Review Article
Mimickers of Lumbar
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Bennett Douglas Grimm, MD
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Brian Joseph Blessinger, MD
Bruce Vaiden Darden, MD
Craig D. Brigham, MD
Jeffrey S. Kneisl, MD
Eric B. Laxer, MD
From OrthoCarolina (Dr. Grimm,
Dr. Blessinger, Dr. Darden,
Dr. Brigham, and Dr. Laxer) and the
Department of Orthopaedics, Carolinas
Healthcare Systems and Levine Cancer
Institute (Dr. Kneisl), Charlotte, NC.
Dr. Blessinger or an immediate family
member has stock or stock options held
in Mazor Surgical Technologies. Dr.
Darden or an immediate family member
has received royalties from Stryker; is
a member of a speakers’ bureau or has
made paid presentations on behalf of
Stryker and Synthes; serves as a paid
consultant to Stryker; has stock or stock
options held in Synthes, Pioneer, and
BioMedFlex; has received research or
institutional support from Synthes and
DePuy; and serves as a board member,
owner, officer, or committee member of
the Cervical Spine Research Society
and the Lumbar Spine Research
Society. Dr. Kneisl or an immediate
family member has received royalties
from Biomet. Dr. Laxer or an immediate
family member has received royalties
from Stryker; serves as a paid consultant
to Stryker and Synthes; and has stock or
stock options held in Pioneer. Neither of
the following authors nor any immediate
family member has received anything of
value from or has stock or stock options
held in a commercial company or
institution related directly or indirectly to
the subject of this article: Dr. Grimm and
Dr. Brigham.
J Am Acad Orthop Surg 2015;23:7-17
http://dx.doi.org/10.5435/
JAAOS-23-01-7
Copyright 2014 by the American
Academy of Orthopaedic Surgeons.
January 2015, Vol 23, No 1
Copyright Ó the American Academy of Orthopaedic Surgeons. Unauthorized reproduction of this article is prohibited.
Radiculopathy
Abstract
Orthopaedic surgeons frequently treat patients who report pain that
radiates from the back into the lower extremity. Although the most
common etiology is either a herniated disk or spinal stenosis, a myriad
of pathologies can mimic the symptoms of radiculopathy, resulting in
differences in the clinical presentation and the workup. Therefore, the
clinician must be able to distinguish the signs and symptoms of lumbar
radiculopathy from pathologies that may have a similar presentation.
Being cognizant of these other possible conditions enables the
physician to consider a breadth of alternative diagnoses when
a patient presents with radiating lower extremity pain.
L umbar radiculopathy refers to
pain in the back or buttocks that
radiates down the leg in a dermatomal
cian’s working from a broad list of
differential diagnoses, especially when
the signs and symptoms are atypical
distribution. The prevalence of true for radicular pain.2,3 Potential mim-
lumbar radiculopathy in the general ickers include musculoskeletal, neu-
population is approximately 3% to rogenic, immunogenic, and iatrogenic
5%.1 Although the two most com- conditions (Table 1). A careful history
mon causes for these symptoms are and physical examination are the first
a herniated disk or, less commonly, and most important steps in dis-
spinal stenosis, many other potential tinguishing these conditions from one
causes mimic lumbar radiculopathy. another.
If the diagnosis of radiculopathy is
presumed, this action may result in
misdiagnosis, leading to unnecessary Lumbar Disk Herniation
tests and treatment and ultimately
a delay in delivery of appropriate care. Lumbar disk herniation most fre-
Although the simultaneous presence quently occurs in patients younger
of low back pain may increase the than 50 years. Symptom onset may be
likelihood of these symptoms origi- acute, may or may not be associated
nating in the lumbar spine, low back with an inciting event, and begins with
pain is common in the general pop- a tear in the posterior annulus. The
ulation. This symptom may create annulus is richly innervated by sen-
a bias toward inappropriately attrib- sory pain fibers; therefore, a common
uting lower extremity symptoms to initial presenting symptom may be
lumbar spine pathology. Furthermore, severe low back pain. As the pathol-
because an asymptomatic lumbar disk ogy progresses, pressure within the
bulge or herniation is a common disk forces a portion of the nucleus
finding on MRI, the presence of such pulposus through the tear into the
changes must be correlated with the spinal canal, where it compresses
patient’s symptoms. These issues and possibly chemically irritates the
highlight the importance of the clini- nerve root, causing radicular pain.4
7
 Mimickers of Lumbar Radiculopathy
Table 1
Mimickers of Lumbar
Radiculopathy
Musculoskeletal: hip and pelvic
pathology
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Osteoarthritis
Osteonecrosis
