DISEASES OF THE NERVE

ROOTS
Kerry Levin

ABSTRACT
Disorders of spinal nerve roots can give rise to disabling pain and weakness. Damage to nerve roots resulting from disc disease and spondylosis can be localized by
attention to anatomic principles and with appropriate testing. Management strategies vary, depending on the clinical situation. Autoimmune, infectious, diabetic,
infiltrative, degenerative, and hereditary disorders are also causes of nerve root
disease. Other neurologic conditions can masquerade as nerve root disease.
Note: Text referenced in the Quintessentials Preferred Responses, which appear
later in this issue, is indicated in yellow shading throughout this chapter.

INTRODUCTION

134

Spinal nerve roots are formed from

sensory and motor axons as they exit
the spinal cord and shift from oligodendroglial myelination to Schwann
cell myelination. They continue
through the intraspinal canal and pass
through segmentally defined neuroforamina. Upon emerging, they are extraspinal and renamed anterior and
posterior primary rami. At the point
where individual anterior primary rami
from different segmental levels merge,
they lose their single nerve root segmental identities and become elements of the cervical or lumbar plexus.
Disease may affect individual nerve
roots, multiple nerve roots, or may involve nerve roots in a diffuse manner.
Nerve root lesions usually can be distinguished from plexus and peripheral
nerve trunk lesions on the basis of
characteristic clinical features. This
chapter will review the basic anatomy
of spinal nerve roots, the processes
that can produce nerve root disease,
and the disorders that may be difficult

to distinguish from nerve root diseases.

ANATOMY
In all, there are 31 pairs of spinal nerve
roots: 8 cervical, 12 thoracic, 5 lumbar,
5 sacral, and 1 coccygeal. Each spinal
nerve root is composed of a dorsal
(somatic sensory) root and a ventral
(somatic motor) root that join in the
intraspinal canal, just proximal to the
intervertebral foramen (Figure 7-1).
In the extraspinal region, just distal to
the intervertebral foramen, the nerve
root divides in two: a small posterior
primary ramus that supplies innervation to the paraspinal muscles and skin
of the neck and trunk, and a large
anterior primary ramus that supplies
sensory and motor innervation to the
limbs and trunk, including intercostal
and abdominal wall muscles. Cell bodies of the motor nerve fibers reside in
the anterior horns of the spinal cord,
while those of the sensory nerve fibers
reside in the dorsal root ganglia
(DRG). DRG are, in general, located
within the intervertebral foramina and

Relationship Disclosure: Dr Levin has nothing to disclose.

Unlabeled Use of Products/Investigational Use Disclosure: Dr Levin has nothing to disclose.

Copyright 2008, American Academy of Neurology. All rights reserved.

are, therefore, not strictly speaking intraspinal. However, at the lumbar and
sacral levels, the DRG tend to reside
proximal to the intervertebral foramina, in intraspinal locations. About 3%
of L3 and L4 DRG are intraspinal,
about 11% to 38% of L5 DRG are intraspinal, and about 71% of S1 DRG
are intraspinal, according to cadaver,
radiographic, and MRI studies (Hamanishi and Tanaka, 1993; Kikuchi et
al, 1994). At the cervical level, this is
less common but can be seen especially at the C5 and C6 levels (Yabuki
and Kikuchi, 1996).
The spinal canal is bound posterolaterally by laminae and the ligamentum
flavum, anterolaterally by pedicles, and
anteriorly by intervertebral discs and
vertebral bodies. The maximal anterior-posterior dimension of the canal at
the C1-C3 levels ranges from 16 mm to
30 mm, and at the C4-C7 levels from 14
mm to 23 mm. The diameter of the
spinal cord at C1 is about 11 mm, at
C2-C6 about 10 mm, and at C6-C7
about 7 mm to 9 mm. The cervical
canal diameter is reduced by 2 mm to
3 mm with extension.
Nerve roots are numbered according to their segmental location in the
spinal cord, while intervertebral foramina are numbered according to the
two vertebral bodies that frame the
intervertebral foramen from above and
below. A cervical root exits above the
vertebral body of the same number,
such that the C3 root exits the spinal
canal via the C23 intervertebral foramen. Since there are only seven cervical vertebrae, the C8 root exits through
the C7-T1 intervertebral foramen. As a
result of this incongruity, all thoracic,
lumbar, and sacral roots exit below the
vertebral body of the same number.
Nutrients reach spinal nerve roots
by a combination of arterial circulation
and diffusion from cerebrospinal fluid.
At each root level, the vascular supply
originates from the dorsal branch of a
segmental artery, which supplies a

FIGURE 7-1

Axial view of the spine at a midcervical level.

lig ligament.
Copyright 2008, Cleveland Clinic. All rights reserved.
Reprinted with permission.

longitudinal radicular artery and collateral radicular arteries, which course

along with the spinal nerve root and
give rise to corkscrewlike interfascicular arteries, stretching and contracting
along with nerve root during body
motion. These vessels supply intraneuronal capillaries that form a network, minimizing watershed zones
and risk of ischemia.
The blood-nerve barrier that protects peripheral nerves against a number of toxic exposures is not intact
around DRG, where open junctions
between and fenestrations within the
ganglionic vascular endothelial cells
have been documented (Jacobs et al,
1976). Hence, dorsal root ganglia are
prone to certain infections (such as
herpes zoster), immune disorders
(such as those associated with pure
sensory neuronopathy), and toxic exposures.
PATHOPHYSIOLOGY
Nerve root fibers are vulnerable to the
same types of injury as other peripheral nerves: entrapment, compression,
transection, invasion (malignancy, infection, inflammation), and ischemia.
Compression of a nerve root may reContinuum: Lifelong Learning Neurol 2008;14(3)

135

 DISEASES OF THE NERVE ROOTS

KEY POINTS:

136

The blood-nerve
barrier that
protects
peripheral nerve
against a
number of toxic
exposures is not
intact around
dorsal root
ganglia.

Since the motor

nerve cell body
(anterior horn
cell, motor
neuron) is within
the spinal cord,
damage to the
nerve root at
any location will
lead to wallerian
degeneration.
Damage to the
dorsal root
ganglia (DRG)
itself or the
sensory axon
distal to the
DRG will result
in wallerian
degeneration of
the sensory
axon.

sult in focal demyelination leading to

conduction block or conduction velocity slowing along the demyelinated
nerve root segment. Conduction block
along sensory or motor fibers causes
motor and sensory deficits, but conduction velocity slowing alone is insufficient to produce weakness or significant sensory loss. However,
sensory pathways that function by
transmission of timed volleys of action
potentials, such as those serving vibration and proprioception, can be disrupted by desynchronization of conduction velocities.
Axon loss also interrupts electrical
impulse transmission from the spinal
cord, leading to sensory and motor
deficits. Wallerian degeneration of the
axon distal to the lesion occurs when
the axon has been disconnected from
its cell body. Since the motor nerve
cell body (anterior horn cell, motor
neuron) is within the spinal cord, damage to the nerve root at any location
will lead to wallerian degeneration.
DRG, in general, reside within the intervertebral foramen, relatively protected from compression from spondylosis and disc protrusion. Only
damage to the DRG itself or the sensory axon distal to the DRG will result
in wallerian degeneration of the sensory axon.
NERVE ROOT DISEASE FROM
DISORDERS OF THE SPINE
Pathologic Features
By far, the leading causes of nerve root
disease are intervertebral disc disease
and spondylosis. Damage to nerve
roots occurs as the result of degenerative change at three main points: the
disc, the uncovertebral joints, and the
zygapophyseal (facet) joints. Resulting
bony overgrowth (osteophytes) or
disc herniation at these points may directly impinge on spinal nerve roots or
the spinal cord. In addition, these
pathologic effects produce instability
Continuum: Lifelong Learning Neurol 2008;14(3)

