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Cervical Spondylotic
Myelopathy: A Common Cause of
Spinal Cord Dysfunction in Older
Persons
- WILLIAM F.
YOUNG, M.D.,
- Temple
University Hospital,
Philadelphia,
Pennsylvania
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Cervical spondylotic
myelopathy is the most
common cause of spinal cord
dysfunction in older
persons. The aging process
results in degenerative
changes in the cervical
spine that, in advanced
stages, can cause
compression of the spinal
cord. Symptoms often develop
insidiously and are
characterized by neck
stiffness, arm pain,
numbness in the hands, and
weakness of the hands and
legs. The differential
diagnosis includes any
condition that can result in
myelopathy, such as multiple
sclerosis, amyotrophic
lateral sclerosis and masses
(such as metastatic tumors)
that press on the spinal
cord. The diagnosis is
confirmed by magnetic
resonance imaging that shows
narrowing of the spinal
canal caused by osteophytes,
herniated discs and
ligamentum flavum
hypertrophy. Choice of
treatment remains
controversial, surgical
procedures designed to
decompress the spinal cord
and, in some cases,
stabilize the spine are
successful in many patients.
(Am Fam Physician
2000;62:1064-70,1073.)
Cervical spondylotic
myelopathy (CSM) is the most
common spinal cord disorder in
persons more than 55 years of
age in North America and perhaps
in the world. As the number of
older persons in the United
States increases, the incidence
of CSM will most likely
increase. In a prospective study
designed to more accurately
define the incidence of CSM,
23.6 percent of 585 patients
with tetraparesis or paraparesis
admitted to a United Kingdom
regional neuroscience center had
CSM.1
The overall prevalence in this
population is unknown.
Pathophysiology of CSM
FIGURE 1. Axial
computerized tomography
scan showing ventral
osteophytes pressing
into the spinal canal. |
Spondylosis refers to the
degenerative changes that occur
in the spine, including
degeneration of the joints,
intervertebral discs, ligaments
and connective tissue of the
cervical vertebrae. There are
three important pathophysiologic
factors in the development of
CSM: (1) static mechanical; (2)
dynamic mechanical; and (3)
spinal cord ischemia.2
Static mechanical
factors result in the reduction
of spinal canal diameter and
spinal cord compression. With
aging, the intervertebral discs
dry out resulting in loss of
disc height. This process puts
greater stress on the articular
cartilage of the vertebrae and
their respective end plates.
Osteophytic spurs develop at the
margins of these end plates (Figure
1). Osteophytes stabilize
adjacent vertebrae whose
hypermobility is caused by the
degeneration of the disc.3
The disc also calcifies,
further stabilizing the
vertebrae. Osteophytes increase
the weight-bearing surface of
the end plates and, therefore,
decrease the effective force
being placed on them. In
addition to osteophytic
overgrowth, the ligamentum
flavum may stiffen and buckle
into the spinal cord dorsally.
Osteophytic overgrowth ventrally
and, in some cases, buckling of
the ligamentum flavum dorsally
can cause direct compression of
the spinal cord resulting in
myelopathy (clinically evident
spinal cord dysfunction).
Symptoms are believed to develop
when the spinal cord has been
reduced by at least 30 percent.4
Dynamic mechanical factors
relate to the fact that the
normal motion of the cervical
spine may aggravate spinal cord
damage precipitated by direct
mechanical static compression.
During flexion, the spinal cord
lengthens, thus stretching over
ventral osteophytic ridges.
During extension, the ligamentum
flavum may buckle into the
spinal cord causing a reduction
of available space for the
spinal cord (Figure 2).
FIGURE 2. Dynamic
mechanical factors in
cervical spondylotic
myelopathy. (Left)
During flexion, the
spinal cord is stretched
over ventral osteophytic
ridges. (Right)
During extension, the
ligamentum flavum may
buckle into the spinal
cord reducing space for
the cord. |
Spinal cord ischemia probably
plays a role in the development
of CSM, particularly in later
stages.5,6
Histopathologic changes in the
spinal cord consistent with
ischemia have been observed in
patients with CSM. However, the
precise mechanism for spinal
cord ischemia is not completely
understood. Other factors
associated with the development
of spondylosis include heavy
labor, posture and genetic
predisposition.7,8
Also, 70 percent of
patients with Down syndrome have
an increased incidence of
spondylosis by 50 years of age.9
Clinical History
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Common
complaints of
patients with
cervical
spondylotic
myelopathy
include neck
stiffness,
crepitus in the
neck with
movement,
brachialgia, a
dull "achy"
feeling in the
arm, and
numbness or
tingling in the
hands.
