Cervical Spondylotic Myelopathy: Pathophysiology, Clinical Presentation, and Treatment

Abstract

Age-related changes in the spinal column result in a degenerative cascade known as spondylosis. Genetic, environmental, and
occupational influences may play a role. These spondylotic changes may result in direct compressive and ischemic dysfunction
of the spinal cord known as cervical spondylotic myelopathy (CSM). Both static and dynamic factors contribute to the pathogenesis.
CSM may present as subclinical stenosis or may follow a more pernicious and progressive course. Most reports of the natural
history of CSM involve periods of quiescent disease with intermittent episodes of neurologic decline. If conservative treatment
is chosen for mild CSM, close clinical and radiographic follow-up should be undertaken in addition to precautions for trauma-related
neurologic sequelae. Operative treatment remains the standard of care for moderate to severe CSM and is most effective in
preventing the progression of disease. Anterior surgery is often beneficial in patients with stenotic disease limited to a
few segments or in cases in which correction of a kyphotic deformity is desired. Posterior procedures allow decompression
of multiple segments simultaneously provided that adequate posterior drift of the cord is attainable from areas of anterior
compression. Distinct risks exist with both anterior and posterior surgery and should be considered in clinical decision-making.

Keywordscervical spine–spondylosis–myelopathy–natural history–operative treatment

Full text

REVIEW ARTICLE
Cervical Spondylotic Myelopathy: Pathophysiology, Clinical
Presentation, and Treatment
Darren R. Lebl, MD &Alex Hughes, MD &Frank P. Cammisa, Jr MD &Patrick F. O’Leary, MD
Received: 19 February 2011/Accepted: 28 April 2011/Published online: 22 June 2011
*Hospital for Special Surgery 2011
Abstract Age-related changes in the spinal column result in
a degenerative cascade known as spondylosis. Genetic,
environmental, and occupational influences may play a role.
These spondylotic changes may result in direct compressive
and ischemic dysfunction of the spinal cord known as cervical
spondylotic myelopathy (CSM). Both static and dynamic
factors contribute to the pathogenesis. CSM may present as
subclinical stenosis or may follow a more pernicious and
progressive course. Most reports of the natural history of CSM
involve periods of quiescent disease with intermittent episodes
of neurologic decline. If conservative treatment is chosen for
mild CSM, close clinical and radiographic follow-up should
be undertaken in addition to precautions for trauma-related
neurologic sequelae. Operative treatment remains the standard
of care for moderate to severe CSM and is most effective in
preventing the progression of disease. Anterior surgery is
often beneficial in patients with stenotic disease limited to a
few segments or in cases in which correction of a kyphotic
deformity is desired. Posterior procedures allow decompres-
sion of multiple segments simultaneously provided that
adequate posterior drift of the cord is attainable from areas of
anterior compression. Distinct risks exist with both anterior
and posterior surgery and should be considered in clinical
decision-making.
Keywords cervical spine.spondylosis.myelopathy.
natural history.operative treatment
Introduction
Cervical myelopathy encompasses a range of symptoms and
examination findings including motor and sensory abnormal-
ities related to dysfunction of the cervical spinal cord. Early
thinking attributed the signs and symptoms of cervical
myelopathy to an intrinsic dysfunction of the nervous system.
It was not until the 1950s that classic anatomic studies
established that spondylosis of the cervical spine is one
possible etiology for compression of the spinal cord and leads
to the development of myelopathic symptoms [6,43].
The pathophysiology of CSM is now thought to be
multifactorial with both static factors causing stenosis and
dynamic factors resulting in repetitive injury to the spinal
cord playing a role. It has been postulated that the absolute
size of the spinal cord may be an important factor in the
development of symptoms from CSM. The symptoms of
this disorder are generally related to the degree of
compression of the various spinal cord tracts. Cadaveric
studies have shown that the transverse cross-sectional area
of the spinal cord and the compressive ratio [compressive
ratio=(sagittal diameter /transverse diameter)× 100%] of the
spinal cord correlate with the severity of pathologic changes
[16]. In addition, autopsy examinations of patients with
CSM have shown gray matter atrophy, neuronal loss, and
white matter demyelination [26,39].
The dynamic factors that contribute to the pathogenesis
of CSM are complex. The spinal cord stretches with flexion
of the cervical spine and shortens and thickens with
HSSJ (2011) 7: 170–178
DOI 10.1007/s11420-011-9208-1
Each author certifies that he or she has no commercial associations
(e.g., consultancies, stock ownership, equity interest, patent/licensing
arrangements, etc.) that might pose a conflict of interest in connection
with the submitted article.
D. R. Lebl, MD (*)
Spine and Scoliosis Surgery,
The Hospital For Special Surgery,
535 East 70th Street,
New York, NY 10021, USA
e-mail: drlebl@stanfordalumni.org
A. Hughes, MD IF. P. Cammisa, Jr MD IP. F. O ’Leary, MD
The Spine Surgery Service, Spine Care Insititute,
The Hospital for Special Surgery,
535 East 70th Street,
New York, NY 10021, USA
D. R. Lebl, MD IA. Hughes, MD IF. P. Cammisa, Jr MD
P. F. O ’Leary, MD
Weill Cornell Medical College,
New York, NY 10065, USA

extension. This principle was demonstrated in a classic
study by Breig in which he examined the effects of
spondylotic bars and positioning of the cervical spine on
the spinal cord geometry and blood flow [7]. He demon-
strated that extension of the cervical spine causes the cord
to relax and shorten. The posterior half of the cord was
found to shorten more than the anterior portion of the cord,
and the axons in the posterior column assumed a spiral
course and occupied a larger cross-sectional area on trans-
verse sectioning. According to this early work, the dynamic
shortening of the posterior cord and dorsal columns in
extension may account for the difficulties with balance in
the CSM patient.
