33 Low Back Pain

Anwar Suhaimi

This chapter elucidates the role of the physiatrist in the prevention, management,
and treatment of low back pain (LBP).

•   EPIDEMIOLOGY
LBP is a symptom, not a disease, and it has many causes. The lifetime prevalence
of LBP approximates 84%. Most attacks are mild to moderate and recur, but they
do not limit activities; thus the majority of individuals with LBP do not seek medi-
cal care. Ten to fifteen percent of acute LBP becomes chronic; 1% of LBP pro-
gresses to permanent disability, consuming up to 90% of health care and social
costs for back pain in the United States. Societal acceptance of back pain disability
and provision of disability benefits for back pain sufferers contribute to the increas-
ing trend of disabling LBP. 

•   ANATOMY AND BIOMECHANICS OF THE LOWER

BACK
The size and shape of the five lumbar vertebrae confer strength to the lumbar spine
for support and protection, while the lumbar lordosis confers flexibility. I­ntervertebral
disks consist of an internal gelatinous nucleus pulposus and an outer annulus fibro-
sus (with its fibrous layers). The annulus fibrosus is a shock absorber (eSlide 33.1);
broken fibers of the annulus result in a herniated nucleus pulposus (eSlide 33.2).
Zygapophyseal joints are paired synovial joints with a capsule, which resist vertebral
rotation and thus limit torsional stress on the lumbar disks. There are two longitudi-
nal ligaments: the anterior and posterior longitudinal ligaments. There are also seg-
mental ligaments: (1) the paired ligamentum flavum joining adjacent laminae, which
are very strong but allow flexion; and (2) the supraspinous, i­nterspinous, and inter-
transverse ligaments, which resist flexion and prevent excessive shear forces during
forward bending. Muscles of the lumbar region can be divided into three functional
groups: (1) those originating from the lumbar spine, which are made up of the ante-
rior muscles (eSlide 33.3); (2) the abdominal brace (eSlide 33.4); and (3) the pelvic
stabilizers. 

•   PAIN GENERATORS OF THE LUMBAR SPINE

Structures with nociceptive innervations are potential sources of pain (eSlide
33.5). Innervations of the pain generators are as follows: (1) sinuvertebral nerve,
innervating the external annulus fibrosus and posterior longitudinal ligament; (2)
medial branch of the dorsal primary ramus, innervating the zygapophyseal joint
and multifida; (3) branches of the dorsal primary ramus, innervating the posterior
vertebral body and lumbar paraspinal musculature and fascia; and (4) gray ramus

228
 CHAPTER 33  Low Back Pain   229

communicans (a branch of the lumbar sympathetic chain), innervating the anterior

longitudinal ligament.

Aging Spine: The Degenerative Cascade

Kirkaldy-Willis described the degenerative changes in the lumbar spine that result
in disk herniation, spondylotic changes, and eventually multilevel spinal stenosis
(eSlide 33.6). Axial compression forces on disks anteriorly or torsional stress on
zygapophyseal joints posteriorly may affect each other or occur simultaneously,
although these structures are anatomically separated. The first change is often an
annulus tear, which typically occurs posterolaterally. Internal disk disruption with-
out herniation of the nucleus pulposus may ensue, causing loss of disk height, joint
instability, and narrowing of the neural foramina and potential nerve root impinge-
ment. Changes at one level place stress on the adjacent levels, causing generalized
multilevel spondylotic changes. Synovial hypertrophy of the zygapophyseal joints
from repetitive microtrauma results in cartilage degeneration, leading to capsular
laxity and joint instability. The laxity, combined with repetitive abnormal joint
motion, leads to bony hypertrophy, which in turn causes narrowing of the central
canal and lateral recess and potential nerve root impingement.
The disk, the adjacent vertebrae (above and below), and the muscles and liga-
ments that act across this area form a functional segment. Segmental dysfunction can
occur when either a segment is too stiff or too mobile. Excessive mobility or func-
tional instability is caused by tissue damage, poor muscle endurance, poor muscle
control, or a combination of all three. Sufficient segmental stiffness is required to
prevent injury and allow for efficient movement. 

