RADICULOPATHY

-JOHN RIBU PARAMPIL

Final Sem
Fellowship In Neurological Rehabilitation

Radiculopathy is a peripheral neurologic syndrome resulting

from mechanical injury and chemical irritation of the
spinal nerve roots. Mechanical injury to the nerve root
occurs with compression, traction, or frictional forces.
Chemical irritation occurs as a response to nerve root
ischemia, vascular stasis, or nerve root exposure to inflammatory
components released during tissue injury. The
classic signs associated with radiculopathy include neck
or back pain with spasm, mild to moderate peripheral
numbness, shooting pain, or extremity weakness in the distribution
of a nerve root. Radiculopathy is often seen in the
post-trauma patient with intervertebral disk herniation.
Direct compression of the nerve root is not necessary
to produce radiculopathic symptoms. A radicular pattern
of pain or deficit will frequently occur with any condition
that produces inflammation in the nerve root area. Osteophytic
projections, degenerative disk disease, and lateral
recess stenosis are common etiologies of radiculopathy in
the degenerative spine.
Localization of the neurologic deficit requires an
understanding of the segmental innervation patterns in the
body and extremities. There is considerable overlap of
innervation from contiguous spinal levels to the skin, muscles,
and skeleton, so that deficit localization is sometimes
difficult. Occasionally, multiple nerve roots are involved,
further complicating the localization process. Confirmation
of subtle or multilevel radiculopathy is based on the
anatomic and functional correlatives between diagnostic

imaging and examination findings. Common correlative

procedures include positive orthopedic tension or compression
signs, neurologic indicators (reflex changes,
motor fatigue, sensory deficits, or pain patterns), electrodiagnostic
findings, and diagnostic imaging findings, including
magnetic resonance (MR), computed tomography
(CT), and plain films. This chapter covers the relevant
anatomy of the nerve root, the pathological processes, and
the most common differential conditions seen with radiculopathy.
SPINAL NERVE ROOT ANATOMY
REGIONAL CHARACTERISTICS
The cervical nerve roots descend the
equivalent of one neuromere (segmental cord level)
before
horizontally traversing their respective neural foramina.
Thus, the C5C6 disk will compress the C6 nerve root.
This arrangement of nerve roots exiting above the
respective
numbered vertebrae changes at the thoracic level as
a result of the anatomic configuration of the eight
cervical nerve roots and seven cervical vertebrae
Sensory input from peripheral and axial receptors
enters the dorsal aspect of the cord through a
configuration
of nerve fibers called the dorsal rootlets. The cell bodies
of sensory axons are not found within the gray matter
of
the dorsal horn of the spinal cord; rather, they are
located
within the dorsal root ganglia (DRG) distal to the spinal
cord within the IVF.
The anterior and posterior rootlets merge just distal to

the DRG to form the spinal nerve. Dorsal root fibers

comprise the largest volume of the spinal nerve. At the
point where the convergence occurs, the sensory and
motor nerve components are no longer separate. The
commingled rootlets interweave in a fascicular pattern
to form the mixed spinal nerve. The spinal
nerve is usually only a few millimeters long and then
divides into the ventral and dorsal rami. In the cervical
and lumbosacral spine, the ventral rami course anterior
to
the spine and intermingle to form the plexes and major
nerves of the extremitites. In the thoracic spine, the
ventral
rami form the intercostal nerves. The dorsal rami are
much
smaller than the ventral rami. The dorsal rami branch
into
two or three branches that supply innervation to the
muscles,
ligaments, zygapophyseal joints, and skin overlying the
spine.
INTERVERTEBRAL FORAMEN ANATOMY
The primary contents of the IVF include the spinal
nerve,
the DRG, connective tissue, fat, the radicular artery,
the
radicular vein, and two to four recurrent meningeal
nerves. This group of structures is referred to as the
nerve root complex .The nerve root typically occupies
approximately one quarter to one third of the volume of
the IVF. This can be
readily observed on sagittal MR images. The nerve-toIVF ratio will vary in the presence of pathologic osseous
& soft-tissue foraminal stenosis. Nerve root distension
or