Femoral acetabular
impingement
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Stress fractures
Greater trochanteric bursitis
Insufficiency fractures
Sacroiliac joints
Vascular
Tumors
Peripheral neuropathy
Metabolic
Compressive
Infectious and autoimmune
disorders
Pyogenic
Shingles
Guillain-Barré syndrome
Transverse myelitis
Iatrogenic
Myogenic
Neuropathic
This process is often associated with
a transition of the patient’s symptoms
from the low back to the buttock and
down the leg, accompanied by pain,
numbness, tingling, and weakness.
Symptoms usually have a mechanical
component that are intensified by
activity and ameliorated with rest.
Any action that increases intradiscal
pressure, such as sneezing or bending
forward, tends to exacerbate the pain.
An important physical examination
finding is nerve root tension; a posi-
tive straight leg raise test is present in
60% of patients5 with disk herniation
at L4-5 and L5-S1. A femoral stretch
test may be positive for disk hernia-
tion at L2-3, L3-4, and occasionally
L4-5. Asymmetric reflexes of the
patellar tendon (ie, L4) or Achilles
tendon (ie, S1) may be noted.
The presence of saddle anesthesia,
bowel or bladder dysfunction, and
8 Journal of the American Academy of Orthopaedic Surgeons
Copyright Ó the American Academy of Orthopaedic Surgeons. Unauthorized reproduction of this article is prohibited.
lower extremity weakness are consis-
tent with cauda equina syndrome,
a potential consequence of a large disk
herniation. It is crucial to identify this
condition because it may require
urgent surgical decompression.
Spinal Stenosis
Neurogenic claudication secondary to
lumbar spinal stenosis, first described
by Verbiest,6 is the most common
indication for spine surgery in patients
older than 65 years.7 It is caused by
narrowing of the spinal canal that is
the result of age-related changes of the
facet joints, the ligamentum flavum,
and the disk.8 Whereas a history of
chronic low back pain is common,
patients experience symptoms mainly
in the buttocks and legs either as
bilateral neurogenic claudication or,
less commonly, as unilateral radicular
pain that may indicate the presence of
a synovial facet cyst.9,10 Neurologic
deficits, such as asymmetric reflexes,
sensory changes, and motor weakness,
are found in .50% of patients with
lumbar spinal stenosis; however, these
findings are nonspecific. Approxi-
mately 20% of patients present with
a positive straight leg raise test or
femoral stretch test.9
Mimickers of Lumbar
Radiculopathy
Musculoskeletal
The most common group of mim-
ickers of lumbar spine pathology
originate in the musculoskeletal
structures around the pelvis, hip
joint, and femur.11 This group in-
cludes hip joint conditions (eg,
osteoarthritis, osteonecrosis, femoral
acetabular impingement), femoral
neck stress fractures, pelvic insuffi-
ciency fractures, bursitis, and sacro-
iliac joint pain.
Hip joint pathology usually may be
differentiated from lumbar pathol-
ogy by the presence of groin pain with
activity. The pain is most evident
during day-to-day activities that
require hip movements, such as
turning in bed, getting in or out of
a car, climbing stairs, and putting on
shoes and socks. Pain may also be
present in the buttock and radiate to
the anterior thigh and knee (Figures 1
and 2). Passive range of motion of
the hip, particularly flexion and
internal rotation, may be diminished
and may reproduce the patient’s
symptoms; this is strongly suggestive
of a pathologic hip joint.12 Brown
et al13 noted that patients who walk
with a limp are seven times more
likely to have hip joint pathology
with or without coexisting spinal
stenosis as the etiology of their pain
rather than spinal stenosis alone
(Table 2).
Osteoarthritis of the hip is the most
common hip joint condition in pa-
tients older than 65 years, with
a prevalence of 5% to 10% of the
population.14 Hip radiographs show
joint space narrowing, osteophyte
formation, subchondral cysts, and
sclerosis. For patients who have co-
existing lumbar stenosis and osteo-
arthritis of the hip, an injection of
local anesthetic into the hip joint
may help differentiate the patient’s
primary pain generator.15
Osteonecrosis, caused by a disrup-
tion of blood flow to the femoral head,
may progress to femoral head collapse
and hip arthritis. Patients aged 20 to
50 years who have risk factors for
osteonecrosis (eg, history of excessive
alcohol intake, chronic steroid use,
sickle cell disease) and groin or but-
tock pain should be evaluated with hip
radiographs; MRI may be done if os-
teonecrosis is suspected but radio-
graphs are normal or inconclusive.16
In early osteonecrosis, a lucency may
be seen on AP hip or pelvic radio-
graphs; a crescent sign (Figure 3)
represents subchondral collapse of
the femoral head. Coronal T1- and
T2-weighted MRI of the pelvis may
 Bennett Douglas Grimm, MD, et al