In flexion, the stretched cord is draped over the posterior
aspects of the PLL and vertebral bodies and held against
any spondylotic protrusions that may be present. The axons
of the cervical cord elongated and the roots are stretched.
Spondylotic bars produced deep grooves on the anterior
surface on the spinal cord in extension, no contact with the
anterior wall in neutral position, and flattening of the cord in
flexion. That is, in extension, the spondylotic bars displaced
the cord, but in flexion, the cord was attenuated over the
spondylotic ridge and the axons were stretched.
These studies laid the groundwork for Breig's theory
that tension on the spinal cord is a key component in the
development of CSM. However, he also demonstrated that
the vascular supply of the cord is an important consid-
eration. The arterioles that branch from the anterior spinal
artery may be subjected to mechanical compression with
flattening of the cord in the sagittal plane leading to
ischemia of cord [7]. These phenomena continue to be
areas of active research and form much of our modern
understanding of the pathogenesis of neuron damage in
CSM mediated by both ischemic and mechanical insults to
the cord.
These and other cadaveric findings have been confirmed
in vivo by dynamic MRI studies in patients with CSM. A
significant increase of spinal stenosis has been observed in
extension (48% of patients) more so than in flexion (24% of
patients) [37]. A congenitally small spinal canal is also an
important predisposing factor to the development of CSM.
In one series of 63 patients with symptomatic CSM, it was
found that 40 (63%) were found to have developmentally
narrow canals [12]. Unique pathologic and kinematic traits
may exist in the patient with a developmentally narrow
canal. Dynamic MRI studies have shown that patients
with a congenitally narrow cervical canal (<13 mm) have
increased segmental mobility in the cervical spine which
may in turn predispose to the development of radio-
graphic dynamic cord compression and potentially clinical
myelopathy [36].
Clinical Presentation and Evaluation
The clinical sequelae related to compression of the cervical
spinal cord represent a broad spectrum. Affected individuals
may have subtle clinical findings such as diminished hand
dexterity or balance difficulties or in severe cases symptoms
of incontinence and complete paralysis. Attempts to
correlate the radiographic findings with clinical presentation
have been made. However, it has yet to be clearly under-
stood why clinical symptoms of myelopathy manifest in
certain individuals with radiographic evidence of stenosis
and not in others. The fact that radiographic spinal canal
narrowing is often asymptomatic underscores the impor-
tance of a thorough history and physical examination in
making the diagnosis of CSM.
Patients with mild symptoms of cervical spondylosis
may report only neck pain and limited range of motion.
Often with chronic CSM, patients may be unaware of subtle
changes in balance or hand dexterity. The clinicians' history
taking should elicit any difficulty with motor tasks such as
clumsiness or slowness with activities such as buttoning
buttons, using keys, or changes in hand writing. Difficulty
with common modern tasks such as using a computer
keyboard, pushing buttons on a cellular phone, or text
messaging may be elicited as early signs of CSM. The
recent use of assistive devices such as a cane, walker, or
wheelchair due to weakness or balance issues may reflect
progression of myelopathy. Often the earliest manifestations
of balance problems are reported by the patient as the recent
necessity to use a handrail while negotiating stairs.
Paresthesias and weakness are often present in the upper
extremities and patients may have concomitant radicular
signs and symptoms. In severe cases of CSM, changes in
bowel or bladder dysfunction may be present.
Physical examination should include assessment of
balance such as heel-to-toe tandem walking, heel-walking,
toe-walking, and Romberg's sign (patient stands with the
eye's closed and arms held forward—loss of balance is
considered a positive test consistent with posterior column
dysfunction). Cervical range of motion should be tested in
flexion, extension, lateral bending, and axial rotation.
Cervical extension is often limited in the patient with
CSM and should be documented should surgical interven-
tion be planned to avoid iatrogenic hyperextension injury
during intubation.
Tests of hand dexterity such as the “15 s grip-and-
release”may be performed [24]. A normal patient should be
able to grip and release their hand approximately 25–30
times in 15s, and patients with CSM may have difficulty
with these rapid movements. “Myelopathy hand”is a
finding in patients with CSM in which loss of motor
strength, sensory changes, wasting of the intrinsic muscles,
and spasticity may dramatically decrease upper extremity
function [54]. The “finger escape sign”may be evident in
which the ulnar two digits drift into abduction and flexion
after the patient holds his or her hand with the MCPs, PIPs,
and DIPs extended for a minute or more; however, the
physiologic basis of this sign remains poorly understood.
Sensory and vibratory testing should be performed in
the upper and lower extremities in addition to reflex
examination. Patients with CSM will often be hyperreflex-
ive in the upper and lower extremities. The pathologic
reflexes are usually dependent on the spinal level of
compression (e.g., a patient with cervical stenosis at C7-
T1 may in fact have normal upper extremity reflexes that
HSSJ (2011) 7: 170–178 171

originate rostral to the site of compression—biceps,
brachioradialis, etc.). Abnormal long-tract signs such as
the Babinski, Hoffman's, and inverted radial reflexes
(tapping the brachioradialis tendon that elicits firing of the
long finger flexors is considered a positive response). Of
note, these clinical signs should not be relied upon solely for
the diagnosis of myelopathy in the patient with stenosis.