enlargement will contribute to an abnormal nerve-toIVF

ratio. The most common causes of an abnormal ratio
include spondylosis and lateral disk herniation. A small
study of cervical IVF anatomy demonstrated
that nerve root compression occurred at the entrance
zone
of the intervertebral foramina. In the anterior aspect of
the
IVF, compression of the nerve roots was caused by
protruding
discs and osteophytes of the uncovertebral region,
whereas the superior articular process, the ligamentum
flavum, and the periradicular fibrous tissues affected
the
nerve posteriorly.
BLOOD SUPPLY OF THE SPINAL NERVE ROOT
The two primary nutrient pathways to the spinal nerve
root occur through vascular supply and diffusion from
the
CSF.The blood supply to the vertebrae and the nerve
roots arise from the segmental artery. The segmental
artery
gives off a dorsal branch, which further branches to
supply
the vertebral arch, with an additional branch supplying
the
posterior vertebral body, and a smaller longitudinally
oriented
arterial branch that supplies the nerve root. The
artery that supplies the posterior intervertebral body
perforates
the posterior longitudinal ligament. The longitudinal
radicular artery provides several collateral radicular

arteries, which may lie anterior and posterior to the

nerve
root, branching to provide perforating interfascicular
arteries. The interfascicular arteries are redundant,
often
coiled in appearance, allowing for nerve root translation
and stretch, without compromising blood flow to the
nerve
root. The interfascicular arteries supply precapillary
arterioles,
which in turn supply intraneuronal capillaries.
Nerve roots receive their blood supply from both ends.
The nerve root has adequate vasculature to prevent a
watershed zone in most cases of slow onset
compression;
however, a large intradural or extradural lesion may
reduce
the blood supply to the nerve root and inhibit CSF flow
to the nerve root sleeve, thus reducing nutrient
delivery.
PATHOPHYSIOLOGY OF NERVE ROOT
COMPRESSION
A nerve fiber begins physically deforming when the
external
pressure exceeds the intraneuronal hydrostatic
pressure.
Electrophysiologic conduction block occurs at different
degrees of external pressure, depending on the axon
diameter. A complete compression block of the
peripheral
nerve occurs at the nerve trunk when approximately
150-mmHg pressure is applied.
Spinal nerve roots have demonstrated conduction block
at only 30 mmHg of pressure.
When compression of the nerve root complex

occurs, direct mechanical effects include conduction

block, interruption of axonal flow, and vascular
sequelae
that include hypoxia and metabolic byproduct
accumulation,
which compromise impulse propagation .
Nerve root compression contributes to a loss of
impulse propagation via impairment of axonal
transport. Anoxia and hypoxia may compromise fast
and slow anterograde
axonal transport as well as retrograde axonal transport.
Axonal transport is required for the replenishment
of neurotransmitter complexes. Axonal transport
may be impaired in various pathologic conditions such
as ischemia,
compression, infection, immunologic cascades, and
axonal degeneration and regeneration.Moderate to
severe compression of a nerve root complex may
induce
direct pathomechanical effects on the nerve fibers,
such
as deformation of the nodes of Ranvier and
invagination
of the paranodal myelin sheaths.
Neurologic function is highly dependent on the
availability
of oxygen. A classic study of the frog nerve by
Grundfest showed that a nerve can function under high
external loads as long as there is a high concentration
of
available oxygen. Even at normal extraneural pressure
levels, if the intraneural oxygen level decreases, the
nerve
will become more susceptible to compressive loads.
Conversely,
even with an adequate systemic circulatory capacity
to make oxygen available to the nerve root complex,

focal vascular insufficiency within the complex will

render
it hypoxic. The combination of vascular insufficiency
and
diminished arterial oxygen saturation will result in
greater
susceptibility to intraneural hypoxia.
Nerve root compression often results in impairment
of intraneural blood flow.
The endoneurial vessels of
nerve roots, in particular the DRG, are more permeable
to plasma proteins than the endoneurial vessels of
peripheral
nerves.Physical deformation of the nerve root
increases the permeability of the microvasculature,
leading
to the formation of edema within the intraneuronal
environment.Large-diameter nerve fibers within the
nerve roots are
more susceptible to compression and deformation than
small-diameter fibers.Mild mechanical compromise of
the nerve root complex can result in selective sensory
and
motor presentations limited to the large-diameter
fibers.
Focal demyelination of large myelinated fibers without
axonopathy results in neural impulses firing in a
dysynchronous
volley.Olmarker et al. have shown that compression of
the
nerve root complex, even at low pressures (e.g., 5 to
10 mmHg), may induce short-term changes within the
intraneural microcirculation. Initially, the intraneural
venous blood flow is compromised. The intravenous
pressures
result in retrograde stasis within the intraneural
capillary

beds and a breakdown of the capillary junctions.