show an area of decreased signal Figure 1

intensity in the weight-bearing dome
of the femoral head. FRONT BACK
Femoral acetabular impingement,
a pathologic contact of the femoral
neck against the acetabulum, is Right Right
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a cause of hip joint pain in younger

Left
patients. Two morphologic mecha-
nisms have been proposed. In cam
impingement, an abnormally shaped
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femoral head contacts the acetabu-

lum; in pincer impingement, the
femoral neck makes contact with
a relatively retroverted acetabular
rim during terminal motion. These
mechanisms lead to labral tears and
cartilage damage to the hip joint,
followed by pain and possible pro-
gression to arthritis. During physical
examination, the pain may be repro-
duced by flexion, adduction, and
internal rotation. An AP radiograph
of the hip may identify a crossover
sign, whereby the radiographic
shadows of the lateral edges of the
anterior and posterior walls intersect,
crossing over each other and indi-
cating a retroverted acetabulum17
(Figure 4). A lateral hip radiograph
may show an abnormal bony
prominence at the femoral head-neck
junction that is responsible for the
impingement. An MRI arthrogram is
the test of choice to evaluate labral
pathology and cartilage defects.18
Stress fractures of the femoral neck,
also known as fatigue fractures,
should be suspected in avid runners
and military trainees who report
insidious onset of groin pain that
worsens with running/marching and
improves with rest. An amenorrheic
adolescent female runner is particu-
larly at risk because of decreased
bone mineral density secondary to an
associated eating disorder.19 These
fractures occur as a result of repeti-
tive submaximal stress that exceeds
the bone’s ability to remodel itself in
response to that stress. In a young
patient, it is critical to consider this
diagnosis because of the risk of dis-
placement and the resultant potential
Please rate your pain now.
No Worst
Pain 1 2 3 4 5 6 7 8 9 10 Ever
Pain diagram of a 51-year-old woman with left buttock and anterior thigh pain for
1 to 3 years. The patient was referred to the spine clinic for a lumbar
decompression. Examination revealed that her typical pain was reproduced with
internal and external rotation of the left hip.
for femoral head osteonecrosis; sig- patients, presents as peritrochanteric
nificant disability is likely, and joint pain that occasionally radiates down
arthroplasty may be required. AP the thigh to the lateral knee. It affects
and lateral radiographs of the hip are 10% to 25% of the population and
the initial imaging choices; MRI is has the clinical findings of tenderness
used for confirmation. Lateral or to palpation over the lateral hip and
tension-sided femoral neck fractures pain on resting on the ipsilateral side,
are at high risk for displacement and particularly at night.21 In a retro-
are treated with surgical stabiliza- spective review, Tortolani et al22
tion; fractures on the medial or diagnosed trochanteric bursitis in
compression side of the femoral neck 20.2% of patients who presented to
may be managed symptomatically the authors’ spine clinic for pre-
with protected weight bearing and sumed lumbar spine pathology.
cessation of the offending activity.20 Women are affected twice as much
Stress fractures of the tibia and the as men. Other pelvic bursa, such as
metatarsals are also common in these the ischial, iliopectineal, and iliop-
populations and should be consid- soas, may more rarely be a cause of
ered in the differential diagnosis. pelvic or thigh pain.23,24
Greater trochanteric bursitis, com- Sacral insufficiency fractures occur
monly found in middle-age aged as a result of normal stresses across