and malalignment of the spine that in

turn produces pain and neurologic sequelae. Whether changes in these different structures are causally interrelated or occur independently is not
known.
It is generally thought that the cascade of spondylotic changes is led by
degenerative change in the nucleus
pulposus of the disc. As the disc degenerates, vertebral body endplates
adjacent to the disc undergo changes,
leading to endplate sclerosis, followed
by osteophyte formation at the margins of the vertebral bodies. Facet joint
degeneration may not be directly related to the above changes but often
coexists. Osteophyte formation at
those joints causes further narrowing
of the spinal canal and lateral recesses.
Risk Factors and Epidemiology
of Radiculopathy
In an epidemiologic study of cervical
radiculopathy in Rochester, Minnesota, physical exertion or trauma preceded onset of radiculopathy in almost
15% of the 561 patients, most often the
result of shoveling snow in the winter
and playing golf in the summer
(Radhakrishnan et al, 1994). Motor vehicle accidents were responsible for
radiculopathy due to spinal fracture,
but not due to disc protrusion. Of the
patients with cervical radiculopathy,
41% had had prior lumbar radiculopathy, and 31% had had prior cervical
radiculopathy.
Lumbosacral radiculopathy is a
very common condition. More than
75% of all disc protrusions causing radiculopathy involve the L5 or S1 nerve
roots. Lumbosacral disc herniation
may occur 10 to 20 times more frequently than cervical disc herniations.
However, cervical radiculopathy is
also a common condition with a maleto-female ratio of 1.7. In the Rochester
study, the annual age-adjusted rate
was 83.2 cases per 100,000, with a
peak frequency of 202.9 per 100,000

per year in the 50- to 54-year-old age

group. Of these cases, 46% involved
the C7 root, 17.6% involved the C6
root, and less than 10% involved each
of the other levels. The cause of radiculopathy was disc protrusion in 22%
and spondylosis, disc, or both in 68%.
Of those, 26% subsequently underwent surgical treatment, but at last follow-up 90% of all patients were
asymptomatic or only mildly affected
by their radiculopathy.
Clinical Localization of
Radiculopathy
Clinicians use reference charts to correlate specific distributions of weakness with the likely anatomic level of
nerve root involvement. Significant
variation exists among the published
reference charts. The lack of agreement from one myotomal chart to another relates to anatomic variations in
humans and differences in the nature
of the research material used in the
collection process. Anatomic charts
have been derived by tracing root and
peripheral nerve innervations of muscles from cadaver studies. Clinical
charts have been derived by correlating the distribution of clinical muscle
weakness in patients with specific
traumatic lesions. EMG charts have
been derived from patterns of muscle
denervation in patients with focal
nerve root lesions. Figures 7-2 and
7-3 show electromyographically derived myotomal charts for the main
cervical and lumbar root levels (Levin
et al, 1996; Tsao et al, 2003).
The Clinical Diagnosis of
Radiculopathy
The initial diagnosis of radiculopathy
rests upon the clinical assessment,
based on the history and physical examination. The anatomic localization
can be inferred in some cases by the
neurologic examination, but the precise structural cause can only be determined by neuroimaging procedures.

Patient history. Obtaining a history consistent with radiculopathy requires exploring the major symptoms
of arm and leg pain, paresthesia,
numbness, and weakness. Pain is
present in virtually all patients with
acute radiculopathy, but it is seldom of
localizing value. The diagnosis of cervical radiculopathy is supported by the
presence of a history of radicular pain
emanating from the neck or shoulder,
with extension into the arm (sometimes in a specific dermatomal distribution). The diagnosis of lumbosacral
radiculopathy is supported by radicular pain that begins in the back or
buttock with radiation into the leg or
foot. The diagnosis is further supported when the symptoms are exacerbated by Valsalva maneuvers
(cough, sneeze, or strain), indicating
stretching of the dura at an intraspinal
point of compression. Radicular symptoms in the arm may also be reported
with neck/head movement. Patients
with lumbosacral radiculopathy may
report the presence of a self-induced
straight-leg raising sign: radicular
symptoms in the leg occurring when
sitting up straight with the legs extended, or even when lying supine if
the symptoms are severe. In the latter
case, relief may be reported when the
knees are flexed.
Paresthesia and numbness are
present less often than pain. They are
usually nonspecific and therefore of
little localizing value. However, these
symptoms are seldom present with
nonradicular causes of neck and back
pain.
The presence of Lhermitte symptoms (spinal or radicular tingling,
shocklike paresthesia with neck flexion), supports dysfunction of the posterior columns of the spinal cord, possibly due to spondylotic cord
compression, but also potentially due
to intraspinal mass lesions or intramedullary processes such as multiple sclerosis. The presence of bowel
Continuum: Lifelong Learning Neurol 2008;14(3)

KEY POINTS:

The diagnosis of
a radiculopathy
is suggested
when symptoms
are exacerbated
by Valsalva
maneuvers
(cough, sneeze,
or strain),
indicating
stretching of the
dura at an
intraspinal point
of compression.

Paresthesia and
numbness are
present less
often than pain
and are usually
nonspecific.
Therefore, like
pain, these
symptoms are
not of great
localizing value.

The presence of
Lhermitte
symptom (spinal
or radicular
tingling,
shocklike
paresthesia with
neck flexion)
suggests
dysfunction of
the posterior
columns of the
spinal cord.

137

 DISEASES OF THE NERVE ROOTS

KEY POINTS:

138

The Spurling test

(neck
compression
maneuver) is
performed by
extending and
rotating the neck
to the side of the
pain, followed by
applying
downward
pressure on the
head.

The shoulder
abduction relief
sign is performed
by asking the
patient to lift the
symptomatic arm
over the head,
resting the hand
on the top of the
head.

The straight-leg
raising sign is
said to apply a
tug on the
sciatic nerve and
its connection
with the L5 and
S1 nerve roots,
where pain is
generated at
points of dural
compression.

Of all the
elements of the
clinical
examination, the
identification of
weakness in a
specific
myotomal
distribution has
the greatest
localizing value
for the diagnosis
of a solitary
cervical or lumbar
spinal nerve root
lesion.

FIGURE 7-2

Needle electrode examination results grouped by the surgically defined root level of
involvement. Closed circle: positive waves or fibrillation potentials, with or without
neurogenic recruitment and motor unit changes; half-closed circle: neurogenic
recruitment changes only; open circle: normal examination.

SUP supraspinatus; INF infraspinatus; DEL deltoid; BRAC brachioradialis; BIC

biceps; PT pronator teres; FCR flexor carpi radialis; TRIC triceps; ANC anconeus;
EDC extensor digitorum communis; EIP extensor indicis proprius; FPL flexor pollicis
longus; APB abductor pollicis brevis; FDI first dorsal interosseus; ADM abductor
digiti minimi; PSP paraspinal muscle.
Reprinted with permission from Levin KH, Maggiano HJ, Wilbourn AJ. Cervical radiculopathies: comparison of
surgical and EMG localization of single-root lesions. Neurology 1996;46(4):10221025. Copyright 1996, AAN
Enterprises, Inc.

Continuum: Lifelong Learning Neurol 2008;14(3)

or bladder urgency, incontinence, new

constipation, or urinary retention may
reflect cervical spinal cord or cauda
equina compression.
The patient may provide important
information regarding the underlying
cause of the symptoms. A history of
recent or remote trauma should be explored, including whiplash incidents
and injuries during contact sports.
Prior episodes of spine pain, prior
spine surgery, and a family history of
spine disease should be sought. A general medical review of systems and
medical history are important to exclude other possible factors, such as
the presence of malignant disease, collagen vascular disease, or infection.
Clinical examination. The initial
part of the examination should be a
limited general physical examination
as dictated by the findings during the
historical interview. A complete neurologic examination should be performed, including inspection and percussion of the spine. A classification of
the typical neurologic attributes of solitary cervical and lumbar root lesions
is listed in Table 7-1.
Specific bedside clinical maneuvers for the provocation of symptoms
of cervical radiculopathy have come
into use, although their accuracy and
safety have not been carefully studied.
Lhermitte sign can be elicited by actively flexing the patients head and
observing for the development of tingling paresthesia down the cervical
spine or into the symptomatic arm.
The Spurling test (neck compression
maneuver) is performed by extending
and rotating the neck to the side of the
pain, followed by applying downward
pressure on the head. This maneuver
may produce limb pain or paresthesia,
as neck extension causes posterior
disc bulging, while lateral flexion and
rotation cause narrowing of the ipsilateral neural foramina. It may be safer to
perform this maneuver by asking patients to actively extend their neck,

FIGURE 7-3

Needle electrode examination results

grouped by the surgically defined root level
of involvement.