•   PROGRESSION OF ACUTE LOW BACK PAIN TOWARD

CHRONICITY
The experience of nociception is the sum of multiple facilitatory and inhibitory
pathways leading to central sensitization; this produces the continued perception of
chronic LBP, even when no pain generator is present in the area. Pain is an individ-
ual experience influenced by psychosocial factors, which explains the variable clini-
cal presentations that cannot be attributed to biomechanical and neurologic factors
alone. Psychosocial factors are linked to transition into chronic pain and disability.
Depression is present in up to 40% of people with chronic LBP. A vicious cycle then
leads to disability and more pain; depressed individuals tend to develop persistent
pain. Depression, anxiety, and distress are strongly related to pain intensity, duration,
and disability. Patients’ beliefs about pain and their coping mechanisms consistently
affect outcomes. Catastrophizing is characterized by excessively negative thoughts
about pain and high fear of movement and injury or reinjury (kinesiophobia); this
predicts more severe or disabling back pain. These sets of maladaptive pain coping
behaviors are the target of multidisciplinary pain programs that effectively decrease
fear-avoidance beliefs and catastrophizing and improve function. 

•   CLINICAL APPROACH TO LOW BACK PAIN

A thorough clinical history should be obtained to help determine the cause of the
LBP. The history should illicit the features of the pain and identify the presence
of serious medical diseases or red flag symptoms (eSlide 33.7). The presence of
230  SECTION IV ISSUES IN SPECIFIC DIAGNOSES

psychosocial factors (yellow flags) that are prognosticators for developing chronic
disabling pain should also be determined (eSlide 33.8). If red flags are present,
further diagnostic evaluation is necessary.
The physical examination (eSlide 33.9) should include a detailed neurologic exam-
ination. The accuracy of the neurologic examination in diagnosing a herniated disk is
moderate, but it can be increased if a combination of findings is present (eSlide 33.10).
Special tests for strength and flexibility are performed to detect deconditioning, poor
endurance, and muscle imbalances in the abdominal, back, and pelvic stabilizer muscles.
Lumbar segmental instability evaluation includes passive intervertebral motion testing
and the prone instability test. Assessment of areas above and below the lumbar spine
include palpation and evaluation of movement of the thoracic spine, determination of
the hip joint range of movement, and screening of the knee and ankle joints. The pres-
ence of nonorganic signs should be sought by identifying symptoms out of proportion
to the injury during the physical examination. Illness behaviors are learned behaviors
and responses used to convey distress, whereas avoidance behaviors are manifestation
of anxiety during the examination (e.g., poor effort during muscle strength testing).
Imaging of the low back is warranted only if specific pathology needs to be con-
firmed. It may include the following: (1) plain radiography after trauma, fractures,
or when other bony lesions are suspected; (2) magnetic resonance imaging (MRI)
for evaluating degenerative disk disease, disk herniation, and radiculopathy; (3)
computed tomography (CT) for bony lesions, especially in patients with excessive
hardware that obscure MRI images or implants that preclude MRI (pacemakers and
clips); and (4) scintigraphy or bone scan for occult fractures, bony metastases, and
infections. Bone scan is a sensitive but not specific imaging modality; single-photon
emission computed tomography (SPECT) is best to identify the z­ygapophyseal
joint as a source of pain. Electromyography is used for evaluating neurogenic
changes and denervation in radiculopathy, which will help identify which anatomic
lesion found on imaging is physiologically significant. Laboratory studies are used
as adjuncts in diagnosing inflammatory and neoplastic diseases. 