January 2015, Vol 23, No 1 9

Copyright Ó the American Academy of Orthopaedic Surgeons. Unauthorized reproduction of this article is prohibited.
 Mimickers of Lumbar Radiculopathy
Figure 2
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A, Lateral radiograph of the lumbar spine demonstrating grade I
spondylolisthesis in the patient from Figure 1. B, AP radiograph showing severe
osteoarthritis of the left hip.
abnormal, weakened bone and are
most commonly seen in elderly
women with osteoporosis. Chronic
steroid use and a history of pelvic
irradiation are also risk factors.
Weber et al25 estimate an annual
incidence rate of 2%. Patients report
vague low back and occasionally
radicular pain, often with no history
of antecedent trauma. The pain may
be so debilitating that patients use
a wheelchair because they are unable
to ambulate. Physical examination
may reveal sacral tenderness. Lum-
bar and pelvis radiographs may be
negative for a fracture. A dedicated
pelvis MRI shows edema around an
acute fracture on fat-suppressed T2-
weighted images or short tau inver-
sion recovery sequences (Figure 5).
Nondisplaced fractures may be
missed on CT;26 therefore, MRI is
indicated if an insufficiency fracture
is suspected. A technetium bone scan
may be ordered if the patient is
unable to undergo MRI.
Sacroiliac joint pain presents as
nonradiating buttock pain over the
10
Copyright Ó the American Academy of Orthopaedic Surgeons. Unauthorized reproduction of this article is prohibited.
posterior superior iliac spine that is
worse with activity. It is a diagnosis of
exclusion. Physical examination find-
ings include a positive FABER test
(flexion, abduction, and external
rotation), Gaenslen test (extension of
the affected leg by hanging it off the
examination table using a downward
force while holding the contralateral
hip in flexion), sacral compression,
thigh thrust, and anterior superior
iliac spine distraction. Van der Wurff
et al27 found that performing three or
more positive stress maneuvers is
85% sensitive and 79% specific for
sacroiliac pain.
Vascular
Intermittent vascular claudication re-
fers to lower extremity pain secondary
to arterial insufficiency in patients with
peripheral arterial disease (PAD). Risk
factors include smoking (ie, 80% to
90% of affected patients are current or
former smokers),28 diabetes, hyper-
lipidemia, and hypertension. Buildup
of atherosclerotic plaque leads to
Journal of the American Academy of Orthopaedic Surgeons
arterial stenosis, precipitating a mis-
match between oxygen supply and
demand in the leg muscles. Pain from
vascular claudication classically radi-
ates from distal to proximal during
ambulation and may be bilateral or
unilateral; the latter may closely
mimic lumbar radiculopathy. Walk-
ing distance before the onset of pain
tends to be more predictable with
PAD compared with that in neuro-
genic claudication. In addition, pa-
tients with vascular claudication may
relieve their symptoms with cessation
of walking; patients with neurogenic
claudication must lean forward or sit
down for pain relief. Careful physical
examination should include evalua-
tion for diminished, asymmetric, or
absent pedal pulses and for the pres-
ence of shiny, hairless, or dystrophic
skin. Redness of the lower extremity
that is alleviated by elevation (ie,
dependent rubor) is common. Non-
invasive ankle-brachial indices (ABIs)
are considered positive when the ABI
ratio is ,0.9. In patients unaffected by
PAD, the lower extremities should
show a pressure differential between
30 to 40 mm Hg compared with the
brachial pressure.29 Jeon et al30 re-
ported a sensitivity and specificity of
85.3% and 85.7%, respectively, of
ABI testing in patients presenting with
claudication symptoms of uncertain
vascular or neurogenic origin.
Tumors
Both benign and malignant extra-
spinal tumors involving the pelvis
and femur may produce symptoms
and signs of lumbar radiculopathy
(Figure 6). Important elements in the
history that may distinguish these
patients include (1) insidious onset
of symptoms without antecedent
trauma; (2) crescendo pain pattern,
particularly at night; (3) no change in
pain pattern with position or activ-
ity; (4) presence of constitutional
symptoms; and (5) identified cancer
risk factors such as prior diagnosis of
 Bennett Douglas Grimm, MD, et al

cancer, tobacco use, and prior irra- Table 2

diation to the pelvis (Table 3).
Differentiating Characteristics Between Hip Arthritis and Spinal Stenosis
Physical examination features that
may be revealing include point Characteristic Hip Arthritis Spinal Stenosis
localization of pain or mass effect Location of pain Groin Buttock
along the course of the sciatic nerve.
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History Giving way Claudication

