagnosis of Low Back Pain

James R. Lehrich, MDHarvard Medical School

Key words: back pain, pain, lumbarspine, lumbar disks

Address reprint requests and correspondenceto Harvard Medical School, MassachusettsGeneral Hospital Neurology Department,Massachusetts General Hospital, 15 ParkmanStreet, WAU-828, Boston, MA 02114

1996 Massachusetts Institute of Technology

Volume 1996, Number 5 Lehrich 3

Clinical EvaluationAs for any neurologic patient, the general physicaland neurologic examinations and history are essen-tial. This discussion will emphasize areas of specialconcern in the evaluation of back pain.

HistoryParticular note should be made of any precedingtrauma, prior attacks of pain, prior evaluations, prioror current treatment, and the duration and progres-sion of symptoms. The patient should be asked aboutweakness; numbness; dysesthesias and paresthesias;bladder, bowel, and sexual dysfunction; and any ac-companying abdominal or flank pain.

PainInquire as to the quality, location, and radiation ofpain, and any exacerbating or relieving factors andactivities. Severe, constant back pain persisting atnight suggests the presence of neoplasm, infection,or lateral recess nerve-root compression. Pain fibersare present in the annulus surrounding the disc (inthe spinal ligaments, facets, and joint capsules) butnot in the intervertebral disc itself. Nerve-root pain isusually brief, sharp, and shooting, is often increasedby coughing, straining, standing, or sitting, and isusually relieved by lying down.

Peripheral-nerve or plexus pain is usually de-scribed as burning, tingling (pins and needles), orasleep or numb in quality; it is usually worse whenthe patient is lying down at night. (See Table 2.) Inpainful radiculopathies and mononeuropathies, thearea of pain and sensory abnormality may extend be-yond the known sensory distribution of the affectedperipheral nerve or beyond the dermatome of the af-fected-root or dorsal-root ganglion, as in postherpeticneuralgia. This phenomenon has been attributed tocentral nervous system plasticity. In most nerve-rootsyndromes, however, a precise description of radiat-ing pain will help localize to a nerve-root level.

Physical ExaminationThe general physical examination can be as impor-tant as the neurologic examination and should in-clude the vasculature (especially the pedal pulses),abdomen, inguinal areas, and rectum (especially if acauda equina syndrome is suspected). The patientshould be undressed.

Watch how the patient moves, sits, and stands.Look for atrophy (measure the calf and thigh cir-cumferences for asymmetry), fasciculations, pelvictilt (bad side is down), involuntary knee flexion (toguard against root traction), scoliosis, and cafe au laitspots (they might indicate neurofibromatosis). Gaittesting should include walking on heels and on toes.

Table 1 Causes of Low Back Pain

Radicularevidence of nerve-root involvement

Intraspinal causes:

Proximal to the disc (conus and cauda equina)neu-rofibroma, ependymoma, meningioma

Disc levelherniated intervertebral disc, spinal steno-sis (canal or lateral recess), synovial cyst of facet joint

Vasculararteriovenous malformation (AVM) of spinalcord, spinal dural AV fistula

Extraspinal causes:

Pelvicvascular, gynecological (endometriosis), sacro-iliac joint, retroperitoneal neoplasms affecting the lum-bosacral plexus, lumbosacral plexitis

Peripheral nervemononeuropathy, polyneuropathy(diabetic and other), trauma, local neoplasm, herpeszoster (shingles)

Nonradicularno evidence of nerve-root involvement

Traumatic causes:

musculoskeletal strain, vertebral-compression fracture,transverse-process fracture

Chronic or subacute causes:

spondylosis and degenerative disc disease, spondylolis-thesis, sacroiliac joint disease, muscular (chronic andrepeated strains), deconditioning, postural,fibromyalgia

Nonmechanical causes:

Referred painabdominal or retroperitoneal (e.g., ab-dominal aortic aneurysm, pancreatic disease, en-dometriosis)

Infectionbone, disc, epidural, urinary tract (espe-cially in women)

Neoplasm of vertebrae or epidural spacemetastatictumor, multiple myeloma, primary bone tumor

Rheumatologic diseaseankylosing spondylitis, degen-erative disease, and other arthritides

Miscellaneous metabolic and vascularosteopeniawith compression fracture, Pagets disease, etc.