•   DIFFERENTIAL DIAGNOSIS AND TREATMENT: BACK

PAIN GREATER THAN LEG PAIN
Nonspecific LBP accounts for 85% of LBP with no specific diagnosis. It is multi-
factorial and may be the result of deconditioning, poor muscle recruitment, emo-
tional stress, injury and aging-related processes such as disk degeneration, arthritis
and ligamentous hypertrophy. Risk factors include obesity, smoking, very seden-
tary lifestyle, very vigorous physical activity, and genetic factors.
Lumbar spondylosis can be caused by degenerative disease of the zygapophyseal
joints. In older patients with other sources of LBP, such as degenerative disks and
lumbar stenosis, it may be difficult to identify the primary pain generator. Axial
back pain is typical, with referred pain extending into the buttocks and legs. Clini-
cally, spondylosis presents with accentuated lumbar lordosis, poor pelvic girdle
mechanics, and multiple myofascial sources for pain. Typically the hip flexors are
tight, which increases the stress on posterior elements thus increasing back pain.
Diagnostic testing includes fluoroscopy-guided zygapophyseal joint injections or
medial branch blocks with local anesthetic. According to the results of diagnostic
joint injections, the prevalence of facet-mediated pain in people with chronic LBP is
15% in younger populations and 40% in older age groups. Lumbar z­ygapophyseal
joint pain mainly originates from the L4-L5 and L5-S1 zygapophyseal joints.
 CHAPTER 33  Low Back Pain   231

Lumbar diskogenic causes of LBP can be divided into three categories: degen-
erative disk disease, internal disk disruption, and disk herniation. Diskogenic pain
is typically distributed in a bandlike pattern and exacerbated by lumbar flexion;
however, unilateral back pain radiating to the buttock can also be present. Atypi-
cally, pain can worsen by extension or side bending, depending on the site of disk
pathology. Internal disk disruption occurs when the disk’s internal architecture is
disrupted, but its external surface remains normal. It is characterized by nucleus
pulposus degradation and radial fissures that extend to the innervated outer third
of the annulus. Pain is generated through chemical nociception from inflammatory
mediators and mechanical stimulation. Disk herniation occurs when disk material
extends beyond the intervertebral disk space, either as a disk bulge or herniation (as
protruded or extruded, sequestrated or nonsequestrated, or contained or uncon-
tained) (eSlide 33.11). Disk herniation is further discussed later.
Imaging investigations alone are unreliable for diagnosing the cause of non-
specific LBP. Clinicians often combine treatment modalities to provide pain relief
and functional improvements. Reassurance and accurate, understandable patient
education help improve treatment adherence, reduce anxiety, and counter mis-
information about back pain. Patients are advised to continue ordinary activity
as normally as possible, leading to quicker recovery and lesser disability. Group
classes providing education about back pain (back schools) are effective in reducing
disability and pain in people with chronic LBP, but they do not prevent the occur-
rence of LBP.
Exercise prevents deconditioning in acute LBP and provides modest pain
relief in chronic LBP while producing additional health benefits and minimal side
effects; thus exercise is a first-line treatment choice. The goals are to strengthen
and increase the endurance of muscles to support the spine, improve flexibility,
establish normal patterns of muscle activity, and improve biomechanical efficiency.
Individualized exercise prescriptions for stretching and strengthening exercises of
the abdominal, low back, and hip muscles performed under supervision appear to
be most effective. Noncompliance is the main reason for failure of exercise treat-
ments. Exercise progression should be conducted in planned, fixed i­ncrements
based on goals, with leeway for temporary exacerbations of pain that may occur
along the way. Increasing exercise levels benefits pain beliefs and behaviors through
decreased fear-avoidance beliefs, anxiety reduction, positive reinforcement for
meeting goals, and personal confrontation to reduce fear of movement, reinjury,
and catastrophizing. Exercise in patients with LBP should consider general health
and fitness goals and include 30 minutes of moderate aerobic activity five times a
week, such as walking or aquatic exercises. No specific aerobic activity is superior
over another.
There is strong evidence that nonsteroidal antiinflammatory drugs (NSAIDs)
provide pain relief for acute and chronic LBP; no particular NSAID is superior.
Side effects of these drugs are well established, but the long-term benefits of
NSAID use are uncertain. Muscle relaxant use remains controversial, as muscle
spasms have not yet been implicated in LBP pathogenesis. Antispasticity medica-
tions have been effective for short-term pain relief in acute back pain. Tricyclic
antidepressants are effective in chronic LBP, whereas selective serotonin reuptake
inhibitors and trazodone are not. Short-acting opioids confer no superior outcomes
for pain or function. Long-acting opioids appear to provide better analgesia and
are well tolerated. Topical Capsicum frutescens (cayenne), Salix alba (white willow
bark), and Harpagophytum procumbens (devil’s claw) reduce pain more than placebo.
232  SECTION IV ISSUES IN SPECIFIC DIAGNOSES

