30

CHAPTER

Degenerative Spine Disease

James K.C. Liu, Edward C. Benzel

CLINICAL PEARLS

l D
 egeneration in the spine is a naturally occurring process
that can be understood through the “three-joint complex,”
which is composed of the intervertebral disk and the two
dorsal articulating joints. Degeneration of any one joint
leads to degeneration of the other two, initiating a cascade
that leads to spinal degenerative disease.
l A
 detailed history and neurological examination can be
used to isolate the level at which the underlying disease
originate. Understanding the presenting symptoms can
help to understand the degree of degeneration present
and then start to formulate the most efficient treatment
plan.
l C
 onservative treatment is a feasible first course of action to
treat the clinical manifestations of first-onset degenerative
spine disease. The most commonly accepted modalities
range from anti-inflammatory therapy to exercises designed
to increase muscle strength and relieve joint loading.  
l S urgical intervention to treat symptoms that result
from degenerative spine disease include diskectomy,
­laminectomy, and fusion procedures. Despite continuing
controversy surrounding which procedure is most effective
in providing long-term relief, the authors believe that
the best course is to understand the underlying disease
and select the least invasive procedure to target that
pathological area.
l F usion remains a heavily debated topic. Multiple studies
have been performed to evaluate the benefits of fusion in
the spine, none of which have provided definitive class I
­evidence to indicate a clear benefit. However, in addition
to the class II and III evidence showing some benefit in
selected patients, spine fusions may be indicated based
on the need to create stability in an unstable region of the
spine.
 

Back pain is the one of the most common reasons for primary
care physician outpatient visits in the United States. A survey
performed in 2002 reported that approximately 26% of
Americans had low back pain and 14% had neck pain.1 In
2002, 890 million office visits were due to back pain. As may
be expected from these statistics, the cost associated with the
diagnosis and treatment of spine-related problems is astro-
nomical. The Journal of the American Medical Association
reported $86 billion in health expenditures in 2005 devoted to
spine-related problems. This amount was an increase of 65%
from 1997.2
The process that leads to the development of neck and
back pain can be segmented and categorized into acquired
and congenital/developmental processes. This chapter focuses
on the naturally occurring events that lead to degeneration of
the spine.
ANATOMY AND PHYSIOLOGY
OF SPINE DEGENERATION
Three-Joint Complex
An understanding of the process of spinal aging involves an
understanding of the relevant anatomy of the affected spine.
In order to understand the sequence of events that leads to
degeneration of the spine, efforts have been made to decon-
struct the spine in order to demonstrate the nature of the
degenerative process, for such a process begins in one segment
of the spine and then spreads to adjacent segments.
The Kirkaldy-Willis three-joint complex theory decon-
structs the spine into three joints that are affected in the
degenerative process. At each level of the spine there exists the
“three-joint complex,” composed of the intervertebral disk

