47 - Low Back Pain

47
Low Back Pain
RAJIV DIXIT
KEY POINTS
Up to 80% of the population will experience low back pain
(LBP), and degenerative changes of the lumbar spine is the
most common cause.
More than 90% of these patients are largely pain free within
8 weeks.
Initial evaluation should identify the few patients with
neurologic involvement or suspicion of systemic disease
(infection, malignancy, or spondyloarthritis) because they
may need urgent or specific intervention.
Psychosocial and other factors that predict risk of chronic
disabling LBP should be assessed.
Imaging is rarely indicated in the absence of significant
neurologic involvement or suspicion of systemic disease.
Imaging abnormalities should be carefully interpreted
because they are frequently present in asymptomatic
individuals.
A precise pathoanatomic diagnosis with identification of the
pain generator cannot be made in up to 85% of patients.
Persistent LBP should be treated with an individually tailored
program that includes analgesia, core strengthening,
stretching, aerobic conditioning, loss of excess weight, and
patient education.
Intensive interdisciplinary rehabilitation with an emphasis on
cognitive-behavioral therapy should be strongly considered
if conservative measures fail.
There is no evidence for the effectiveness of epidural
corticosteroid injections in patients without radiculopathy.
A large number of injection techniques, physical therapy
modalities, and nonsurgical interventional therapies lack
evidence of efficacy.
The major indication for back surgery is presence of a serious
or progressive neurologic deficit.
Back surgery in the absence of neurologic deficits, especially
spinal fusion for degenerative changes, is not clearly
effective.
EPIDEMIOLOGY
Low back pain (LBP) is one of the most common conditions
encountered in clinical medicine. It affects the area between
the lower rib cage and gluteal folds.
An estimated 65% to 80%1 of the population will experience LBP during their lifetime. LBP is the most prevalent
chronic pain syndrome and the leading cause of limitation
of activity in patients younger than the age of 45. It is also
the second most frequent reason for a visit to the physician’s
office and the third most common surgical indication.2 The
incidence of LBP increases with age, and LBP more commonly affects women.
The natural history of back pain, especially the duration
and chronicity, remains somewhat controversial. Regardless, studies show that pain and function improve substantially in most patients within 1 month,3 and more than 90%
are better at 8 weeks.4 These patients, however, remain
susceptible to future relapses that also tend to be brief. The
remaining 7% to 10% develop chronic LBP and it is these
individuals who are largely responsible for the high costs
associated with LBP. The most recent reliable data, from
1998, estimated the direct cost of managing LBP in the
United States to be $90 billion5 with substantial additional
indirect costs due to lost time from work and decreased
productivity.
A number of risk factors have been associated with LBP
including heredity, psychosocial factors, heavy lifting,
obesity, pregnancy, weaker trunk strength, and cigarette
smoking.6 Persistence of disabling LBP has been associated
with the presence of maladaptive pain coping behavior,
nonorganic signs, functional impairment, poor general
health status, and psychiatric comorbidities.7
ANATOMY
The lumbar spine is composed of five vertebrae. Each vertebra consists of a body anteriorly and a neural arch that
encloses the spinal canal posteriorly (Figure 47-1). Their
cartilaginous end plates cover the superior and inferior surfaces of the vertebral body.
Adjacent vertebrae are united by an intervertebral disk.
The outer circumference of the disk is made up of concentric layers of dense, tough fibrous tissue, the annulus fibrosus.
The annulus encloses a shock-absorbing gelatinous nucleus
pulposus. In addition to this discovertebral joint anteriorly,
at each level of the lumbar spine, there are two posterolaterally placed synovial facet (apophyseal) joints. These are
formed by articulation of the superior and inferior articular
processes of adjacent vertebrae.
The vertebral column is further stabilized by ligaments
and paraspinal muscles (erector spinae, trunk, and abdominal muscles). The anterior and posterior longitudinal ligaments run the length of the spinal column. They anchor
the anterior and posterior vertebral body surfaces and intervertebral disks. The ligamentum flavum interconnects the
laminae while the interspinous and supraspinous ligaments
interconnect the spinous processes. The intertransverse
ligaments interconnect the transverse processes.
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Nucleus pulposus
Vertebral
body
Annulus fibrosus
Spinal canal
Facet joint
Cauda equina
Pedicle
Intervertebral
foramen
Intervertebral
disk
Spinous
process
Lamina
A
Ligamentum
flavum
Facet joint
Spinous process
B
Figure 47-1 Anatomy of the lumbar spine. A, Cross-sectional view through a lumbar vertebra. B, Lateral view of the lumbar spine.
The sacroiliac joints join the spinal column to the pelvis.
The anterior and inferior part of the joint is lined with
synovium, whereas the posterior and superior part is fibrous.
There is little or no movement at the sacroiliac joint.
The spinal canal in the lumbar region contains the cauda
equina (the bundle of lumbar and sacral nerve roots that
occupy the vertebral canal below the cord), blood vessels,
and fat. Because the spinal cord ends at the L1 level, cord
compression is generally not a feature of lumbar pathology.
At each level a pair of nerve roots leaves the spinal canal
and exits through the intervertebral foramina.
CLINICAL EVALUATION
LBP has a large number of causes, and the spectrum of clinical presentation is broad. Many individuals will have selflimited episodes of acute LBP that resolve without specific
treatment, whereas others may present with recurrent or
chronic LBP. A thorough history is the most important part
of the clinical evaluation of these patients. Imaging is often
unnecessary.
HISTORY
The major focus in the initial evaluation of a patient with
LBP is to identify the small fraction8 (<5%) of patients who
may have neural compression or underlying systemic disease
(infection, malignancy, or spondyloarthritis) as the cause of
back pain. These patients require early diagnostic testing
and may require specific treatment (e.g., antibiotics for vertebral osteomyelitis) or urgent treatment (e.g., surgical
decompression in a patient with major or progressive neural
compression). As such, clues to the presence of underlying
systemic disease9-11 (Table 47-1), often referred to as “red
flags,” should be carefully sought. It is also important to
look for any social or psychologic distress such as job
dissatisfaction, pursuit of disability compensation, and
depression that may amplify or prolong the pain.11
Mechanical LBP is due to an anatomic or functional
abnormality in the spine that is not associated with inflammatory or neoplastic disease. It typically increases with
physical activity and upright posture and tends to be
relieved by rest and recumbency. More than 95% of LBP
is mechanical,8 and degenerative change in the lumbar
spine is the most common cause of mechanical LBP.9 Severe
and acute mechanical LBP in a postmenopausal woman
would be suspicious for a vertebral compression fracture
secondary to osteoporosis. Nocturnal pain suggests the possibility of underlying infection or neoplasm as the cause
of LBP.
Inflammatory LBP,12 as seen in the spondyloarthritides,
is more common in men younger than 40 years of age. It is
associated with marked morning stiffness that usually lasts
for more than 30 minutes. The pain frequently improves
with exercise but not with rest. Pain is often worse during
the second half of the night, and some patients complain of
alternating buttock pain.
It is important to ask the patient if the back pain radiates
into the lower extremities, suggesting pseudoclaudication
Table 47-1 Red Flags for Potentially Serious
Underlying Causes of Low Back Pain
Spinal Fracture
Significant trauma
Prolonged glucocorticoid use
Age > 50 yr
Infection or Cancer
History of cancer
Unexplained weight loss
Immunosuppression
Injection drug use
Nocturnal pain
Age > 50 yr
Cauda Equina Syndrome
Urinary retention
Overflow incontinence
Fecal incontinence
Bilateral or progressive motor deficit
Saddle anesthesia
Spondyloarthritis
Severe morning stiffness
Pain improves with exercise, not rest
Pain during second half of night
Alternating buttock pain
Age < 40 yr
CHAPTER 47 (neurogenic claudication) secondary to spinal stenosis or
sciatica (usually secondary to a herniated disk). Young
adults are more likely to experience disk herniations, and
elderly patients are more likely to have spinal stenosis. Sciatica results from nerve root compression and produces pain
in a dermatomal (radicular) distribution, usually to the level
of the foot or ankle. The pain is lancinating, shooting, and
sharp in quality. It is frequently accompanied by numbness
and tingling and may be accompanied by sensory and motor
deficits. Sciatica due to disk herniation typically increases
with cough, sneezing, or the Valsalva maneuver. Sciatica
should be differentiated from non-neurogenic sclerotomal
pain. This pain can arise from pathology within the disk,
facet joint, or lumbar paraspinal muscles and ligaments.
Like sciatica, sclerotomal pain is often referred into the
lower extremities, but unlike sciatica, sclerotomal pain is
nondermatomal in distribution, it is dull in quality, and the
pain usually does not radiate below the knee or have associated paresthesias. Most radiant pain is sclerotomal.9 Bowel
or bladder dysfunction should suggest the possibility of the
cauda equina syndrome.
PHYSICAL EXAMINATION
A physical examination usually does not lead to a specific
diagnosis. Nevertheless, a general physical examination
including a careful neurologic examination may help identify those few but critically important cases of LBP that are
secondary to a systemic disease or have clinically significant
neurologic involvement (see Table 47-1).
Inspection may reveal the presence of scoliosis. This can
be either structural or functional. A structural scoliosis is
associated with structural changes of the vertebral column
and sometimes the rib cage as well. In adults structural
scoliosis is usually secondary to degenerative changes,
although some adults may have a history of adolescent idiopathic scoliosis. With forward flexion, structural scoliosis
persists. In contrast, functional scoliosis, which usually
results from paravertebral muscle spasm or leg length discrepancy, usually disappears. A tuft of hair in the lumbar
spine region may indicate a congenital structural abnormality such as spina bifida occulta.
Palpation can detect paravertebral muscle spasm. This
often leads to loss of the normal lumbar lordosis. Point
tenderness on percussion over the spine has sensitivity
but not specificity for vertebral osteomyelitis. A palpable
step-off between adjacent spinous processes suggests
spondylolisthesis.
Limited spinal motion (flexion, extension, lateral
bending, and rotation) is not associated with any specific
diagnosis because LBP due to any cause may limit motion.
Range of motion measurements, however, can help in monitoring treatment.6 Chest expansion of less than 2.5 cm has
specificity but not sensitivity for ankylosing spondylitis.12
The hip joints should be examined for any decrease in
range of motion because hip arthritis, which normally
causes groin pain, may occasionally present as LBP. Trochanteric bursitis with tenderness over the greater trochanter of the femur can be confused with LBP. The presence of
more widespread tender points, especially in a female
patient, suggests the possibility that LBP may be secondary
to fibromyalgia.