Recent studies have demonstrated a sensitivity as low as 58%
of the Hoffman's sign for clinical myelopathy when the
investigators are blinded [18]. There is some evidence
however that the sensitivity of the Hoffman's sign is improved
while performed with a dorsiflexion force to the DIP joint
(compared to 20.5% in volarflexion) to 76.9%. However, the
specificity of this clinical sign is thought to be higher with a
volarflexion force—96.7% (compared to 78.0% in dorsiflex-
ion) [45]. Cranial nerve examination should be performed for
assessment of possible brain or brainstem lesions.
Several clinical measures of disease severity have been
developed such as the Japanese Orthopaedic Association
(JOA) [25], Nurick [38], and Chile's modified Japanese
Orthopaedic Association (mJOA) [10] scoring systems. These
popular scales provide the clinician with a metric to quantify
the extent and progression of disease (Tables 1,2,and3).
However, they are not without their limitations. The mJOA
translates the Japanese functional grading of the ability to use
chopsticks to a more pertinent evaluation in western cultures
(ability to use fork and knife). For instance, there remains
inter-observer potential for variation in these systems when
assessing items such as “mild”versus “severe”sensory loss.
These tools should be utilized to augment a carefully
documented history and physical exam and by no means
serve to replace astute clinical acumen.
Plain X-ray radiographic evaluation of the patient with
CSM should include AP and lateral views. Narrowing of
the disc space, facet joint arthrosis, bone spurs, ossification
of the posterior longitudinal ligament (OPLL), and kyphotic
alignment may be visualized on a standard lateral plane X-
ray. Spondylotic changes often lead to a stiffening of the
involved segments. Adjacent segments of the spine may be
hypermobile to compensate for the decreased motion at the
spondylotic levels. This hypermobility can result in a
dynamic compression of the spinal column and may not
be seen on routine MRI imaging. Therefore, flexion-
extension radiographs should be included in the radio-
graphic evaluation of the patient with CSM. Additional
oblique views are useful in for visualizing foraminal
narrowing. Comparison of standing radiographs to supine
radiographs provides important information about the
stability and motion of the cervical spine under a physio-
logic load.
Magnetic resonance imaging is an important part of the
workup. Disc herniations, facet joint hypertrophy, folding of
the ligamentum flavum, cord edema, and the sagittal
diameter of the cord are indicative of the extent of the
pathology. The presence of bone spurs or any ossification of
the posterior longitudinal ligament (OPLL) as a source of
compression are best visualized on cervical CT scan and are
important for operative planning. CT myelography is a useful
modality to characterize compression of the spinal cord more
accurately than MRI scanning and in patients unable to get an
MRI scan. Moreover, a CT myelogram may be utilized as a
dynamic study—allowing the visualization of contrast flow
through the CSF in flexion, extension, and lateral bending.
Radiographic attempts to characterize patients with
cervical stenosis have included the Torg–Pavlov ratio
(diameter of the cervical canal:width of vertebral body
<0.80 is indicative of stenosis) [42]. Although the use of a
ratio avoids problems with variation in magnification when
measurements are made from plain radiographs, these
measures were developed in a select population of 23
athletes and have since been reported to be unreliable and to
correlate poorly with the true diameter of the canal [4].
An “absolute stenosis”has been defined as a sagittal
canal diameter <10 mm and a “relative stenosis”as a canal
diameter <13 mm, and a normal sagittal diameter in the
mid-cervical spine of 17–18 mm [1,55]. However, these
absolute measurements of sagittal plane diameter are subject
to genetic variation between individuals of different sizes. In
his classic study, Boden reported a high false positive rate of
stenosis using such absolute measurements in asymptomatic
individuals. In his study, cervical canal stenosis was observed
on MRI imaging in 14% of individuals less than age 40 and
28% of those over the age of age 40. Disc degeneration or
narrowing was also observed at one or more levels in 25% of
individuals less than age 40 and in almost 60% of those over
the age of 40 [5]. As such, the diagnosis of CSM requires
consideration of history, physical examination, and imaging
studies for each individual patient.
Natural History
To date, the natural history of CSM has not been clearly
defined, and many of the existing studies are limited. Most
Table 1 Nurick's classification system for myelopathy [38]
Grade Root signs Cord involvement Gait Employment
0 Yes No Normal Possible
I Yes Yes Normal Possible
II Yes Yes Mild abnormality Possible
III Yes Yes Severe abnormality Impossible
IV Yes Yes Only with assistance Impossible
Reproduced with permission of Oxford University Press via Copyright Clearance Center. The pathogenesis of the spinal cord disorder associated
with cervical spondylosis. Brain 1972;95:87–100. Nurick S. Copyright 1972 by Oxford University Press.
172 HSSJ (2011) 7: 170–178

authors agree that there is a tendency of patients with CSM
to progress to more severe disease, however, the proportion
of patients that deteriorate and the rate of decline remains a
subject of debate. Predominantly Class III evidence sug-
Table 2 The Japanese Orthopaedic Association (JOA) scale for spondylotic myelopathy [25]
Points
Motor Upper extremity Unable to eat with spoon or chopsticks 0
Possible to eat with spoon not chopsticks 1
Possible to eat with chopsticks—but not adequate 2
Possible to eat with chopsticks, but awkward 3
Normal 4
Lower extremity Impossible to walk 0
Need a cane or aid on flat ground 1
Need a cane or aid on stairs 2
Possible to walk without a cane or aid but slow 3
Normal 4
Sensory Upper extremity Apparent sensory loss 0
Minimal sensory loss 1
Normal 2
Lower extremity Apparent sensory loss 0
Minimal sensory loss 1
Normal 2
Trunk Apparent sensory loss 0
Minimal sensory loss 1
Normal 2
Bladder function Complete retention 0
Severe disturbance 1
Mild disturbance 2
Normal 3
Total 17
Reproduced with permission and copyright © of the British Editorial Society of Bone and Joint Surgery. Hukuda S, Mochizuki T, Ogata M,
Shichikawa K, Shimomura Y. Operations for cervical spondylotic myelopathy: a comparison of the results of anterior and posterior procedures.