487
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488   PART 5  Spine
Superior
vertebral notch
Intervertebral
Facet joint disk
Ligamentum
flavum
Intervertebral
foramen
Inferior vertebral notch
FIGURE 30-1  Three-joint complex. Each motion segment is com-
posed of a three-joint complex, which consists of one intervertebral
disk space and two dorsal zygapophyseal joints. Degeneration in
one of these joints often leads to accelerated degeneration in the
adjacent joints. This results in a relatively predictable progression
of degeneration.
and two dorsal zygapophyseal joints.3 Kirkaldy-Willis pro-
posed that the three joints are linked, in that degeneration of
one joint leads to degeneration of the other two joints, and
ultimately results in the global manifestations of degenerative
spine disease (Fig. 30.1).
Degeneration, as stated, typically begins in one joint. This,
in and of itself, may lead to clinical manifestations. It, how-
ever, is the interplay of the three-joint complex as a whole
that leads to degenerative disease, as it typically presents in
the clinical setting. The three-joint complex is first examined
individually here, and then a discussion of the interaction of
pathological changes that lead to spinal stenosis follows.
Disk Degeneration
The intervertebral disk has three components: the nucleus
pulposus, which is surrounded by the annulus fibrosis, and
the cartilaginous end plates.4 The nucleus pulposus is a semi-
gelatinous structure situated near the center of the disk com-
plex. It is a remnant of the notochord and is composed mainly
of mucopolysaccharides with salt and water. The surround-
ing annulus fibrosis is a multilayered circular structure that
surrounds the nucleus pulposus. It is composed of fibrocarti-
laginous lamellae and is stiffer than the nucleus. It is usually
thicker ventrally than dorsally.4
The process of disk degeneration is a part of the natural
aging process. Repetitive loading results in forces that foster
degeneration. As part of the normal aging process, the inter-
vertebral disk becomes desiccated as collagen and proteo-
glycans are replaced with fibrous tissue. As axial pressure
continues to be repetitively applied to the disk, the less com-
pliant annulus fibrosis develops circumferential tears that are
most frequently observed in the dorsolateral aspect of the
annulus.5 These tears can enlarge and eventually develop into
radial tears. These tears are areas through which the nucleus
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pulposus may herniate. Since the nucleus pulposus is situated
relatively dorsal in the disk space, herniation typically occurs
dorsally into the spinal canal. The presence of the posterior
longitudinal ligament forces disk herniations laterally. The
aforementioned anatomical and biomechanical factors often
lead to the common classical dorsolateral disk herniation.
Annular tears also lead to a weakening of the annulus
fibrosus and to circumferential bulging of the annulus, which
in turn results in a loss of disk height. Disk bulging can lead to
osteophyte formation at the attachment of the annulus to the
vertebral body. This contributes to narrowing of the central
canal, as well as the neural foramen.
Dorsal Joint Degeneration
The dorsal aspect of the intervertebral joint is composed of
articulating facets from the superior and inferior vertebral
segments. The joints are diarthrodial joints with articular
cartilage, a synovial membrane, and a capsule.6 Studies have
shown that natural aging of the dorsal joints passes through
a progression that includes synovial reaction, fibrillation of
the articular cartilage, osteophyte formation, and ultimately,
laxity of the joint capsule. This inevitably results in instability
of the joint complex and can lead to subluxation of the joint.
Osteophytic formation from the joint protruding into the spi-
nal canal can also contribute to stenosis, particularly in the
lateral recesses of the spinal canal.
Combined Three-Joint Complex Degeneration
The three-joint complex degeneration concept implies that
the individual aging process of the intervertebral disk and
dorsal facet joints are interlaced to contribute to the clinical
manifestation of spondylosis. As disk degeneration occurs,
loss of disk height contributes to subluxation of the dorsal
joints. The instability caused by the loss of disk height com-
pounds the natural process of facet joint degeneration, which
includes capsular laxity. Eventually, subluxation of the dor-
sal joints can occur. This results in subluxation of the rostral
vertebral body ventrally with respect to the caudal vertebral
body (spondylolisthesis). Such translation of the vertebral seg-
ments can result in further narrowing of the neural foramina,
manifesting as lateral nerve root entrapment. Lateral nerve
root entrapment can also result from loss of disk height. Disk
resorption reduces the rostral-caudal dimension of the neural
foramina, thus further contributing to this presentation.
Three Stages of Degenerative Spine Disease
Using the three-joint complex as a basis for degenerative spine
disease, Kirkaldy-Willis categorized the degeneration of the
spine into three stages to rationalize the natural history of
spine degeneration, as well as to provide an algorithm to tailor
treatment for each stage (Fig. 30.2).
The Dysfunction Stage
The first stage is that of dysfunction. The clinical manifes-
tations both clinically and physiologically are minor at this
stage. This stage is characterized by synovial reaction in
the dorsal joints and small tears in the intervertebral disks.