A high index of suspicion is required,
Exacerbating symptom Tying shoes Standing
particularly if pain is out of pro-
Gait Limping Lean forward
portion to or anatomically inconsis-
Physical examination Pain with passive Variable
tent with spine imaging studies. The
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key diagnostic steps are to obtain
an accurate history and to perform
a careful physical examination.
Based on these considerations, fur-
ther workup of the pelvis, hip, and
femur should include radiographs,
supplemented with more advanced
imaging (ie, bone scan, MRI, CT) as
indicated.
Peripheral Neuropathy
Metabolic disorders represent the
predominant etiology of extremity
pain arising from peripheral neuro-
genic origin. Although several causes
of peripheral neuropathy exist, diabe-
tes mellitus is the most common cause;
peripheral neuropathy affects up to
66% of patients with diabetes.31 In
distal sensory peripheral neuropathy,
which is present in 80% of patients
with diabetic peripheral neuropathy,
demyelination of large myelinated
nerve fibers that are responsible for
vibration, touch, and proprioception
leads to a sensation of pins and nee-
dles bilaterally in the lower extremi-
ties in a stocking distribution.32,33
Patients reporting these sensations
often falsely attribute their symptoms
to a spinal etiology.34 Proximal dia-
betic neuropathy, also known as
diabetic amyotrophy, presents as
unilateral or bilateral buttock, thigh,
and/or leg pain. Other common signs
and symptoms include burning ante-
rior thigh pain at night and weakness
and atrophy of the proximal muscle
girdles. As a result, patients report
difficulty with ambulation and
climbing stairs. Men older than 50
years with poorly controlled type 2
range of motion
diabetes are most commonly affected;
many report a history of weight loss
around the time of the onset of
symptoms.35 The pain usually sub-
sides within 3 to 6 months; therefore,
the prognosis for these patients is
good.
Compressive
Peroneal neuropathy most com-
monly arises from trauma about the
knee and ankle. Between 30% to
60% of nontrauma patients experi-
ence compression of the common
peroneal nerve by ganglion cysts
originating from the proximal tibio-
fibular joint.36,37 Tibialis anterior
weakness may result from a common
peroneal neuropathy or from an L4
or L5 radiculopathy. Clinical dis-
tinction between the two etiologies
may be made by assessment of the
strength of the ipsilateral hip
abductor muscle and the tibialis
anterior muscle; both of these mus-
cles receive primary innervation
from the L5 nerve root. Jeon et al38
reported ipsilateral hip abductor
weakness in 85.6% of patients with
a foot drop caused by an L5 radic-
ulopathy, but only 3% of patients
with foot drop caused by a peroneal
neuropathy had concomitant hip
abductor weakness. A palpable mass
and a positive Tinel sign at the lateral
proximal fibula may be present in
97% of patients with peroneal nerve
compression.39 MRI of the lumbar
spine is indicated in a patient with
a foot drop. Electrodiagnostic stud-
ies can help distinguish proximal
etiologies from distal etiologies if the
MRI is equivocal. If the MRI of the
lumbar spine is normal and/or elec-
trodiagnostic studies are consistent
with compressive peroneal neurop-
athy at the knee, then MRI of the
knee should be performed to rule out
a ganglion cyst of the proximal tib-
iofibular joint.
Anterolateral thigh paresthesia,
secondary to compression of the lat-
eral femoral cutaneous nerve
(LFCN), is known as meralgia par-
esthetica (MP); it most commonly
occurs in middle-aged men with an
incidence of 0.43 per 10,000 per-
sons.40 The LFCN, a purely sensory
nerve, originates in the lumbar
plexus from any combination of the
L1, L2, or L3 nerve roots; therefore,
it may be confused with radiculop-
athy from these levels.41 It courses
underneath or over the inguinal lig-
ament along an aponeurotic fascial
tunnel in which compression of the
nerve may occur. Symptoms, often
described as numbness or burning
along the anterior thigh, are usually
improved with sitting.42 External
sources that may compress the
LFCN include tight-fitting pants,
belts, or girdles. Obesity, diabetes,
and pregnancy are risk factors for
MP. Iatrogenic injury may occur
with prone positioning during sur-
gery. The presence of hip flexor
weakness is more consistent with an
L2 or L3 radiculopathy than with