J Bone Joint Surg [Br] 1985;67-B:609-15. (Table V)
Table 3 Chile's modified Japanese Orthopaedic Association (mJOA) scale for spondylotic myelopathy [10]
Points
Motor Upper extremity Unable to feed oneself 0
Unable to use knife and fork; able to use spoon 1
Able to use knife and fork with much difficulty 2
Able to use knife and fork with slight difficulty 3
Normal 4
Lower extremity Unable to walk 0
Can walk on flat floor with walking aid 1
Can walk up and/or down stairs with handrail 2
Lack of stability and smooth gait 3
Normal 4
Sensory Upper extremity Severe sensory loss or pain 0
Mild sensory loss 1
Normal 2
Lower extremity Severe sensory loss or pain 0
Mild sensory loss 1
Normal 2
Trunk Severe sensory loss or pain 0
Mild sensory loss 1
Normal 2
Bladder function Unable to void 0
Marked difficulty with micturition (retention) 1
Difficulty with micturition (frequency, hesitation) 2
Normal 3
Total 17
Reproduced with permission of Wolters Kluwer Health via Copyright Clearance Center. Chiles BW, 3rd, Leonard MA, Choudhri HF, et al.
Cervical spondylotic myelopathy: patterns of neurological deficit and recovery after anterior cervical decompression. Neurosurgery
1999;44:762–9.
HSSJ (2011) 7: 170–178 173

gests that patients with CSM experience stable quiescent
periods with an intervening slow and stepwise decline in
function [34]. However, some authors have described stable
neurological dysfunction for extended periods of time in
most individuals and rapid decline in others. Clarke and
Robinson reported a retrospective series of 120 patients
with CSM. Of those patients, 75% experienced long periods
of consistent disease with a series of intervening episodes
during which they experienced new symptoms and signs.
Of those 75%, two out of three patients also deteriorated
between episodes. An additional 20% of patients with CSM
followed a slow, steady progression of disease (with one in
five patients showing a late improvement). The remaining
5% showed rapid deterioration of symptoms and signs
followed by long stable periods. This study was, however,
limited by a heterogenous patient population and the lack of
objective outcome measures [11].
Lees and Turner studied 44 patients (age 31–80 years)
with radiographic cervical spondylosis and a neurologic
exam consistent with myelopathy (extensor plantar
responses) and characterized a pattern of progression in
patients with symptoms for more than 10 years [31]. They
demonstrated that very few patients have a steady pro-
gression of symptoms. The more common scenario in their
study was that myelopathic disease was quiescent for periods
of time with intermittent periods of rapid decline in neuro-
logical function.
Barnes and Saunders reported that the majority of
patients remain stable for years with deterioration more
prevalent with female gender and increased ROM [2]. A
longer duration of symptoms has also been reported to
portend a poor prognosis [47,49]. More recent investiga-
tions have suggested that 62% of patients with mild CSM
will not deteriorate or undergo surgery at 10 years, and that
mal-alignment and instability are adverse prognostic factors
[41]. One systematic review of the literature regarding the
natural history of CSM suggest a mixed course with many
patients having quiescent disease for long periods of time
and others experiencing a slow, stepwise decline [34].
Conservative Management
Nonsurgical care for patients with radiographic evidence of
cervical stenosis without clinical signs or symptoms of
myelopathy is a treatment option. Such patients should be
advised regarding the potential of a hyperextension force to
result in spinal cord injury (e.g., central cord syndrome)
with even minor trauma (such as a low-energy fall or rear-
impact motor vehicle collision). Patients with mild clinical
disease such as hyperreflexia or slight balance disturbance
may be observed with close clinical and radiographic
follow-up. The biologic and physiologic age, activity level,
and functional status should all be taken into consideration
when considering non-operative treatment.
Prospective studies in which patients were randomized
into conservative and operative treatment groups have
suggested that patients with mild CSM do not frequently
progress at early time points (2–3 years) [27,28,32].
However, other studies have suggested that conservative
therapy will be successful in preventing progression in 70%
of patients at a minimum of 1-year follow-up with the
remainder requiring surgery due to progressive symptoms.
Given the paucity of definitive data regarding the natural
history of CSM, a discussion with the patient regarding the
severity of symptoms, the degree of disability, and the
potential for progression or spinal cord injury should be
undertaken prior to conservative treatment. Collar immobi-
lization could be considered in patients with radiographic
evidence of severe stenosis despite mild clinical symptoms
given the potential for catastrophic neurologic injury. It
should be noted that even a hard cervical collar restricts
cervical range of motion only a limited amount and cervical
spine injury is possible in the patient with a stenotic canal
despite collar usage. Potential adverse effects of prolonged
collar immobilization such as muscle deconditioning and
restrictions in motion due to their cumbersome nature in
young active patients with mild myelopathy should be
considered.