This contributes to exudation and extravascular
intraneural
edema formation.Rapid spinal nerve root compression
influences the
degree of clinical deficit and recovery characteristics.
Rapid-onset compression (between 0.05 and 0.10 sec)
causes a more pronounced effect than slow-onset
compression
(over a 20-sec interval) with similar level pressures.
Rapid-onset as well as sustained compressive insult
results in pronounced intraneural edema, impaired
vascular flow, conductive changes, and reduced
capacity
for nerve conduction recovery.This is an important
consideration relative to intermittent and slow-onset
compression syndromes compared with rapid-onset
disk herniation
and spine injuries after motor vehicle collisions.
The magnitude of compression is also important in
the development of symptoms. Changes in spinal nerve
root conduction occur at pressures between 15 and
75 mmHg. Motor conduction velocity recovers more
rapidly
than sensory conduction when nerve root compression
pressures reach 100 to 200 mmHg.
Spinal nerve root compression can be present without
overt symptoms.In such cases, however, there is
invariably
an absence of trauma, but the presence of a
longstanding
condition, such as osteophytosis or lateral recess
stenosis,
producing a slow-onset of compression.
SITES OF NERVE ROOT VULNERABILITY

The spine contains many osteoligamentous spaces that

accommodate and protect delicate neurovascular
structures.
These spaces include the central vertebral canal, the
IVF, and the foramen transversarium. The morphologic
relationships
of these osteoligamentous spaces differ in various
intravertebral and intervertebral locations . The
spatial relationship of the nervous tissue to osseous
and
nonosseous elements of the spinal canal and the IVF is
an important consideration in the development of
radicular
compression.
The dynamic properties of these spaces are
strongly dependent on the anatomic characteristics and
relationships of the tissues making up their margins.
The
dynamics of the intervertebral motion segment affect
the
relative instantaneous size and volume of the intrinsic
osteoligamentous canals and foramina.
The volume of the IVF increases slightly during flexion
and decreases during extension. These changes are
more pronounced in the cervical spine. Yoo and
colleagues found that, in the neutral position and at
extremes of flexion and extension in the cervical spine,
20 of axial rotation produced a decrease in the mean
size
of the foramen on the ipsilateral side and an increase
on
the contralateral side. Compared with the
measurement at
neutral position, 30 of extension caused a 13.2%
decrease
in the cervical foraminal dimensions, and 30 of flexion

caused a 10.6% increase.This IVF narrowing explains

one of the mechanisms
involved in reproducing radicular pain with Spurlings
clinical maneuver. This orthopedic test is performed by
turning the patients head to the side of complaint and
extending it backward with gradual downward pressure.
A controlled downward blow to the vertex of the head
can
also be used to reproduce symptoms.
PATHOMECHANICS AFFECTING THE NERVE ROOT
COMPLEX
Breig demonstrated that when the spine moves there is
no significant axial displacement of the spinal nerve
root
relative to the canal. During extension, however, the
nerve
root increases in cross-sectional diameter, and
consequently
there is a slackening and widening of the nerve
root sleeve. During forward flexion, the dural sleeves
and
nerve roots were found to straighten gradually. This
adaptability
of the nerve roots greatly reduces friction between
the nerve roots and their adjacent sheaths during
movement.
Severe fibrotic adherence of the nerve roots and
their perineural structures results in excessive traction
at
the nerve root attachment to the spinal cord.
Some of the signs and symptoms of radiculopathy
develop from irritation created by immobilization of the
nerve root and dural sleeve. Because the dura mater is
mechanosensitive, traction of the dura over a spaceoccupying
lesion, such as a herniated disk or osteophyte, may

result in pain originating from the dura.

