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2. medicine
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SIEMIONOW SPINE SURGERY 
Kris Siemionow, MD
Chicago, Illinois
Cervical Spondylotic Myelopathy
Correspondence should be addressed to:
K. B. Siemionow, M.D.
Assistant Professor of Orthopaedics and Neurosurgery
University of Illinois, Chicago
Email: [email protected]
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Dr. Krzysztof (Kris) B. Siemionow MD is Assistant Professor of
Orthopaedics and Neurosurgery at the University of Illinois in
Chicago. Dr. Siemionow completed fellowships in Spine Surgery and
he specializes in the surgical management of spinal conditions
affecting the neck, spine, and back in adults, children, and
adolescents. Dr. Siemionow is Board Certified by the American Board
of Orthopaedic Surgery.
Dr. Siemionow completed a residency in Orthopaedic Surgery at the
Cleveland Clinic in Cleveland, Ohio, ranked one of the top hospitals
in the nation by US News. While in Cleveland, Dr. Siemionow
completed a combined orthopedic/neurosurgical spine fellowship at
the Cleveland Clinic Spine Institute. After completing residency, Dr.
Siemionow and his family moved to Chicago. In Chicago, Dr.
Siemionow completed fellowship training in Adult Spine Surgery at
Rush University Medical Center and a Pediatric Spine Fellowship at
the Shriners Hospital for Children.
Dr. Siemionow participates in an annual spine surgery mission to
Uganda, East Africa, where he treats both children and adults
suffering from spinal trauma, scoliosis, tumors, and infection.
Dr. Siemionow has published numerous scientific articles pertaining
to spine surgery and basic science spine research. He was awarded
an NIH grant to study, “ The effects of inflammation on glial fibrillary
acidic protein expression in satellite cells of the dorsal root ganglion.”
Some of his current research is focused on the aging spine, the
effects of less invasive surgical techniques, and robotic spine
surgery.
Dr. Siemionow has been awarded several patents for developing
devices and technologies used in nerve and spine surgery. Currently
he is working on applications for terahertz electromagnetic waves
with scientists at Case Western Reserve University.
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Cervical Spondylotic Myelopathy
Introduction
You might have been diagnosed with cervical spondylotic myelopathy or CSM by your
doctor. What is CSM? Cervical spondylotic myelopathy is a slowly progressive process
resulting from age related spinal degeneration that can lead to significant functional
disability and, in some cases, paralysis. It is now well established, that CSM is the result
of a reduction in the space available for the spinal cord in the spinal canal. This causes
pressure on the spinal cord itself and results in damage to the blood supply, nerves, and
the nerve cells that form the spinal cord. [1, 2]. CSM is the most common type of spinal
cord dysfunction affecting individuals over 55 years of age[2-4]. The most common
reason for the reduction in spinal cord diameter is age related degeneration of the spinal
joints and discs. These joints wear out just like other joints in the body and form bone
spurs, the discs decrease in height and bulge. With time, the combination of these factors
results in narrowing of the passage for the spinal cord.
Without definitive surgical treatment, progressive deterioration is common. Conservative
treatment is generally ineffective, and surgical intervention remains the most reliable and
predictable method to halt further neurologic deterioration.
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MRI of the cervical spine. The arrows are showing spinal cord compression caused
by degenerative changes. In this case the discs are collapsed and bulging and the
ligaments are thick and buckled.
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History
The natural history of cervical myelopathy is best summarized as a gradual, progressive
worsening of symptoms and decline in functional status. The most common pattern is a
stepwise progression of symptoms followed by periods of stable or worsening function
and in rare instances, improvement[5, 6]. In a review of 120 patients, Clarke and
Robinson identified a slow pattern of stepwise decline in function with intervals of stable
neurologic function in 50% of patients, and a rapid pattern with stable intervals in 25% of
patients[6]. In contrast, 20% of patients had a slow, continuous progression of symptoms
without a stable period, while 5% were found to have a rapid deterioration of neurologic
function. Lees and Turner similarly defined stepwise neurological dysfunction with
quiescent intervals.[5] The authors additionally demonstrated that patients with long
standing disease (>10 years) were more likely to be severely disabled than those earlier in
the disease process.