THREE JOINT COMPLEX DEGENERATION
Dysfunction Disk hernation Diskectomy
Abnormal motion Laminectomy
De-stabilization
spondylolisthesis with fusion
Canal stenosis
Laminectomy +/–
Re-stabilization Lateral recess
fusion
stenosis
FIGURE 30.2  The three stages of degenerative spine disease. The
first stage is dysfunction, which results primarily in simple disk her-
niations, often necessitating a surgical diskectomy. Progression of
the degenerative process results in destabilization and abnormal
spinal motion. This may necessitate the performance of a fusion
procedure to stabilize the spine. The most advanced stage of
degeneration is that of restabilization. The spine become more sta-
ble due to osteophyte formation, but in doing so creates a central
and lateral recess stenosis, which often necessitates decompres-
sion, with or without a supplemental fusion. Red arrows designate
the most likely surgical strategy for each phase of the degenerative
process.
Clinical symptoms present at this stage are typically minor or
absent and are best treated conservatively.
The Destabilization Stage
The second stage is the destabilization stage or rather the stage
of instability. Kirkaldy-Willis defines this stage as being asso-
ciated with greater degeneration in the three-joint complex,
manifesting as laxity and subluxation in the dorsal joints and
progressive disk degeneration. As its name implies, this stage
is characterized by abnormal spinal motion. As segmental
degeneration continues, the natural mobility of the spine is
gradually lost. This is further compounded by advanced disk
degeneration and loss of disk height, which can lead to spon-
dylolisthesis. This creates a dysfunctional mechanical envi-
ronment in the region of the motion segment, hence the term
dysfunctional motion segment. Treatment options for spondy-
lolisthesis include core strengthening and flexibility programs
that are designed to stabilize or normalize the dysfunctional
motion segment and strategies that are designed to immobi-
lize the spine (dysfunctional motion segment), with or without
restoration of the intervertebral height, and fusion of abnor-
mal motion segments.
The Restabilization Stage
The third stage is restabilization. In this, the most advanced
stage of degeneration as defined by Kirkaldy-Willis, spine
instability is actually reduced via osteophyte formation sec-
ondary to a prior increased joint laxity and loss of disk inter-
space height. Clinically, resolution of symptoms can occur
due to a gradually decreased spinal motion. The instability
observed during the destabilization stage can be replaced by
radiculopathy from spinal nerve entrapment or claudication
symptoms from central canal and lateral recess stenosis.
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CHAPTER 30  Degenerative Spine Disease   489
CLINICAL PRESENTATION
The manifestation of clinical symptoms depends upon the type
and degree of ongoing degeneration. A careful history and
clinical examination enables the examiner to determine the
stage of degeneration and the underlying disease. Determin-
ing the fundamental disease process facilitates the formulation
of a focused plan of treatment, without the performance of
unnecessary surgical intervention, to prevent advanced symp-
tomatic segmental degeneration.
The first stage of degeneration as described by Kirkaldy-
Willis, dysfunction, is characterized in the disk joint by annu-
lar tears and herniation of the nucleus pulposus. This leads
to intervertebral disk herniation, one of the most common
reasons for back pain, leg pain, and spine surgery. Disk her-
niation typically occurs in the dorsolateral aspect of the disk
interspace. The strength of the posterior longitudinal ligament
causes a paramedian migration and herniation of the nuclear
material, which may result in impingement of a single nerve
root, causing pain known as radiculopathy. Compression of
the nerve root typically manifests as pain, but can also result
in numbness or weakness in the distribution of the affected
nerve root.
With cervical spine involvement, the patient often com-
plains of a shooting pain that travels from the shoulder to the
fingers. The exact location of the shooting pain can help to
isolate the level of the disk herniation. Cervical disk hernia-
tions most often occur at the C5-C6 and C6-C7 levels.7 In the
lumbar spine disk herniations most commonly occur at the
L4-L5 interspace8 and manifest as shooting pain that often
begins in the buttock region and passes down the legs, with or
without extension into the feet. Once again, the distribution
can help to localize the level of herniation. Thoracic disk her-
nations are much less common than cervical or lumbar disk
herniations. In a study of 82 patients with thoracic disk her-
niations, 76% of the presenting complaints consisted of pain.
Of the patient who presented with pain, 41% presented with
localized back pain, thus relegating surgical management to
the “precarious” category in most clinical cases.9
Further degeneration, resulting in further diffuse disk bulg-
ing into the spinal canal, combined with osteophyte formation
from dorsal joint laxity and inflammation of the ligamentum
flavum, can lead to circumferential spinal canal narrowing
manifesting as neurogenic claudication. Neurogenic claudica-
tion manifests as pain that is exacerbated by walking or stand-
ing, and relieved with postural changes that allow increasing