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In patients with a history of LBP that radiates into the
lower extremities (sciatica, pseudoclaudication, or referred
sclerotomal pain) a straight leg–raising test should be performed. With the patient lying on his or her back, the heel
is placed in the palm of the examiner’s hand. With the knee
fully extended the leg is raised progressively. This places
tension on the sciatic nerve (that takes origin from L4, L5,
S1, S2, and S3) and thereby stretches the nerve roots (especially L5, S1, and S2). If any of these nerve roots is already
irritated, such as by impingement from a herniated disk,
further tension on the nerve root by straight leg–raising will
result in radicular pain that extends below the knee. The
test is positive if radicular pain is produced when the leg is
raised less than 70 degrees. Dorsiflexion of the ankle further
stretches the sciatic nerve and increases the sensitivity of
the test. Pain experienced in the posterior thigh or knee
during straight leg–raising is generally from hamstring tightness and does not represent a positive test. The straight
leg–raising test is sensitive but not specific for clinically
significant disk herniation at the L4-5 or L5-S1 level (the
sites of 95% of clinically meaningful disk herniations).
False-negative tests are more frequently seen with herniation above the L4-5 level. The straight leg–raising test is
usually negative in patients with spinal stenosis. The crossed
straight leg–raising test (with sciatica reproduced when the
opposite leg is raised) is highly specific but insensitive for a
clinically significant disk herniation.6,11,13,14
The neurologic evaluation (Figure 47-2) of the lower
extremities in a patient with sciatica can identify the specific nerve root involved. The evaluation should include
motor testing with focus on dorsiflexion of the foot (L4),
great toe dorsiflexion (L5), and foot plantar flexion (S1);
determination of knee (L4) and ankle (S1) deep tendon
reflexes; and tests for dermatomal sensory loss. The inability
to toe walk (mostly S1) and heel walk (mostly L5) indicate
muscle weakness. Muscle atrophy can be detected by circumferential measurements of the calf and thigh at the same
level bilaterally.6
Patients involved with litigation or with psychologic distress occasionally exaggerate their symptoms. They may
display nonorganic signs where the objective findings do not
match the subjective complaints such as with nonanatomic
motor or sensory loss. A number of tests to detect this have
been described by Waddell and co-workers.15 The most
reproducible tests are the presence of superficial tenderness,
overreaction during the examination, and observation of a
discrepancy in the straight leg–raising test done in the
seated and supine positions.
DIAGNOSTIC TESTS
Imaging
The major function of diagnostic testing, especially imaging,
is the early identification of pathology in those few patients
who have evidence of a major or progressive neurologic
deficit and those in whom an underlying systemic disease is
suspected (see Table 47-1). Otherwise, imaging is not
required unless significant symptoms persist beyond 6 to 8
weeks. This approach avoids unnecessary early testing
because more than 90% of the patients will have recovered
spontaneously by 8 weeks.6,8 Furthermore, neither magnetic
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Lower extremity
dermatome
S1
L5
Disc
Nerve root
Motor loss
Sensory loss
Reflex loss
L3-4
L4
Dorsiflexion
of foot
Medial foot
Knee
L4-5
L5
Dorsiflexion
of great toe
Dorsal foot
None
L5-S1
S1
Plantarflexion
of foot
Lateral
foot
Ankle
L4
Figure 47-2 Neurologic features of lumbosacral radiculopathy.
resonance imaging (MRI) nor plain radiographs obtained
early in the course of LBP evaluation improves clinical
outcome, predicts recovery course, or reduces the overall
cost of care.2,16
A significant problem with all imaging studies is that
many of the anatomic abnormalities identified in patients
with LBP are also commonly present in asymptomatic individuals and are frequently unrelated to the back pain.9
Often these abnormalities result from age-related degenerative changes, which begin to appear even in early adulthood
and are among the earliest degenerative changes in the
body.17 Although clinically challenging and sometimes
impossible, one should refrain from making causal inferences based solely on imaging abnormalities in the absence
of corresponding clinical findings because this may lead to
unnecessary, invasive, and costly interventions.
Given the weak association between imaging abnormalities and symptoms, it is not surprising that in up to 85% of
patients a precise pathoanatomic diagnosis with identification of the pain generator cannot be made.11 Patients should
understand that the reason for imaging is to rule out serious
conditions and that common degenerative findings are
expected. Ill-considered attempts to make a diagnosis on
the basis of imaging studies may reinforce the suspicion of
serious disease, magnify the importance of nonspecific findings, and label patients with spurious diagnoses.
Plain radiographs and MRI are the major modalities used
in the evaluation of patients with LBP. In patients with
persistent LBP of greater than 6 to 8 weeks’ duration despite
standard therapies, radiography may be a reasonable first
option if there are no symptoms suggesting radiculopathy or
spinal stenosis.18 Anteroposterior and lateral views are
usually adequate. Oblique views substantially increase radiation exposure and add little new diagnostic information.
Gonadal radiation in a woman from a two-view radiograph
of the lumbar spine is equivalent to radiation exposure from
a chest radiograph taken daily for more than 1 year.18
Abnormalities on radiography such as single-disk degeneration, facet joint degeneration, Schmorl’s nodes (protrusion of the nucleus pulposus into the spongiosa of a vertebra),
spondylolysis, mild spondylolisthesis, transitional vertebrae
(the “lumbarization” of S1 or “sacralization” of L5), spina
bifida occulta, and mild scoliosis are equally prevalent in
individuals with and without LBP.8,9,19
MRI without contrast is generally the best initial test for
patients with LBP who require advanced imaging. It is the
preferred modality for the detection of spinal infection and
cancers, herniated disks, and spinal stenosis.8 MRI testing
for LBP should largely be limited to patients in whom there
is a suspicion of systemic disease (such as infection or malignancy), for the preoperative evaluation of patients who are
surgical candidates on clinical grounds11,18 (e.g., the presence of a significant or progressive neurologic deficit), or for
those patients with radiculopathy or spinal stenosis who are
candidates for epidural corticosteroids.18 Disk abnormalities
are commonly noted on MRI studies but often have little
or no relationship with the patient’s symptoms. A disk bulge
is a symmetric, circumferential extension of disk material
beyond the interspace. A disk herniation is a focal or asymmetric extension. Herniations are subdivided into protrusions and extrusions. Protrusions are broad-based, whereas
extrusions have a “neck” so that the base is narrower than
the extruded material. Bulges (52%) and protrusions (27%)
are common in asymptomatic adults, but extrusions are
rare.8 MRI with the intravenous contrast agent, gadolinium,
may be useful for the evaluation of patients with prior back
surgery (with no hardware present) to help in the differentiation of scar tissue from recurrent disk herniation.
MRI is generally preferred over computed tomography
(CT) scanning in the evaluation of patients with LBP.
However, when bone anatomy is critical, CT is superior.
Unlike MRI, CT can safely be done in patients with a
ferromagnetic implant, although imaging artifacts may
make interpretation difficult. CT myelography is therefore
sometimes preferred in patients with surgically placed spinal
hardware.
Bone scanning is used primarily to detect infection, bony
metastases, or occult fractures and to differentiate them
from degenerative changes. Bone scans have limited specificity due to poor spatial resolution, and thus abnormal
findings often require further confirmatory imaging such
as MRI.
CHAPTER 47 Electrodiagnostic Studies
Electrodiagnostic studies can be helpful in the evaluation
of some patients with lumbosacral radiculopathy. The main
procedures are electromyography and nerve conduction
studies. These studies can confirm nerve root compression
and define the distribution and severity of involvement.
Whereas studies such as MRI can only provide anatomic
information, electrodiagnostic studies provide physiologic
information that may support or refute the findings on
imaging. Electrodiagnostic testing is therefore mostly considered in patients with persistent disabling symptoms of
radiculopathy where there is discordance between the clinical presentation and findings on imaging. Electromyography
and nerve conduction studies can also be helpful in differentiating the limb pain of peroneal nerve palsy or lumbosacral plexopathy from that of L5 radiculopathy. These studies
are also useful in evaluating possible factitious weakness.
Electrodiagnosis is unnecessary in a patient with an obvious
radiculopathy. It should be noted that electromyographic
changes depend on the development of muscle denervation
following nerve injury and may not be detected for 2 to 3
weeks after the injury. Another limitation is that electromyographic abnormalities may persist for over a year following decompressive surgery.20
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Table 47-2 Causes of Low Back Pain
Mechanical
Lumbar spondylosis*
Disk herniation*
Spondylolisthesis*
Spinal stenosis*
Fractures (mostly osteoporotic)
Nonspecific (idiopathic)
Neoplastic
Primary
Metastatic
Inflammatory
Spondyloarthritides
Infectious
Vertebral osteomyelitis
Epidural abscess
Septic diskitis
Herpes zoster
Metabolic
Osteoporotic compression fractures
Paget’s disease
Referred Pain to Spine
From major viscera, retroperitoneal structures, urogenital system,
aorta, or hip
*Related to degenerative changes.
Laboratory Studies
Laboratory studies are used mostly in identifying patients
with systemic causes of LBP. A patient with normal blood
cell counts, erythrocyte sedimentation rate, and radiographs
of the lumbar spine is unlikely to have underlying infection
or malignancy as the cause of LBP.21
DIFFERENTIAL DIAGNOSIS
LBP usually originates from pathology within the lumbar
spine or associated muscles and ligaments (Table 47-2).
Rarely pain is referred to the back from visceral disease. In
the vast majority of patients with LBP, the pain is mechanical.11 Degenerative change in the lumbar spine is the largest
contributor to the mechanical causes of LBP8 (see Table
47-2) and indeed the most commonly identified cause of
back pain.
Lumbar Spondylosis
The current common usage of the term lumbar spondylosis
incorporates degenerative changes in both the anteriorly
placed discovertebral joints and the posterolaterally placed
facet joints.6 These degenerative or osteoarthritic changes
are seen radiographically as disk or joint space narrowing,
subchondral sclerosis, and osteophytosis (Figure 47-3).
Imaging evidence of lumbar spondylosis is common in
the general population, increases with age, and may be
unrelated to back symptoms. Radiographic abnormalities
such as single disk degeneration, facet joint degeneration,
Schmorl’s nodes, mild spondylolisthesis, and mild scoliosis
are equally prevalent in persons with and without back
pain.22 The situation is further complicated by the observation that patients with severe mechanical LBP may have
minimal radiographic changes, and conversely patients with
advanced changes may be asymptomatic.
The clinical spectrum of mechanical LBP is wide.
Patients may present with acute LBP (with recurrent attacks
in some), whereas chronic LBP (often with periods of acute
exacerbation) may develop in others. Somatic referral may
lead to sclerotomal pain that radiates into the buttocks and
lower extremities. Lumbar spondylosis predisposes patients
to intervertebral disk herniation, spondylolisthesis, and
spinal stenosis.
In some patients with facet joint osteoarthritis the pain
may radiate into the buttock and posterior thigh, be alleviated with forward flexion, and be exacerbated by bending
ipsilateral to the involved joint (facet syndrome).
The terms internal disk disruption and diskogenic low back
pain are used interchangeably and remain controversial
diagnoses.13 The disorder is diagnosed by provocative diskography. Following contrast injection into several disks in
sequence, the radiographic appearance and induced pain at
each level are assessed. If injection into a disk reproduces a
patient’s usual LBP, the test is considered positive. Advocates of this technique interpret a positive diskogram as
defining the particular disk as the primary pain generator,
and spinal fusion or disk arthroplasty is frequently recommended.2 However, injection into a disk can simulate the
quality and location of pain known not to originate from
that disk.23 Furthermore, diskographic abnormalities and
induced pain are frequently seen in asymptomatic persons
and, more importantly, the diskogenic pain attributed to
disk disruption frequently improves spontaneously.8,11
Therefore the clinical importance and appropriate management of this condition remains unclear.