AL adductor longus; IL iliacus; VL vastus lateralis;

RF rectus femoris; VM vastus medialis; PT tibialis
posterior; TA tibialis anterior; EDB extensor digitorum
brevis; PL peroneus longus; EHL extensor hallucis
longus; GMED gluteus medius; ST semitendinosus;
TFL tensor fascia lata; MG medial gastrocnemius;
LG lateral gastrocnemius; AD abductor digiti quinti;
BFSH biceps femoris (short head); BFLH biceps
femoris (long head); GM gluteus maximus; AH
abductor hallucis; PSP paraspinal.
Reprinted with permission from Tsao B, Levin KH, Bodner RA. Comparison
of surgical and electrodiagnostic findings in single root lumbosacral
radiculopathies. Muscle Nerve 2003;27(1):60 64. Copyright 2003, John
Wiley & Sons, Inc.

then laterally flex and rotate toward

the side of the pain, followed by application of pressure through the examiners hands on the vertex of the
head. When radiating pain or limb
numbness develops, the maneuver
should be stopped. This maneuver is
said to be rather specific but not sensitive. The shoulder abduction relief
Continuum: Lifelong Learning Neurol 2008;14(3)

139

 DISEASES OF THE NERVE ROOTS

TABLE 7-1

140

Typical Clinical Attributes of Solitary Root Lesions

Root

Pain

Numbness

Weakness

Reflex Loss

C5

Neck, shoulder

Axillary distribution

Shoulder abduction,
external rotation, elbow
flexion, forearm
supination

Biceps,
brachioradialis

C6

Neck, shoulder,
lateral upper arm,
lateral forearm,
thumb, and lateral
hand

Lateral forearm,
thumb, and index
finger

Shoulder abduction,
external rotation, elbow
flexion, forearm
supination and
pronation

Biceps,
brachioradialis

C7

Neck, shoulder,
middle finger, hand

Index and middle

finger, palm

Elbow and wrist (radial

aspect) extension,
forearm pronation, wrist
flexion

Triceps

C8

Shoulder, medial
forearm, fourth and
fifth digits, medial
hand

Medial forearm,
fourth and fifth
digits, medial hand

Finger extension, wrist

(ulnar aspect) extension,
distal finger flexion,
distal thumb flexion,
finger abduction and
adduction

Triceps

T1

Medial arm and

forearm, axillary
chest wall, medial
forearm

Medial forearm,
fourth and fifth
digits

Thumb abduction, distal

thumb flexion, finger
abduction and
adduction

L23-4

Back, anterior thigh,

occasionally medial
lower leg

Anterior thigh,
occasionally medial
lower leg

Hip flexion, hip

adduction, knee
extension

Patellar

L5

Back, buttock, lateral

thigh, dorsum foot,
great toe

Lateral calf, dorsum

foot, web space
between first and
second toe

Hip abduction, knee

flexion, foot
dorsiflexion, toe
extension and flexion,
foot inversion and
eversion

Medial hamstrings
(semitendinosus/
semimembranosus
tendons)

S1

Back, buttock, lateral

or posterior thigh,
posterior calf, lateral
or plantar foot

Posterior calf,
lateral or plantar
aspect of foot

Hip extension, knee

flexion, foot plantar
flexion

Achilles tendon

sign is performed by asking the patient

to lift the symptomatic arm over the
head, resting the hand on the top of
the head. Reports indicate this may be
a useful therapeutic maneuver, as well
as a diagnostic one, for lower cervical
radiculopathy (Fast et al, 1989).
The straight-leg raising sign is the
main clinical bedside maneuver for the
Continuum: Lifelong Learning Neurol 2008;14(3)

provocation of symptoms of lumbosacral radiculopathy. With the patient in

the supine position, the fully extended
leg is passively elevated until radicular
symptoms in the leg are reported, usually by 30 to 40 degrees of elevation.
This maneuver is said to apply a tug
on the sciatic nerve and its connection
with the L5 and S1 nerve roots, where

pain is generated at points of dural

compression. A reverse straight-leg
raising sign is performed by passively
elevating the leg when the patient is in
the prone position, applying a tug on
the femoral nerve and its connections
to the L2, L3, and L4 nerve roots. The
straight-leg raising maneuver may produce nonspecific back pain in patients
with mechanical or musculoskeletal
symptoms, but not radicular, radiating
symptoms. To explore the possibility
that leg and hip pain is due to hip joint
disease, the knee in the flexed and
elevated position is rotated medially or
laterally, a maneuver that is painful in
patients with hip joint disease.
Of all the elements of the clinical
examination, the identification of
weakness in a specific myotomal distribution has the greatest localizing
value for the diagnosis of a solitary
cervical or lumbar spinal nerve root
lesion. Limb weakness provides the
most reliable correlation with the anatomic level of spinal nerve root involvement. The presence of weakness
is strong support for a neurologic disorder, but the examination seldom
fully differentiates radiculopathy from
plexopathy or mononeuropathy. True
neurogenic weakness may be difficult
to distinguish clinically from reduced
voluntary effort due to pain.
Diagnostic Testing For
Radiculopathy
Neuroimaging procedures. For imaging of the lumbar spine, MRI and CT
myelography (CT scan after intrathecal
administration of contrast media) are
equally sensitive for the diagnosis of
disc herniation (Bischoff et al, 1993).
For routine initial assessment, MRI is
less invasive and more informative
than CT because it can also identify
other intraspinal pathologies, including inflammatory, malignant, and vascular disorders. However, MRI studies
also frequently identify asymptomatic
lesions (Boden et al, 1990). In one

study, 28% of normal subjects had MRI

evidence of disc herniation (Jensen et
al, 1994). CT myelography is indicated
in patients with implanted electrical
devices and is preferred over MRI in
patients with surgically placed spinal
hardware that produces magnetic artifacts.
Electrodiagnosis. The primary
electrodiagnostic (EDX) procedures
are nerve conduction studies (NCS)
and electromyography (EMG). These
procedures provide a high yield of
clinical information about radiculopathy when neurologic weakness is
present for at least 3 weeks. The yield
is much lower in patients with pain or
sensory loss as the only manifestations
of radiculopathy. EDX studies provide
no diagnostic information in patients
with nonspecific spine pain, except to
exclude the presence of muscle and
nerve pathology. In such patients,
EMG can distinguish pain-related reduced muscular effort from true neurogenic weakness. In patients with
weakness due to radiculopathy, NCS
and EMG together can provide excellent localization of the specific spinal
nerve root that is damaged, distinguish
between old and new axon loss nerve
damage, and provide indirect support
for the presence of demyelinating conduction block at the root level (Levin,
2000). Finally, EDX testing can identify
mimickers of radiculopathy, such as
mononeuropathy, plexopathy, and
motor neuronopathy.
A number of studies have assessed
the relative value of EDX studies in the
diagnosis of lumbosacral radiculopathy. EMG studies tend to have a low
false-positive rate of diagnosis compared with MRI (Khatri et al, 1984).
Studies tend to demonstrate that EMG
and imaging studies have a comparable diagnostic sensitivity, varying between 50% and 85%, depending on
the patient population (Kuruoglu et al,
1994; Nardin et al, 1999; Wilbourn and
Aminoff, 1998). Neither MRI nor EMG
Continuum: Lifelong Learning Neurol 2008;14(3)

KEY POINT:

In patients with
weakness due to
radiculopathy,
nerve
conduction
studies and EMG
together can
provide excellent
localization of
the specific
spinal nerve root
that is damaged,
distinguish
between old and
new axon loss
nerve damage,
and provide
indirect support
for the presence
of demyelinating
conduction
block at the root
level.

141

 DISEASES OF THE NERVE ROOTS

can stand alone in the diagnosis of
radiculopathy, as each provides
unique anatomic and physiologic information (Albeck et al, 2000).
Somatosensory evoked potentials
are another EDX technique, carried
out by repetitive stimulation of the tibial nerve at the ankle and recording of
the propagated sensory potentials up
the leg, into the cauda equina, through
central sensory pathways in the spinal
cord and brain, to the sensory cortex.
This procedure has been investigated
as a tool for the assessment of electrical conduction through the damaged
segment of spinal nerve root in the
intraspinal canal. Unfortunately, there
are conflicting results in the literature
regarding the ability of this technique
to localize specific nerve root compression, raising questions about its
clinical value (Aminoff et al, 1985;
Dumitru and Dreyfuss, 1996; Katifi and
Sedgwick, 1987).