Anticonvulsants, tramadol, lidocaine (lignocaine) patches, and topical irritant or

antiinflammatory creams have not yet been proven effective clinically.
Trigger point injections (dry needling, lidocaine alone, or lidocaine with corti-
costeroid) are the most studied techniques and are effective in providing long-term
pain relief for back pain. The efficacy of acupuncture is doubtful; however, it can
supplement other forms of treatment and has a low rate of complications. Botuli-
num toxin injection and prolotherapy have not yet been proven effective in treating
nonspecific back pain. Spinal manipulation has modest effectiveness, whereas trac-
tion is not effective. Lumbar support is no more effective than other treatments;
compliance is poor and it does not prevent the occurrence of back pain. Transcu-
taneous electrical nerve stimulation (TENS) provides temporary pain relief and
better function; however, long-term efficacy remains to be evaluated. Massage is
effective in pain relief and functional restoration, with beneficial results persisting
after 1 year in patients with subacute and chronic LBP. Complementary move-
ment therapies effective for LBP include yoga, the Alexander technique, and the
Feldenkrais method.
An interdisciplinary pain treatment program with the goal of functional res-
toration is helpful for severe chronic pain. Treatment of comorbidities, such as
depression, anxiety, and sleep disturbances, decreases pain and increases function.
A sedentary lifestyle, obesity, noninsulin-dependent diabetes, and cardiovascular
disease contribute to greater all-cause morbidity.
Most patients with nonspecific LBP rapidly improve within 1 month, with an
approximately slower decline of pain over the next 2 months. Between 3 to 12
months, little change in pain is expected. The risk of recurrence within 3 months
can be as high as 34% and within 1 year as high as 84%. 

•   SPINAL FRACTURES
Spondylolysis is a defect of the pars interarticularis. It is usually due to heredi-
tary dysplasia and repetitive stress on the immature spine, although an acute frac-
ture from a severe hyperextension injury is an uncommon possible cause. Bilateral
defects lead to isthmic spondylolisthesis. Spondylolysis commonly occurs at the
L5-S1 level. It presents as back pain exacerbated by extension and alleviated by
rest, with focal tenderness, a palpable step defect, pain with lumbar extension, and
hamstring tightness. Oblique radiographs can show the pars defect, whereas a thin-
slice CT through the abnormal level is diagnostic and allows staging to predict
healing (eSlide 33.12). Approximate healing rates are 70% for acute defects, 30%
for progressive defects, and 0% for terminal lesions.
Conservative management involves relative rest and avoidance of extension for
3 months, which is the shortest healing duration for pars lesions. Bracing can be
considered for pain unrelieved by 2 weeks of rest. The treatment goal is a radio-
graphically stable bony union. Deconditioning is a concern and can be addressed
through aerobic conditioning, a core stabilization program, training of neuromus-
cular proprioceptive control, and sport-specific drills. Patients with chronic LBP
may benefit from specific training of the lumbar multifidi and deep abdominal
muscles. Surgery is rarely indicated except in the presence of spondylolisthesis or
radiculopathy. Vigilant monitoring during the adolescent growth spurt or when
the listhesis is greater than 50% is recommended to detect progressive slippage;
this involves flexion–extension plain x-ray films every 6–12 months until skeletal
maturity.
 CHAPTER 33  Low Back Pain   233