Indications for Surgery
The decision for operative treatment of CSM must take into
consideration the patient's age, baseline function, rate of
deterioration, severity of symptoms, and overall health. It is
generally agreed upon that patients with ongoing symptoms
refractory to conservative measures, those with progressive
symptoms, bowel or bladder dysfunction, or overt weak-
ness should be considered for operative intervention. The
natural history studies discussed previously suggest
periods of stable function with intervening episodes of
rapid deterioration that exist which makes operative
treatment for patients with symptomatic CSM a common
practice.
Patients with CSM are generally counseled that oper-
ative treatment is most effective to prevent further decline in
function, but may not result in substantial spontaneous
improvement from their current level of function. Surgery
may be recommended earlier for patients with myelomala-
cia (seen as edema within the cord on MRI) or severe
radiographic stenosis. There is some data to suggest that
intramedullary high signal intensity is a poor prognostic
indicator for neurological recovery [52]; however, the
relative importance remains controversial. In general, signal
change within the spinal cord itself may not necessarily
correlate with neurological function or postoperative recov-
ery; however, it should be noted and documented as
evidence of the extent of CSM pathology.
A Cochrane Review of randomized controlled trials for
the role of surgery in mild CSM concluded that the early
results of surgery were superior to non-operative treatment
in terms of pain, weakness, and sensory loss. However, no
significant differences were found at 1 year. Another trial
reviewed found no significant differences between operative
and non-operative care up to 2 years after treatment.
Overall, the data from the reviewed trials was inadequate
174 HSSJ (2011) 7: 170–178

to provide definitive conclusions on the role for operative
treatment of CSM [15].
Surgical Techniques
There have been many different surgical techniques
described for the treatment of CSM. Regardless of the
surgical approaches chosen, the goal of operative treatment
is the decompression of the spinal cord (while preserving
alignment and stability) with consideration of both static
and dynamic factors. Surgical intervention in patients with
moderate to severe myelopathy can be expected to halt the
progression of symptoms. Fujiwara et al. [17] analyzed the
factors involved in the prognosis of CSM in 50 patients by
CT myelography and found that in patients with a trans-
verse area of the cord <30 mm
2
, the results were poor. Age
and preoperative neurological function were also found to
play a role on outcome. Patients with larger transverse area
of the cord, younger patients, patients with shorter duration
of symptoms, and single rather than multiple levels of
involvement can be expected to have a better prognosis
with surgical intervention [17,30].
Special consideration is given to the positioning of the
patient with CSM. Documentation of the preoperative
cervical range of motion is essential. The spondylotic
patient with a tight cervical canal may sustain severe
neurological injury if excessive extension is achieved
during intubation on the operating table. Fiber-optic
intubation is a useful adjunct in the CSM patient with
limited extension. Discussion between the surgeon and
anesthesia team will permit safe intubation, induction of
anesthesia, and positioning.
Broadly speaking, surgical options may be divided into
anterior, posterior, or combined anterior and posterior
approaches. The choice of approach remains a source of
active debate among practitioners. Factors involved in the
decision-making progress include sagittal alignment, num-
ber of diseased segments, stenosis morphology, history of
prior surgery, and bone quality. The overall cervical spine
alignment in the sagittal plane is thought to be an important
consideration when choosing between an anterior and
posterior approach. Traditionally, in the setting of a fixed
cervical kyphosis, an anterior procedure or combined
anterior and posterior procedures have been performed
(Fig. 1). In the presence of a fixed cervical kyphosis, an
anterior procedure will allow direct decompression of the
spinal canal in addition to indirect decompression by
correction of the deformity. A posterior procedure in this
setting has the theoretical risk of leaving the spinal cord
compressed anteriorly against any spondylotic bars or disc
bulges in the kyphotic segment of the spine. Postoperative
MRI scanning has demonstrated that posterior migration of
the thecal sac following laminectomy may be inadequate to
clear compression from anterior osteophytes in patients with
neutral to kyphotic alignment and may account for some
instances of poor outcome after laminectomy for CSM [3].
A recent large prospective observational multicenter
study of 280 patients sought to address the issue of anterior
versus posterior surgery [13]. At 12-month follow-up,
patients with CSM showed significant improvements in
both disease-specific and general health-related outcome
measures with either anterior or posterior surgery (mJOA,
Nurick scale, NDI, and SF-36). Patients treated with
anterior surgery generally had more focal pathology, limited
to a few levels, compared to patients treated with posterior
surgery.
There have been reports of patients with myelopathy
being treated by one-level [51] and multiple-level [50]
cervical disc arthroplasty. Although several studies to date
have shown the equivalence of cervical disc arthroplasty
and arthrodesis for the treatment of cervical radiculopathy
Fig. 1. A patient presenting with CSM with predominantly C5–C6
and C6–C7 stenosis on sagittal T2-weighted MRI scan and a regional
fixed cervical kyphosis from C4–C6
Fig. 2. Sagittal T2-weighted MRI scan of a patient with predom-
inantly C6–C7 stenosis, retrovertebral compression at C6 and C7, and
preservation of cervical lordosis
HSSJ (2011) 7: 170–178 175

[21,44,48], there remains a concern that motion preserva-
tion at the myelopathic spinal segment may allow continued
microtrauma to the spinal cord. Recent multicenter cross-
sectional studies have shown similar improvements in
neurological status in patiens undergoing arthrodesis and
arthroplasty at the 2-year time point [46]. Despite early
encouraging results, the future role that motion preservation
will play in the myelopathic patient remains to be
determined and is still considered investigative at the
present time.