Focal high signal in the posterior annulus fibrosus as seen
on T2-weighted MRI images, sometimes referred to as a
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A
B
Figure 47-3 Lumbar spondylosis. Anteroposterior (A) and lateral (B) radiographs of the lumbar spine show the cardinal features of disk-space narrowing, marginal osteophytes, and end plate sclerosis. (Courtesy Dr. John Crues, University of California, San Diego.)
high-intensity zone, is believed to represent tears in the
annulus fibrosus and to correlate with positive findings on
provocative diskography.8 The high prevalence of highintensity zones in asymptomatic individuals limits its clinical value.24
Spinal instability is seen in some patients with lumbar
spondylosis. It is identified by demonstrating abnormal vertebral motion (anteroposterior displacement or excessive
angular change of adjacent vertebrae) on lateral radiographs
in flexion and extension. However, such spinal motion may
be seen in asymptomatic persons and its natural history and
relationship to the causation of LBP is unclear. Thus the
diagnosis of spinal instability (in the absence of fractures or
spondylolisthesis) as a cause of LBP and its treatment by
spinal fusion remains controversial.
occurs at L4-526 (with more torsion at the L4-5 level). Probably related to this, 90% to 95% of clinically significant
compressive radiculopathies occur at these two levels.11
Disk herniation is rare in young individuals with the
frequency increasing with age. The peak frequency of herniation at the L5-S1 and L4-L5 levels is between the ages
of 44 and 50 with a progressive decline in frequency
thereafter.27
The genesis of sciatica is felt to have both a mechanical
(disk material impinging on a nerve root) and biologic component. Inflammation, vascular invasion, immune responses,
and an array of cytokines have been implicated.
Disk Herniation
Intervertebral disk herniation occurs when the nucleus
pulposus in a degenerated disk prolapses and pushes out
the weakened annulus, usually posterolaterally. Imaging evidence of disk herniation has a high prevalence in the
general population with one study finding MRI evidence of
disk herniation in 27% of asymptomatic individuals.25
Occasionally, however, the herniated disk can cause nerve
root impingement leading to lumbosacral radiculopathy
(Figures 47-4 and 47-5). A herniated intervertebral disk is
the most common cause of sciatica.8
The lumbosacral spine is susceptible to disk herniation
because of its mobility. Seventy-five percent of flexion and
extension occurs at the lumbosacral joint (L5-S1), and 20%
Figure 47-4 Schematic drawing showing posterolateral disk herniation resulting in nerve root impingement.
CHAPTER 47 A
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B
Figure 47-5 Lumbar disk extrusion. A, The sagittal T2-weighted magnetic resonance image shows an extruded disk at the L4-5 level. B, The axial
image through the L4-5 level shows disk extrusion to the left side of the neural canal and compressing the exiting L5 nerve root against the left lamina.
(Courtesy Dr. John Crues, University of California, San Diego.)
The clinical features of disk herniation resulting in lumbosacral radiculopathy have already been discussed (see
history, physical examination, and Figure 47-2). It should
be noted that immediate imaging is unnecessary in patients
without a clinically significant neurologic deficit and no red
flags to suggest an underlying systemic pathology (see Table
47-1). L1 radiculopathy is rare and presents with symptoms
of pain, paresthesias, and sensory loss in the inguinal
region.28 L2, L3, and L4 radiculopathies are uncommon and
more likely to be seen in older patients with lumbar spinal
stenosis.
The natural history of disk herniation is favorable with
progressive improvement expected in most patients.
Sequential MRI studies reveal that the herniated portion
of the disk regresses with time and there is partial or complete resolution in two thirds of cases after 6 months.11,29
Only approximately 10% of patients have sufficient pain
after 6 weeks of conservative care, and for this group
decompressive surgery is considered.11 Even a sequestered
fragment (piece of herniated material that breaks off and
is free in the epidural space) tends to be reabsorbed with
time.30
Rarely a large midline disk herniation, usually L4-5,9
compresses the cauda equina resulting in cauda equina syndrome. Patients usually present with LBP, bilateral radicular
pain, and bilateral motor deficits with leg weakness. Physical examination findings are often asymmetric. Sensory loss
in the perineum (saddle anesthesia) is common, and urinary
retention with overflow incontinence is usually present.11
Fecal incontinence may also occur. Other causes of cauda
equina syndrome include neoplasia, epidural abscess, hematoma, and rarely lumbar spinal stenosis. Cauda equina syndrome is a surgical emergency because neurologic results are
affected by the time to decompression.6
Spondylolisthesis
Spondylolisthesis is the anterior displacement of a vertebra
on the one beneath it. There are two major types: isthmic
and degenerative.
Isthmic spondylolisthesis (Figure 47-6) is caused by bilateral spondylolysis. Spondylolysis is a defect in the pars interarticularis that is most commonly seen at L5. It is typically
a fatigue fracture acquired early in life that is more commonly seen in boys. Spondylolysis progresses to spondylolisthesis in approximately 15% of patients.31
Degenerative spondylolisthesis develops in some patients
with severe degenerative changes with subluxation at the
facet joints allowing anterior or posterior movement of one
vertebra over another. It is usually seen in an older age group
(typically older than age 60), is more common in women,
and most frequently involves the L4-5 level.9
Most patients, especially those with a minor degree of
spondylolisthesis, are asymptomatic. Some may complain of
an aching mechanical LBP. Neurologic complications may
occur in some with greater degrees of spondylolisthesis.
Nerve root impingement is more likely to be seen in patients
with isthmic spondylolisthesis (especially L5 nerve root),
whereas in degenerative spondylolisthesis the more likely
clinical presentation is of spinal stenosis. Rarely extreme
slippage results in cauda equina syndrome. In view of its
potential dynamic nature, spondylolisthesis may be missed
if standing radiographs are not obtained.
Spinal Stenosis
Lumbar spinal stenosis is defined as a narrowing of the
central spinal canal, its lateral recesses, and neural foramina
that may result in a compression of lumbosacral nerve roots.
Spinal stenosis can occur at one or multiple levels, and the
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L5
S1
A
B
Figure 47-6 A, Spondylolysis with bilateral defects in the pars interarticularis (arrows). B, Spondylolysis of the L5 vertebra (arrow) resulting in isthmic
spondylolisthesis at L5-S1.
narrowing may be asymmetric. It is important to recognize
that 20% to 30% of asymptomatic adults older than age 60
have imaging evidence of spinal stenosis. The prevalence of
symptomatic lumbar spinal stenosis is not established. It is,
however, the most frequent indication for spinal surgery in
patients older than age 65.
Congenital idiopathic spinal stenosis (Table 47-3) is
not uncommon and results from congenitally short
pedicles. These patients tend to become symptomatic early
(third to fifth decade of life) when superimposed mild
degenerative changes that would normally be tolerated
result in sufficient further narrowing of the spinal canal to
cause symptoms.32
Degenerative changes are the cause of spinal stenosis in
the vast majority of cases. The intervertebral disk loses
height as it degenerates. This results in a bulging or buckling
of the now redundant and often hypertrophied ligamentum
flavum into the posterior part of the canal. Any herniation
of the degenerated disk narrows the anterior part of the
canal while hypertrophied facets and osteophytes may compress nerve roots in the lateral recess or intervertebral
foramen (Figures 47-7 and 47-8). Any degree of spondylolisthesis will further exacerbate spinal canal narrowing.
The hallmark of spinal stenosis is neurogenic claudication (pseudoclaudication). The symptoms of neurogenic
claudication are usually bilateral but often asymmetric. The
primary complaint is of pain in the buttocks, thighs, and
legs. The pain may be accompanied by paresthesias. Neurogenic claudication is induced by standing erect or walking
and relieved by sitting or flexing forward. This forward
flexion increases the spinal canal dimensions and may lead
to the patient adopting a simian stance. It is therefore not
Table 47-3 Causes of Lumbar Spinal Stenosis
Congenital
Idiopathic
Achondroplastic
Acquired
Degenerative
Hypertrophy of facet joints
Hypertrophy of ligamentum flavum
Disk herniation
Spondylolisthesis
Scoliosis
A
C
Iatrogenic
Postlaminectomy
Postsurgical fusion
Miscellaneous
Paget’s disease
Fluorosis
Diffuse idiopathic skeletal hyperostosis
Ankylosing spondylitis
B
Figure 47-7 Spinal stenosis secondary to a combination of disk herniation (A), facet joint hypertrophy (B), and hypertrophy of the ligamentum
flavum (C).
CHAPTER 47 A
| Low Back Pain
673
B
Figure 47-8 Degenerative spinal stenosis. A, The sagittal T2-weighted magnetic resonance image shows decreased anteroposterior diameter of the
neural canal at the L4-5 level due to redundancy of the ligamentum flavum. B, The axial image through the L4-5 disk shows decreased cross-sectional
area of the thecal sac from hypertrophic changes of the facet joints posterolateral to the thecal sac. (Courtesy Dr. John Crues, University of California,
San Diego.)
surprising that these patients often feel relief by stooping
forward while holding onto a shopping cart (the “shopping
cart sign”) and may exhibit surprising endurance while pedaling a stationary bicycle. Symptoms of neurogenic claudication probably represent intermittent mechanical and
ischemic disruption of lumbosacral nerve root function.33
The patients also often have a sense of weakness in the
lower extremities, and unsteadiness of gait is a frequent
complaint. The finding of a wide-based gait in a patient
with LBP has a more than 90% specificity for lumbar spinal
stenosis.34 Factors that favor a diagnosis of neurogenic claudication over vascular claudication include preservation of
pedal pulses, provocation of symptoms by standing erect just
as readily as by walking, relief of symptoms with flexion of
the spine, and location of maximal discomfort to the thighs
rather than the calves.
The physical examination of a patient with lumbar
spinal stenosis is often unimpressive.6 Severe neurologic
deficits are not commonly seen. Lumbar range of motion
may be normal or reduced, and the result of straight leg–
raising is usually negative. Deep tendon reflexes and vibration sense may be reduced. Mild weakness is seen in some.
The significance of these findings is often difficult to determine in elderly patients. However, in a few patients with
spinal stenosis a fixed nerve root injury may occur, resulting
in a lumbosacral radiculopathy or rarely a cauda equina
syndrome.
The diagnosis of lumbar spinal stenosis is most often
suspected when a history of neurogenic claudication is elicited. The diagnosis is best confirmed by MRI.
Spinal stenosis is generally an indolent condition where
the symptoms evolve gradually and the natural history is
benign. In a study of patients with lumbar spinal stenosis
followed for 49 months without surgical intervention,
symptoms remained unchanged in 70%, improved in 15%,
and worsened in 15%.35 As such, prophylactic surgical intervention is not warranted.32
Diffuse Idiopathic Skeletal Hyperostosis
Diffuse idiopathic skeletal hyperostosis (DISH) is characterized by calcification and ossification of paraspinous ligaments and the entheses.36 It is a noninflammatory condition
of unknown etiology that is not associated with HLA-B27
positivity.