Psychogenic

Adapted from Macnab and McCullock, 1990.

Palpate the lower spine, paraspinal muscles, sciaticnotches, and sciatic nerve looking for tenderness,muscle spasms, and radiating pain. Muscle tender-ness may be associated with nerve-root irritation(calf muscles with S1, anterior tibial muscles withL5, and quadriceps with L4).

Nerve Root StretchingRoots may be impinged upon or tethered by herni-ated discs or other lesions, so that stretching the rootcauses pain. This should be tested by having the pa-tient bend forward or by straight-leg raising (SLR).

4 Contemporary Neurology Volume 1996, Number 5

SLR is performed by raising the extended leg of a su-pine patient to determine whether this action elicitspain in the leg, buttock, or back, and, if so, at whatangle from the horizontal the pain occurs. The painis usually worsened by dorsiflexion at the ankle andrelieved by flexion of the knee and hip. Positive SLRresults usually indicate S1 or L5 root irritation. Painoccuring in the contralateral, symptomatic leg whenthe asymptomatic leg is raised is considered a posi-tive crossed SLR test, which usually indicates thepresence of a disc herniation medial to the nerveroot, often with an extruded disc fragment. ReverseSLR tests detect L3 or L4 root irritation. The patientlies prone or on his side, and the thigh is extended atthe hip joint. If the patient has hip or groin pain, theexaminer should rotate the hip; pain on hip rotationsuggests hip disease rather than radiculopathy.

Motor ExaminationIt is helpful to bear in mind certain features of themotor examination of the lower extremities in pa-tients with low back pain. Since it is difficult to de-tect proximal leg weakness when the patient is lyingdown, it may be necessary to ask her to attempt torise from a squatting position. Similarly, gastrocne-mius weakness is easiest to detect with repeated ris-ing up on the toes. Toe flexors and extensors usuallybecome weak before the foot muscles do. If the glu-teus maximus (supplied by S1) is weak, one buttockmay sag; gluteus medius (L5) weakness may cause alurching or waddling (Trendelenburg) gait. In a pa-tient with root pain, do not test the dorsiflexors ofthe foot with the knee extended, since this maystretch the S1 or L5 root and increase sciatic pain.For the same reason, quadriceps strength should betested with the patient prone. Muscles are inner-vated by more than one nerve root, so total paralysisimplies a lesion of multiple roots or of peripheralnerves. Even if a single root has been severed, thereis little weakness. Atrophy is rarely seen unlesssymptoms have been present for more than threeweeks. Severe atrophy should raise the suspicion ofan extradural neoplasm.

Sensory ExaminationA dermatomal distribution of loss of pinprick andtouch sensation indicates and localizes root involve-ment (Figure 1). Because there is a wide overlap ofroot distributions, a single root lesion usually causesmild hypalgesia. The examiner may not be able todetect any sensory deficit, even though the patienthas sensory symptoms.

Tendon reflexesAsymmetry of the ankle and knee jerks can be help-ful in identifying the affected nerve root.

Nerve-Root SyndromesIn S1 nerve-root syndromes (see Table 3), leg pain isoften worse than low back pain. Pain and paresthes-ias are felt in the buttock, posterior thigh, posterolat-eral calf and heel, and sometimes in the lateral footand last two toes. Numbness and pinprick hypalgesiamay be in the fifth toe and lateral foot, and, to alesser degree, in the posterolateral calf and postero-lateral thigh. There may be weakness of the toe flex-ors, the gastrocnemius, and (rarely) the hamstrings aswell as toe adbuction and eversion of the foot. Theankle jerk is often diminished or absent.