the diameter of the spinal canal or neural foramina. The
affected patient often reports that pain is relieved when in the
sitting position. Also, patients report that walking while lean-
ing forward, often supporting their weight while pushing a
shopping cart, allows for relief of back pain (“shopping cart
sign”). An important distinction must be made between neu-
rogenic claudication and vascular claudication. Vascular clau-
dication is a result of vascular insufficiency and manifests as
leg pain with motion that is relieved by rest. It is important to
properly assess the vascular supply by inspecting distal pedal
pulses in order to differentiate between the two entities. In
addition, other clinical observations may be used to differ-
entiate the two diagnoses. For example, pushing a shopping
cart (i.e., “shopping cart sign”) does not relieve vascular clau-
dication symptoms. Other manifestations of vascular disease
490   PART 5  Spine
A B
should be sought as well, including loss of foot/toe hair, skin
discoloration, and a clinical history of other disorders and risk
factors associated with ischemic vascular disease.
The degenerative process advances in the destabilization
stage and involves laxity of the dorsal joints, which, in turn,
leads to joint subluxation. This subluxation, combined with
advanced disk degeneration resulting in disk desiccation and
narrowing of the intervertebral space, can lead to slippage of
one vertebral body relative to another, or spondylolisthesis.
Spondylolisthesis manifests as instability of the joints, which,
in turn, leads to abnormal or dysfunctional motion. The result
of this process can eventually lead to mechanical back pain.
Mechanical back pain is defined as pain that results from activ-
ity and is relieved with rest. This pain is attributed to joint
instability and abnormal motion of one vertebral body upon
another, which can be the result of the degenerative changes
described previously but can also result from traumatic or
congenital causes. The treatment for mechanical back pain
includes restoration of stability to the segment through fusion
and fixation.
DIAGNOSTIC FINDINGS
The initial evaluation of back and leg pain begins with static
plain radiographs (Fig. 30.3). Static radiographs provide an
evaluation of spinal alignment and the intervertebral disk
spaces. An assessment of an affected intervertebral space serves
to provide a rough estimation of the extent of disk degenera-
tion, and therefore desiccation, that is present at a given level.
Static radiographs consisting of flexion and extension views of
the cervical or lumbar spine can reveal loss of normal align-
ment during motion. Such may be indicative of dorsal, or even
ventral, joint instability.
Computed tomography (CT) provides a very useful evalu-
ation of the bony anatomy (Fig. 30.4). CT is effective in
evaluating for bony osteophytes, presence of calcification,
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FIGURE 30.3  Lateral (A) and antero-
posterior (B) plain radiograph views
of the lumbar spine. Plain radio-
graphs are effective in evaluating
for alignment of the spine in both
the sagittal and coronal orienta-
tion. The intervertebral height (A) is
an indication of degenerative disk
disease.
and dimensions of bony architecture that may be required for
surgical planning. CT myelography is an effective alternative
to assess the neural elements when magnetic resonance imag-
ing (MRI) is either contraindicated (due to medical implants)
or would be less efficacious owing to artifact from previous
instrumentation. CT myelography can detect central as well
as foraminal stenosis.
MRI is widely considered the gold standard for the imag-
ing evaluation of spinal canal stenosis (Fig. 30.5). MRI can
most effectively visualize the soft tissues surrounding the
spinal canal, as well as the intervertebral disks, ligamentum
flavum, and facet joints. In degenerative spine disease, the
location of disk herniation can be evaluated. The origin of the
spinal canal stenosis, whether from the intervertebral disks,
hypertrophy of the posterior longitudinal ligament or of the
ligamentum flavum, or facet hypertrophy, can be specifically
localized by MRI.
Diskography is a more invasive diagnostic strategy. At
times, when the clinical presentation does not match the find-
ings on the aforementioned routine imaging techniques, or
indeterminate findings on standard imaging modalities are
present, some feel that diskography may be used to identify
and characterize the disease. Diskography involves injecting
contrast material into the intervertebral disks in question. The
amount of contrast agent tolerated by a disk is an indication
of degeneration. A normal cervical disk may tolerate 0.2 to
0.5 mL of fluid, whereas a degenerated disk can accept 0.5 to
1.5 mL of fluid.10 If the pain produced following contrast
injection is concordant with the typical pain experienced by
the patient, the injected level is considered by some to be the
pathological segment. Disk pressure at which pain is elicited
is also used to predict the pathological level, because damaged
disks allegedly produce pain at lower pressures than normal
disks.11 The effectiveness of diskography to predict positive
surgical outcomes is controversial at best, with varying predic-
tive reliability. One of the greatest criticisms of diskography
is that the grading system employs a subjective criterion for
 CHAPTER 30  Degenerative Spine Disease   491