DISH has been associated with obesity, diabetes mellitus,
and acromegaly.37 It is rarely diagnosed before the age of 30,
is more commonly seen in men, and the prevalence rises
with age.38
The thoracic spine is most commonly involved, although
the cervical and lumbar regions may also be affected. Ossification of the anterior longitudinal ligament is best seen on
a lateral radiograph of the thoracic spine. This together with
bridging enthesophytes in the spine give the appearance of
flowing wax on the anterior and right lateral aspects of the
spine. Involvement of the left lateral aspect in patients with
situs inversus has led to speculation that the descending
aorta plays a role in the location of the calcification. Intervertebral disk spaces and facet joints are preserved (unless
there is coexisting lumbar spondylosis) and the sacroiliac
joints appear normal. This helps differentiate DISH from
spondylosis and the spondyloarthritides. Almost any extraspinal osseous or articular site may be affected.39 Irregular
new bone formation (“whiskering”) is often best seen at the
iliac crests, ischial tuberosities, and femoral trochanters.
Ossification of tendons and ligaments at sites of attachment
(such as the patella, olecranon process, and calcaneus) and
periarticular osteophytes (such as the lateral acetabulum
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PART 6 | DIFFERENTIAL DIAGNOSIS OF REGIONAL AND DIFFUSE MUSCULOSKELETAL PAIN
and inferior portion of the sacroiliac joint on pelvic radiographs) may also be seen. Severe ligamentous calcification
may be seen in the sacrotuberous and iliolumbar ligaments
and heterotopic bone formation following hip replacement
in patients with DISH has been described.40
DISH may be entirely asymptomatic. The most common
complaint encountered is of pain and stiffness involving
the spine, often the thoracic region. Usually there is only
a moderate limitation of spinal motion. Extensive ossification of the anterior longitudinal ligament together with
large anterior enthesophytes may occasionally compress
the esophagus and cause dysphagia.36 Ossification of the
posterior longitudinal ligament is almost exclusively seen in
the cervical spine and may occur either as a discrete disorder
or as part of DISH. This can rarely lead to cervical myelopathy. Pain and tenderness may be present at the entheses,
and these patients may have findings of lateral or medial
humeral epicondylitis, Achilles tendinitis, or plantar
fasciitis.
If treatment of DISH is necessary at all, it is symptomatic. Most patients respond to acetaminophen, nonsteroidal
anti-inflammatory drugs (NSAIDs), and judicious use of
glucocorticoid injections for painful enthesopathy.
Nonspecific Low Back Pain
This is also referred to as idiopathic LBP. As mentioned
earlier, a precise pathoanatomic diagnosis, with identification of the pain generator, cannot be made in up to 85% of
the patients. This is largely because of the nonspecific
nature of the symptoms in patients with LBP and the weak
association of these symptoms with findings on imaging.
Thus terms such as lumbago, strain, and sprain have come
into use. Strain and sprain have never been histologically
characterized. Therefore nonspecific LBP is a more accurate
label for these patients who have a mostly self-limited syndrome of acute mechanical LBP. The severity of pain can
vary from mild to severe, and whereas sometimes the back
pain develops immediately after a traumatic event such as
lifting a heavy object or a twisting injury, other patients
may just wake up with LBP. Most patients are better within
1 to 4 weeks3 but remain susceptible to similar future episodes. Less than 10% of patients develop chronic nonspecific LBP.
Neoplasm
Neoplasms are an uncommon, but nevertheless important,
cause of LBP. In a primary care setting, neoplasia accounts
for less than 1% of the patients with LBP.11
In a large prospective study of patients in a walk-in
clinic, a history of cancer, unexplained weight loss, failure
to improve after 1 month of conservative therapy, and age
older than 50 years were each associated with a higher
likelihood for cancer.41 By far the most important predictor
for the likelihood of underlying cancer as the cause of LBP
was a prior history of cancer.
The typical patient with LBP secondary to spinal malignancy presents with a persistent and progressive pain
that is not alleviated by rest and indeed is often worse at
night. In some patients a spinal mass can result in a lumbosacral radiculopathy or cauda equina syndrome. Acute LBP
may be the presentation in a patient with a pathologic
compression fracture. Rarely, leptomeningeal carcino­
matosis (in patients with breast cancer, lung cancer, lymphoma, or leukemia) may present with a lumbosacral
polyradiculopathy.42
Most cases result from involvement of the spine by metastatic carcinoma4 (especially prostate, lung, breast, thyroid,
or kidney) or multiple myeloma. Metastatic vertebral
lesions, more commonly seen in the thoracic spine, account
for 39% of bony metastases in patients with primary neoplasms.43 Spinal cord tumors, primary vertebral tumors, and
retroperitoneal tumors may rarely be the cause of LBP.11
Osteoid osteoma, a benign tumor of bone, typically pre­
sents with LBP in the second or third decade of life. The
pain is often accompanied by a functional scoliosis secondary to paravertebral spasm. Patients may present with pain
even before the osteoid osteoma is visible radiographically.
Osteoid osteomas predominantly involve the posterior elements of the spine, usually the neural arch. A sclerotic
lesion measuring less than 1.5 cm with a lucent nidus is
pathognomonic.44 A bone scan, CT scan, or MRI should be
ordered if an osteoid osteoma is suspected but not detected
on radiography.
Plain radiographs are less sensitive than other imaging
tests in detecting neoplastic lesions because approximately
50% of trabecular bone must be lost before a lytic lesion
is visible.8 Metastatic lesions may be lytic (radiolucent),
blastic (radiodense), or mixed. The majority of metastases
are osteolytic. Vertebral bodies are primarily involved
because of their rich blood supply associated with red
marrow, and unlike infections the disk space is usually
spared. It should be noted that a purely lytic lesion such
as multiple myeloma will not be detected by a bone scan.
MRI offers the greatest sensitivity and specificity in the
evaluation of spinal tumors and is generally the modality
of choice.
Infection
Vertebral osteomyelitis (spinal osteomyelitis, spondylodiskitis) may be acute (usually pyogenic) or chronic (pyogenic,
fungal, or granulomatous). Acute vertebral osteomyelitis
evolves over a period of a few days or weeks and is the major
focus of this discussion.
Vertebral osteomyelitis usually results from hematogenous seeding, direct inoculation at the time of spinal surgery,
or contiguous spread from an infection in the adjacent soft
tissue. The lumbar spine is the most common site of vertebral osteomyelitis followed by the thoracic and cervical
spine.45 Staphylococcus aureus is the most common microorganism followed by Escherichia coli. Coagulase-negative
staphylococci and Propionibacterium acnes are almost always
the cause of exogenous osteomyelitis after spinal surgery,
particularly if internal fixation devices are used.45
A source of infection is detected in about half the cases
with endocarditis diagnosed in up to a third of cases of
vertebral osteomyelitis.45 Other common sites for the
primary focus of infection are the urinary tract, skin, soft
tissue, a site of vascular access, bursitis, or septic arthritis.46
Most patients with hematogenous pyogenic vertebral os­
teomyelitis have underlying medical disorders such as diabetes, coronary artery disease, immunosup­­pressive disorders,
CHAPTER 47 malignancy, and renal failure.45,46 Intravenous drug abuse is
also a risk factor for vertebral osteomyelitis.
Vertebral osteomyelitis may be complicated by an epidural or paravertebral abscess. This may result in neurologic
complication.
Back pain is the initial symptom in most patients. The
pain tends to be persistent, present at rest, exacerbated by
activity, and at times well localized. Point tenderness on
percussion over the spine has sensitivity but not specificity
for vertebral osteomyelitis. Fever is present in only about
half of the patients,45 partly because most patients are using
analgesic medications. Because most cases of vertebral
osteomyelitis result from hematogenous seeding, the dominant manifestations initially may be of the primary infection. An epidural abscess may result in a radiculopathy or
cauda equina syndrome.
Leukocytosis is seen in only about two-thirds of the
patients. However, almost all the patients have increases in
the erythrocyte sedimentation rate and C-reactive protein,
with the latter best correlating with clinical response to
therapy.46 If blood cultures are negative in a patient suspected of having vertebral osteomyelitis, a bone biopsy
(CT-guided or open) with appropriate culture studies and
histopathologic analysis is indicated.
Plain radiography is usually the initial imaging study.
Radiographic changes, however, occur relatively late and
are nonspecific. Typically there is loss of disk height and loss
of cortical definition followed by bony lysis of adjacent
vertebral bodies. MRI is the most sensitive and specific
imaging technique to detect spinal infections. The classic
finding of pyogenic osteomyelitis is involvement of two
vertebral bodies with their intervening disk.8 In a patient
with neurologic impairment, MRI should be done early to
rule out an epidural abscess. Whenever possible, antimicrobial therapy should be directed against an identified susceptible pathogen. There are no data from randomized,
controlled trials to guide decisions about specific antimicrobial regimens or the duration of therapy.46 Intravenous
therapy of at least 4 to 6 weeks, and possibly additional oral
antibiotic therapy, is usually recommended. Surgery may be
necessary to drain an abscess, although CT-guided catheter
drainage may be sufficient in some cases. Surgical débridement is always required when infection is associated with
a spinal implant with removal of the implant whenever
possible.46
Tuberculosis and nontubercular granulomatous infections (blastomycosis, cryptococcosis, actinomycosis, coccidioidomycosis, and brucellosis) of the spine should be
considered in the appropriate clinical and geographic
setting.
Lumbar nerve roots are commonly involved in patients
with herpes zoster. In most cases a single unilateral dermatome is involved. Pain is often severe and may precede the
appearance of a maculopapular rash that evolves into vesicles and pustules.
Inflammation
The spondyloarthritides cause inflammatory LBP (see Table
47-1) and are discussed in detail elsewhere (see Chapters 74
to 78).
| Low Back Pain
675
Metabolic Disease
The major consideration in this category is the occurrence
of acute mechanical LBP secondary to a vertebral compression fracture in a patient with osteoporosis (Chapter 101).
Most patients are postmenopausal women.
Paget’s disease of bone (Chapter 101) is most often
detected in an asymptomatic patient by the incidental
finding of either an elevated alkaline phosphatase or characteristic radiographic abnormality. The spine is the second
most commonly affected site after the pelvis. Within the
spine the L4 and L5 vertebrae are most commonly involved.47
Paget’s disease of the spine may involve single or multiple
levels. The vertebral body is almost always involved together
with a variable portion of the neural arch. Radiographically
Paget’s disease is seen as areas of enlargement of the bone
with thickened, coarsened trabeculae. Usually a mixed
picture of sclerotic and lytic Paget’s disease is encountered.
The vertebrae may enlarge, weaken, and fracture. LBP may
occur due to the pagetic process itself (with periosteal
stretching and vascular engorgement), microfractures, overt
fractures, secondary osteoarthritis of the facet joints, spondylolysis with or without spondylolisthesis, or sarcomatous
transformation (rare).47 Neurologic complications secondary to Paget’s disease of the lumbar spine include sciatica
secondary to nerve root impingement, spinal stenosis, and
rarely a cauda equina syndrome.