Causes
The cause of cervical myelopathy is often multifactorial, but can be categorized
into mechanical and vascular etiologies. [7]. Spinal cord compression can arise from birth
defects, progressive degenerative changes, acute cervical disc herniation, hardening of
ligaments (OPLL) or cervical deformity (kyphosis/translation).
Congenital(present at birth), or developmental canal stenosis may be an
underlying contributor to many, but not all, patients with symptomatic disease. A
congenitally narrow canal provides less space than a normally open canal to
accommodate for compressing strucutres or deformity.
Progressive cervical degeneration (spondylosis), a common cause of CSM,
contributes to compression by progressive cervical disc disease, degeneration of the
facet( small joints located in the back of the spinal column) joints, degeneration of the
joints of Luschka or uncinate joints(located outside of the disc), formation of bone spurs
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(ostephytes), and thickening or infolding of the ligaments (like ligamentum flavum)[8, 9].
Additionally, compression can arise from other structures such as acute disc herniations
or ligament calcification. All of these compressive structures act as a space-occupying
mass within the fixed volume of the cervical spinal canal.
Cross section through spinal column of a cadaver demonstrating bone
spurs(white arrow) and ligament thickening and buckling(black arrow).
These changes contribute to spinal cord compression.
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Cervical deformities such subaxial subluxation, seen in rheumatoid disease, can
contribute to CSM by further diminishing the spinal canal volume. Deformities such as
cervical kyphosis may result in a mechanical stretch to the spinal cord and subsequent
CSM symptoms. These mechanical factors may be worsened by neck motion resulting in
repetitive trauma to the cervical cord.
In addition to pure mechanical effects on the spinal cord, CSM symptoms may also be
due to spinal cord ischemia(lack of sufficient blood flow). These ischemic changes are
likely secondary to direct compression or direct spinal cord stretch and may lead to
further nerve cell injury.[10]
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They may account for the stepwise progression of symptoms seen in patients with
otherwise stable radiographic findings. Maintenance of spinal cord blood flow, possibly
through collateral circulation, may explain how some patients remain asymptomatic
despite significant cord compression or deformation.
Clinical Presentation
Due to its wide spectrum of causes, this degenerative process results in various clinical
presentations. In the early stages, neck pain is a common complaint, with cervical
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radiculopathy(pain radiating down the arm) and myelopathy seen in more advanced
disease. Some patients report neck pain as a significant component of their symptoms,
while others have little or no such symptoms[11]. Numbness or paresthesias in the hands,
that is often associated with a loss of hand coordination, is another common complaint.
This may be manifested as an inability to distinguish items such as coins in ones pocket,
or an inability to perform delicate tasks such as tying shoes or buttoning a shirt[4].
Complaints of difficulty with writing, or an unexplained change in handwriting are also
common[8]. Patients may report that they cannot tell the temperature of water, although
they can tell that their hand is submersed[12].
Patients may complain of arm pain, which is most commonly travels down one of the
arms (radiculopathy). [11]. Concomitant radiculopathy is one of the most common
presenting symptoms and may be seen in more than 40% of patients with CSM [13,
14].10,18. The same degenerative changes that contribute to central stenosis and result in
spinal cord compression, such as a bone spur or herniated disc, may impinge on the
neural foramen causing nerve root compression and the resultant radiculopathy. The
presence of a concomitant radiculopathy can influence both treatment decision making as
well as surgical planning.
Problems with walking are very common and are often one of the first signs of
spinal cord compression. Gait disturbance such as a loss of balance or unsteadiness when
walking are the most common lower extremity complaints reported by patients with CSM
and myelopathy should be considered in the differential diagnosis of a patient with a
history of multiple, unexplained falls [14, 15]. Hip muscle weakness can be profound in
these patients and may contribute to difficulty with getting out of a chair[8]. Additionally,
a number of patients with CSM may present with primary complaints of low back and leg
pain symptoms, often due to associated lumbar nerve compression. Although the
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frequency of symptomatic lumbar nerve compression is unknown, the incidence of
anatomic stenosis has been reported to be 5 to 25% of patients.[16, 17].