The nerve root near a disk herniation is sensitive to
mechanical deformation,
as observed in patients under epidural anesthesia
during laminectomy and disk excision.
For patients with paresthesia secondary to
neuroforaminal
compression, extension-induced narrowing may
magnify symptoms. Concomitant adduction of the
painful
arm and contralateral lateral flexion may cause
stretching
of the nerve root within the narrowed foramen, thereby
worsening symptoms. Conversely, shoulder abduction
and
cervical flexion may lessen symptoms.
Nerve root tension signs are common in cervical and
lumbosacral radiculopathy. Cervical motions that
reduce
foramen size also tend to elicit symptoms associated
with
neuropathology at the IVF.
In lumbosacral radiculopathies, a positive straight leg
raise test is highly correlative to nerve root
compression.
SPINAL DEGENERATION AND RADICULOPATHY
Spondylosis and posterolateral exostosis are common
causes of IVF stenosis, lateral recess stenosis, or
central
spinal canal stenosis. Routine radiographs or CT scans
often demonstrate disk-spur complexes or isolated
osteophytosis.
Osteophytic changes are more prevalent within
particular segmental levels of the spine. The levels of
the

cervical spine most frequently affected are C5C6 and

C6C7. In the thoracic spine, the T8 level is most
vulnerable.
In the lumbar spine, the L4L5 and L5S1 levels are
the regions most often involved.The larger the
osteophytic
bar or projection, the greater the potential for a
mass effect on neural structures and their blood supply.
The
osteoarthritic spine is particularly vulnerable to trauma.
The four general classifications of compression
syndromes
associated with spondylosis are lateral or radicular
syndrome, medial or spinal syndrome, combined
medial
lateral syndrome or myeloradiculopathy, and vascular
syndromes.
Lateral recess stenosis has four subcategories:
(1) lateral stenosis from hypertrophic enlargement of
the
superior facet, (2) subarticular stenosis, (3) dynamic
stenosis that occurs from increased intersegmental
motion
or clinical instability, and (4) fixed stenosis that occurs
when degeneration and stenosis are severe.
Osteophytosis is more prevalent where Sharpeys
fibers attach to the vertebral body.This transitional
region of bone and periosteum is usually several
millimeters
from the discovertebral junction. In this region,
osteophytes
generally begin as clawlike, horizontal, calcific
projections off the vertebral body. As the spur develops,
it begins to project in a vertical or inferior direction,
forming
an osseous bar as both vertebral margins fuse.
Progressive

osteophytosis results in an expansile mass effect on

neighboring
neurovascular tissues. Posterior or posterolateral
projections are often visualized on MR images as
tenting
of the posterior longitudinal ligament (PLL).
Ligamentous
tenting may be a significant source of chronic pain
because
of the irritation to the free nerve endings in the PLL.
Spondylotic myelopathy and radiculopathy can occur
when
osteophytic projections progress to the point of
compressing
both vascular and neural elements within the IVF, the
lateral
recess, and the central spinal canal.
FIBROSIS AND RADICULOPATHY
During spinal movement, the nerve roots slide within
their
dural sleeves. Compressive lesions that deform the
nerve
root, its adjacent sleeve, or the surrounding vasculature
induce edema formation, which in turn may lead to
fibroblast
invasion and fibrosis in the nerve root and IVF.
Fibrotic adhesions between the nerve root and dural
sleeve
inhibit this sliding motion and compromise the elasticity
of the nerve root and dural sleeve. In this situation, the
nerve root and dural sleeve are subjected to abnormal
tensions that induce the cyclic development of
inflammation.
Inflamed nerve roots are in turn sensitized to
compression

or traction and cause pain syndromes.When fibrotic

tissue compartmentalizes
the peridural space in the region of the descending or
exiting nerve root, the nerve root is immobilized and
susceptible
to compression from acute or recurrent disk. pathology.
If a nerve root cannot move out of the path of
a mass effect, it is rendered more susceptible to
compression
and is also at risk for traction-type injuries because
of loss of elasticity. The elastic limit of a normal nerve
root is approximately 15% of its resting length, and any
stress beyond 21% of its resting length may bring
about
complete failure.Mild compressive lesions may only
slightly decrease
the extent of movement between the nerve root sleeve
and
nerve root. A chronic compressive lesion may induce
fibrotic adherence and mechanical approximation that
severely impairs nerve root movement.This results in
nerve root traction microinjuries against the pedicles,
vertebral
arches, and/or posterior vertebral body projections.
Fibrosis of the nerve root sleeve results in cumulative
microinjury and a vicious cycle of scar-tissue formation.
Painless extremity movement is dependent on normal
biomechanics
within the IVF and nerve root elasticity. A loss
of neural elasticity can lead to traction-induced
nociception
and microavulsion of scar tissue, stimulating an
inflammatory cascade.
TRAUMA AND RADICULOPATHY