January 2015, Vol 23, No 1 11

Copyright Ó the American Academy of Orthopaedic Surgeons. Unauthorized reproduction of this article is prohibited.
 Mimickers of Lumbar Radiculopathy
Figure 3
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Lateral radiograph of the right hip
demonstrating a crescent sign
(arrows), a subchondral collapse of
the weight-bearing dome of the
femoral head. (Reproduced with
permission from Malizos KN,
Karantanas AH, Varitimidis SE,
Dailiana ZH, Bargiotas K, Maris T:
Osteonecrosis of the femoral head:
Etiology, imaging and treatment. Eur
J Radiol 2007;63[1]:16-28.)
MP. A positive Tinel sign over the
lateral aspect of the inguinal liga-
ment supports the diagnosis of MP.
Nouraei et al43 described a pelvic
compression test in which the patient
lies in the contralateral decubitus
position while downward pressure is
applied to the pelvis, relaxing the
inguinal ligament and putting pres-
sure on the LFCN. The authors re-
ported sensitivity and specificity of
95% and 93%, respectively, for the
relief of discomfort caused by MP in
patients with a positive pelvic com-
pression test and surgical release.
Several other lower extremity
compressive neuropathies have been
reported. Examples include entrap-
ment of the peroneal nerve in the
anterior compartment of the lower
leg and entrapment of the tibial nerve
in the tarsal tunnel. Piriformis syn-
drome, irritation of the sciatic nerve
by an aberrant piriformis muscle,
trauma, or overuse cause symptoms
12
Copyright Ó the American Academy of Orthopaedic Surgeons. Unauthorized reproduction of this article is prohibited.
Figure 4
A, Illustration showing relative acetabular retroversion. B, AP radiograph of the
left hip demonstrating crossover or a figure-of-eight sign (dashed line); abnormal
intersection of the anterior wall/posterior wall of the acetabulum indicates
a retroverted acetabulum. AW = anterior wall, PW = posterior wall (Reproduced
with permission from Tannast M, Siebenrock KA, Anderson SE:
Femoroacetabular impingement: Radiographic diagnosis. What every
radiologist should know. AJR Am J Roentgenol 2007;188[6]:1540-1552.)
very similar to those of lumbar radiculopathy, particularly in immu-
radiculopathy.44,45 In a systematic nocompromised patients who report
review of 55 studies with a total of unremitting low back pain, fever,
126 patients, Hopayian et al45 chills, and/or pain that is worse at
identified three common symptoms night. Osteomyelitis and discitis are
that patients experienced, including likely causes of axial nonradiating
buttock pain (50% to 95% of pa- back pain with fever, but they also may
tients), aggravation of pain with produce radiculopathy with epidural
sitting (39% to 97% of patients), extension of the infection.46,47 In
and point tenderness over the addition to axial pain (89% of pa-
greater sciatic notch (59% to 92% tients), radiculopathy and neurologic
of patients); these symptoms were deficit (80% of patients) are the most
present together with a 22% fre- common presenting symptoms of
quency. A positive straight leg raise epidural abscess, followed by fevers
was present 42% to 62% of the and chills (67% of patients).48 The
time. The authors suggest that the most commonly identified organism
diagnosis be considered when in spinal pyogenic infections is
a lumbar MRI is negative for evi- Staphylococcus aureus. Laboratory
dence of nerve root compression studies, including erythrocyte sedi-
and when patients have atypical mentation rate, C-reactive protein
histories. level, and white blood cell count with
differential, and MRI with contrast
should be ordered when infection is
Infectious and Autoimmune suspected.
Disorders Shingles (ie, herpes zoster) occurs
Infectious etiologies, such as osteo- when the dormant varicella-zoster
myelitis, spondylodiscitis, and epidu- virus in nerve cell bodies of the
ral abscess should be considered in dorsal root ganglia reactivates and
the differential diagnosis of lumbar causes a painful, vesicular rash in
Journal of the American Academy of Orthopaedic Surgeons
 Bennett Douglas Grimm, MD, et al

Figure 5
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A right vertical sacral insufficiency fracture demonstrated on a coronal oblique T1-weighted magnetic resonance image (A)
and a coronal oblique short tau inversion recovery image (B). C, CT of the sacrum showing the fracture. (Reproduced with
permission from Murthy NS: Imaging of stress fractures of the spine. Radiol Clin North Am 2012;50[4]:799-821.)

Figure 6

A, Coronal T1-weighted magnetic resonance image demonstrating a large dumbbell-shaped hemangioendothelioma of the
right sciatic notch. B, AP standing radiograph of the pelvis and left femur demonstrating a femoral chondrosarcoma that was
diagnosed after the patient reported no relief of leg pain following spinal decompression, fusion, and instrumentation. C, AP
radiograph of the right proximal femur in a patient who received a lumbar epidural steroid injection for foraminal stenosis at
L5/S1. The metastatic lesion in the femur is from non-small cell lung cancer.