Visceral Pathology
Disease in organs that share segmental innervation with the
spine can cause pain to be referred to the spine. In general,
pelvic diseases refer pain to the sacral area, lower abdominal
diseases to the lumbar area, and upper abdominal diseases
to the lower thoracic spine area. Local signs of disease such
as tenderness to palpation, paravertebral muscle spasm, and
increased pain on spinal motion are absent.
Vascular, gastrointestinal, urogenital, or retroperitoneal
pathology may on occasion cause LBP. A partial list of
causes includes an expanding aortic aneurysm, pyelonephritis, ureteral obstruction due to renal stones, chronic prostatitis, endometriosis, ovarian cysts, inflammatory bowel
disorders, colonic neoplasms, and retroperitoneal hemorrhage (usually in a patient taking anticoagulants).
Most abdominal aortic aneurysms are asymptomatic but
may become painful as they expand. Aneurysmal pain is
usually a harbinger of rupture. Rarely the aneurysm may
develop leakage. This produces severe pain with abdominal
tenderness. Most patients with aortic dissection present
with a sudden onset of severe “tearing” pain in the chest or
upper back. Pain originating from a hollow viscus such as
the ureter or colon is often colicky.
Miscellaneous
LBP may be part of the clinical spectrum in innumerable
conditions. It would not be practical or useful to discuss
these entities here. Considered next are some of the more
important or controversial causes of LBP.
The piriformis syndrome is felt to be an entrapment
neuropathy of the sciatic nerve related to anatomic variations in the muscle-nerve relationship or to overuse. The
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PART 6 | DIFFERENTIAL DIAGNOSIS OF REGIONAL AND DIFFUSE MUSCULOSKELETAL PAIN
piriformis is a narrow muscle that originates from the anterior part of the sacrum and inserts into the greater trochanter. It is an external rotator of the hip. There is, however,
debate about the existence of the piriformis syndrome as a
discrete entity because of the lack of objective, validated,
and standardized tests. The diagnosis is clinical. Patients
complain of pain and paresthesias in the gluteal region that
radiate down the leg to the foot. Unlike sciatica from lumbosacral nerve root compression, the pain is not restricted
to a specific dermatome. The straight leg–raising test is
usually negative. There may be tenderness over the sciatic
notch. Physical examination maneuvers for the diagnosis of
piriformis syndrome are based on the notion that stretching
the irritated piriformis muscle may provoke sciatic nerve
compression. This can be done by internally rotating the
hip (Freiburg’s sign) or by flexion, adduction, and internal
rotation (FAIR maneuver) of the hip. Physical therapy that
focuses on stretching the piriformis muscle and NSAIDs are
generally the treatments offered.
Sacroiliac joint dysfunction is a controversial diagnosis.
It is a term used to describe pain in the sacroiliac region
related to abnormal sacroiliac joint movement or alignment. However, tests of pelvic symmetry or sacroiliac joint
movement have low intertester reliability and fluoroscopically guided sacroiliac joint injections have been unreliable
in diagnosis and treatment.48,49 Radiographic degenerative
changes of the sacroiliac joint are often noted in the evaluation of patients with LBP. It remains unresolved as to
whether these changes are the primary cause of the
back pain.50
Lumbosacral transitional vertebrae include sacralization
of the lowest lumbar vertebral body and lumbarization of
the uppermost sacral segment. The association of these variants with LBP remains controversial.
A “back mouse” is a mobile subcutaneous fibro-fatty
nodule in the lumbosacral area. The nodule may be tender.
Although there are case reports,51 the association with LBP
remains unproven.
Epidural lipomatosis may be seen in obese patients, but
it is more commonly seen as a rare side effect of long-term
use of corticosteroids. There is an increase in epidural
adipose tissue that causes a narrowing of the spinal canal.
This is usually an incidental finding, although it may lead
to compression of neural structures.
LBP during pregnancy is common. The pain usually
starts between the fifth and seventh months of pregnancy.52
The etiology of LBP in pregnancy is unclear. Biomechanical, hormonal, and vascular factors have been implicated.
Most women have resolution of their pain postpartum.
Fibromyalgia (see Chapter 52) and polymyalgia rheumatica (see Chapter 88) are two frequently encountered
rheumatologic conditions in which LBP may be a prominent part of the clinical syndrome.
TREATMENT
Specific treatment is available only for the small fraction of
patients with LBP who have either evidence of clinically
significant neural compression or an underlying systemic
disease (cancer, infection, visceral disease, and spondyloarthritis). In the vast majority of patients with LBP, either the
precise pathoanatomic cause (i.e., the pain generator)
cannot be determined or, when the cause is determined, no
specific treatment is available. These patients are managed
with a conservative program centered on analgesia, education, and physical therapy. The goal of treatment is relief of
pain and restoration of function. Surgery is rarely necessary
(Figure 47-9).
One should be wary of the proliferation of unproven
medical, surgical, and alternative therapies. Most have not
been rigorously tested in well-designed randomized controlled trials. Uncontrolled studies can produce a misleading
impression of efficacy due to fluctuating symptoms and the
largely favorable natural history of LBP in most patients.
For management purposes, patients with LBP are considered to have either acute LBP (duration <3 months),
chronic LBP (duration >3 months), or a nerve root compression syndrome.
Acute Low Back Pain
The typical patient seeks medical attention for sudden onset
of severe mechanical LBP. Examination usually reveals
paravertebral muscle spasm, often resulting in loss of the
normally present lumbar lordosis and severe decrease in
range of motion secondary to pain. The prognosis for acute
LBP is excellent. Indeed, only about a third of these patients
seek medical care and more than 90% recover within 8
weeks or earlier.53
Patients with acute LBP are advised to stay active and
continue ordinary daily activities within the limits permitted by pain. This leads to more rapid recovery than bed
rest.54 Bed rest of more than 1 or 2 days is discouraged.
Pharmacologic therapy is used for symptomatic relief.
Unfortunately, no medication has consistently been shown
to result in large average benefits on pain and evidence of
beneficial effects on function is even more limited.5 Acetaminophen and NSAIDs are first-line options for analgesia.
Short-term use of opioids is reasonable in patients with
severe disabling LBP or in those at high risk of complications due to NSAIDs. For patients with acute LBP, shortacting opioids are generally recommended. Muscle relaxants
are moderately effective for short-term symptomatic relief
but have a high prevalence of adverse effects including
drowsiness and dizziness.5 It is unclear whether these medications truly relax muscles or their effects are related more
to sedation or other nonspecific effects. Benzodiazepines
have similar efficacy to muscle relaxants for short-term pain
relief but are associated with risks for abuse, addiction, and
tolerance.18
Back exercises are not helpful in the acute phase, and a
physical therapy referral is usually unnecessary in the first
month. Later an individually tailored program that focuses
on core strengthening, stretching exercises, aerobic conditioning, functional restoration, and loss of excess weight is
recommended to prevent recurrences.6,11 The purpose of
back exercises is to stabilize the spine by strengthening
trunk muscles. Flexion exercises strengthen the abdominal
muscles, and extension exercises strengthen the paraspinal
muscles. Numerous exercise programs have been developed
and appear to be equally effective.
Patient education including use of education booklets is
strongly recommended.18 The information provided should
include causes of LBP, basic anatomy, favorable natural
CHAPTER 47 | Low Back Pain
677
Low back pain
Focused history and physical
examination to categorize patients
Patients with “red flags” that indicate
risk of systemic disease
(infection, malignancy, spondyloarthritis)
or vertebral compression fracture
• Plain radiography
• ESR
• Consider MRI if abnormal
or high index of suspicion
Patients with neurologic signs
and symptoms
• Cauda equina
syndrome
suspected
• Presence of
serious or
progressive
neurologic
deficit
Systemic disease
confirmed
No systemic
disease
Specific
treatment
Conservative
care
Radiculopathy without serious
or progressive neurologic deficit
MRI and urgent
surgical
consultation
Plain radiography,
ESR if concern for
osteomyelitis
Conservative
care for
4-6 weeks
Serious or
progressive
neurologic
deficit
MRI and
surgical
consultation
MRI if no improvement
Consider surgical consultation
especially with neurologic
progression
Patients with nonspecific/
mechanical LBP
Spinal stenosis
suspected
Conservative care
No serious
neurologic
deficit
If not improved
plain radiography
and ESR to
exclude systemic
disease
Conservative
care
Continue
conservative
care if
symptoms
manageable
MRI and surgical consultation
for development of disabling
neurogenic claudication
Consider
interdisciplinary
rehabilitation
with cognitive
behavioral
therapy for
severe
disabling
chronic LBP
Figure 47-9 Algorithm for the differential diagnosis and treatment of low back pain. ESR, erythrocyte sedimentation rate; LBP, low back pain; MRI,
magnetic resonance imaging.
history, minimal value of diagnostic testing, importance of
remaining active, effective self-care options, and coping
techniques.
Spinal manipulation is provided mainly by chiropractors
and osteopaths. It may involve low-velocity mobilization or
manipulation with a high-velocity thrust that stretches
spinal structures beyond the normal range and is frequently
accompanied by a cracking or popping sound. For acute
LBP, current evidence suggests that manipulative therapy is
no more effective than conventional medical therapy.18
There is no evidence that ongoing manipulation reduces
the risk of recurrence of LBP.55 There is insufficient evidence regarding the efficacy of massage and acupuncture in
the treatment of acute LBP.18
Application of heat by heating pads or blankets is a
reasonable self-care option for short-term relief of acute
LBP. There is, however, insufficient evidence to recommend
application of cold packs or the use of corsets and braces.18
Traction provides no significant benefit for LBP patients
with or without sciatica.56
Injection therapy is used mostly in subacute (>6 weeks)
and chronic LBP. Epidural corticosteroid injections have
gained remarkable, but unjustified, popularity. The rationale
for their use is that the genesis of radicular pain, when a
herniated disk impinges on a nerve root, is at least partly
related to locally induced inflammation. Indeed, there is
evidence of moderate benefit compared with placebo injection for short-term relief of leg pain in patients with radiculopathy due to a herniated nucleus pulposus.57 However,
epidural corticosteroid injections offer no significant functional benefit, nor do they reduce the need for surgery. It
is important to note that there is no evidence for the effectiveness of epidural corticosteroid injections in LBP patients
without radiculopathy.
A variety of other injection therapies using glucocorticoids or anesthetic agents, often in combination, are used
in individuals with LBP with or without radicular pain and
other symptoms in the leg. These include injection of trigger
points, ligaments, sacroiliac joints, facet joints, and intradiskal steroid injections. There is no convincing evidence of
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PART 6 | DIFFERENTIAL DIAGNOSIS OF REGIONAL AND DIFFUSE MUSCULOSKELETAL PAIN
the efficacy of these interventions.58,59 Medial branch block
for presumed facet joint pain and nerve root blocks for
therapeutic or diagnostic purposes are also not recommended.59 Unfortunately these invasive and expensive procedures are commonly used in interventional pain clinics.