Spinal trauma may lead to nerve root injury secondary

to
avulsion, contusion, stretch, and/or compressive injury.
Nerve root contusion and stretch injuries represent
transient
physical pathomechanisms. Compressive insult may
be transient or may persist after the original trauma.
Signs
of root compression may occur as a result of neural
injury
anywhere from the rootlets on the spinal cord to the
spinal
nerve in the distal portion of the IVF. Common causes of
persistent post-traumatic nerve root compression
include
hematoma, disk herniation, displaced vertebral
fracture,
or vertebral dislocation. Any condition that distorts and
narrows the dimensions of the IVF may result in nerve
root compromise. Unilateral facet dislocation, vertebral
body fracture, and ligamentous disruption with a shift
of
bony elements may produce transient, partial, or
complete
occlusion of the IVF or cause a traction injury of the
nerve
root. Preexisting spondylosis with spurring or spinal
stenosis due to other causes may infringe on the
reserve
space surrounding the neural elements, increasing the
risk
for concussive and stretch injury of the nerve root.
Perineural fibrosis and postsurgical scarring
may adhere the nerve root sleeve to the surrounding
tissues,
predisposing the nerve root to tensile strain injury

from reduced gliding capacity of the nerve during

vertebral
motion. Patients with chronic radiculopathy may have
significant fibroproliferation within the lateral recess
and
IVF which lowers the threshold for subsequent nerve
root
injury and aggravated symptoms.Individuals with
ankylosing spondylitis are prone to
fractures.This may be due to greater focal stress placed
upon select bony regions due to the general spinal
rigidity
created by the ankylosis. The greater risk for fracture in
ankylosing spondylitis is associated with an increased
risk
for associated nerve root injury. Diminished bone
strength
increases the risk for acquiring reduced IVF dimensions
secondary to fracture. The World Health Organization
(WHO) has classified bone density characteristics into
the
following four primary categories: (1) normal, (2)
osteopenic, (3) osteoporotic without fractures, and (4)
severely osteoporotic.Low bone mineral density and
reduced trabecular density are associated with
increased
risk for acquiring a fracture due to loss of subcortical
bony
support.During the aging process, trabecular bone loss
is similar between men and women although women
commonly acquire greater loss of trabecular
connectivity.
Whiplash injury is a common pseudomechanistic term
that describes a constellation of symptoms following
injury sustained in a motor vehicle accident (MVA).
Considerable
debate can be found in the scientific literature

regarding the very definition of whiplash, including its

mechanism of onset, prevalence, extent of related
injuries,
and how to name this complex trauma disorder.Injuries
to the body result from rapid acceleration or
deceleration
forces transmitted through the head, neck, and body
within a few hundred milliseconds after vehicle impact.
Rear-end collisions are responsible for approximately
85% of reported whiplash injuries.MVAs are one of the
most frequent causes of radiculopathy. Although more
than one third of patients acutely complain of
paresthesias
following an MVA, neurogenic thoracic outlet syndrome
is more commonly the cause than cervical
radiculopathy.
Symptoms associated with whiplash can be classified
in a loose time frame of acute and late whiplash
syndromes.
Patients with cervical spondylosis are more likely
to present with late-onset abnormal clinical findings
after
whiplash injury.Osteophytosis and bony hypertrophic
changes which narrow the IVF may contribute to
contusion
and/or avulsive injury to the nerve root. After vertebral
trauma, plain radiographic studies should be performed
in any patient with reduced range of motion (ROM) or
lateralizing pain symptoms. Oblique projections and
flexion
extension plain films are essential for evaluating the
posttraumatic
patient with mild radicular symptoms.
INTERVERTEBRAL DISK HERNIATION AND
RADICULOPATHY
Disk herniation is well documented as one of the most