In L5 nerve-root syndrome, low back pain is oftenworse than leg pain. Pain and paresthesias radiate tothe posterolateral thigh, groin, lateral calf, dorsomed-ial foot, and first two toes. Numbness and hypalgesiamay be found in the great toe and medial foot, and,to a lesser extent, the anterolateral calf. Weaknessmay be noted in the extensor hallucis longus (EHL),the tibialis anterior (TA), and peroneal muscles, caus-ing a foot drop. There is usually no reflex loss.

In L4 and L3 nerve-root syndromes, low back painis worse than leg pain. There may be some anteriorthigh pain. Numbness and hypalgesia may be presentover the anteromedial thigh and knee. Weaknessmay be detected in the quadriceps and iliopsoasmuscles. The knee jerk is often diminished or absent.

InconsistenciesSince some patients with back pain may exaggeratetheir symptoms, especially in medicolegal or workerscompensation cases, it is important to detect inconsis-tencies in the clinical presentation (Macnab andMcCullock, 1990; Waddell et al, 1980). The historymay indicate that the patient is able to engage inactivities inconsistent with the severity of his com-plaints. Symptoms may be described in an exaggeratedor histrionic manner. During the examination, tender-ness may be elicited by minimal pressure or over areaswhere pain would not be expected. Axial loading, bypressing down on top of the head, or rotating the bodyat the hips or shoulders should not elicit low back

Table 2 Root Pain and Peripheral Nerve Pain

Root Pain Peripheral Nerve Pain

Duration Brief Continual

Quality Sharp, shooting Burning, asleep,numb

Worse with Coughing, straining, Lying in bed atstanding, sitting night

Relieved bylying down Yes No

Volume 1996, Number 5 Lehrich 5

Figure 1 Dermatomal and peripheral nerve sensory distributions (from Keegan, JJ, Garrett, FD. Anat. Rec. 102:411, 1948; andHaymaker, W, Woodhall, B. Peripheral Nerve Injuries. 2d ed. Philadelphia. Saunders. 1953).

Table 3 Nerve-Root Syndromes

Pain and Motor ReflexRoot Paresthesias Hypesthesia Disturbance Loss Stretch

S1 Buttock, post. Lat. foot, 4th and 5th Toe flexors, Ankle SLR

thigh, postlat. toes, (sometimes) gastrocnemius, jerk

calf, heel, lat. postlat. calf and (rarely) hamstrings

foot, 4th and 5th toes. post. thigh and toe

Leg pain worse abductors

than back pain

L5 Postlat. thigh, First toe, EHL, TA, None SLR

groin, lat. calf, medial foot, peroneii

dorsomed. foot, anterolat. calf (foot drop)

first 2 toes.

Back pain worse

than leg pain

L4 Anteromed. thigh, Anteromed. thigh, Quadriceps, Knee Reverse

L3 anteromed. shin. knee iliopsoas jerk SLRBack pain worsethan leg pain

6 Contemporary Neurology Volume 1996, Number 5

pain. It may be helpful to distract the patient, to seewhether there is more mobility in spontaneous activi-ties than elicited during the formal examination. Thepatient may be observed during dressing (especiallyshoes and socks) and getting on and off the examina-tion table. Straight-leg raising (SLR) should be testedwhen she is in a sitting position (e.g., while testing theplantar responses or measuring the calf circumfer-ences) as well as when supine. There should be no sig-nificant difference in the degree of hip flexion withsitting or supine SLR or when the patient bends for-ward while standing. Nondermatomal or otherwisenonanatomic distributions of sensory loss should alsobe noted. In the motor examination, sudden givingway, jerky movements, or weakness appearing to in-volve many muscle groups should raise suspicion.Note whether the patient appears to overreact duringthe examination, including what appears to be a dis-proportionate verbalization of pain on minimal provo-cation, dramatic facial expressions, muscle tension andtremors, collapsing when asked to bear weight, andrequiring a companion for dressing and undressing.These observations must be considered in the contextof the overall examination. Severe pain can cause ex-treme reactions in some patients.