A number of physical therapy modalities are currently
used in the treatment of patients with subacute and chronic
LBP. These include transcutaneous electrical nerve stimulation (TENS), percutaneous electrical nerve stimulation,
interferential therapy, low-level laser therapy, shortwave
diathermy, and ultrasound. There is insufficient evidence of
efficacy to recommend their use.
Vertebral compression fractures secondary to osteoporosis are common. There is resolution of pain with fracture
healing within a few weeks in most patients. Vertebroplasty
and balloon kyphoplasty are two increasingly popular, invasive, and expensive procedures that are being used for the
treatment of persistent pain associated with these fractures.
Both procedures involve the percutaneous placement of
needles into the vertebral body through or lateral to the
pedicles, as well as the injection of bone cement to stabilize
the fracture. Kyphoplasty differs from vertebroplasty in that
the cement is injected into a void in the vertebral body
created by inflation of a balloon. Several early studies had
suggested a positive treatment effect for vertebroplasty.60
However, two blinded, randomized, placebo-controlled
trials of vertebroplasty for painful osteoporotic spinal fractures found no beneficial effect of vertebroplasty as compared with a sham procedure.61,62 Therefore on the basis of
current evidence, the routine use of vertebroplasty or indeed
kyphoplasty for relief of pain from osteoporotic compression
fractures cannot be justified.
Chronic Low Back Pain
The clinical spectrum in patients with chronic LBP is wide.
Some complain of severe, unrelenting pain, but most have
a nagging mechanical LBP that may radiate into the buttocks and upper thighs. Patients with chronic LBP may
experience periods of acute exacerbation. These exacerbations are managed according to the principles discussed
earlier. A significant number of patients with chronic LBP
remain functional and continue working, but overall the
results of treatment are unsatisfactory and complete relief
of pain is unrealistic for most. Patients with chronic LBP
are largely responsible for the high costs associated with
LBP. It is therefore incumbent on physicians who treat these
patients to judiciously use proven therapies.
For most patients, first-line medication options are acetaminophen or NSAIDs. They may provide some degree of
analgesia, but the evidence for their long-term efficacy is
not compelling. Opioid analgesics or tramadol are an option
when used judiciously in patients with severe disabling pain.
Because of substantial risks including aberrant drug-related
behaviors with long-term use in patients vulnerable to abuse
or addiction, potential benefits and harms of opioid analgesics should be carefully weighed before starting therapy.18,63
There is no evidence that long-acting, around-the-clock
dosing is more effective than short-acting or as-needed
dosing, and continuous exposure to opioids could induce
tolerance and lead to dose escalations.5 Muscle relaxants are
not recommended for long-term use in patients with chronic
stable LBP. Antidepressants that inhibit norepinephrine
uptake are thought to have pain-modulating properties
independent of their effects on depression. As such, lowdose tricyclic antidepressants are an option for chronic LBP,
although the treatment effect is small and adverse side
effects are common.5 There is no evidence of efficacy of
selective serotonin reuptake inhibitors for LBP. Depression
is, however, common in patients with chronic LBP and
should be treated appropriately. Duloxetine, a serotoninnorepinephrine reuptake inhibitor, may have marginal efficacy in patients with chronic LBP.64,65 There is insufficient
evidence to recommend antiepileptic medications such as
gabapentin and topiramate for pain relief in patients with
LBP with or without radiculopathy.5
An individually tailored physical therapy program and
patient education, as discussed in the section earlier on the
treatment of acute LBP, are particularly important aspects
in the management of a patient with chronic LBP. The use
of physical therapy modalities and injection techniques (as
discussed earlier) is not recommended for patients with
chronic LBP. Lumbar supports and traction are ineffective.
For most patients with LBP a medium-firm mattress or a
back-conforming mattress (waterbed or foam) may be superior to a firm mattress.66,67
A number of physical treatments have been used in treating chronic LBP. Spinal manipulation has been shown to
be superior to sham manipulation but is no more effective
than conservative medical therapy.68 There is less evidence
for the efficacy of massage and acupuncture.68
There has been a proliferation of nonsurgical interventional therapies for back pain. Chemonucleolysis is used for
the treatment of herniated disks with intradiskal injections
of chymopapain (extracted from papaya). Chymopapain
enzymatically digests the nucleus pulposus while leaving the
annulus fibrosus intact. Potentially life-threatening anaphylactic reactions have occurred rarely. Chemonucleolysis has
lost favor in the United States but remains popular in
Europe. Radiofrequency denervation has most commonly
been used for the treatment of presumed facet joint pain by
targeting the medial branch of the primary dorsal ramus. It
involves fluoroscopic placement of an electrode near the
nerve and application of heat by using a radiofrequency
current to coagulate the nerve. There is a lack of convincing
evidence about the effectiveness of this invasive procedure.58 Intradiskal electrothermal therapy (IDET) and percutaneous intradiskal radiofrequency thermocoagulation
(PIRFT) involve placement of an electrode into the intervertebral disk of patients with presumed diskogenic pain
and using electric or radiofrequency current to provide heat
to thermocoagulate and shrink intradiskal tissue and destroy
nerves. Current evidence does not support the use of IDET
or PIRFT.58,69 Prolotherapy (also referred to as sclerotherapy)
involves repeated injections of an irritant sclerosing agent
into ligaments and tendinous attachments. It is based on
the hypothesis that back pain in some patients stems from
weakened ligaments and repeated injections of a sclerosing
agent will strengthen the ligaments and reduce pain. On
the basis of trial data, a guideline from the American Pain
Society recommends against prolotherapy for chronic LBP.58
Spinal cord stimulation is a procedure involving
the placement of electrodes, percutaneously or by laminectomy, in the epidural space adjacent to the area of the
CHAPTER 47 spine presumed to be the source of pain and applying an
electric current in order to achieve sympatholytic and other
neuromodulatory effects.58 Power for the spinal cord stimulator is supplied by an implanted battery. Spinal cord stimulation is associated with a greater likelihood for pain relief
compared with reoperation or conventional medical management in patients with failed back surgery syndrome
with persistent radiculopathy.58 At present there is no
good evidence for the use of spinal cord stimulation for
chronic LBP not related to the failed back surgery or failed
back surgery syndrome without radiculopathy. Approximately a third of the patients involved in studies have
experienced a com­plication following spinal cord stimulation implanta­­tion including electrode migration, infection,
wound breakdown, and lead- and generator pocket–related
complications.58
Intraspinal drug infusion systems, using a subcutaneously
implanted pump with attached catheter, have been used in
some patients with chronic intractable LBP for the intrathecal delivery of analgesics, usually morphine. Adequate evidence to support this intervention is not available.
Chronic LBP is a complex condition that involves biologic, psychologic, and environmental factors. For patients
with persistent and disabling nonradicular LBP despite recommended noninterdisciplinary therapies, the clinician
should strongly consider intensive interdisciplinary rehabilitation with an emphasis on cognitive-behavioral
therapy.59 Interdisciplinary rehabilitation (also called multidisciplinary therapy) is an intervention that combines and
coordinates physical, vocational, and behavioral components and is provided by multiple health professionals
with different clinical backgrounds. Cognitive-behavioral
therapy is a psychotherapeutic intervention that involves
working with cognitions to change emotions, thoughts, and
behaviors. There is strong evidence of improved function
and moderate evidence of pain improvement with intensive
interdisciplinary rehabilitation programs.23 Functional restoration (also called work hardening) is an intervention that
involves simulated or actual work in a supervised environment in order to enhance job performance skills and
improve strength, endurance, flexibility, and cardiovascular
fitness in injured workers. When combined with a cognitivebehavioral component, functional restoration is more
effective than standard care alone for reducing time lost
from work.68
As previously discussed, the precise identification of the
pain generator in an LBP patient with degenerative changes
involving the lumbar spine and no radicular pain is usually
not possible in contradistinction to the patient with radicular symptoms. It is therefore not surprising that as a general
rule the results of back surgery are disappointing when the
goal is relief of back pain rather than relief of radicular
symptoms resulting from neurologic compression. As such,
the role of surgical treatment for chronic disabling LBP
without neurologic involvement in patients with degenerative disease remains controversial. The most common
surgery performed is spinal fusion. Interbody fusion is
achieved from either a posterior or an anterior approach or
both combined for a circumferential fusion. All fusion techniques involve placement of a bone graft between the vertebrae. Instrumentation refers to the use of hardware such
as screws, plates, or cages that serve as an internal splint
| Low Back Pain
679
while the bone graft heals. Bone morphogenetic proteins
are sometimes used to speed fusion. The rationale for fusion
is based on its successful use at painful peripheral joints.
The current evidence is that for nonradicular back pain
with degenerative changes, fusion is no more effective than
intensive interdisciplinary rehabilitation but is associated
with small to moderate benefits compared with standard
nonsurgical care.70 Furthermore, the majority of patients
who undergo surgery do not experience an optimal outcome
defined as no pain, discontinuation or occasional pain medication use, and return of high-level function.59
Lumbar disk replacement using a prosthetic disk is a
newer alternative to fusion. Disk replacement is approved
in the United States for patients with disease limited to one
disk between L3-S1 and no spondylolisthesis or neurologic
deficit. No data support the hypothetical advantage that,
unlike spinal fusion, prosthetic disks will protect adjacent
levels from further degeneration by preserving motion. At
present there is insufficient evidence regarding long-term
benefits and harms of disk replacement to support
recommendations.
Nerve Root Compression Syndromes
Disk Herniation
Patients with a herniated disk with radicular pain secondary
to nerve root compression should be treated nonsurgically,
as described in the section on acute LBP unless they have
a serious or progressive neurologic deficit. Only about 10%
of patients have sufficient pain after 6 weeks of conservative
care that surgery is considered.11 A decision to continue
with nonsurgical therapy beyond 6 weeks in these patients
does not increase risk for paralysis or cauda equina syndrome.59 Surgery in these patients is associated with moderate short-term (through 6 to 12 weeks) benefits compared
with nonsurgical therapy, though differences in outcome
diminish with time and are generally no longer present after
1 to 2 years.56,59
Open diskectomy or microdiskectomy is the usual surgery
performed on patients with serious or progressive neurologic
deficit or electively on patients with persistent disabling
pain secondary to radiculopathy (Table 47-4). Open dis­
kectomy generally involves a laminectomy, whereas micro­
diskectomy, using a smaller incision and an operating
microscope, involves a hemilaminectomy to remove the
disk fragment compressing the nerve root. There are no
Table 47-4 Indications for Surgical Referral
Disk Herniation
Cauda equina syndrome (emergency)
Serious neurologic deficit
Progressive neurologic deficit
Greater than 6 weeks of disabling radiculopathy (elective)
Spinal Stenosis
Serious neurologic deficit
Progressive neurologic deficit
Persistent and disabling pseudoclaudication (elective)
Spondylolisthesis
Serious or progressive neurologic deficit
680
PART 6 | DIFFERENTIAL DIAGNOSIS OF REGIONAL AND DIFFUSE MUSCULOSKELETAL PAIN
clear differences in the outcome between open diskectomy
and microdiskectomy. There is insufficient evidence to
evaluate the efficacy of sequestrectomy, or various laserassisted, endoscopic, percutaneous, and other minimally
invasive methods.70,71
Epidural corticosteroid injections may offer moderate
benefit for short-term relief of radicular pain but do not offer
significant functional benefit and do not reduce the need
for surgery.57
Anti–tumor necrosis factor therapy is under investigation in patients with lumbar radiculopathy. A small randomized controlled trial with addition of a short course of
adalimumab to the treatment regimen of patients with
severe and acute sciatica resulted in a small decrease in leg
pain and fewer surgical procedures.72 However, another randomized controlled trial found no difference between infliximab and a saline infusion.73
Spinal Stenosis
It is critical to understand the natural history of degenerative lumbar spinal stenosis before making treatment decisions. The symptoms of spinal stenosis remain stable for
years in most patients and may improve in some. Dramatic
improvement is uncommon. Even when symptoms progress,
there is little likelihood of rapid deterioration of neurologic
function. Therefore conservative nonoperative treatment is
a rational choice for most patients.