a dermatomal pattern. Therefore, it is
important to inquire about the presence
of a skin rash or blisters and inspect the
patient’s skin from the back and
buttock down the leg. Patients older
than 60 years and immunosuppressed
patients (ie, patients with cancer,
human immunodeficiency virus [HIV],
diabetes) are particularly susceptible.
Lumbar radiculitis occurs in 20% of
patients and can cause burning dyses-
thesias and even motor weakness.49,50
Sprenger DeRover et al51 described
two patients with L5 radiculitis with
foot drop caused by a herpes zoster
infection.
HIV can cause a distal symmetric
polyneuropathy similar to diabetic
neuropathy; it is typically found in
patients with profound immunosup-
pression manifested by CD41 counts
of ,200 cells/mL and high viral lev-
els.52 Whereas this is the most com-
mon neuropathy associated with HIV,

January 2015, Vol 23, No 1 13

Copyright Ó the American Academy of Orthopaedic Surgeons. Unauthorized reproduction of this article is prohibited.
 Mimickers of Lumbar Radiculopathy
Table 3
Medications That May Cause Iatrogenic Neuropathy
Cardiovascular
Chemotherapeutic Drugs
Bortezomib Amiodarone
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Ixabepilone Perhexiline
Platinum compounds (cisplatin,
carboplatin, and oxaliplatin)
WnYQp/IlQrHD3i3D0OdRyi7TvSFl4Cf3VC1y0abggQZXdgGj2MwlZLeI= on 03/19/2023
Suramin
Taxanes
Thalidomide (1 analogue
lenalidomide)
Vinca alkaloids
5-Azacytidine
5-Fluorouracil
Clioquinol
Cytarabine
Etoposide
Gemcitabine
Ifosfamide
Misonidazole
Teniposide
CNS = central nervous system
several other neuropathic disorders
exist. Rapidly progressive lumbosa-
cral polyneuropathy presents as cauda
equina syndrome that is characterized
by saddle anesthesia, lower extremity
weakness, and loss of bowel or
bladder function; it occurs in patients
with severe immunosuppression and
a history of cytomegalovirus infec-
tion.53,54 This presentation warrants
a lumbar MRI or CT myelogram to
rule out a compressive spinal etiology.
The diagnosis is made by examination
of the cerebrospinal fluid and a posi-
tive polymerase chain reaction test for
cytomegalovirus infection.
HIV-associated radiculitis and
myelopathy have also been reported
from co-infection by herpes zoster,
herpes simplex virus, syphilis, and
tuberculosis.52 Other neuropathic
entities associated with HIV infection
include Guillain-Barré syndrome
(GBS) and chronic inflammatory
demyelinating polyneuropathy.55,56
14
Copyright Ó the American Academy of Orthopaedic Surgeons. Unauthorized reproduction of this article is prohibited.
Drugs Antibiotics and Antivirals
Dapsone
Isoniazid
Linezolid
Metronidazole
Nucleoside reverse
transcriptase inhibitors (NRTI)
ddl, ddC, d4T
Chloroquine
Chloramphenicol
Fluoroquinolones
Griseofulvin
Nitrofurantoin
Podophyllin resin
GBS (incidence = 1:100,000)
is characterized by demyelination of
peripheral nerves, and transverse
myelitis (TM) (incidence = 1 to
5/1,000,000) is characterized by
demyelinating myelopathy involving
the spinal cord, most commonly at the
thoracic level.56,57 GBS presents as the
acute onset of paresthesia in the hands
and/or feet that ascends symmetrically
to involve the proximal muscle girdles;
it may rapidly worsen to affect the
diaphragm with the potential for
respiratory failure. Flaccid paralysis,
areflexia, and autonomic dysfunction
also may be present. The pathogenesis
is believed to arise from an autoim-
mune mechanism because GBS com-
monly follows a viral illness such as
herpes simplex and cytomegalovirus
infections; however, it has also
been associated with Borrelia burg-
dorferi and Campylobacter jejuni
infections.58,59 These infections stim-
ulate antigenic mimicry that leads to
Journal of the American Academy of Orthopaedic Surgeons
Miscellaneous
CNS Agents Agents
Nitrous oxide Colchicine
Chlorprothixene Dichloroacetate
Glutethimide Etanercept
Phenelzine Infliximab
Phenytoin Pyridoxine
excess
Allopurinol
Interferons:
alfa2a, 2b
Leflunomide
Sulfasalazine
Triazole
antifungals
cross reactivity of native tissue; this
produces an immune response
against myelinated peripheral nerves
and results in the slowing of nerve
conduction velocities. The diagnosis
is made by clinical presentation,
cerebrospinal fluid analysis (ie, pro-
tein count .0.4 g/L and cell count
,10/mL), electrodiagnostic studies,
and blood laboratory studies to
exclude chemical toxicities.1,57
An idiopathic or a peri-infectious
autoimmune etiology is most likely
responsible for GBS and TM.57 Symp-
toms include back pain, weakness,
sensory loss, dysesthesias of the lower
extremities, and bladder and possibly
bowel dysfunction. Hyperreflexia is
often present below the level of the
lesion when TM symptoms develop
over several weeks, but patients may
be areflexic when symptoms are rapid
in onset.57,60
MRI of the whole spinal cord
should be obtained to rule out