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Patients with CSM will
generally have these symptoms:
neck stiffness; unilateral or
bilateral deep, aching neck, arm
and shoulder pain; and possibly
stiffness or clumsiness while
walking (Table 1). CSM
usually develops insidiously. In
the early stages of CSM,
complaints of neck stiffness are
common because of the presence
of advanced cervical
spondylosis.10
Other common complaints include
crepitus in the neck with
movement; brachialgia, which is
characterized as a stabbing pain
in the pre- or postaxial border
of the arm, elbow, wrist or
fingers; a dull "achy" feeling
in the arm; and numbness or
tingling in the hands.
Pain following a
stereotypical dermatomal
distribution is referred to as a
radiculopathy rather than a
myelopathy. For example, in
patients with a disc herniation
between the sixth and seventh
vertebrae, pain radiates into
the shoulder, upper arm, elbow,
and index and middle fingers. It
is typically unilateral.
Numbness and weakness follow the
same distribution. Some patients
will exhibit signs and symptoms
of radiculopathy and myelopathy.
The hallmark symptom of CSM
is weakness or stiffness in the
legs.10,11
Patients with CSM may also
present with unsteadiness of
gait. Weakness or clumsiness of
the hands in conjunction with
the legs is also characteristic
of CSM. Symptoms may be
asymmetric particularly in the
legs. Loss of sphincter control
or frank incontinence is rare;
however, some patients may
complain of slight hesitancy on
urination.
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TABLE 1
Clinical
Presentation of
Cervical
Spondylotic
Myelopathy
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Common
symptoms
Clumsy or weak
hands
Leg weakness or
stiffness
Neck stiffness
Pain in
shoulders or
arms
Unsteady gait
Common signs
Atrophy of the
hand musculature
Hyperreflexia
Lhermitte's sign
(electric
shock-like
sensation down
the center of
the back
following
flexion of the
neck)
Sensory loss
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Physical and Neurologic
Examination
The physical and neurologic
examination is used to confirm
the presence of spinal cord
dysfunction. Flexion of the neck
may cause a generalized
"electric shock-like" sensation
down the center of the back,10
referred to as
Lhermitte's sign (Table 1).
Atrophy of the hands,
particularly the intrinsic
musculature, may be present.
Sensory abnormalities have a
variable pattern on examination.
Loss of vibratory sense or
proprioception in the
extremities (especially the
feet) can occur. Superficial
sensory loss may be asymmetric
and persons are variably
affected. The sensory
examination may be confounded by
the presence of diabetes
mellitus and a concurrent
peripheral neuropathy.
A characteristic physical
finding of CSM is hyperreflexia.
The biceps and supinator
reflexes (C5 and C6) may be
absent, with a brisk triceps
reflex (C7). This pattern is
almost pathognomonic of cord
compression because of cervical
spondylosis at the C5-C6
interspace.12
Ankle clonus and Babinski's sign
(pathologic extension of the
great toe elicited by stroking
the foot) in the feet may also
be revealed. Hoffmann's sign (a
reflex contraction of the thumb
and index finger after nipping
the middle finger) is a subtle
indicator of spinal cord
dysfunction. A stiff or spastic
gait is also characteristic of
CSM in its later stages.
When cervical spondylosis is
isolated to the C6-7, C7-T1
spinal levels, the arm reflexes
may be normal. A hyperactive
pectoralis muscle reflex
elicited by tapping the
pectoralis tendon in the
deltopectoral groove causing
adduction and internal rotation
of the shoulder is a sign of
cord compression in the upper
cervical spine (C2-3, C3-4
spinal levels).13
The "dynamic" Hoffmann's sign
(when a typical Hoffmann's sign
is elicited after having the
patient flex and extend the neck
multiple times) may be an
indicator of early CSM.14
Hyperreflexia may be absent in
CSM patients who have concurrent
diabetes, causing a peripheral
neuropathy (Table 1).
FIGURE 3.
Sagittal magnetic
resonance imaging
showing narrowing of the
spinal canal as a result
of anterior herniated
discs/osteophytes (left)
and posterior buckling
of hypertrophied
ligamentum flavum (right).