There is a paucity of good data to guide the conservative
management of lumbar spinal stenosis. Physical therapy is
the mainstay of management, but evidence for the efficacy
of specific standardized regimens is not available. Most regimens include core strengthening, stretching, aerobic con­
ditioning, loss of excess weight, and patient education.
Exercises that involve lumbar flexion such as bicycling are
better tolerated. Strengthening of abdominal muscles may
be helpful by promoting lumbar flexion and reducing lumbar
lordosis. Lumbar corsets that maintain slight flexion may
provide symptomatic relief. They should only be used for a
limited number of hours a day to avoid atrophy of paraspinal
muscles.
Acetaminophen, NSAIDs, and mild narcotic analgesics
are used for symptomatic relief of pain.
Lumbar epidural corticosteroid injections are used on the
assumption that symptoms may result from inflammation at
the interface between the nerve root and compressing
tissues.32 A small randomized controlled trial showed a
reduction in pain and improvement in function at 6 months
following use of epidural steroid injections.74 However,
observational data suggest that epidural injections do not
influence functional status or the need for surgery at 1 year.75
Surgery is indicated for the few patients with lumbar
spinal stenosis who have a serious or progressive neurologic
deficit. However, most surgery for lumbar spinal stenosis is
elective. The indication for elective surgery is to relieve
persistent and disabling symptoms of neurogenic claudication that have not responded to conservative care. In
patients without fixed neurologic deficits, delayed surgery
produces similar benefits to surgery selected as the initial
treatment.32,76 The surgical goal is to decompress the central
spinal canal and the neural foramina to eliminate pressure
on the nerve roots. This is accomplished by laminectomy,
partial facetectomy of hypertrophied facet joints, and excision of the hypertrophied ligamentum flavum and any protruding disk material. Laminectomy with lumbar fusion
should generally be reserved for patients who have spinal
stenosis with spondylolisthesis. Unfortunately there is an
alarming increase in spinal fusion surgery with routine use
of complex fusion techniques in the absence of evidence of
greater efficacy. The techniques include instrumentation,
bone graft augmentation with bone cement and human
bone morphogenetic proteins, and combined anterior and
posterior fusion (often at multiple levels). These techniques
are associated with increased perioperative mortality, major
complications, rehospitalization, and cost.77-79
Overall, for patients with spinal stenosis, with or without
spondylolisthesis, who have disabling symptoms of neurogenic claudication despite conservative care, there is some
evidence supporting the effectiveness of decompressive
laminectomy in reducing pain and improving function
through 1 to 2 years.32,59,70 Beyond this time frame the benefits appear to diminish.
A less invasive alternative to decompressive laminectomy is the implantation of a titanium interspinous spacer
at one or two vertebral levels. This spacer distracts adjacent
spinous processes and thereby imposes lumbar flexion,
which in turn potentially increases the spinal canal dimensions. There is preliminary evidence of efficacy in patients
with one- or two-level spinal stenosis, without spondylolisthesis, and with a history of relief of neurogenic claudication
with flexion.70 There are no trials comparing the interspinous spacer with decompressive surgery.
Spondylolisthesis
The vast majority of patients with spondylolisthesis and
chronic LBP are treated conservatively. Rarely a patient
may need decompression surgery with fusion if a serious or
progressive neurologic deficit develops from nerve root
impingement or the patient develops disabling pseudoclaudication secondary to spinal stenosis. A randomized trial
involving patients with isthmic spondylolisthesis and disabling isolated LBP or sciatica for at least a year suggested
better results from fusion surgery than from nonsurgical
care,80 although the differences in outcome narrowed over
a 5-year follow-up period.81
OUTCOME
The natural history of acute LBP is favorable. There is
substantial improvement in pain and function within a
month in the majority of patients,3 and more than 90% are
better at 8 weeks.4 Only about a third of patients with acute
LBP seek medical care. Presumably the rest improve on
their own. Relapses that also tend to be brief are common
and may affect up to 40% of patients within 6 months.
Improvement is also the norm for patients with sciatica
secondary to a herniated disk.82 A third of these patients are
significantly better in 2 weeks, and 75% improve after 3
months.8 Only about 10% of these patients ultimately
undergo surgery.
The symptoms of spinal stenosis tend to remain stable in
70%, improved in 15%, and worsened in 15%.35
CHAPTER 47 The 7% to 10% of patients who develop chronic pain
are largely responsible for the high costs associated with
LBP and remain a major challenge. Factors that predict
persistence of chronic disabling LBP include maladaptive
pain coping behaviors, presence of nonorganic signs, functional impairment, poor general health status, psychiatric
comorbidities, job dissatisfaction, disputed compensation
claims, and a high level of “fear avoidance” (an exaggerated fear of pain leading to avoidance of beneficial
activities).23,83
SUMMARY
The outcome for most patients with LBP is good. The management of patients with chronic LBP, however, remains a
challenge. The results of conservative and surgical management in these patients are unsatisfactory. There has been a
proliferation and increasing utilization of a large number of
expensive but unproven nonsurgical interventional techniques and physical therapy modalities.
Surgical intervention is indicated in the presence of a
serious or progressive neurologic deficit. However, surgery
in the absence of neurologic deficits, especially spinal fusion
for degenerative changes, is controversial and not clearly
effective. Rates of back surgery (including spinal fusion) in
the United States are the highest in the world and continue
to rise rapidly.70 A particularly worrisome trend is the
routine use of complex fusion techniques (with associated
increased perioperative mortality, major complications, and
cost) in the absence of evidence of greater efficacy.77-79 The
use of sham surgery in controlled trials is controversial for
ethical reasons. However, randomized trials incorporating a
sham operation may be justifiable to test the efficacy of
spinal fusion because the surgery is not performed for a lifethreatening condition, the primary clinical outcomes are
subjective, and the rate of complications is high.79
An Australian study indicated that a television campaign advising people with back pain to stay active and keep
working reduced work-injury claims and medical expenses
and had a sustained effect of altering physicians’ and
patients’ perceptions regarding back pain.84 Perhaps public
health initiatives may help prevent episodes of LBP from
becoming chronic and disabling.23
References
1. Kelsey JL, White AA: Epidemiology and impact of low back pain,
Spine 5:133–142, 1980.
2. Wildstein MS, Carragee EJ: Low back pain. In Firestein GS, Budd
RC, Harris ED, et al, editors. Kelley’s textbook of rheumatology, ed 8,
Philadelphia, 2008, Elsevier, pp 617–625.
3. Pengel LH, Herbert RD, Maher GC, Refshauge KM: Acute low back
pain: systematic review of its prognosis, BMJ 7410:323–327, 2003.
4. Isaac Z, Katz J, Borenstein DG: Lumbar spine disorders. In Hochberg
MC, Silman AJ, Smolen JS, et al, editors. Rheumatology, ed 4, Philadelphia, 2010, Elsevier, pp 593–618.
5. Chou R: Pharmacological management of low back pain, Drugs
70(4):384–402, 2010.
6. Dixit RK: Approach to the patient with low back pain. In Imboden
J, Hellmann D, Stone J, editors. Current diagnosis and treatment in
rheumatology, ed 2, New York, 2007, McGraw-Hill, pp 100–110.
7. Chou R, Shekelle P: Will this patient develop persistent disabling
low back pain? JAMA 303(13):1295–1302, 2010.
8. Jarvik JG, Deyo RA: Diagnostic evaluation of low back pain with
emphasis on imaging, Ann Intern Med 137:586–597, 2002.
| Low Back Pain
681
9. Dixit RK, Schwab JH: Low back and neck pain. In Stone JH, editor.
A clinician’s pearls and myths in rheumatology. New York, 2009,
Springer.
10. Dixit RK, Dickson DJ: Low back pain. In Adebajo A, editor. ABC
of rheumatology, ed 4, Hoboken, NJ, 2010, Wiley-Blackwell.
11. Deyo RA, Weinstein DO: Low back pain, N Engl J Med 344(5):363–
370, 2001.
12. Gran JT: An epidemiological survey of the signs and symptoms of
ankylosing spondylitis, Clin Rheumatol 4:161–169, 1985.
13. Deyo RA, Rainville J, Kent DL: What can the history and physical
examination tell us about low back pain? JAMA 268:760–765, 1992.
14. Vroomen PC, de Krom MC, Knottnerus JA: Diagnostic value of
history and physical examination in patients suspected of sciatica due
to disk herniation: a systematic review, J Neurol 246:899–906, 1999.
15. Waddell G, McCullogh JA, Kummel E, Venner RM: Non-organic
physical signs in low back pain, Spine 5:117–125, 1980.
16. Chou R, Fu R, Carrino JA, Deyo RA: Imaging strategies for low back
pain: systematic review and meta-analysis, Lancet 373:463–472,
2009.
17. Deyo RA: Diagnostic evaluation of LBP, Arch Intern Med 162:1444–
1447, 2002.
18. Chou R, Qaseem A, Snow V, et al: Diagnosis and treatment of low
back pain: a joint clinical practice guideline from the American
College of Physicians and the American Pain Society, Ann Intern
Med 147(7):478–491, 2007.
19. Frymoyer JW, Newberg A, Pope MH, et al: Spine radiographs in
patients with low back pain: an epidemiological study in men, J Bone
Joint Surg Am 66:1048–1055, 1984.
20. Tullberg T, Svanborg E, Issacsson J, et al: A preoperative and postoperative study of the accuracy and value of electrodiagnosis in
patients with lumbosacral disc herniation, Spine 18:837–842, 1993.
21. Deyo RA: Early diagnostic evaluation of low back pain, J Gen Intern
Med 1:328–338, 1986.
22. Van Tulder MW, Assendelft WJ, Koes BW, et al: Spinal radiographic
findings and nonspecific low back pain. A systematic review of observational studies, Spine 22:427–434, 1997.
23. Carragee EJ: Persistent low back pain, N Engl J Med 352(18):1891–
1898, 2005.
24. Carragee EJ, Paragiondakis SJ, Khurana S: 2000 Volvo Award winner
in clinical studies: lumbar high-intensity zone and discography in
subjects without low back problems, Spine 25:2987–2992, 2000.