Laboratory EvaluationLaboratory tests are not necessary in every patient.They are important to verify the diagnosis if surgeryis contemplated and are sometimes necessary toclarify the differential diagnosis. Since X rays, CT andMRI scans, myelograms, and other tests may be ab-normal in asymptomatic patients, the results must beinterpreted with the entire clinical presentation inmind. Some guidelines are outlined in Table 4. (For adetailed discussion, see Laboratory Evaluation ofLow Back Pain in this issue.)

ManagementMost patients with back pain will respond to conser-vative treatment. Guidelines appropriate to the pri-mary care physician as well as to the neurologist areoutlined in Table 5. (For a more detailed discussion,see Management of Low Back Pain in this issue.)

Table 4 Laboratory Evaluation of Low Back Pain

Symptoms Laboratory Tests Indicated

Pain is chronic, incompletely ESR, Glucose, IEP, PSA,relieved by lying down, or Urine Bence-Jones proteins,constant nocturnal LS spine X rays, possible

or bone scan

Patient is more than sixty yearsof age, has unexplained weightloss, or has a history of cancer(situations in which myelomaor other neoplasms should beof concern)

Motor, bladder, bowel, or MRI (contrast-enhanced ifsexual-function deficits there has been prior back

surgery) or CT*

History suggestive of lumbar MRI or CT *spinal stenosis

Patient has had a fusion, Flexion-extensionand instability might be LS spine X rayscausing pain

Surgery is being considered Lumbar myelogram, CT(especially in cases of spinalcanal stenosis, lateral recessstenosis, multiple abnormaldiscs, or possible neoplasm)

*See Miller et al, 1989.

Table 5 Management Guidelines

Moderate pain; Pain medications, muscleno neurologic deficit or relaxants, heat, backmild to moderate deficit precautions; neurology

consultation, if deficit;follow-up examination in 2weeks, if deficit; if symptomsimprove, refer to physicaltherapy (back exercises, backschool), or back exercises athome

Severe pain; Bed rest up to 10 daysno neurological deficit or (depending on pain severitymild to moderate deficit and response to rest),

pain medications, musclerelaxants, heat; neurologyconsultation, if deficit;Follow-up examination in 2weeks, if deficit; if symptomsimprove, physical therapy orhome exercises

Severe deficit (neurologic, Neurology or neurosurgerybladder, bowel, sexual) consultation and MRI on an

urgent basis; if a large-massor lesion is found, refer to a

neurosurgeon or orthopedicsurgeon

Increasing neurologic Neurology consultation; MRI ordeficit; severe pain not CT; if large-mass lesion found,improved by 1+ week refer to neurosurgeon orof bed rest orthopedic surgeon; if no large

lesion, up to one more week ofbed rest, then refer to physicaltherapy or home exercises

No improvement or MRI or CT if not already done;incomplete improvement consider referral to neurologist,after bed rest, gradual neurosurgeon, or orthopedicambulation, physical surgeon; consider epiduraltherapy, and home steroidsexercises

Volume 1996, Number 5 Lehrich 7

ReferencesKlein BP, Jensen RC, Sanderson LM: Assessment of

workerscompensation claims for back strains/sprains.J Occup Med 26:443, 1984.

Hart LG, Deyo RA, Cherkin DC: Physician office visits forlow back pain. Frequency, clinical evaluation, andtreatment patterns from a US National Survey. Spine20:11, 1995.

American Medical Association. Guides to the evaluation ofpermanent impairment, 4th ed. Chicago: AMA, 1993.

Macnab I, McCullock J: Backache, 2nd ed. Baltimore: Wil-liams and Wilkins, 1990.

Waddell G, McCulloch JA, Kumel EG, et al: Nonorganicsigns in low back pain. Spine 5:117, 1980.

Miller GM, Forbes GS, Onofrio BM. Magnetic resonanceimaging of the spine. Mayo Clin Proc 64:986, 1989.