Figure 7
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Sagittal T2-weighted magnetic
resonance image of the thoracic
spine demonstrating increased
signal within the spinal cord caused
by transverse myelitis (arrow).
(Reproduced with permission from
Jacob A, Weinshenker BG: An
approach to the diagnosis of acute
transverse myelitis. Semin Neurol
2008;28[1]:105-120.)
a compressive etiology in both GBS
and TM. MRI findings in GBS are
usually negative, whereas in TM
they may show focal or multilevel
increased spinal cord signal on
T2-weighted images (Figure 7).
When the diagnosis of GBS or TM is
suspected, urgent neurology referral
and access to intensive critical care is
indicated because respiratory failure
and paralysis may ensue.
Iatrogenic
Iatrogenic causes of lower extremity
pain that may be misdiagnosed as
lumbar radiculopathy may be divided
into two categories: myogenic and
neuropathic. Systemic medications
prescribed for a variety of acute and
chronic medical conditions constitute
most iatrogenic neuropathies and
myopathies (Table 3).
According to the IMS Institute
for Healthcare Informatics, lipid
regulators are the most commonly
January 2015, Vol 23, No 1
Copyright Ó the American Academy of Orthopaedic Surgeons. Unauthorized reproduction of this article is prohibited.
prescribed class of medication in the
United States, with simvastatin
being the single most commonly
prescribed medication after hydro-
codone/acetaminophen.61 A common
adverse effect of the statin class of
drugs is myopathy, occurring in 5%
to 10% of patients.62 According to
the Prediction of Muscular Risk in
Observational Conditions (PRIMO)
study involving 7,924 French pa-
tients, those taking simvastatin re-
ported the highest incidence of
myopathy (18%), whereas those
taking fluvastatin had the lowest
incidence (5.1%). Weakness and
cramping pain in the thighs or calves
was reported in 75% of affected
patients, whereas another 25% re-
ported diffuse myalgias.63 Onset of
symptoms occurs at a mean of 6.3
months after initiation of statin
therapy; however, symptoms may
occur as early as 1 week or as late as 4
years.64 Symptoms usually resolve
once the statins are stopped, helping
to support the diagnosis.
Modern treatment regimens for pa-
tients infected with HIV have mark-
edly reduced morbidity and mortality
associated with the disease; however,
potent antiretrovirals have neuro-
pathic adverse effects that patients
may attribute to a spinal origin. The
nucleoside analogues zalcitabine, di-
danosine, and stavudine have been
shown to have a dose-dependent effect
on the incidence and time to onset of
distal symmetric polyneuropathy.54
Chemotherapeutic agents used to
treat cancer, especially platinum-
containing compounds (eg, cisplatin,
carboplatin, oxaliplatin), are also
well-known potential causes of sen-
sory neuropathy; this can be a dose-
limiting adverse effect. Thalidomide
used in the treatment of multiple
myeloma may have the adverse effect
of both a distal sensory and a motor
neuropathy.65,66 A distal sensory
polyneuropathy may be an adverse
effect from chronic use of amiodarone
as a treatment of atrial fibrillation;
Bennett Douglas Grimm, MD, et al
however, a rapid form of neuropathy
with lower extremity weakness, are-
flexia, and ataxia has been reported.67
Summary
The most common cause of lumbar
radiculopathy is a herniated disk,
which tends to follow a predictable
onset and pattern. However, there
are several other diagnoses that
may cause lumbar radiculopathy-
type symptoms and are therefore
mimickers of lumbar radiculopathy.
These mimickers each have a differ-
ent onset and pattern of symptoms.
Performing a thorough history and
physical examination, supplemented
when needed with additional diag-
nostic tests, and/or referral to
appropriate specialists, can help dif-
ferentiate them. Providing high-
quality, cost-effective medical care
requires identifying these mimickers
when they are the cause of a patient’s
symptoms.
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