25. Jensen MC, Brandt-Zawadski MN, Obuchowski N, et al: Magnetic
resonance imaging of the lumbar spine in people without back pain,
N Engl J Med 331:69–73, 1994.
26. Winstein PR: Anatomy of the lumbar spine. In Hardy RW, editor.
Lumbar disc disease, ed 2, New York, 1993, Raven Press, p 5.
27. Dammers R, Koehler PJ: Lumbar disc herniation: level increases with
age, Surg Neurol 58:209–212, 2002.
28. Tarulli AW, Raynor EM: Lumbosacral radiculopathy, Neurol Clin
25:387, 2007.
29. Bozzao A, Gallucci M, Masciocchi C, et al: Lumbar disc herniation:
MR imaging assessment of natural history in patients treated without
surgery, Radiology 185:135–141, 1992.
30. Oegema TR: Intervertebral disc herniation: does the new player up
the ante? Arthritis Rheum 62:1840–1842, 2010.
31. Fredrickson BE, Baker D, McHolick WJ, et al: The natural history
of spondylosis and spondylolisthesis, J Bone Joint Surg Am 66:699,
1984.
32. Katz JN, Harris MB: Lumbar spinal stenosis, N Engl J Med 358(8):818–
825, 2008.
33. Rydevik, B: Neurophysiology of cauda equina compression, Acta
Orthop Scand Suppl 251:52, 1993.
34. Katz JN, Dalgas M, Stucki G, et al: Degenerative lumbar spinal stenosis: diagnostic value of the history and physical examination,
Arthritis Rheum 38:1236–1241, 1995.
35. Johnsson KE, Rosen I, Uden A: The natural course of lumbar spinal
stenosis, Clin Orthop Relat Res Jun:82–86, 1992.
36. Utsinger PD: Diffuse idiopathic skeletal hyperostosis, Clin Rheum Dis
11:325, 1985.
37. Julkunen H, Heinonen OP, Pyorala K: Hyperostosis of the spine in
an adult population: its relation to hyperglycemia and obesity, Ann
Rheum Dis 30:605, 1971.
38. Kiss C, O’Neill TW, Mituszova M, et al: The prevelance of diffuse
idiopathic skeletal hyperostosis in a population-based study in
Hungary, Scand J Rheumatol 31:226, 2002.
682
PART 6 | DIFFERENTIAL DIAGNOSIS OF REGIONAL AND DIFFUSE MUSCULOSKELETAL PAIN
39. Resnick D, Shapiro RF, Wiesner KB, et al: Diffuse idiopathic skeletal
hyperostosis (DISH) [ankylosing hyperostosis of Forestier and RotesQuerol], Semin Arthritis Rheum 7:153, 1978.
40. Bundrick TJ, Cook DE, Resnik CS: Heterotopic bone formation in
patients with DISH following total hip replacement, Radiology
155:595, 1985.
41. Deyo RA, Diehl AK: Cancer as a cause of back pain: frequency,
clinical presentation, and diagnostic strategies, J Gen Intern Med
3:230–238, 1988.
42. Grossman SA, Krabak MJ: Leptomeningeal carcinomatosis, Cancer
Treat Rev 25:103, 1999.
43. Olson DO, Shields AF, Scheurich CJ, et al: Imaging of tumors of the
spinal canal and cord, Radiol Clin North Am 26:965, 1988.
44. Klein MH, Shankman S: Osteoid osteoma: radiologic and pathologic
correlation, Skeletal Radiol 21:23, 1992.
45. Mylona E, Samarkos M, Kakalou E, et al: Pyogenic vertebral osteomyelitis: a systemic review of clinical characteristics, Semin Arthritis
Rheum 39:10–17, 2009.
46. Zimmerli W: Vertebral osteomyelitis, N Engl J Med 362(11):1022–
1029, 2010.
47. Dell’Atti C, Cassar-Pullicino VN, Lalam RK, et al: The spine in
Paget’s disease, Skeletal Radiol 36:609–626, 2007.
48. Slipman CW, Sterenfeld EB, Chou LH, et al: The predictive value
of provocative sacroiliac joint stress maneuvers in the diagnosis of
sacroiliac joint syndrome, Arch Phys Med Rehab 79:288, 1998.
49. Riddle DL, Freburger JK: Evaluation of the presence of sacroiliac
joint region dysfunction using a combination of tests: a multicenter
intertester reliability study, Phys Ther 82:772, 2002.
50. O’Shea FD, Boyle E, Salonen DC, et al: Inflammatory and degenerative sacroiliac joint disease in a primary back pain cohort, Arthritis
Care Res 62:447–454, 2010.
51. Curtis P, Gibbons G, Price F: Fibro-fatty nodules and low back pain.
The back mouse masquerade, J Fam Pract 49:345, 2000.
52. Fast A, Shapiro D, Docommun EJ, et al: Low back pain in pregnancy,
Spine 12:368, 1987.
53. Coste J, Delecoeuillerie G, Cohen deLara A, et al: Clinical course
and prognostic factors in acute low back pain: an inception cohort
study in primary care practice, BMJ 308:577, 1994.
54. Malmivaara A, Hakkinen U, Aro T, et al: The treatment of acute
low back pain—bed rest, exercises, or ordinary activity? N Engl J Med
332(6):351–355, 1995.
55. Cherkin DC, Deyo RA, Battie M, et al: A comparison of physical
therapy, chiropractic manipulation, and provision of an educational
booklet for the treatment of patients with low back pain, N Engl J
Med 339:1021–1029, 1998.
56. Clarke JA, van Tulder MW, Blomberg SE, et al: Traction for low back
pain with or without sciatica, Cochrane Database Syst Rev
(23):CD003010, 2007.
57. Carette S, Leclaire R, Marcouxs S, et al: Epidural corticosteroid
injections for sciatica due to herniated nucleus pulposus, N Engl J
Med 336(23):1634–1640, 1997.
58. Chou R, Atlas SJ, Stanos SP, et al: Nonsurgical interventional therapies for low back pain. A review of the evidence for an American
Pain Society Clinical Practice Guideline, Spine 34(10):1078–1093,
2009.
59. Chou R, Loeser JD, Owens DK, et al: Interventional therapies,
surgery, and interdisciplinary rehabilitation for low back pain. An
evidence based clinical practice guideline from the American Pain
Society, Spine 34(10):1066–1077, 2009.
60. Weinstein JN: Balancing science and informed choice in decisions
about vertebroplasty, N Engl J Med 361(6):619–621, 2009.
61. Kallmes DF, Comstock BA, Heagerty PJ, et al: A randomized trial of
vertebroplasty for osteoporotic spinal fractures, N Engl J Med
361(6):569–579, 2009.
62. Buchbinder R, Osborne RH, Ebeling PR, et al: A randomized trial of
vertebroplasty for painful osteoporotic vertebral fractures, N Engl J
Med 361(6):557–568, 2009.
63. Martell BA, O’Connor PG, Kerns RD, et al: Systematic review:
opioid treatment for chronic back pain: prevalence, efficacy, and
association with addiction, Ann Intern Med 146:116–127, 2007.
64. Skljarevski V, Desaiah D, Liu-Seifert H, et al: Efficacy and safety of
duloxetine in chronic low back pain, Spine 35(13):E578–E585, 2010.
65. Skljarevski V, Ossanna M, Liu-Seifert H, et al: A double-blind, randomized trial of duloxetine versus placebo in the management of
chronic low back pain, Eur J Neurol 16(9):1041–1048, 2009.
66. Kovacs FM, Abraira V, Pena A, et al: Effect of firmness of mattress
on chronic non-specific low back pain: randomized, double-blind,
controlled, multicentre trial, Lancet 362:1599, 2003.
67. Bergholdt K, Fabricius RN, Bendix T: Better backs by better beds?
Spine 33:703, 2008.
68. Chou R, Huffman LH: Nonpharmacologic therapies for acute and
chronic low back pain: a review of the evidence for an American
Pain Society/American College of Physicians Clinical Practice
Guideline, Ann Intern Med 147(7):492–514, 2007.
69. Urrutia G, Kovacs F, Nishishinya MD, Olabe J: Percutaneous thermocoagulation intradiscal techniques for discogenic low back pain,
Spine 32:1146, 2007.
70. Chou R, Baisden J, Carragee EJ, et al: Surgery for low back pain. A
review of the evidence for an American Pain Society Clinical Practice Guideline, Spine 34(10):1094–1109, 2009.
71. Peul WC, van Houwelingen HC, van den Hout WB, et al: Surgery
versus prolonged conservative treatment for sciatica, N Engl J Med
356:2245–2256, 2007.
72. Genevay S, Viatte S, Finckh A, et al: Adalimumab in severe and
acute sciatica, Arthritis Rheum 62:2339–2346, 2010.
73. Korhonen T, Karppinen J, Paimela L, et al: The treatment of discherniation-induced sciatica with infliximab: one-year follow-up
results of FIRST II, a randomized controlled trial, Spine 31(24):2759–
2766, 2006.
74. Koc Z, Ozcakir S, Sivrioglu K, et al: Effectiveness of physical therapy
and epidural steroid injections in lumbar spinal stenosis, Spine
34(10):985–989, 2009.
75. Armon C, Argoff CE, Samuels J, Backonja MM: Assessment: use of
epidural steroid injections to treat radicular lumbosacral pain: report
of the Therapeutics and Technology Assessment Subcommittee of
the American Academy of Neurology, Neurology 68:723–729, 2000.
76. Amundsen T, Weber H, Nordal JH, et al: Lumbar spinal stenosis:
conservative or surgical management? A prospective 10 year study,
Spine 25:1424, 2000.
77. Carragee EJ: The increasing morbidity of elective spinal stenosis
surgery. Is it necessary? JAMA 303(13):1309–1310, 2010.
78. Deyo RA, Mirza SK, Martin BI, et al: Trends, major medical complications, and charges associated with surgery for lumbar spinal stenosis
in older adults, JAMA 303(13):1259–1265, 2010.
79. Deyo RA, Nachemson A, Mirza S: Spinal fusion surgery—the case
for restraint, N Engl J Med 350(7):722–726, 2004.
80. Moller H, Hedlund R: Surgery versus conservative management in
adult isthmic spondylolisthesis—a prospective randomized study: part
1, Spine 25:1711–1715, 2000.
81. Ekman P, Moller H, Hedlund R: The long-term effect of posterolateral fusion in adult isthmic spondylolisthesis: a randomized controlled
study, Spine J 5(1):36–44, 2005.
82. Vroomen P, deKrom M, Knottnerus JA: Predicting the outcome of
sciatica at short-term follow-up, Br J Gen Pract 52:119, 2002.
83. Chou R, Shekelle P: Will this patient develop persistent disabling
low back pain? JAMA 303(13):1295–1302, 2010.
84. Buchbinder R, Jolley D: Population based intervention to change
back pain beliefs: three year follow up population survey, BMJ
328:321, 2004.
The references for this chapter can also be found on www.expertconsult.com.