[corrected] |
Imaging and Diagnostic
Studies
Magnetic resonance imaging
(MRI) of the cervical spine is
the procedure of choice during
the initial screening process of
patients with suspected CSM.15
MRI is noninvasive and provides
images of the spine and spinal
cord in several planes (Figure
3). In addition to giving an
assessment of the degree of
spinal canal stenosis, an MRI
can identify intrinsic spinal
cord lesions that can also
present with myelopathy (e.g.,
tumors). High signal changes
seen in the spinal cord of
patients with CSM may indicate
myelomalacia or permanent spinal
cord damage.
Computed tomography (CT) is
complementary to MRI (Table 2).
CT may give a more accurate
assessment of the amount of
canal compromise because it is
superior to MRI in evaluating
bone (osteophytes).16
Myelography or the intrathecal
injection of a contrast agent is
used in conjunction with CT.
Since the advent of MRI, the use
of myelography has decreased;
however, it still provides
useful information in some
instances for surgical planning.
Plain radiographs alone are of
little use as an initial
diagnostic procedure.
Electromyography is rarely
useful in most patients with
CSM; however, it may help in the
exclusion of specific syndromes
such as peripheral neuropathy.
Somatosensory evoked potentials
(SSEPs) provide a more direct
assessment of spinal cord
function (e.g., dorsal column
function) than electromyography.17
However, SSEPs are nonspecific
and therefore their use as a
diagnostic tool is undetermined.
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A characteristic
physical finding
of cervical
spondylotic
myelopathy is
hyperreflexia.
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Differential Diagnosis
The presence of myelopathy on
neurologic examination is not
unique to CSM. Therefore, it is
important to exclude other
diagnoses that present in a
similar fashion. In one study,
it was found that 14.3 percent
of patients who underwent
surgery for CSM were later found
to have other diagnoses.18
This finding could be an
explanation for the lack of
neurologic improvement after
surgery in some cases.
Because cervical spondylosis
is a universal finding in the
elderly population, it is
important to correlate cervical
spondylotic changes with
sensorimotor abnormalities
identified on examination.10
If there is a lack
of correlation, there may be a
demyelinating process (e.g.,
multiple sclerosis). MRI is
useful in this situation for
identifying areas of
demyelination in the spinal cord
and cerebrum. In addition, a
cerebrospinal fluid examination
(e.g., oligoclonal bands) and
visual evoked responses are
important diagnostic adjuncts.
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TABLE 2
Diagnostic
Criteria for
Cervical
Spondylotic
Myelopathy
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Characteristic
symptoms (leg
stiffness, hand
weakness)
Characteristic
signs
(hyperreflexia,
atrophy of
hands)
MRI or CT
(showing spinal
stenosis and
cord compression
as a result of
osteophyte
overgrowth, disc
herniation,
ligamentum
hypertrophy)
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MRI = magnetic
resonance
imaging; CT =
computed
tomography. |
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Amyotrophic lateral sclerosis
(ALS) is another
neurodegenerative disorder that
can be confused with CSM. The
absence of extremity sensory
abnormalities on neurologic
examination of a patient with
myelopathy should alert the
physician to the possibility of
ALS. The presence of
fasciculations on examination
and a denervation pattern on
electromyography serve as
confirmatory evidence for ALS (Table
3).
Other conditions that can
mimic CSM on presentation are
primary spinal cord tumors,
syringomyelia, extramedullary
conditions (e.g., metastatic
tumors), subacute combined
degeneration of the spinal cord
(vitamin B12
deficiency), hereditary spastic
paraplegia, normal pressure
hydrocephalus and spinal cord
infarction (Table 4).10
Most of these conditions can
easily be distinguished from CSM
based on characteristic MRI
findings.
Treatment
Evaluating the efficacy of
any particular treatment
strategy for CSM is difficult
because reports show that as
many as 18 percent of patients
with CSM will improve
spontaneously, 40 percent will
stabilize and approximately 40
percent will deteriorate if no
treatment is given.19
Unfortunately, the current
understanding of CSM does not
allow physicians to predict the
course of a patient. Also, the
literature regarding various
treatment strategies (surgical
and nonsurgical) for CSM is
flawed because of a lack of
prospective controlled studies.