142

Management of Radiculopathy
Approaches to the management of radiculopathy vary depending on the
acuity of illness and the degree of neurologic deficit. In general, the likelihood for spontaneous recovery is
high, except in situations with severe
neurologic impairment. For acute radiculopathy, treatment recommendations can be specified for the sensory/
painful radicular pattern, the mild
motor deficit pattern, and the marked
motor/progressive pattern of illness.
Treatment strategies are summarized
in Tables 7-2 to 7-4.
Acute sensory/painful radicular pattern. The management of the
sensory/painful radicular pattern is not
significantly different from the approach to acute mechanical back pain,
since the likelihood of spontaneous
resolution of all symptoms is very
high. Treatment includes rest for several days and avoidance of lifting and
activities that increase the pain. Radiculopathy is often extremely painful.
Continuum: Lifelong Learning Neurol 2008;14(3)

Nonsteroidal anti-inflammatory drugs

can be useful. Muscle relaxants do not
provide a significant benefit over nonsteroidal drugs (Bigos et al, 1994). Depending on the severity of pain, narcotic analgesia may be required during
the first 10 to 14 days, when radicular
pain is most intense.
Next in importance to analgesics
in the management of acute radiculopathy is modification of activity to
lessen active nerve root impingement.
The patient should avoid activities that
exacerbate pain. In general, physical
therapy in the first 1 to 2 weeks is not
recommended. Avoidance of activity
does not imply prolonged complete
bed rest, which may prolong disability
(Vroomen et al, 1999). Patients often
identify pain-relieving positions for
themselves. Some individuals commonly report that semi-sitting, reclining, or some positions in bed provide
a good degree of sciatic or femoral
pain relief. Other patients find recumbence in bed more painful, preferring
to be up and around, even performing
light work duties.
Patients with the sensory/painful
radicular pattern have no neurologic
deficits, aside from a segmental pattern of sensory dysfunction, so the
likelihood that neuroimaging will lead
to a consideration for surgery is very
low.
For patients with acute sensory
cervical radiculopathy, treatment with
cervical traction and spinal manipulation is not recommended in the presence of spinal cord compression or
large disc protrusion, and should not
be considered unless the intraspinal
anatomy has already been defined by
neuroimaging. In the patient with
acute cervical radiculopathy due to
neural foraminal stenosis from facet or
uncovertebral osteophytes, cervical
traction may provide temporary relief
by modestly increasing the separation
between vertebral bodies. This therapy can be self-administered with a

TABLE 7-2

Treatment Approaches for Acute Lumbosacral

Radiculopathy (Less Than 4 Weeks)

Painful/Sensory Pattern
Nonsteroidal anti-inflammatory drugs
Additional narcotic analgesia for severe pain
Brief (bed) rest (1 to 2 days)
Avoidance of aggravating activities
Consideration of a 10- to 14-day course of oral corticosteroids
Gradual mobilization
Medical follow-up if no improvement over 2 to 3 weeks

Mild Motor Deficit Pattern

Above strategies
Consideration of MRI scan of lumbar spine
EMG examination after 3 weeks if no or little improvement
Physical therapy assessment when pain has stabilized

Marked Motor Deficit

Urgent MRI scan of the lumbar spine
Neurosurgical or orthopedic consultation for compressive lesion
Above strategies
EMG at 3 weeks
Physical therapy assessment when pain has stabilized

TABLE 7-3

Treatment Approaches for Subacute Lumbosacral

Radiculopathy (Greater Than 4 Weeks)

Medical/Neurologic Reassessment

MRI Scan of the Lumbar Spine if Not Already Done

Neurosurgical or Orthopedic Consultation for Compressive Lesion
More Aggressive Mobilization
Medical Program of Rehabilitation
Nonsteroidal anti-inflammatory drugs
Consideration of gabapentin, pregabalin and/or duloxetine, and tricyclics
for neuropathic pain
Active physical therapy
Education

Continuum: Lifelong Learning Neurol 2008;14(3)

143

 DISEASES OF THE NERVE ROOTS

KEY POINTS:

144

For patients with

acute sensory
cervical
radiculopathy,
treatment with
cervical traction
and spinal
manipulation is
not
recommended in
the presence of
spinal cord
compression or
large disc
protrusion and
should not be
considered unless
the intraspinal
anatomy has
already been
defined by
neuroimaging.
In patients with
an acute
radiculopathy
the decision
regarding
surgery requires
the following
considerations:
(1) the likelihood
of spontaneous
improvement,
(2) the likelihood
of disability from
a fixed
neurologic
deficit, and (3)
the risk of
progression of
the deficit
without surgery.
Change in the
pain and
neurologic
deficits (for
better or worse)
over time will
help inform the
final decision.

TABLE 7-4

Treatment Approaches for Cervical Radiculopathy

Acute Radiculopathy With Sensory Symptoms and Signs

Perform cervical radiographs and MRI: with trauma, myelopathy, prolonged
symptoms
Avoid heavy lifting and activities that increase pain
Avoid bed rest and immobilization of the head and neck
Use nonsteroidal anti-inflammatory drugs for pain control
Consider high-dose, fast-taper corticosteroids for unresponsive symptoms
Consider cervical traction if pathology is limited to foraminal stenosis
Reassess in 1 month

Acute Radiculopathy With Neurologic Deficits

Perform MRI cervical spine
Refer for neurosurgical consultation for compressive myelopathy
Avoid heavy lifting and activities that increase pain
Avoid bed rest and immobilization of the head and neck
Use nonsteroidal anti-inflammatory drugs for pain control
Consider high-dose, fast-taper corticosteroids for unresponsive symptoms
Consider cervical traction if pathology is limited to foraminal stenosis
Reassess in 1 month

Subacute or Chronic Radiculopathy (Greater Than 4 Weeks)

Progressive mobilization
Physical therapy for mobility, posture
Consider transcutaneous electrical nerve simulation
Refer for neurosurgical/orthopedic consultation for structural and
continued clinical evidence of root or spinal cord compression

pulley system traction device. The initial counterweight should not exceed
5 to 7 pounds but can be increased as
tolerated to 15 or more pounds. Fifteen- to 20-minute episodes of traction
should be repeated throughout the
day as needed. Reports indicate that,
during cervical traction and for some
minutes after, some anterior cervical
vertebral separation does occur. In
one study, greater separation appeared with 50 pounds than with 30
pounds of traction, but traction applied for more than 7 seconds at a time
provided no further separation (ColaContinuum: Lifelong Learning Neurol 2008;14(3)

chis and Strohm, 1966). With 7 seconds of 30 pounds of applied traction

alternating with 5 seconds of rest,
maximal separation occurred at 25
minutes, but the effect was lost within
20 minutes of the last applied traction.
Although the efficacy of cervical traction has not been proven, it is a standard therapy, and many patients claim
benefit. If traction induces increased
symptoms or pain, it should be discontinued. A systematic review of the literature could not support firm conclusions on the efficacy of cervical
traction because of methodologic in-

adequacies in the published studies

(van der Heijden et al, 1995).
Acute mild motor deficit pattern. The management of the mild
motor deficit pattern also begins with
conservative measures as outlined
above. The likelihood of spontaneous
recovery is high. Systemic corticosteroids (1-week course of oral prednisone) have not been shown to be
more effective than placebo, based on
a single randomized controlled study
(Haimovic and Beresford, 1986). However, as a temporizing maneuver, and
for its effects as an anti-inflammatory
agent and mild mood raiser, corticosteroids may be beneficial in the early
phase of radiculopathy. A typical
course would be prednisone 60 mg to
80 mg daily for 5 to 7 days, followed
by a fast taper to discontinuation over
the next 7 to 14 days. Prophylaxis
against gastritis is recommended, and
special precautions are needed in diabetics, but otherwise the short course
of treatment is not likely to produce
complications.
With acute, mild motor deficits the
need for neuroimaging is dictated
more by the perceptions of the patient
and physician than by its value in clinical decision making. As the concern
about permanent or progressive deficits increases, the need for defining
the anatomic disease underlying the
radiculopathy becomes more acute.
Acute marked motor/progressive pattern. The management of the
marked motor/progressive pattern requires simultaneous treatment of the
pain symptoms and diagnosis of the
underlying anatomic cause of the condition. An MRI scan of the lumbosacral
spine will identify most pathologic
states that may require surgical intervention. EMG studies will not be of
value in the diagnosis of acute radiculopathy until at least 3 weeks have
passed from the onset of weakness.
The decision regarding surgery requires the following considerations:

(1) the likelihood of spontaneous improvement, (2) the likelihood of disability from a fixed neurologic deficit,
and (3) the risk of progression of the
deficit without surgery. Change in the
pain and neurologic deficits (for better
or worse) over time will help inform
the final decision. After 3 weeks, EMG
studies can help the decision-making
process by identifying the distribution
and extent of spinal nerve root damage, the degree of acute axon loss, and
the likelihood of conduction block. A
linear correlation does not exist between the size of disc herniation or
nerve compression and the amount of
spinal nerve root damage. Small compressive lesions can at times produce
severe, irreversible nerve damage if
they affect arterial blood supply to the
nerve. An ischemic nerve lesion, although severe, would not be likely to
improve as a result of removal of the
compressive lesion (Case 7-1).
Subacute radiculopathy. In general, radiculopathy has a monophasic
course with eventual improvement
(Cherkin et al, 1998). Patients with at
least moderate neurologic deficits may
have long-standing residual impairment. At 3 to 4 weeks after onset, unimproved patients who have not yet
had neuroimaging should have that
done to assess the underlying structural abnormalities. If a causative
structural lesion is identified, surgical
consultation should be considered.
Patients with continued spinal nerve
root compression or spinal nerve root
infarction are likely to have some degree
of persistent pain. Drugs with particular
effectiveness against neuropathic pain
should be considered, including gabapentin, pregabalin, duloxetine, and tricyclic antidepressants. Continuing narcotic
medications should be avoided but in
individual cases may be effective at a
specific dosage. Patients will respond to
mobilization and other physical therapy
techniques but may be limited by their
neurologic deficits. Physical therapy
Continuum: Lifelong Learning Neurol 2008;14(3)

KEY POINTS:

In patients with
acute
radiculopathy,
EMG studies will
not be of value
until at least 3
weeks have
passed from the
onset of
weakness. After
3 weeks, EMG
studies can help
the decisionmaking process
by identifying
the distribution
and extent of
spinal nerve root
damage, the
degree of acute
axon loss, and
the likelihood of
conduction
block.

A linear
correlation does
not exist
between the size
of disc
herniation or
nerve
compression and
the amount of
spinal nerve root
damage.

145

 DISEASES OF THE NERVE ROOTS

KEY POINT:

146

Small
compressive
lesions can at
times produce
severe,
irreversible nerve
damage if they
affect arterial
blood supply to
the nerve. An
ischemic nerve
lesion, although
severe, would
not be likely to
improve as a
result of removal
of the
compressive
lesion.

Case 7-1
A 65-year-old man with a history of L4 5 discectomy developed acute
severe back pain with radiation into the left posterior thigh and over the
dorsum of the foot. On examination, a left footdrop with weakness in
foot inversion and eversion, toe extension, and flexion was identified. The
pain improved over several weeks, but the footdrop persisted. The patient
was referred for electrodiagnostic testing 4 weeks after onset of
symptoms.
NCS demonstrated reduced amplitude of the left peroneal motor
responses when recording over the extensor digitorum brevis muscle in
the foot and over the tibialis anterior muscle, when compared with the
opposite side. The superficial peroneal sensory response was absent on
the left and normal on the right, while the sural sensory responses were
normal and symmetric. Needle EMG showed fibrillation potentials in the
left anterior tibialis, posterior tibialis, extensor hallucis longus,
semitendinosus, and gluteus medius muscles, with sparing of the biceps
femoris (short head and long head) muscles. Fibrillation potentials could
not be identified at left low lumbar and sacral paraspinal levels.
An MRI study of the lumbar spine showed advanced lumbar canal
stenosis at the L4 5 level with focal lateral disc herniation into the left
L5-S1 lateral recess.
Comment. This patient demonstrated clinical signs suggesting an L5
radiculopathy. EDX testing confirmed an L5 distribution of active motor
axon loss, with additional evidence of loss of the L5 sensory response on
NCS. Loss of the superficial peroneal sensory response is usually seen with
common peroneal neuropathy at or above the fibular head, sciatic
neuropathy, and sacral plexopathy. Loss of this sensory response,
however, can be seen with intraspinal canal lesions affecting the L5 root
when the L5 dorsal root ganglion is situated within the intraspinal canal
and vulnerable to compressive injury (Levin, 1998). For this patient, if pain
has subsided and there is no progression of weakness, surgery can be
deferred and physical therapy can be initiated on a trial basis.

should address issues of mobility and

strengthening of weak muscles.
In postoperative patients with continuing radicular pain, compressive
disease such as residual disc fragments, hematoma, and arachnoiditis
must be excluded. Neuroimaging is required to investigate treatable causes
of pain. In nonoperated patients with
continued radicular pain, several nonsurgical treatment modalities can be
considered.
Epidural corticosteroid injection. The American Academy of Neurology has a practice parameter that
addresses the issue of epidural steroid
injections to treat radicular lumbosacral pain (Armon et al, 2007) (AppenContinuum: Lifelong Learning Neurol 2008;14(3)

dix). Few placebo-controlled, prospective studies are available to assess

the value of epidural corticosteroid injections, and those that are available
have been criticized for design flaws
(Malanga and Nadler, 1999; Nelemans
et al, 2000). These procedures used an
interlaminar injection approach, often
without
fluoroscopic
guidance,
whereby a needle is advanced between the lamina of two adjacent vertebrae into the dorsal epidural space.
One meta-analysis found no trend favoring epidural steroids (Koes et al,
1995). Another study included patients
with radiculopathy from disc herniation and claudication from lumbar ca-

nal stenosis. It identified some effect

on pain and/or findings within days to
12 weeks after treatment, but found no
difference in pain or deficits when
compared with placebo at 12 weeks
(Cuckler et al, 1985). A randomized
double-blind trial studied 158 patients
with lumbar radiculopathy of 4 to 52
weeks duration, with evidence of radicular deficits on clinical examination
and CT evidence of disc herniation
(Carette et al, 1997). Six weeks after
three epidural injections of either corticosteroid or saline, patients having
received corticosteroid had somewhat
more improvement in leg pain, but at
3 months there was no significant difference between the two groups.
Twenty-five percent of patients in
both groups eventually went on to
lumbar spine surgery. With the interlaminar approach it has been shown
that only 70% of cases have epidural
delivery of steroid without fluoroscopic guidance (Karasek, 2001).
Transforaminal epidural injections
have been promoted as a more selective, and therefore more effective,
treatment technique. The likelihood of
steroid delivery at the root level is
thought to be higher, since the needle
is placed under fluoroscopic guidance
in the epi-radicular space just above
the dorsal root ganglion in the neural
foramen. One placebo-controlled
study of 55 patients assessed the need
for surgery for pain or neurologic deficits after treatment (Riew et al, 2000).
Eight of 28 treated patients ultimately
underwent surgery while 18 of 27 placebo-treated patients ultimately received surgery. Concerns raised with
this study included a non-homogeneous patient population (disc herniation and foraminal stenosis), atypical
pain scale assessment tools, and multiple surgeons making operative decisions (Joelson, 2001).
Epidural corticosteroid injections
at the cervical levels have been performed for several decades, but not to

the extent they have been used at the

lumbar levels. Epidural injection of a
combination of corticosteroid and anesthetic can lead to temporary reduction of pain in some patients. The few
trials that have been performed have
not been well controlled and have
lacked homogeneous study populations. One study involving injections
performed at the C5-6 and C6-7 interspaces produced pain relief for 1
month or longer in 38% of patients
(Shulman, 1986).
A retrospective study of 100 patients attempted to identify a patient
profile that predicted response to cervical epidural injection of a combination of corticosteroid and anesthetic
(Ferrante et al, 1993). Based on clinical
outcomes determined by subjective reports of pain relief and return to activities of daily living, only the presence
of radicular pain predicted a better
outcome from epidural injection.
Other measured predictors, including
age, abnormal sensory examination,
change in muscle stretch reflexes, motor changes on examination, and abnormal EMG findings, were not found
to be significant. Predictors of a poor
outcome included normal radiologic
examination findings and the presence
of a herniated disc. In those who experienced greater than 50% pain relief,
the response occurred irrespective of
the cervical level involved. In patients
with symptoms and neurologic signs
of true radiculopathy, whether or not a
structural abnormality was seen radiographically, the probability of at least
50% improvement was 62%, while the
probability was only 35% for patients
with only radicular pain symptoms
and radiologic structural changes. The
poorest probability was seen in patients with radicular symptoms without structural changes and in patients
with nonspecific axial pain symptoms.
One study described a 76% success
rate for paravertebral transforaminal
Continuum: Lifelong Learning Neurol 2008;14(3)

KEY POINT:

Potential
complications of
epidural steroid
injections
include spinal
headache,
epidural or
intrathecal
hematoma,
transient
worsening of
radiculopathy,
and steroid
effects. While
reported
complications of
cervical
injections are
rare, they can be
severe, including
spinal cord and
brainstem
infarction.