A B
FIGURE 30.4  Computed tomography (CT) of the cervical and lumbar spine. CT scans are effective for evaluating bony structure in the spine.
In the CT scan of the cervical spine (A), a single-level ventral fusion with plating has been performed. CT is more effective compared to
magnetic resonance imaging (MRI) for evaluating instrumentation due to the lack of artifact on CT imaging. Successful fusion can also
be effectively evaluated by CT imaging by observing whether the interbody graft is consistent with the vertebral bodies above and below.
Careful assessment of the bony anatomy is required when instrumentation is planned. Autofusion of the spine as seen in the lumbar spine
(B) at the L1-L2 level can be detected on CT and provides useful information prior to surgical intervention.

FIGURE 30.5  Severe lumbar spine

degenerative changes. The sag-
ittal view (A) magnetic resonance
imaging (MRI) displays multilevel
stenosis from anterior and pos-
terior disease as well as loss of
intervertebral disk height. Axial
view (B) shows facet hypertrophy
with edema in the facet joints
indicated by the hyperintensity.

A B

pain, and therefore can be skewed, depending on the patient
and the examiner. It is emphasized that diskography should be
used with the understanding that it does not provide clinically
proven diagnostic utility.
TREATMENT OPTIONS
Nonoperative Management
Conservative management plays a significant role in the man-
agement of degenerative spine disease. Studies of the natu-
ral course of spinal stenosis have shown that up to 47% of
patients with symptoms of lumbar spinal stenosis, including
neurogenic claudication and radiculopathy, had improvement
of symptoms without any intervention.12 Although the physi-
ology of spontaneous improvement of symptoms of spinal
stenosis is unclear, it has been postulated that progressive disk
dehydration may lead to shrinking of the disk and a decrease
in nerve root compression.13
Medical treatment of degenerative spine disease ranges
from symptomatic relief to reduction of inflammation. Nar-
cotics can be effective for controlling back or extremity pain,
but these drugs represent short-term resolutions, because they
only postpone the inevitable course of the degenerative dis-
ease, whether it is toward improvement or further worsening
of symptoms.
Nonsteroidal anti-inflammatory medications have been
shown to be effective in providing relief for acute back pain.14
Narcotic medication can be used to supplement those drugs
when there is more severe pain, but the effectiveness of nar-
cotics only serves to mask the degenerative process until it
progresses or improves spontaneously. Furthermore, nar-
cotic medications often contribute to the perpetuation of the