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TABLE 3
Differential
Diagnosis: CSM
vs. ALS
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Feature
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CSM
|
ALS
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Age |
Older
than 55 |
Older
than 55 |
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MRI
findings |
Spondylosis |
Spondylosis |
|
Fasciculations |
Absent |
Present |
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Atrophy
of arms |
Present |
Present |
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Atrophy
of legs |
Absent |
Present |
|
Denervation |
Absent |
Present |
|
CSM = cervical
spondylotic
myelopathy; ALS
= amyotrophic
lateral
sclerosis; MRI =
magnetic
resonance
imaging.
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TABLE 4
Conditions That
Mimic Cervical
Spondylotic
Myelopathy on
Presentation
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Amyotrophic
lateral
sclerosis
Extrinsic
neoplasia
(metastatic
tumors)
Hereditary
spastic
paraplegia
Intrinsic
neoplasia
(tumors of
spinal cord
parenchyma)
Multiple
sclerosis
Normal pressure
hydrocephalus
Spinal cord
infarction
Syringomyelia
Vitamin B12
deficiency
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Nonsurgical Treatment
In patients who are mildly
affected by CSM, a "careful
watching" approach can be taken.
A variety of nonsurgical
strategies have been used with
variable success for the
treatment of CSM. These include
cervical traction, cervical
immobilization (collar or neck
brace), skull traction and
physical therapy. Cervical
immobilization is the most
commonly used treatment in the
United States. Some studies
demonstrate the benefits of
wearing a brace, while other
studies show that immobilization
does not improve the patient's
condition.20
It has also been reported that
symptomatic patients may
deteriorate neurologically
during bracing, causing many to
advocate earlier surgical
intervention.20,21
A nonsurgical approach is
usually inadvisable.
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The primary goal
of surgery is to
decompress the
spinal cord,
thus giving the
neural elements
more room.
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Surgical Treatment
Once frank myelopathy occurs,
surgical intervention is
necessary. The primary goal of
surgery is to decompress the
spinal cord, thus giving the
neural elements more room.
Traditionally, cervical
laminectomy, a posterior
approach, has been used for
surgical treatment of CSM.
However, over the past 20 years,
it has been increasingly
recognized that laminectomy is
not appropriate for all
patients. Further neurologic
deterioration after laminectomy
is attributed to a development
of latent instability of the
spine with development of
kyphotic spinal deformities and
to the inability of posterior
approaches to directly address
anterior vector compression
secondary to osteophytic
overgrowth.
FIGURE 4.
Postoperative magnetic
resonance imaging of
patient in Figure 3
showing adequate
decompression of the
spinal cord after
multilevel posterior
laminectomy.[corrected] |
For this reason, anterior
approaches to the spine have
been increasingly used.22
Through an anterior cervical
approach, one can directly
address and remove osteophytes
and disc material for
decompression of the spinal
cord. Also, with the addition of
interposition bone grafts and,
in some cases, cervical plates
(instrumentation) to promote
spinal fusion, the development
of instability of the neck can
be prevented. A variety of
factors must be considered when
deciding whether to use an
anterior or posterior approach,
but the primary goal of both
approaches is to provide
adequate space for the spinal
cord (Figure 4).
Many surgical series show
"improvement," or at least
stabilization of symptoms with
posterior and anterior
approaches. After reviewing the
surgical literature, one
investigator found that the rate
of successful outcome after
surgery was at best 50 percent
with the potential for
significant postsurgical
morbidity.22
The older surgical literature
has been criticized because of
the uncertainty of whether
nonspondylotic myelopathy
conditions (e.g., multiple
sclerosis, ALS) had been
sufficiently excluded before
surgery.22
A variety of factors
determine success after surgery.
Factors that may portend a less
than satisfactory surgical
outcome include severe
preoperative neurologic
deficits, abnormal signal
changes within the spinal cord
and/or spinal cord atrophy seen
on MRI, and severity of cord
compression seen on radiographic
studies.23-25
Final Comment
CSM is a common cause of
disability in older persons.
Because spondylosis is a
universal finding as patients
age, it is important to
correlate clinical history and
neurologic findings with
radiographic studies. MRI is the
most useful radiographic study
for quantifying the degree of
stenosis and excluding other
pathologies. Current treatment
remains controversial with
regard to surgical and
nonsurgical management. In the
future, prospective randomized
trials may be required to
definitively establish treatment
guidelines. Currently, surgical
decompression is appropriate for
many symptomatic patients.