147

 DISEASES OF THE NERVE ROOTS

KEY POINT:

148

Diabetic
polyradiculopathy
may present as
an isolated L3-4
radiculopathy
but often
spreads over
weeks to
months into
other root
distributions.
Infections may
involve single or
multiple nerve
roots.

epidural steroid injections (Bush and

Hillier, 1996).
Potential complications of epidural steroid injections include spinal
headache, epidural or intrathecal hematoma, transient worsening of radiculopathy, and steroid effects. While reported complications of cervical
injections are rare, they can be severe,
including spinal cord and brainstem
infarction (Rathmell et al, 2004).
Surgical management. A number of carefully controlled, multicenter
trials have studied the value of surgery
for lumbosacral radiculopathy. In a recent study, patients with severe sciatica for 6 to 12 weeks with lumbosacral
radiculopathy confirmed by a neurologist were randomly assigned to receive either conservative treatment
(with or without eventual surgery) or
early minimal unilateral transflaval surgery with magnification (Peul et al,
2007). Patients with severe weakness
and cauda equina syndrome were excluded. At 1 year, outcomes were similar for the two groups, although the
rates of pain relief and of perceived
recovery were faster for those assigned to early surgery. In another
study, patients with lumbar spondylolisthesis, lumbar canal stenosis,
and neurogenic claudication with neurologic signs were randomly assigned
to conservative treatment or decompressive surgery with spinal fusion
(Weinstein et al, 2007). This study
demonstrated significantly greater improvement in pain and function
among the surgically treated patients,
but the analysis was complicated by
an unexpectedly high rate of crossover
from the conservative treatment group
to the surgery group. For both of these
studies, back pain did not improve as
much as leg pain, indicating that the
greatest benefit is likely to occur for
nerve rootrelated symptoms (Deyo,
2007).
The factors that increase the likelihood that surgery will be performed
Continuum: Lifelong Learning Neurol 2008;14(3)

for cervical radiculopathy include

identification of an anatomic lesion
that corresponds with the clinical picture in the presence of one or more of
the following: obvious neurologic deficit, progression of the deficit over
time, unresolved pain, and spinal cord
compression on neuroimaging in the
presence of associated myelopathic
neurologic deficits (Carette and Fehlings, 2005). In a Cochrane Database
of Systematic Reviews, only two studies met criteria for inclusion (Fouyas et
al, 2002). One study compared surgical and nonsurgical therapies in 81 patients with cervical radiculopathy
without myelopathy (Persson et al,
1997). At 3 months after therapy, there
was 42%, 18%, and 2% reduction in the
visual-analogue pain scores for surgical, physical therapy, and hard collar
patients, respectively. However, at 1
year, the three groups did not differ in
regard to any measure, including pain,
function, or mood.
OTHER DISORDERS OF NERVE
ROOTS
Few disorders, other than skeletal disease of the spine, present as a single
nerve root disorder. Diabetic polyradiculopathy may present as an isolated
L3-4 radiculopathy but often spreads
over weeks to months into other root
distributions. Infections may involve
single or multiple nerve roots. In particular, herpes zoster infection often
involves a single nerve root distribution when it manifests in an extremity.
Polyradiculopathy
Polyradiculopathy refers to damage to
multiple root segments simultaneously
or in progressive order, occurring in a
single limb, or more frequently bilaterally, and sometimes diffusely. The
causes are diverse and at times unclear. In general, this process affects
the lumbosacral segments, with the
cervical segments involved later or not
at all. In some neurologic disorders,

TABLE 7-5

Differential Diagnosis of Polyradiculopathies

Polyradiculopathy

Polyneuropathy

Myelopathy

Disorders with true root involvement

Arachnoiditis

Inflammatory polyneuropathy

Diabetes

HNPP

Procainamide polyradiculoneuropathy

Spondylosis

Radiation

Vascular malformation (conus medullaris)

Malignant invasion

Paraneoplastic syndromes

Sarcoidosis

Lyme disease

Viral infection (HZV, CMV, HSV, EBV)

Mycoplasma infection

Vasculitis

Angiotropic lymphoma

Pompe disease (-glucosidase deficiency)

Polyglucosan body disease (glycogenbranching enzyme deficiency)

Adrenal insufficiency
a

Disorders mimicking root involvement

Porphyric polyneuropathy

-Lipoprotein deficiency

X-Linked bulbospinal neuronopathy

Motor neuron disease

Juvenile monomelic amyotrophy

Spinal cord infarction

Multiple sclerosis

Syringomyelia

HNPP hereditary neuropathy with tendency to pressure palsy; HZV herpes zoster virus; CMV cytomegalovirus; HSV
herpes simplex virus; EBV Epstein Barr virus.
a

Data from Sahenk Z, Mendell JR, Rossio JL, Hurtubise P. Polyradiculopathy accompanying procainamide-induced lupus erythematosus: evidence for
drug-induced enhanced sensitization to peripheral nerve myelin. Ann Neurol 1977;1(4):378 384.

polyradiculopathy coexists with lesions in distal peripheral nerves, lesions in the CNS, or both. Table 7-5

lists some causes of polyradiculopathy

and disorders that fall into the differential diagnosis.
Continuum: Lifelong Learning Neurol 2008;14(3)

149

 DISEASES OF THE NERVE ROOTS

150

Compressive polyradiculopathies. Spondylosis of the spine is often multifocal, and multiple roots may
suffer compressive damage concurrently. This is especially true at the
lumbosacral level, where spondylosis
causes lumbar canal stenosis and multilevel neuroforaminal stenosis. With
lesions from L1 to the sacrum, a large
disc herniation or marked concentric
constriction of the canal from spondylotic stenosis may cause compression of
the cauda equina. This kind of lesion
can produce bilateral polyradiculopathy
at several levels simultaneously, at times
also affecting innervation of the urinary
and rectal sphincters.
At the cervical level, bilateral compressive polyradiculopathy may occur
due to diffuse spondylosis, perhaps
associated with congenital narrowing
of the intraspinal canal or hypertrophy
of the ligamentum flavum. This condition is often associated with cervical
myelopathy. Occasionally the occurrence of acute or subacute myelopathy
and motor axon loss in root distributions may not be due to direct compression, but rather to venous congestion in the spinal cord secondary to the
compression, leading to ischemia and
infarction of long tracts and anterior
horn cells. The effects of venous congestion span multiple segmental levels, explaining how a focal compressive lesion at one level of the cervical
spinal cord can produce anterior horn
cell loss at a number of levels distal to
the compression (Stark et al, 1981).
Other causes of polyradiculopathy. The polyradiculopathy associated with diabetes can be among the
most disabling of all the neuropathic
complications of that condition. Although almost always confined to the
thoracic, lumbar, and sacral segments,
in severe cases cervical myotomes are
also affected (Dyck et al, 1999; Riley
and Shields, 1984). Diabetic polyradiculopathy is usually associated with
underlying diabetic polyneuropathy
Continuum: Lifelong Learning Neurol 2008;14(3)

(so-called diabetic polyradiculoneuropathy), but may be seen in isolation

in as many as 25% of cases (Bastron
and Thomas, 1981). This condition is
often associated with damage at the
lumbosacral plexus level as well, leading some authors to refer to the condition as diabetic lumbar radiculoplexoneuropathy (Dyck et al, 1999)
(Case 7-2).
Any process that can infiltrate or
compress nerve roots or their sheaths
can lead to polyradiculopathy. Infectious causes include Lyme disease,
tuberculosis, syphilis, and fungal infections. Cytomegalovirus polyradiculopathy associated with underlying
HIV infection presents as a painful,
rapidly progressive paraparesis with
urinary and rectal sphincter dysfunction (Eidelberg et al, 1986). Malignancy produces polyradiculopathy by
compression and invasion. Malignancies with a predilection for bone (myeloma, metastatic breast, prostate,
lung cancer) are especially likely to
cause polyradiculopathy, myelopathy,
or both, because of their tendency to
spread into contiguous regions. Malignant cells may also gain entry into the
intraspinal canal by hematogenous
spread.
Polyradiculoneuropathies
The diagnosis of polyradiculoneuropathy indicates the presence of coexisting features of polyradiculopathy
and peripheral polyneuropathy. The
clinical presentation includes weakness in both proximal and distal root
distributions of the legs (and in some
disorders the arms as well), often in a
distal to proximal gradient, associated
with features of sensory axon loss.
Electrodiagnostically, the picture is
characterized by loss of sensory responses, combined with features of
motor axon loss, or demyelinating
conduction block in multiple root distributions, or both. The leading causes
include acute inflammatory demyeli-

KEY POINTS:

Case 7-2
About 4 weeks after total abdominal hysterectomy, a 58-year-old woman
developed back discomfort and pain in the right anterior thigh that
progressed in severity over a 2-week period of time. The patient was a
diet-controlled diabetic, but in the immediate postoperative period
glucose control deteriorated and insulin therapy was initiated. The pain
was burning and felt as though it was just under the surface of the skin.
Position changes did not affect the pain, and it was severe in bed at night.
Over the same period, the right knee began to give out and several falls
occurred. Over several weeks the leg failed to hold her up without
support of a walker. Over the subsequent 2 weeks, she reported a
progressive tendency to catch her foot and toes on rugs, and she noted
that she could not lift her foot to clear a curb.
The examination showed strength graded 3/5 in right knee extension,
4/5 in hip flexion, knee flexion, and foot dorsiflexion. Toe extension was
graded 4/5, and toe flexion and foot plantar flexion were nearly normal.
Sensation was blunted in the stocking distribution to light touch and pin
bilaterally, and more marked sensory loss was noted over the right
anterior thigh. Muscle stretch reflexes were graded 1 in the arms, 1 at the
left knee, and absent at the right knee and both ankles.
MRI studies of the lumbar spine demonstrated multilevel spondylosis
with mild canal stenosis at L3-L5. MRI studies of the pelvis showed
postoperative changes without discernible hematoma.
NCS showed absence of the sensory responses at both feet. Peroneal
and tibial motor responses recording over foot muscles were within
normal limits, but the right femoral motor response showed more than a
50% reduction of the amplitude compared with the opposite side. Needle
EMG showed prominent fibrillation potentials in the right quadriceps
muscles, the iliacus, adductor longus, tibialis anterior muscle, and extensor
hallucis longus. On the left, mild fibrillation potentials were identified in
the quadriceps muscles only. Laboratory studies identified a fasting
glucose of 155 mg/dL and the hemoglobin A1c level was 8.0.
Comment. A diagnosis of diabetic lumbar polyradiculoneuropathy was
made. Aggressive pain management was instituted, and diabetic control
was improved. Over the course of 6 months, improvement occurred in
right leg function with physical therapy, and the patient could ambulate
with a cane.

nating polyradiculoneuropathy (Guillain Barre syndrome) and chronic

inflammatory demyelinating polyradiculoneuropathy. Both demyelinating and pure axon loss forms of inflammatory polyradiculoneuropathy
are now recognized (Griffin et al,
1996). As noted above, diabetes produces a primarily axon-loss polyradiculoneuropathy.
Some hereditary disorders produce a picture of polyradiculoneuropathy. Hereditary neuropathy with
tendency to pressure palsy can present

in this fashion (Le Forestier et al,

1997). -Lipoprotein deficiency (Tangier disease) is associated with a motor
and sensory neuronopathy in a progressive segmental pattern that often
affects the upper extremities first, and
mimics a pattern of polyradiculopathy
(Case Records of the Massachusetts
General Hospital, 1996; Schmalbruch
et al, 1987). Porphyric polyneuropathy
is characterized by marked proximal
and distal weakness, sometimes asymmetric, affecting the arms more than
the legs. Sensory responses are variContinuum: Lifelong Learning Neurol 2008;14(3)

Some hereditary
disorders
produce a
picture of
polyradiculoneuropathy.

When a
polyradiculopathy
pattern is
associated with
corticospinal
tract deficits, the
differential
diagnosis
expands to a
consideration of
motor neuron
disease of the
ALS type,
cervical and/or
thoracic
polyradiculopathies, and
myelopathies.

151

 DISEASES OF THE NERVE ROOTS

ably affected, but the clinical presentation is predominantly motor.
Differential Diagnosis
A number of conditions mimic the
clinical picture seen with polyradiculopathy and should be considered
when making a diagnosis. Motor neuron disorders present with a picture of
asymmetric or symmetric progressive
segmental weakness, involving either
the cervical or lumbosacral myotomes
first. Disorders with only lower motor
neuron involvement include spinal
muscular atrophy, juvenile amyotrophy of the upper extremity, and progressive muscular atrophy (lower motor neuron variant of ALS) (Hirayama
et al, 1987; Suarez et al, 1997).
When a polyradiculopathy pattern
is associated with corticospinal tract
deficits, the differential diagnosis expands to a consideration of motor neuron disease of the ALS type, cervical
and/or thoracic polyradiculopathies,
and myelopathies. To distinguish
these disorders, neuroimaging, EDX
studies, and occasionally CSF analysis
are required. Several EMG features

may help distinguish one disorder

from the other. Compressive polyradiculopathy is a more chronic process,
and there may not be much evidence
of active motor axon loss (fibrillation
potentials). In contrast, in midstage
ALS, fibrillation potentials are prominent, as is motor unit configuration
instability as a feature of active reinnervation. Second, the degree of motor unit dropout is usually greater in
ALS than in most radiculopathies.
Other conditions that may fall into this
category include polyglucosan body
disease (glycogen-branching enzyme
deficiency) (Bruno et al, 2004) and
Pompe disease (-glucosidase deficiency) (Karpati et al, 1977; Moses and
Parvari, 2002).
Other disorders of the spinal cord
can mimic polyradiculopathy with
associated myelopathy. Examples include syringomyelia; radiation radiculo-myelopathy; severe demyelinating disease (multiple sclerosis);
intramedullary glioma, as well as other
malignancies; and arteriovenous malformations affecting the spinal cord.

REFERENCES

152

Albeck MJ, Taher G, Lauritzen M, Trojaborg W. Diagnostic value of electrophysiological

tests in patients with sciatica. Acta Neurol Scand 2000;101(4):249 254.
Aminoff MJ, Goodin DS, Barbaro NM, et al. Dermatomal somatosensory evoked
potentials in unilateral lumbosacral radiculopathy. Ann Neurol 1985;17(2):171176.
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 2007;68(10):723729.
Bastron JA, Thomas JE. Diabetic polyradiculopathy: clinical and electromyographic
findings in 105 patients. Mayo Clin Proc 1981;56(12):725732.
Bigos SJ, Bowyer OR, Braen GR, et al. Acute low back problems in adults. Clinical practice
guideline 14. AHCPR Publication 95 0642. Rockville, MD: Agency for Health Care Policy
and Research, 1994.
Bischoff RJ, Rodriguez RP, Gupta K, et al. A comparison of computed tomographymyelography, magnetic resonance imaging, and myelography in the diagnosis of
herniated nucleus pulposus and spinal stenosis. J Spinal Disord 1993;6(4):289 295.

Continuum: Lifelong Learning Neurol 2008;14(3)

Boden SD, Davis DO, Dina TS, et al. Abnormal magnetic-resonance scans of the lumbar
spine in asymptomatic subjects. A prospective investigation. J Bone Joint Surg Am 1990;
72(3):403 408.
Bruno C, van Diggelen OP, Cassandrini D, et al. Clinical and genetic heterogeneity of
branching enzyme deficiency (glycogenosis type IV). Neurology 2004;63(6):10531058.
Bush K, Hillier S. Outcome of cervical radiculopathy treated with periradicular/epidural
corticosteroid injections: a prospective study with independent clinical review. Eur Spine
J 1996;5(5):319 325.
Carette S, Fehlings MG. Clinical practice. Cervical radiculopathy. N Engl J Med
2005;353(4):392399.
Carette S, Leclaire R, Marcoux S, et al. Epidural corticosteroid injections for sciatica due
to herniated nucleus pulposus. N Engl J Med 1997;336(23):1634 1640.
Case records of the Massachusetts General Hospital. Weekly clinicopathological
exercises. Case 16 1996: a 36-year-old woman with bilateral facial and hand weakness
and impaired truncal sensation. N Engl J Med 1996;334(21):1389 1394.
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 1998;339(15):10211029.
Colachis SC Jr, Strohm BR. Effect of duration of intermittent cervical traction on
vertebral separation. Arch Phys Med Rehabil 1966;47(6):353359.
Cuckler JM, Bernini PA, Wiesel SW, et al. The use of epidural steroids in the treatment of
lumbar radicular pain: a prospective, randomized, double-blind study. J Bone Joint Surg
Am 1985;67(1):63 66.
Deyo R. Back surgerywho needs it? N Engl J Med 2007;356(22):2239 2243.
Dumitru D, Dreyfuss P. Dermatomal/segmental somatosensory evoked potential
evaluation of L5/S1 unilateral/unilevel radiculopathies. Muscle Nerve 1996;19(4):442
449.
Dyck PJ, Norell JE, Dyck PJ. Microvasculitis and ischemia in diabetic lumbosacral
radiculoplexus neuropathy. Neurology 1999;53(9):21132121.
Eidelberg D, Sotrel A, Vogel H, et al. Progressive polyradiculopathy in acquired immune
deficiency syndrome. Neurology 1986;36(7):912916.
Fast A, Parikh S, Marin EL. The shoulder abduction relief sign in cervical radiculopathy.
Arch Phys Med Rehabil 1989;70(5):402 403.
Ferrante FM, Wilson SP, Iacobo C, et al. Clinical classification as a predictor of
therapeutic outcome after cervical epidural steroid injection. Spine 1993;18(6):730 736.
Fouyas IP, Statham PF, Sandercock PA. Cochrane review on the role of surgery in cervical
spondylotic radiculomyelopathy. Spine 2002;27(7):736 747.
Griffin JW, Li CY, Ho TW, et al. Pathology of the motor-sensory axonal Guillain-Barre
syndrome. Ann Neurol 1996;39(1):1728.
Haimovic KC, Beresford HR. Dexamethasone is not superior to placebo for treating
lumbosacral radicular pain. Neurology 1986;36(12):15931594.
Hamanishi C, Tanaka S. Dorsal root ganglia in the lumbosacral region observed from the
axial views of MRI. Spine 1993;18(13):17531756.