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492   PART 5  Spine
cyclical process leading to the development of a chronic pain
syndrome in patients who do not improve. Their use, there-
fore, should be very carefully considered.
Other medical treatments include muscle relaxants. Mus-
cle relaxants have shown benefit for the treatment of acute
neck and back pain.15 Systemic oral steroids have also been
utilized for the treatment of radicular pain. Some think that
the anti-inflammatory effects may reduce nerve root irritation,
although several studies have not demonstrated a proven clini-
cal effect.16-18
A critical tool for nonoperative management of degen-
erative spine disease is physical reconditioning, often via the
employment of a physical therapist. The goal associated with
the application of self-induced physical focuses in order to
strengthen core muscle groups is to help alleviate pathological
loading of the affected dysfunctional joints. Flexibility exer-
cises play an integral role as well. Improving segmental flexi-
bility at adjacent segments can diminish pain and help preserve
normal motion.
Epidural steroid injections (ESIs) have been shown to be
effective, particularly for radicular pain. The anti-inflammatory
effects of the steroids are likely to be effective against the che-
moinflammatory responses emanating from a herniated disk.
As expected from its mechanism of action, the effects of ESIs
are usually acute and, hence, short term in nature. Because
they do not alter the overall progression of the spine degenera-
tion, their temporary clinical benefits are limited, and there-
fore, they serve best when used to supplement the use of an
alternative conservative treatment, such as physical therapy.
Facet joint injections remain a controversial mode
of treatment for back pain. Injections are composed of a
long-acting local anesthetic, combined with steroids. Stud-
ies have reported no evidence of clinical improvement of
back pain,19 with only 33% of patients reporting greater
than a 50% relief of pain.20 This approximates results that
are consistent with the placebo effect. The key to the effi-
cacy of facet injections may reside in the proper selection of
patients with the so-called facet syndrome. Lippitt defined
the manifestations of the facet syndrome as “pain in the
hips and buttocks area, cramping thigh pain, and back stiff-
ness that is worse in the morning, without lower extremity
­paresthesias.” One of the alleged key signs associated with
the facet syndrome is the observation that the pain is exac-
erbated with lumbar spine extension.21 A factor that may
confound the efficacy of facet joint injections is the likeli-
hood that injected material may leak out of the facet joint.
This leaking may result in direct nerve root block or diffu-
sion of anesthetic material into the paraspinous soft tissues.
Such “leakage” would obviously skew outcomes. Neverthe-
less, facet joint injection persists as a popular therapeutic
and diagnostic modality.
One of the less understood therapies patients have often
attempted prior to their presentation to a spine specialist is
spinal manipulative therapy (SMT). SMT is primarily pro-
vided by chiropractors, but can also be administered by physi-
cal therapists and osteopathic physicians. Manipulation can
be categorized into three main types of therapies: therapeutic
massage, mobilization, and manipulative procedures. These
manipulation techniques range from the application of pres-
sure isolated to the paraspinal musculature to maneuvers that
stress the spinal joints and ligaments. The therapeutic benefit
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of SMT stems from the hypothesis that neck or back pain is
caused by either a limited range of motion or abnormal dorsal
intervertebral joint motion. A natural joint motion consists
of an active range of motion, followed by a passive range of
motion that can be reached with external mobilization. A dys-
functional joint leads to pain because it is unable to reach the
entire range of motion. SMT “resets” the joint by extending
the joint beyond the passive range of motion, into the “para-
physiological range of motion.” This stresses the joint to its
limit, just short of joint disruption. At this point, joint cavita-
tion occurs, and the often encountered sounds of joint mobili-
zation, which are likely the result of gas released into the joint
space,22 occur. The effectiveness of spinal manipulation has
been questioned, and definitive clinical studies that show sig-
nificant long-term improvement are lacking. Clinical evidence
indicates that there may be short-term relief for the manage-
ment of low back pain, but there is no evidence of significance
that demonstrates efficacy.23 One of the difficulties associated
with assessing the effectiveness of SMT is related to the fact
that there exists no universal treatment strategy—the types
and numbers of treatments administered vary most dramati-
cally across the board.
Operative Treatment
Surgical treatment options for degenerative spine disease
range widely in complexity and may correlate with the extent
of disease progression. Via the matching of the clinical evalu-
ation with imaging findings, the disease can be isolated and
the most appropriate nonsurgical or surgical approach chosen
and employed.
In the initial stage of spinal degeneration, disk desiccation
leads to predominantly dorsolateral disk herniations causing
radicular symptoms (Fig. 30.6). Single-level disk herniations
can be treated nonoperatively or with cervical or lumbar dis-
kectomy. The latter are relatively “simple” operations that are
associated with a relatively high degree of short-term success.
Long-term success is more variable.
More complex pathological processes may require surgical
decompression via laminectomy or surgical stabilization. The
options are myriad. The decision to fuse should not be taken
lightly, however. A failed instrumented lumbar fusion often
results in further surgery and chronic pain. Such patients are
very difficult to manage moving forward.
Diskectomy
Diskectomy procedures can be typically categorized into ven-
tral and dorsal approaches. In the cervical spine, the ventral
approach is often utilized because of its ability to decom-
press broad-based disk herniations. The ventral approach is
performed through a paramedian incision that requires little
muscle splitting, which leads to a relatively low amount of
postoperative pain and morbidity. The most commonly
encountered postoperative complication is dysphagia second-
ary to retraction of the esophagus, which has been shown
to occur in anywhere from 1% to 79% of cases following
anterior cervical procedures, but dramatically improves in the
majority of cases.24 The other main consideration of the ven-
tral cervical approach, and possibly a contraindication to the
approach, is damage to the recurrent laryngeal nerve resulting
 CHAPTER 30  Degenerative Spine Disease   493