Anterior procedures include single or multilevel anterior
cervical discectomy and fusion (ACDF) or hemi-corpec-
tomy or corpectomy and fusion depending on the desired
regions of decompression. Anterior surgery is generally
recommended for patients with disease limited to a few
segments (Fig. 2) and patients with a fixed cervical
kyphosis. Choice of interbody graft and cervical plate for
graft containment for ACDF procedures is chosen based on
the individual patient and surgeon's preferences. Commeri-
cally available allograft interbody spacers avoid the donor
site morbidity associated with conventional iliac crest
harvesting. Synthetic interbody spacers are also an option,
most commonly composed of a PEEK (polyether–ether-
ketone) polymer, carbon fiber, or a PEEK/carbon fiber
hybrid material. Autograft through open or percutaneous
iliac crest aspiration offers the theoretical benefitof
improved biology for enhancing a fusion. With regard to
plate choice, locking plates (in which the screw head is
threaded and forms a “fixed-angle device”with the plate)
may prevent graft subsidence in older patients with
osteoporotic bone whereas variable angle plates will allow
some settling of the graft for compression at the graft site
once a patient is upright and the spine experiences a
physiologic load. Newer dynamic anterior cervical plates
offer a design that allows load sharing between the vertebral
body and the plate despite subsidence of the interbody bone
graft [8,9]. Although a clinical advantage of dynamic plate
stabilization over locked plate fixation has not been clearly
established, both techniques have inherent risks of late
instrumentation-related complications.
Patients with predominantly dorsal compression due to
ligamentum flavum infolding and patients with multiseg-
mental stenotic disease may be better suited for a posterior
procedure in the setting of a neutral to lordotic alignment.
Posterior procedures for CSM include central decompres-
sion alone by removal of the posterior elements (laminec-
tomy), decompression and fusion (laminectomy and fusion),
and decompression by hinging open of the lamina (lami-
naplasty). Laminaplasty is a relatively motion-preserving
procedure in which the dorsal arch of the lamina is fixed by
plate, wire, cable, spacer between the lamina and the lateral
mass, or suture technique to maintain its protective role
over the dorsal thecal sac.
Complications of Surgery
In addition to complications of bleeding, infection, nerve
damage, dural leak or fistula seen with any spinal surgery,
unique risks exist with anterior and posterior procedures for
CSM. ACDF or anterior corpectomy by conventional
Smith-Robinson approach carries the risk of recurrent
laryngeal nerve injury, superior laryngeal nerve injury,
esophageal injury, vertebral artery injury [53], hardware
breakage or migration, pseudoarthrosis, graft dislodgement,
Horner's syndrome, and airway compromise [14]. Most
patients undergoing anterior cervical surgery will experi-
ence moderate dysphagia that is usually self-limited and
should be made aware of this preoperatively.
Laminectomy for the treatment of CSM has been
associated with reports of neurologic re-stenosis, or the
development of a “post-laminectomy”membrane [56] and
soft tissue impingement on the unprotected thecal sac
remains a possibility. Post-laminectomy kyphosis is a
potential complication following multilevel posterior
decompression procedures [35]. Fusion should be consid-
ered in patients undergoing laminectomy with any pre-
existing instability or in patients in whom a wide decom-
pression is desired. Fusion procedures in the cervical spine
(either anterior or posterior) carry the theoretical risk (albeit
controversial) of adjacent segment degeneneration (ASD).
Symptomatic ASD has been shown to occur at an incidence
of 2.9% per year and survivorship analysis predicts that
25% of patients will develop ASD within 10 years after an
ACDF for instance [23]. A portion of these patients will
require revision surgery for symptomatic ASD [19,20].
Risks unique to laminaplasty include premature lamina
closure after open-door technique with resultant re-stenosis
[33] and axial neck pain [40]. Cervical nerve root palsy
(most commonly C5 palsy) remains a risk predominantly of
posterior cervical decompression [29] but has also been
reported to occur following anterior decompression [22].
Summary
Age-related changes in the spinal column result in a
degenerative cascade with resultant disc dessication, facet
joint hypertrophy, ligamentum flavum infolding, and
kyphotic collapse. Genetic, environmental, and occupa-
tional influences may play a role in this degenerative
process. These spondylotic changes may result in direct
compressive and ischemic dysfunction of the spinal cord
known as CSM. Both static and dynamic factors play a role
in the pathogenesis and should be considered when
considering treatment options. CSM may present as
subclinical stenosis seen on imaging studies or may follow
a more pernicious and progressive course. Most reports of
the natural history of CSM involve periods of quiescent
disease with intermittent episodes of neurologic decline. If
conservative treatment is chosen for mild CSM, close
clinical and radiographic follow-up should be undertaken
in addition to precautions for trauma-related neurologic
sequelae with even low-energy impact. Operative treatment
remains the standard of care for moderate to severe CSM
and is most effective in preventing the progression of
disease. Anterior surgery is often beneficial in patients with
stenotic disease limited to a few segments or in cases in
176 HSSJ (2011) 7: 170–178

which correction of a kyphotic deformity is desired.
Posterior procedures allow decompression of multiple seg-
ments simultaneously given adequate posterior drift of the
cord is attainable with both anterior and posterior surgery
and should be included in the clinical decision-making.
References
1. Arnold JG, Jr. The clinical manifestations of spondylochondrosis
(spondylosis) of the cervical spine. Ann Surg 1955;141:872–89.
2. Barnes MP, Saunders M. The effect of cervical mobility on the
natural history of cervical spondylotic myelopathy. J Neurol
Neurosurg Psychiatry 1984;47:17–20.