Continuum: Lifelong Learning Neurol 2008;14(3)

153

 DISEASES OF THE NERVE ROOTS

Hirayama K, Tomonaga M, Kitano K, et al. Focal cervical poliopathy causing juvenile
muscular atrophy of distal upper extremity: a pathological study. J Neurol Neurosurg
Psychiatry 1987;50(3):285290.
Jacobs JM, Macfarlane RM, Cavanagh JB. Vascular leakage in the dorsal root ganglia of
the rat, studied with horseradish peroxidase. J Neurol Sci 1976;29(1):95107.
Jensen MC, Brant-Zawadzki MN, Obuchowski N, et al. Magnetic resonance imaging of
the lumbar spine in people without back pain. N Engl J Med 1994;331(2):69 73.
Joelson E. Epidural steroid injections: con. Paper presented at: 53rd Annual Meeting of
the American Academy of Neurology; May 2001; Philadelphia, PA.
Karasek ME. Epidural steroid injections: pro. Paper presented at: 53rd Annual Meeting
of the American Academy of Neurology; May 2001; Philadelphia, PA.
Karpati G, Carpenter S, Eisen A, et al. The adult form of acid maltase (alpha-1,4glucosidase) deficiency. Ann Neurol 1977;1(3):276 280.
Katifi HA, Sedgwick EM. Evaluation of the dermatomal somatosensory evoked potential
in the diagnosis of lumbo-sacral root compression. J Neurol Neurosurg Psychiatry 1987;
50(9):1204 1210.
Khatri BO, Baruah J, McQuillen MP. Correlation of electromyography with computed
tomography in evaluation of lower back pain. Arch Neurol 1984;41(6):594 597.
Kikuchi S, Sato K, Konno S, Hasue M. Anatomic and radiographic study of dorsal root
ganglia. Spine 1994;19(1):6 11.
Koes BW, Scholten RJ, Mens JM, Bouter LM. Efficacy of epidural steroid injections for
low-back pain and sciatica: a systematic review of randomized clinical trials. Pain 1995;
63(3):279 288.
Kuruoglu R, Oh SJ, Thompson B. Clinical and electromyographic correlations of
lumbosacral radiculopathy. Muscle Nerve 1994;17(2):250 251.
Le Forestier N, LeGuern E, Coullin P, et al. Recurrent polyradiculoneuropathy with the
17p11.2 deletion. Muscle Nerve 1997;20(9):1184 1186.
Levin KH. L5 radiculopathy with reduced superficial peroneal sensory responses:
intraspinal and extraspinal causes. Muscle Nerve 1998;21(1):37.
Levin KH. Radiculopathy. In: Levin KH, Luders HO, eds. Comprehensive clinical
neurophysiology. Philadelphia: WB Saunders, 2000:189 200.

154

Levin KH, Maggiano HJ, Wilbourn AJ. Cervical radiculopathies: comparison of surgical
and EMG localization of single-root lesions. Neurology 1996;46(4):10221025.
Malanga GA, Nadler SF. Nonoperative treatment of low back pain. Mayo Clin Proc 1999;
74(11):11351148.
Moses SW, Parvari R. The variable presentations of glycogen storage disease type IV: a
review of clinical, enzymatic and molecular studies. Curr Mol Med 2002;2(2):177188.
Nardin RA, Patel MR, Gudas TF, et al. Electromyography and magnetic resonance
imaging in the evaluation of radiculopathy. Muscle Nerve 1999;22(2):151155.
Nelemans PJ, de Bie RA, de Vet HC, Sturmans F. Injection therapy for subacute and
chronic benign low back pain [Update in: Cochrane Database Syst Rev
2006;(2):CD001824]. Cochrane Database Syst Rev 2000;(2):CD001824.
Persson LC, Carlsson CA, Carlsson JY. Long-lasting cervical radicular pain managed with
surgery, physiotherapy, or a cervical collar: a prospective, randomized study. Spine 1997;
22(7):751758.

Continuum: Lifelong Learning Neurol 2008;14(3)

Peul WC, van Houwelingen HC, van den Hout WB, et al. Surgery versus prolonged
conservative treatment for sciatica. N Engl J Med 2007;356(22):22452256.
Radhakrishnan K, Litchy WJ, OFallon WM, Kurland LT. Epidemiology of cervical
radiculopathy: a population-based study from Rochester, Minnesota, 1976 through
1990. Brain 1994;117(pt 2):325335.
Rathmell JP, Aprill C, Bogduk N. Cervical transforaminal injection of steroids.
Anesthesiology 2004;100(6):15951600.
Riew KD, Yin Y, Gilula L, et al. The effect of nerve-root injections on the need for
operative treatment of lumbar radicular pain: a prospective, randomized, controlled,
double-blind study. J Bone Joint Surg Am 2000;82-A(11):1589 1593.
Riley D, Shields RW. Diabetic amyotrophy with upper extremity involvement [abstract].
Neurology 1984;34(suppl 1):216.
Sahenk Z, Mendell JR, Rossio JL, Hurtubise P. Polyradiculoneuropathy accompanying
procainamide-induced lupus erythematosus: evidence for drug-induced enhanced
sensitization to peripheral nerve myelin. Ann Neurol 1977;1(4):378 384.
Schmalbruch H, Stender S, Boysen G. Abnormalities in spinal neurons and dorsal root
ganglion cells in Tangier disease presenting with a syringomyelia-like syndrome.
J Neuropathol Exp Neurol 1987;46(5):533543.
Shulman M. Treatment of neck pain with cervical epidural steroid injection. Reg Anesth
1986;11:9294.
Stark RJ, Kennard C, Swash M. Hand wasting in spondylotic high cord compression: an
electromyographic study. Ann Neurol 1981;9(1):58 62.
Suarez G, Kokmen E, Atkinson J, Piepgras D. Juvenile amyotrophy of upper extremities:
suggestive evidence for a vascular pathogenesis. J Neurol Sci 1997;150(suppl 1):269.
Tsao B, Levin KH, Bodner RA. Comparison of surgical and electrodiagnostic findings in
single root lumbosacral radiculopathies. Muscle Nerve 2003;27(1):60 64.
van der Heijden GJ, Beurskens AJ, Koes BW, et al. The efficacy of traction for back and
neck pain: a systematic, blinded review of randomized clinical trial methods. Phys Ther
1995;75(2):93104.
Vroomen PC, de Krom MC, Wilmink JT, et al. Lack of effectiveness of bed rest for
sciatica. N Engl J Med 1999;340(6):418 423.
Weinstein JN, Lurie JD, Tosteson TD, et al. Surgical versus nonsurgical treatment for
lumbar degenerative spondylolisthesis. N Engl J Med 2007;356(22):22572270.
Wilbourn AJ, Aminoff MJ, American Association of Electrodiagnostic Medicine. AAEM
minimonograph 32: the electrodiagnostic examination in patients with radiculopathies.
Muscle Nerve 1998;21(12):16121631.
Yabuki S, Kikuchi S. Positions of dorsal root ganglia in the cervical spine: an anatomic
and clinical study. Spine 1996;21(13):15131517.

Continuum: Lifelong Learning Neurol 2008;14(3)

155