FIGURE 30.6  Single-level disk her-

niation in the cervical (A) and lum-
bar spine (B).

A B

A B C
FIGURE 30.7  Sagittal magnetic resonance imaging (MRI) of the cervical spine (A) indicating multilevel stenosis primarly from disk herniations.
A three-level anterior diskectomy and fusion procedure was performed. Postoperative radiographs (B and C) show a three-level fusion with
ventral plating.

in vocal cord paralysis. This paralysis has also been shown to
improve with time in the majority of cases25 (Fig. 30.7).
The dorsal approach to the cervical spine has also been
shown to be effective in eliminating unilateral nerve root com-
pression. The technique is effective for eliminating postero-
lateral disk herniations either through foraminotomies with
or without a diskectomy procedure. The dorsal approach
eliminates the morbidity associated with the ventral approach,
mainly dysphagia, and risk to the ventral neurovascular struc-
tures, but requires muscle splitting, which can add a variable
amount of postoperative pain. Simple foraminotomies and
diskectomies also do not require fusion, theoretically decreas-
ing risk of adjacent segment degeneration. Minimally inva-
sive techniques have been developed to reduce the amount of
muscle dissection carried out and have shown to have up to a
97% success rate alleviating radiculopathy symptoms.26
Diskectomy procedures in the lumbar spine can also be
categorized into anterior and posterior approaches, although
unlike the cervical spine, the posterior approach is the more
often utilized. Lumbar diskectomies involve a unilateral
muscle dissection exposing the lamina of the given level to
allow a hemilaminectomy, through which the herniated disk
is removed. The Spine Patient Outcomes Research Trial
(SPORT) was a prospective, randomized trial that evaluated
lumbar diskectomies against nonoperative treatment.27 This
trial concluded that patients undergoing lumbar diskectomies
enjoyed reduction of pain, improvements in physical function-
ing, and a greater improvement in their disability index than
patients undergoing conservative treatment. Given the pres-
ence of the cauda equina in the lumbar region as opposed to
the spinal cord present in the cervical region, the posterior
approach is more versatile in the sense that even more cen-
tralized disk herniations can be decompressed owing to the
amount of manipulation that can be tolerated by the thecal
sac.
Laminectomy
Laminectomies decompress the spine via the removal of the
lamina and spinous process. Laminectomy can be applied
equally in the cervical, thoracic, and lumbar spine, typically
for multilevel reduction of spinal canal stenosis. In the cervi-
cal spine, multilevel laminectomy has been shown to be effec-
tive particularly for canal decompression resulting in cervical