3. Batzdorf U, Batzdorff A. Analysis of cervical spine curvature in
patients with cervical spondylosis. Neurosurgery 1988;22:827–36.
4. Blackley HR, Plank LD, Robertson PA. Determining the sagittal
dimensions of the canal of the cervical spine. The reliability of
ratios of anatomical measurements. J Bone Joint Surg Br
1999;81:110–2.
5. BodenSD,McCowinPR,DavisDO, et al. Abnormal magnetic-
resonance scans of the cervical spine in asymptomatic subjects.
A prospective investigation. J Bone Joint Surg Am
1990;72:1178–84.
6. Brain WR, Northfield D, Wilkinson M. The neurological
manifestations of cervical spondylosis. Brain 1952;75:187–225.
7. Breig A, Turnbull I, Hassler O. Effects of mechanical stresses on
the spinal cord in cervical spondylosis. A study on fresh cadaver
material. J Neurosurg 1966;25:45–56.
8. Brodke DS, Gollogly S, Alexander Mohr R, et al. Dynamic
cervical plates: biomechanical evaluation of load sharing and
stiffness. Spine 2001; 26:1324–9.
9. Brodke DS, Klimo P, Jr., Bachus KN, et al. Anterior cervical
fixation: analysis of load-sharing and stability with use of static
and dynamic plates. J Bone Joint Surg Am 2006;88:1566–73.
10. Chiles BW, 3rd, Leonard MA, Choudhri HF, et al. Cervical
spondylotic myelopathy: patterns of neurological deficit and
recovery after anterior cervical decompression. Neurosurgery
1999;44:762–9
11. Clarke E, Robinson PK. Cervical myelopathy: a complication of
cervical spondylosis. Brain 1956;79:483–510.
12. Edwards WC, LaRocca H. The developmental segmental sagittal
diameter of the cervical spinal canal in patients with cervical
spondylosis. Spine (Phila Pa 1976) 1983;8:20–7.
13. Fehlings MG KB, Arnold PM, Yoon ST, Vaccaro AR. Anterior vs
Posterior Surgical Approaches to Treat Cervical Spondylotic
Myelopathy: Outcomes of the Prospective Multi-center AOSPine
North America CSM Study in 280 Patients. Cervical Spine
Research Society 38th Annual Meeting 2010:86–8.
14. Fountas KN, Kapsalaki EZ, Nikolakakos LG, et al. Anterior
cervical discectomy and fusion associated complications. Spine
(Phila Pa 1976) 2007;32:2310–7.
15. Fouyas IP, Statham PF, Sandercock PA. Cochrane review on the
role of surgery in cervical spondylotic radiculomyelopathy. Spine
(Phila Pa 1976) 2002;27:736–47.
16. Fujiwara K, Yonenobu K, Hiroshima K, et al. Morphometry of the
cervical spinal cord and its relation to pathology in cases with
compression myelopathy. Spine (Phila Pa 1976) 1988;13:1212–6.
17. Fujiwara K, Yonenobu K, Ebara S, et al. The prognosis of surgery
for cervical compression myelopathy. An analysis of the factors
involved. J Bone Joint Surg Br 1989;71:393–8.
18. Glaser JA CJ, Bailey KL, Morrow DL. Cervical spinal cord
compression and the Hoffman sign. Iowa Ortho J 2001;21:49–51.
19. Goffin J, Geusens E, Vantomme N, et al. Long-term follow-up
after interbody fusion of the cervical spine. J Spinal Disord Tech
2004;17:79–85.
20. Gore DR, Sepic SB. Anterior discectomy and fusion for painful
cervical disc disease. A report of 50 patients with an average
follow-up of 21 years. Spine (Phila Pa 1976) 1998;23:2047–51.
21. Hacker RJ. Cervical disc arthroplasty: a controlled randomized
prospective study with intermediate follow-up results. Invited
submission from the joint section meeting on disorders of the
spine and peripheral nerves, March 2005. J Neurosurg Spine
2005;3:424–8.
22. Hashimoto M, Mochizuki M, Aiba A, et al. C5 palsy following
anterior decompression and spinal fusion for cervical degener-
ative diseases. Eur Spine J 2010;19:1702–10.
23. Hilibrand AS, Carlson GD, Palumbo MA, et al. Radiculopathy
and myelopathy at segments adjacent to the site of a previous
anterior cervical arthrodesis. J Bone Joint Surg Am 1999;81:519–
28.
24. Hosono N, Sakaura H, Mukai Y, et al. A simple performance test
for quantifying the severity of cervical myelopathy. J Bone Joint
Surg Br 2008;90:1210–3.
25. Hukuda SMT, Ogata M, Schichikawa K, Shimomura T. Oper-
ations for cervical spondylotic myelopathy: a comparison of the
results of anterior and posterior procedures. J Bone Joint Surg Br
1985;67B:609–15.
26. Ito T, Oyanagi K, Takahashi H, et al. Cervical spondylotic
myelopathy. Clinicopathologic study on the progression pattern
and thin myelinated fibers of the lesions of seven patients
examined during complete autopsy. Spine (Phila Pa 1976)
1996;21:827–33.
27. Kadanka Z, Bednarik J, Vohanka S, et al. Conservative treatment
versus surgery in spondylotic cervical myelopathy: a prospective
randomised study. Eur Spine J 2000;9:538–44.
28. Kadanka Z, Mares M, Bednanik J, et al. Approaches to
spondylotic cervical myelopathy: conservative versus surgical
results in a 3-year follow-up study. Spine (Phila Pa 1976)
2002;27:2205–10; discussion 10–1.