In advanced cases of CSM, patients may have bladder or bowel impairment –
symptoms that are usually associated with a poor prognosis for recovery[18]. Urinary
symptoms vary and may consist of urinary frequency, urgency, incontinence, or urinary
retention. The incidence of these symptoms varies with 15 to 50% being reported in the
literature [19, 20]. Bladder dysfunction was demonstrated in 15% and bowel dysfunction
in 18% out of 269 patients with CSM[19]. In a clinical series involving CSM patients
older than age 55, 20% exhibited bladder dysfunction with urinary retention of varying
degrees[21, 22]. The “presence of neurogenic bladder was closely correlated with severe
leg symptoms”[23].
Other Causes Mimicking CSM
Diagnosing CSM is a challenge that requires a high degree of clinical suspicion. There
are other diseases that can mimic CSM. Complaints of difficulty with ambulating and
reduced hand dexterity should alert the examining physician to the possibility of an
underlying myelopathy. There are several other conditions that can mimic CSM on initial
presentation such as multiple sclerosis, ALS(Lou Gehrig’s disease), or polio among
others. [44, 45]. Most of these conditions can easily be distinguished from CSM based on
characteristic MRI findings which document spinal cord compression.
Treatment
If you were diagnosed with CSM then you need to consult a spine surgeon. Make
sure that your surgeon is board certified and has completed a fellowship in spine surgery.
Since CSM is a progressive problem, early surgical intervention is warranted in a patient
who presents with significant spinal cord compression and symptoms. In patients with
radiographic evidence of canal narrowing, with or without cord compromise, and only
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mild symptoms, such as neck stiffness and no radicular or myelopathic symptoms, initial
conservative management with close follow-up is appropriate and has shown equivalent
results to operative treatment.[46] Nonsurgical treatments for patients with mild
symptoms include cervical immobilization, pain medication, and physical therapy. There
is often apprehension associated with nonsurgical management , for both the patient and
the physician since it has been reported that symptomatic patients may deteriorate
neurologically during conservative treatment, causing many to advocate earlier surgical
intervention[47]. Many have also advocated surgical management in asymptomatic
patients to prevent spinal cord injury from minor trauma despite the lack of evidence to
support this recommendation. There is no strong clinical evidence (grade I, II, or III) to
support prophylactic spinal cord decompression and, therefore, asymptomatic patients are
best managed through serial clinical examination.
Surgical treatment for patients with moderate to severe symptoms is often
recommended. A number of treatment options exist – anterior decompression and fusion,
posterior laminectomy, posterior laminaplasty, posterior laminectomy and fusion, and
combined anterior and posterior procedures. Alignment of the spine, location of cord
compression (front vs back), flexibility of the spine, the presence of
deformity(angulation), the number of levels involved, and surgeon preference all
influence decision making. Deciding the approach, number of levels, fusion vs nonfusion techniques remain controversial, with little widespread agreement. Each has
demonstrated potential benefits and as well as risks. Overall, outcomes of surgical
decompression, among symptomatic patients, have been demonstrated to be superior to
nonoperative treatment in functional status, pain relief, and neurological status.[48]
Negative predictors of postoperative recovery include: poorer preoperative neurological
status, longer duration of symptoms, and advance patient age.[8]
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Summary
Cervical spondylotic myelopathy is a slowly progressive process resulting from
age related degenerative changes in the spine that can lead to significant functional
disability. Once myelopathic symptoms are present, most patients with will require
surgery to decompress the spinal cord and prevent further functional deterioration.
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Figure Legend
Figure 1. Sagittal T2 weighted MRI showing compression of the spinal cord at C3-C4
with increased signal in the cord (arrow) indicative of myelomalacia.
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NOTES
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