Cervical Spondylotic Myelopathy: A

Common Cause of Spinal Cord Dysfunction

in Older Persons
WILLIAM F. YOUNG, M.D., Temple University Hospital, Philadelphia, Pennsylvania
Am Fam Physician. 2000 Sep 1;62(5):1064-1070.
See related patient information handout on cervical spondylotic myelopathy, written by the
author of this article.
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.
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
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

FIGURE 1.
Axial computerized tomography scan showing ventral osteophytes pressing into the spinal canal.
View Large
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.
View Large
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
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.
TABLE 1 Clinical Presentation of Cervical Spondylotic Myelopathy
View Table
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.

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).

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.

FIGURE 3.
Sagittal magnetic resonance imaging showing narrowing of the spinal canal as a result of anterior
herniated discs/osteophytes and posterior buckling of hypertrophied ligamentum flavum.
View Large
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.
TABLE 2 Diagnostic Criteria for Cervical Spondylotic Myelopathy
View Table
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.

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.
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).
TABLE 3 Differential Diagnosis: CSM vs. ALS
View Table
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.
TABLE 4 Conditions That Mimic Cervical Spondylotic Myelopathy on Presentation
View Table

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.

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.

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.
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).

FIGURE 4.
Postoperative magnetic resonance imaging of patient in Figure 3 showing adequate
decompression of the spinal cord after multilevel posterior laminectomy.

View Large
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.2325

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.
The Author
WILLIAM F. YOUNG, M.D., is associate professor of neurosurgery and physiology at Temple
University School of Medicine, Philadelphia. He is also director of the neurospine program at
Temple University Hospital, Philadelphia. Dr. Young received his medical degree from Cornell
University Medical College, New York, N.Y., and received training in neurosurgery and spinal
reconstructive surgery at Temple University Hospital.
Address correspondence to William F. Young, M.D., Temple University Hospital, 3401 N. Broad
St., Philadelphia, PA 19140. Reprints are not available from the author.

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