common etiologies of radiculopathy.For example,

in a study by Modic and colleagues,72% of patients
with acute radiculopathy had a herniated nucleus
pulposus.
Direct correlation among the size of the disk lesion,
clinical presentation, and treatment outcome is not
always
clear.Many patients older than 60 years may have one
or more relatively asymptomatic herniations. It should
be
noted, however, that intermittent pain and loss of
functional
capacity accompany virtually all relatively
asymptomatic
herniations.
A normal intervertebral disk has a high capacity for
accepting axial loads. Many studies have been
performed on the behavior of the disk under variable
stressors. One of these showed that the normal
intervertebral disk loses
about 0.6 mm of vertical height and bulges
approximately
0.34 mm in a radialward direction under a compressive
axial load of 1700 N.This study determined that the
disk
withstands a maximum compressive force of 7000 N
before failure; by comparison, the maximum force
needed
to produce failure of the endplate was 2500 N.These
findings indicate that compression alone does not
produce
disk prolapse in the experimentally prepared spine.
Adams and Hutton were able to experimentally
produce
disk herniation in a two-vertebrae specimen by
applying

sudden compression to the specimen with

simultaneous
lateral and full forward flexion. The disk prolapse
occurred
on the open disk wedge side opposite the side of lateral
flexion. Clinically, disk herniation is often seen after a
lifting
injury or motor vehicle accident in which lateral flexion
and
forward flexion positions of the spine occur at the time
of
traumatic compression or shear. The classification of
disk herniations is often confusing and imprecise. The
term disk herniation implies that a rupture or tear of
annular fibers occurs allowing the migration
of nuclear material beyond the vertebral margin. The
nuclear material may protrude out and cause a
distention
of the outer annulus fibrosis or rupture through the
annulus
and extrude behind the posterior longitudinal ligament.
Additionally, in cases with a greater degree of
extrusion,
the nuclear material may become separated from the
disk
of origin and migrate into the epidural space or lateral
recess as a free fragment. The confusion in describing
the
previously mentioned lesions stems from the limited
resolution
of diagnostic imaging technology and the poor
standardization of terminology. This resolution
inadequacy
is most problematic in confirming small-to-moderate
sized subannular herniations and confirming whether
an extrusion has separated from the disk as a free
fragment.

The second problem is the plethora of terms used

to describe a disk herniation. Some of the terms
encountered
are disk herniation, protrusion, extrusion, nuclear
extrusion, prolapse, bulging disk, slipped disk, ruptured
disk, and sequestered disk.
It is classified disk lesions into four main groups
based on their appearance on MR imaging. They are
annular
bulge; protrusion (herniation); extrusion; and free disk
fragment (sequestration). These categories can be
applied
to the description of disk lesions throughout the spine.
The next consideration in describing a disk lesion is
whether the herniation is contained by the annulus or
uncontained and in a subligamentous position under
the
posterior longitudinal ligament (PLL). When disk
material
has migrated around or through the PLL, it is called
transligamentous
extrusion. The sizes of disk herniations are
categorized as small, moderate, and large. The location
of
the disk herniation in relation to midline spinal anatomy
should be described. The majority of disk lesions
involve
herniation in a central posterior or posterolateral
direction.
Herniations that occur in a lateral direction or through
the
anterior portion of the intervertebral disk are not as
common.
The pathoanatomical relationship of the herniation
to the adjacent neural and spinal elements should be
evaluated
and described. Compression of the nerve root or

spinal cord is described as mild, moderate, and severe.

Effacement of the thecal sac, nerve root, or cord is also
clinically significant because of compression of the
surrounding
vasculature and contact with the inflammatory
interface of discal material.
SPONDYLOLISTHESIS AND RADICULOPATHY
Radiculopathy and spondylolisthesis are relatively
uncommon, as compared to nerve root compression
from
disk herniation in the lumbar spine. However, in cases
of
spondylotic spondylolisthesis, radiculopathy occurs in
60
to 70% of patients.Spondylolisthesis refers to the
anterior
displacement or listhesis of a vertebral body in
relationship
to the vertebral body immediately below. The term
listhesis refers to slippage or displacement without
reference
to direction. Spondylolisthesis may occur without a
defect
in the neural arch or secondary to a defect in the neural
arch.
If there is a defect in the neural arch, the term
spondylotic
spondylolisthesis should be applied. With an intact
neural
arch, the term non-spondylotic spondylolisthesis should
be used.
Cervical spondylolisthesis is rare, but when present, it
is often found at the C6 level.

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