8 Contemporary Neurology Volume 1996, Number 5

Journal of Contemporary Neurology is a peer-reviewed and electronically pub-lished scholarly journal that covers a broad scope of topics encompassingclinical and basic topics of human neurology, neurosciences and related fields.

EditorKeith H. Chiappa, M.D.

Associate EditorDidier Cros, M.D.

Electronic Mailchiappa@helix.mgh.harvard.edu

Editorial Board

Robert AckermanMassachusetts General Hospital, Boston

Barry ArnasonUniversity of Chicago

Flint BealMassachusetts General Hospital, Boston

James BernatDartmouth-Hitchcock Medical Center,New Hampshire

Julien BogousslavskyCHU Vaudois, Lausanne

Robert BrownMassachusetts General Hospital, Boston

David BurkePrince of Wales Medical Research Institute, Sydney

David CaplanMassachusetts General Hospital, Boston

Gregory CascinoMayo Clinic, Rochester

Phillip ChanceThe Childrens Hospital of Philadelphia, Philadelphia

Thomas ChaseNINDS, National Institutes of Health, Bethesda

David CornblathJohns Hopkins Hospital, Baltimore

F. Michael CutrerMassachusetts General Hospital, Boston

David DawsonBrockton VA Medical Center, Massachusetts

Paul DelwaideHpital de la Citadelle, Liege

John DonoghueBrown University, Providence

Richard FrithAuckland Hospital, New Zealand

Myron GinsbergUniversity of Miami School of Medicine

Douglas GoodinUniversity of California, San Francisco

James GrottaUniversity of Texas Medical School, Houston

James GusellaMassachusetts General Hospital, Boston

John HalperinNorth Shore University Hospital / CornellUniversity Medical College

Stephen HauserUniversity of California, San Francisco

E. Tessa Hedley-WhiteMassachusetts General Hospital, Boston

Kenneth HeilmanUniversity of Florida, Gainesville

Daniel HochMassachusetts General Hospital, Boston

Fred HochbergMassachusetts General Hospital, Boston

John HoffmanEmory University, Atlanta

Gregory HolmesChildrens Hospital Boston

Bruce JenkinsMassachusetts General Hospital, Boston

Ryuji KajiKyoto University Hospital

Carlos KaseBoston University School of Medicine, Boston

J. Philip KistlerMassachusetts General Hospital, Boston

Jean-Marc LgerLa Salptrire, Paris

Simmons LessellMassachusetts Eye and Ear Infirmary, Boston

Ronald LesserJohns Hopkins Hospital, Baltimore

David LevineNew York University Medical Center

Ira LottUniversity of California, Irvine

Phillip LowMayo Clinic, Rochester

Richard MacdonellAustin Hospital, Victoria, Australia

Joseph MasdeuSt. Vincents Hospital, New York

Kerry R. MillsRadcliffe Infirmary, Oxford

Jos OchoaGood Samaritan Hospital, Portland

Barry OkenOregon Health Sciences University, Portland

John PenneyMassachusetts General Hospital, Boston

Karlheinz ReinersBayerische Julius-Maximilians-Universitt, Wurzburg

Allen RosesDuke University Medical Center, Durham

Thomas SabinBoston City Hospital, Boston

Raman SankarUniversity of California at Los Angeles

Joan SantamariaHospital Clinic Provincial de Barcelona

Kenneth TylerUniversity of Colorado Health Science Center, Denver

Francois VialletCH Aix-en-Provence

Joseph VolpeChildrens Hospital, Boston

Michael WallUniversity of Iowa, Iowa City

Stephen WaxmanYale University, New Haven

Wigbert WiederholtUniversity of California, San Diego

Eelco WijdicksMayo Clinic, Rochester

Clayton WileyUniversity of California, San Diego

Anthony WindebankMayo Clinic, Rochester

Shirley WrayMassachusetts General Hospital, Boston

Anne YoungMassachusetts General Hospital, Boston

Robert YoungUniversity of California, Irvine