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494   PART 5  Spine
A B
FIGURE 30.8  Multilevel cervical stenosis viewed on sagittal magnetic resonance imaging (MRI) (A). Laminectomies were performed from the
C3 to C6 levels and fused with lateral mass screws. Postoperative lateral and anteroposterior (AP) radiographs are shown (B and C).
spondolytic myelopathy, as well as for other pathological dis-
orders such as ossification of the posterior longitudinal liga-
ment. Although shown to be effective in improving signs of
myelopathy, the development of postoperative kyphosis has
been reported to be between 14% and 47%.28 This has led
to the use of cervical laminectomy combined with fusion and
laminoplasty. Although all three techniques have been shown
to be effective in decompressing the spinal canal, laminectomy
with fusion and laminoplasty have become more commonplace
owing to their reduced incidence of postoperative kyphosis.
Laminoplasty involves detachment of the lamina on only
one side by creating a trough, and thinning the lamina on
the contralateral side to allow for “hinging” at the attached
lamina site. This allows the detached lamina to be elevated
and secured using small bone grafts to maintain the decom-
pressed state. The preservation of the posterior elements has
been shown to effectively decompress the spinal canal without
the consequences of fusion such as loss of range of motion and
adjacent segment degeneration. In one study, laminoplasty
was shown to be associated with a 27% improvement in pre-
venting the incidence of postoperative kyphosis.29
Laminectomy in the lumbar spine is most common proce-
dure performed by spine and neurological surgeons. Laminec-
tomy alone in the lumbar spine is most effective for neurogenic
claudication resulting from spinal stenosis. Lumbar laminec-
tomy involves removal of the lamina as well as performing a
medial facetectomy to eliminate lateral recess stenosis.
Fusion
Fusion remains a heavily debated topic. Multiple studies have
been performed to evaluate the benefits of fusion in the spine,
none of which has provided definitive class I evidence to indi-
cate a clear benefit. The consideration to perform a fusion is
typically based on the need to create stability in an unstable
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C
region of the spine. In the cervical spine, fusion can be consid-
ered for ventral and dorsal approaches. A review of 13 class
II and III studies comparing the outcome of anterior cervical
diskectomies with and without fusion performed by Matz and
associates, demonstrated that there was no clinically signifi-
cant advantage of including fusion. Only two class III stud-
ies demonstrated that anterior cervical diskectomy alone had
a short length of hospital stay and operative time.30 Fusion
has become a commonplace procedure with cervical lami-
nectomies owing to the incidence of postoperative kyphosis
(Fig. 30.8). Although no class I or II evidence exists to sup-
port the use of cervical laminectomy with fusion, there is
class III evidence to indicate that fusion reduces postoperative
kyphosis.28,31,32
A great deal of controversy surrounds the indications
for fusion in the lumbar spine. The indication for fusion is
typically during the end of the second stage of the Kirkaldy-
Willis process, which is the phase of maximal destabilization.
Degeneration of the joint complexes and disk space leads to
excessive movement of one vertebral body upon another, cre-
ating mechanical back pain. The pain created is partially axial
pain caused by disk degeneration and abnormal joint motion
but can also have a radicular component due to foraminal
stenosis and nerve root entrapment during mobility. Lumbar
fusion can be used to augment the transition to the second
stage of spinal degeneration into the third stage, restabiliza-
tion. Fusion typically involves a laminectomy to decompress
the spinal canal and the lateral recess (Fig. 30.9). Autograft
bone is used either in the dorsolateral spaces or the interspaces
to facilitate bony fusion while the construct immobilizes the
spinal segment. There are no clear data to support the pre-
sumption that fusion results in better outcomes compared
to simple laminectomy alone. A multicenter trial is currently
underway to compare fusion with laminectomy alone for
grade I spondylolisthesis.33
 CHAPTER 30  Degenerative Spine Disease   495

FIGURE 30.9  Sagittal magnetic resonance imag-

ing (MRI) of the lumbar spine (A) showing a
grade I spondylolisthesis at the L4-L5 level. This
patient was treated with decompression fusion
at those levels (B).

A B

SELECTED KEY REFERENCES
Ghogawala Z. Spinal laminectomy vs. instrumented pedicle screw
fusion. Available at http://www.spine-slip-study.org/2.
Johnsson KE, Rosen I, Uden A. The natural course of lumbar spi-
nal stenosis. Clin Orthop Relat Res. 1992;279:82-86.
Ritchie JH, Fahrni WH. Age changes in lumbar intervertebral
discs. Can J Surg. 1970;13(1):65-71.
Weinstein JN, Lurie JD, Tosteson TD, et al. Surgical versus non-
operative treatment for lumbar spinal stenosis: four-year
results of the spine patient outcomes research trial. Spine.
2010;35(14):1329-1338.
Yong-Hing K, Kirkaldy-Willis WH. The pathophysiology of
degenerative disease of the lumbar spine. Orthop Clin North
Am. 1983;14(3):491-504.
Please go to expertconsult.com to view the complete list of
references.

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Para uso personal exclusivamente. No se permiten otros usos sin autorización. Copyright ©2017. Elsevier Inc. Todos los derechos reservados.