Spondylolisthesis, or anterior slippage of one vertebra on another, can be classi-

fied into six groups, according to etiology. The commonest is isthmic spondylolis-
thesis, which is the result of spondylolysis. Dysplastic spondylolisthesis is caused by
congenital facet joint dysplasia. Degenerative spondylolisthesis is due to interseg-
mental instability from degenerative facet or disk disease, commonly occurring at
the L4-L5 level. Traumatic spondylolisthesis is caused by an acute fracture. Patho-
logic spondylolisthesis is attributable to bone disease that decreases bony strength.
Postsurgical spondylolisthesis is the result of extensive spinal decompression.
Typically, spondylolisthesis presents with axial pain, although intermittent
radicular symptoms may occur from nerve root irritation caused by instability at
the listhetic segment. Clinical findings and treatment are similar to those for spon-
dylolysis; the degree of listhesis can be graded from 1 through 5 on the basis of lat-
eral plain x-ray findings (eSlide 33.13). Risk factors for significant slip progression
are the degree of slip, degenerative disk disease at the level of the slip, adolescent
age group, and ligamentous laxity. Surgical fusion is only considered for grade 3
or greater slip, recalcitrant pain after rehabilitation, persistent radiculopathy, or
progressive instability.
Osteoporotic compression fractures are associated with an increased risk of sub-
sequent fractures, especially hip fractures (which carry high morbidity and mor-
tality rates). Compression fractures contribute to a higher incidence of back pain
in older adult women; up to 30% are caused by secondary osteoporosis due to
oral corticosteroid use, hyperthyroidism, metastases, or multiple myeloma. Bone
mineral density studies are diagnostic and allow assessment of treatment. Treat-
ment includes a combination of medications, lifestyle modifications, and exercises
aimed at balancing pain relief and medication side effects. Calcitonin reduces pain
with adjunctive use of TENS. Occasionally intercostal nerve blocks are effective.
Vertebroplasty is recommended for severe pain unresponsive to conservative man-
agement; however, the possibility of spinal nerve roots and cord compression, and
pulmonary embolism must be considered.
Other spinal fractures are caused by trauma, with the outcomes depending on
concurrent neurologic injury at the time of injury, the time elapsed between the
injury and surgery, and the presence of instability. The Denis three-column struc-
tural concept is used for the classification of spinal fractures.
Bone metastases from lung, breast, prostate, and renal cell malignancies are
common in the spine. Pain is caused by periosteal stretching and the mass effect of
the tumor. Metastases should be highly suspected in patients with a previous his-
tory of cancer, back pain unrelieved by rest, new onset of back pain after 50 years
of age, systemic features (e.g., weight loss), and failure to improve with conservative
care. Neurologic deficits occur in 5%–10% of individuals because of mechanical
pressure from the tumor or bone extruded from a collapsed vertebra. MRI is a sen-
sitive assessment tool and may show early changes in the bone marrow.
Spinal infections include osteomyelitis, diskitis, pyogenic facet arthropathy,
and epidural infections. Prompt treatment is paramount to prevent mortality and
morbidity from complications. Hematogenous spread occurs via the spinal artery
from urinary tract infections, infected intravenous lines, or endocarditis. Diabetics,
hemodialysis recipients, intravenous drug users, and immunocompromised indi-
viduals have an increased risk of spinal infections. The lumbar spine is commonly
affected, presenting with back pain. A raised erythrocyte sedimentation rate is typi-
cally the sole abnormal laboratory finding. Local spread may lead to abscesses in
the epidural space and paraspinal or psoas muscles. The first sign is a periosteal
234  SECTION IV ISSUES IN SPECIFIC DIAGNOSES