29. Kaneyama S, Sumi M, Kanatani T, et al. Prospective Study and
Multivariate Analysis of the Incidence of C5 Palsy After Cervical
Laminoplasty. Spine (Phila Pa 1976) 2010.
30. Koyanagi T, Hirabayashi K, Satomi K, et al. Predictability of
operative results of cervical compression myelopathy based on
preoperative computed tomographic myelography. Spine (Phila
Pa 1976) 1993;18:1958–63.
31. Lees F, Turner JW. Natural History and Prognosis of Cervical
Spondylosis. Br Med J 1963;2:1607–10.
32. Matsumoto M, Toyama Y, Ishikawa M, et al. Increased signal
intensity of the spinal cord on magnetic resonance images in
cervical compressive myelopathy. Does it predict the outcome of
conservative treatment? Spine (Phila Pa 1976) 2000;25:677–82.
33. Matsumoto M, Watanabe K, Tsuji T, et al. Risk factors for closure
of lamina after open-door laminoplasty. J Neurosurg Spine
2008;9:530–7.
34. Matz PG, Anderson PA, Holly LT, et al. The natural history of
cervical spondylotic myelopathy. J Neurosurg Spine 2009;11:104–
11.
35. Mikawa Y, Shikata J, Yamamuro T. Spinal deformity and
instability after multilevel cervical laminectomy. Spine (Phila Pa
1976) 1987;12:6–11.
36. Morishita Y, Naito M, Hymanson H, et al. The relationship
between the cervical spinal canal diameter and the pathological
changes in the cervical spine. Eur Spine J 2009;18:877–83.
37. Muhle C, Weinert D, Falliner A, et al. Dynamic changes of the
spinal canal in patients with cervical spondylosis at flexion and
extension using magnetic resonance imaging. Invest Radiol
1998;33:444–9.
38. Nurick S. The pathogenesis of the spinal cord disorder associated
with cervical spondylosis. Brain 1972;95:87–100.
39. Ogino H, Tada K, Okada K, et al. Canal diameter, anteroposterior
compression ratio, and spondylotic myelopathy of the cervical
spine. Spine (Phila Pa 1976) 1983;8:1–15.
40. Ohnari H, Sasai K, Akagi S, et al. Investigation of axial
symptoms after cervical laminoplasty, using questionnaire survey.
Spine J 2006;6:221–7.
41. Oshima Y TK, Seichi A, Morii J, Chikuda H, Kawaguchi H,
Nakaura K. Natural Course and Prognostic Factors for Mild
Cervical Spondylotic Myelopathy. Cervical Spine Research
Society 2010;38th Annual Meeting:83.
HSSJ (2011) 7: 170–178 177

42. Pavlov H, Torg JS, Robie B, et al. Cervical spinal stenosis: determination
with vertebral body ratio method. Radiology 1987;164:771–5.
43. Payne EE, Spillane JD. The cervical spine; an anatomico-patho-
logical study of 70 specimens (using a special technique) with
particular reference to the problem of cervical spondylosis. Brain
1957;80:571–96.
44. Porchet F, Metcalf NH. Clinical outcomes with the Prestige II
cervical disc: preliminary results from a prospective randomized
clinical trial. Neurosurg Focus 2004;17:E6.
45. Regan CM DGD, Lim MR. Cervical Spine Research Society, 38th
Annual Meeting. Paper # 60 2010:199.
46. Riew KD, Buchowski JM, Sasso R, et al. Cervical disc
arthroplasty compared with arthrodesis for the treatment of
myelopathy. J Bone Joint Surg Am 2008;90:2354–64.
47. Roberts A. Myelopathy due to cervical spondylosios treated by
collar immobilization. Neurology 1966;16:951–4.
48. Robertson JT, Papadopoulos SM, Traynelis VC. Assessment of
adjacent-segment disease in patients treated with cervical fusion or ar-
throplasty: a prospective 2-year study. J Neurosurg Spine 2005;3:417–23.
49. Sadasivan KK, Reddy RP, Albright JA. The natural history of
cervical spondylotic myelopathy. Yale J Biol Med 1993;66:235–42.
50. Sekhon LH. Two-level artificial disc placement for spondy-
lotic cervical myelopathy. J Clin Neurosci 2004;11:412–5.
51. Sekhon LH. Cervical arthroplasty in the management of
spondylotic myelopathy: 18-month results. Neurosurg Focus
2004;17:E8.
52. Shin JJ. Intramedullary high signal intensity and neurological
status as prognostic factors in cervical spondylotic myelopathy.
Acta Neurochir (Wien) 2010;152(10):1687–94.
53. Smith MD, Emery SE, Dudley A, et al. Vertebral artery injury
during anterior decompression of the cervical spine. A retro-
spective review of ten patients. J Bone Joint Surg Br
1993;75:410–5.
54. Stark RJ, Kennard C, Swash M. Hand wasting in spondylotic high
cord compression: an electromyographic study. Ann Neurol
1981;9:58–62.
55. Wolf BS, Khilnani M, Malis L. The sagittal diameter of the bony
cervical spinal canal and its significance in cervical spondylosis. J
Mt Sinai Hosp N Y 1956;23:283–92.
56. Yonenobu K, Hosono N, Iwasaki M, et al. Neurologic complica-
tions of surgery for cervical compression myelopathy. Spine
(Phila Pa 1976) 1991;16:1277–82.
178 HSSJ (2011) 7: 170–178