reaction on plain x-ray films, followed by irregular endplate erosions and narrow-
ing of the disk space, which are pathognomonic. MRI is the recommended imaging
technique. Treatment is usually a 4- to 6-week course of intravenous antibiotics.
The choice of antibiotic is determined by blood cultures or bone biopsy, and treat-
ment is guided by the erythrocyte sedimentation rate response. Surgery is indicated
in the presence of spinal instability, progressive neurologic deficit, or failure of
medical treatment.
Osteomyelitis secondary to a contiguous focus of infection is seen after surgical
procedures and with extension of infection from adjacent soft tissues. Risk fac-
tors are smoking, obesity, poor nutrition, uncontrolled diabetes, administration of
corticosteroids, a history of malignancy, and radiation treatment in the area of sur-
gery. Treatment requires surgical débridement, followed by a course of antibiotics.
D­iskitis can be the result of contiguous spread of infection or iatrogenic infection
after diskectomy and diskography. Although the incidence is low, morbidity from
disk infection is significant because of the difficulty with using antibiotics to treat
the infection because of the relative avascularity of disks.

Spondyloarthropathies
Spondyloarthropathies are commonly associated with the presence of the HLA-
B27 allele; in genetically susceptible individuals, environmental and immunologic
factors interact to produce clinical manifestations. Ankylosing spondylitis is three
times more common in men and begins in the late teens or early 20s. It typically
presents with morning stiffness and dull low back or buttock ache. These are fol-
lowed by decreased spinal mobility, decreased chest expansion, and tenderness of
the sacroiliac joints. Bony tenderness and enthesitis at the heel, greater trochan-
ter, iliac crest, and tibial tuberosity are common. Systemic disease manifestations
include anterior uveitis, heart disease, and inflammatory bowel disease. Radio-
graphic changes include squaring of the vertebral bodies, syndesmophyte forma-
tion, and eventually a bamboo spine appearance. Sacroiliitis appears late on plain
radiographs. MRI is more sensitive, and its findings are now considered diagnostic
of ankylosing spondylitis.
Initial treatment includes exercises that promote spinal extension. Exercise
enhances mobility, improves function, and prevents severe deformity. Indometh-
acin is particularly helpful in reducing pain and inflammation, thereby allowing
exercises to be performed and function maintained. Peripheral arthritis necessi-
tates sulfasalazine and methotrexate use. Disease-modifying agents, such as tumor
necrosis factor inhibitors, control articular inflammation but do not prevent joint
ankylosis. Fluoroscopy-guided sacroiliac joint injections relieve acute symptoms
but have no long-term benefits. 

•   DIFFERENTIAL DIAGNOSIS AND TREATMENT: LEG

PAIN GREATER THAN BACK PAIN
Lumbosacral radiculopathy results from mechanical compression or a chemi-
cally mediated inflammatory process of the nerve root. Disk herniation exposes
the nucleus pulposus fluid and initiates an autoimmune-mediated inflammatory
cascade leading to swelling of nearby nerves. This alters their electrophysiologic
function, leading to sensitization of these neurons and enhanced pain generation,
even in the absence of specific mechanical compression. Mechanical compression
induces structural and vascular changes, as well as inflammation. These lead to
 CHAPTER 33  Low Back Pain   235

intraneural blood flow disturbances, causing local ischemia and intraneural edema
that triggers an inflammatory cascade. Local structural effects of mechanical
compression include demyelination and blockage of axonal transport; mechani-
cal stimulation enhances the production of substance P, which modulates sensory
nociceptive feedback.
The commonest cause of nerve root compression is disk protrusion; in less
than 1% of patients, compression is caused by an infection, malignancy or
fracture. The commonest levels of disk herniation are L4-L5 and L5-S1, com-
monly affecting the L5 and S1 nerve roots. Posterolateral herniation is the most
common type of herniation, affecting the nerve root before it enters the neural
foramen. Extraforaminal herniation affects the exiting nerve root, and central
disk herniation can affect multiple nerve roots because of the organization of
the cauda equina. True cauda equina syndrome occurs in 1% of herniations. It
causes bowel, bladder, and sexual dysfunction and is a surgical emergency, with
the greatest recovery of neurologic deficits occurring if decompressive surgery is
performed within the first 48 hours.
Conservative treatment can decrease pain and improve function in the acute
phase of lumbosacral radiculopathy. Favorable outcomes have been reported with
aggressive nonoperative care involving an active exercise program and f­luoroscopy-
guided transforaminal epidural steroid injections, resulting in short-term pain
improvement and decreased inflammation; they potentially reduce the need for
surgery and facilitate an active rehabilitation program (eSlide 33.14). Surgical
management is reserved for significant persistent radicular symptoms, neurologic
progression, or cauda equina syndrome. Decompressive procedures significantly
improve pain and slightly accelerate the resolution of neurologic deficits.
Lumbar spinal stenosis results from degenerative changes that lead to narrow-
ing of the spinal canal. Spinal venous congestion and radicular artery obstruction
cause ischemic neuritis, producing neurogenic claudication. Neurogenic claudica-
tion is exacerbated by walking, prolonged standing, or any activity with relative
lumbar extension and relieved by forward bending. Foraminal or lateral recess ste-
nosis causes radicular pain in a typical dermatomal distribution.
Electrodiagnostic investigations can differentiate spinal stenosis from periph-
eral neuropathy and characterize the stenosis. Conservative management is war-
ranted for mild to moderate symptoms, with the goals of pain control and reducing
functional limitations. Oral medications, flexion-based lumbar stabilization, and
hip mobility and aerobic exercises together with epidural steroid injections have
demonstrated short-term improvement in pain and walking tolerance. Decompres-
sive surgery is reserved for intractable pain and profound or progressive neurologic
deficit or lifestyle impairment. Fusion is indicated if instability is present. Surgery
improves pain but does not affect functional outcomes and is less effective for axial
back pain.
Nonlumbar spine causes of “radicular” leg symptoms mimic lumbar radiculopa-
thy because they generate pain referral patterns similar to the lumbosacral derma-
tomes. Sacroiliac joint disorders are a potential pain generator; however, the exact
pathologic structure in these disorders is uncertain. The diagnosis is confirmed by
observing pain relief after injecting local anesthetic into the joint. Sacroiliac pain
does not radiate above the lumbosacral junction and overlaps substantially with
lumbosacral radicular pain patterns. Hip joint pain is typically referred to the groin,
posterior pelvis, or anterior thigh, making it easily confused with L1-L3 nerve root
involvement. Plain hip radiographs and hip range of movement help differentiate
236  SECTION IV ISSUES IN SPECIFIC DIAGNOSES

intraarticular hip pain pathology from lumbar radiculopathy. Pyriformis syndrome

can cause sciatica from local pressure on the sciatic nerve, producing buttock pain
or pain radiating into the posterior thigh to below the knee in a distribution simi-
lar to the L5 or S1 dermatomal pattern. Pain can be elicited on palpation of the
sciatic notch, through various examination maneuvers, or during electrodiagnostic
investigations. Greater trochanteric pain syndrome is a regional pain syndrome
around the greater trochanter that is often caused by gluteus medius and minimus
tendinopathy or tears. It can also be the result of myofascial pain, causing gluteal
muscle inhibition and deconditioning and manifesting as hip abductor weakness.
Greater trochanteric pain syndrome and the iliotibial band syndrome can be con-
fused with an L4 or L5 radiculopathy. Myofascial pain syndromes may arise from
active trigger points within the surrounding muscle or fascia, with referral patterns
mimicking lumbosacral dermatomes.
Peripheral vascular disease presents with vascular claudication, which is simi-
lar to neurogenic claudication. Both types of symptoms are exacerbated by walk-
ing; however, neurogenic claudication is relieved by forward flexion, whereas
intermittent vascular claudication is not (it is only relieved by walking cessation,
even when standing erect). Peripheral polyneuropathy causes paresthesias in the
lower limbs and often occurs in older individuals with diabetes. Electrodiagnostic
studies can differentiate this condition from lumbar stenosis and may be espe-
cially indicated in patients with MRI findings suggestive of stenosis. These stud-
ies may be particularly useful if epidural steroid injections are contemplated, as
the injections will reduce symptoms caused by spinal stenosis but not those due
to a polyneuropathy.
LBP in pregnancy is a common problem and needs to be differentiated from
pelvic girdle pain. It is caused by increased biomechanical strain from anterior
movement of the pregnant woman’s center of gravity or from hormones altering
the lumbopelvic ligaments and causing instability of the lumbosacral spine. Risk
factors include a history of previous back pain or pregnancy-related back pain and
LBP during menses. Pain usually peaks at 36 weeks’ gestation and decreases after-
wards; it is usually substantially improved 3 months postpartum. Persistent back
pain may occur in women with both low back and pelvic girdle pain, back pain
in early pregnancy, weakness of the back extensor muscles, older individuals, and
those with work dissatisfaction. Individualized physical therapy, water aerobics,
acupuncture, and massage can be used to decrease pain. Medications should be
discussed with the obstetrician.
The prevalence of pediatric LBP is cited between 30% to 51%, with the great-
est increase occurring during puberty and the maximal growth spurt. Risk factors
for nonspecific LBP include older age, female sex, parents with LBP, hyperlordotic
posture, history of spinal trauma, participation in competitive sports, high level of
physical activity, and depression. Sitting exacerbates the back pain, and there is a
positive correlation between LBP in adolescence and during adulthood. Specific
causes of LBP in the pediatric population are listed in eSlide 33.15.
Spondylolysis and isthmic spondylolisthesis in young athletes are common
causes of persistent LBP. Scheuermann disease is a painless exaggerated thoracic
kyphosis, which causes a compensatory lumbar hyperlordosis; a higher prevalence
of degenerative disk changes are present in those individuals with pain. Painful
idiopathic scoliosis is indicative of a possible underlying tumor, infection, or spon-
dylolisthesis. The most frequent malignant lesion affecting the pediatric spine is
Ewing’s sarcoma.
 CHAPTER 33  Low Back Pain   237

Clinical Pearls
• Low back pain is a symptom of multifactorial etiology that significantly affects func-
tion and drains health care resources if poorly managed.
• The annulus fibrosus of intervertebral disks are shock absorbers. Lumbar muscle
a­ctivities influence intradiskal pressures; lifting a load close to the body decreases
forces on the lumbar spine and reduces intradiskal pressure.
• Ankle dorsiflexion weakness, calf muscle wasting, an abnormal ankle jerk reflex, and
a positive crossed straight leg test correlate with the presence of a lumbosacral
r­adiculopathy.
• Lumbar spinal stenosis results from narrowing of the spinal canal and causes n­eurogenic
claudication from mechanical compression, venous congestion, and r­adicular artery
obstruction.This type of claudication worsens with lumbar extension (e.g., prolonged
standing, walking downhill) and is relieved by forward flexion or sitting.
• Lumbosacral radiculopathy results from annular tears allowing herniation of the
nucleus pulposus. Herniation most commonly occurs at the L4-L5 and L5-S1 disks,
thereby affecting the L5 and S1 nerve roots. Extraforaminal herniation affects the
exiting nerve root, and central disk herniation can affect multiple nerve roots within
the cauda equina.
•  Spondylolysis is a defect of the pars interarticularis resulting from repetitive
e­xtension. It occurs most commonly at the L5-S1 level. Bilateral pars defects lead to
isthmic spondylolisthesis. Plain oblique radiographs show the pars defect; computed
tomography scans are diagnostic and allow staging to predict healing.
• Spinal metastases should be suspected in patients with a previous malignancy, back
pain unrelieved by rest, new onset of back pain after age 50 years, and systemic
features. Bone scans are sensitive but not specific for detecting bony metastases.
•  Randomized controlled trials have only validated the effectiveness of lumbar
s­tabilization exercises, core strengthening, and motor control exercises in chronic
low back pain and spinal manipulation in acute low back pain.
• Treatment modalities are generally combined. Reassurance and patient education
are the cornerstones for a therapeutic relationship and successful outcomes. Exer-
cise prevents deconditioning and provides modest pain relief plus additional general
health and fitness benefits. Walking is best to achieve aerobic fitness; fast walking
results in lower spine loading, while arm swinging facilitates efficient storage and us-
  age of elastic energy.

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