62

CH A P T ER

Spinal Stenosis: Pathophysiology, Clinical

Diagnosis, and Differential Diagnosis
Chetan K. Patel, MD
Eeric Truumees, MD

Spinal stenosis is one of the most common conditions in the

elderly. It is defined as a narrowing of the spinal canal. The
term stenosis is derived from the Greek word for narrow,
which is stenos. The first description of this condition is
attributed to Antoine Portal in 1803. Verbiest1-10 is credited
with coining the term spinal stenosis and the associated narrowing of the spinal canal as its potential cause. KirkaldyWillis11-15 subsequently described the degenerative cascade in
the lumbar spine as the cause for the altered anatomy and
pathophysiology in spinal stenosis.
Narrowing in the spine can occur in the central canal,
lateral recess, or foramen, leading to compression of the neural
elements in those locations. The symptoms produced vary by
the location of the neural compression. Neural compression
in the central canal leads to the commonly seen clinical presentation of low back pain radiating into bilateral legs. Patients
typically also describe heaviness and weakness in their legs
that worsens with ambulation and improves with leaning
forward or resting. Degeneration of the spine with aging leads
to alteration in the anatomy causing gradually progressive narrowing of the spinal canal.
The term spinal stenosis refers to an anatomic diagnosis that
increases with age and can occur in asymptomatic individuals.16,17 The exact reason for why some with this condition have
debilitating symptoms while others have no symptoms is not
well understood. These differences in presentation may be
related to the different abilities of individuals to compensate
for the anatomic changes that have occurred. When symptoms
do present, they usually occur on the basis of the location of
neural compression. Patients with central canal stenosis typically present with neurogenic claudication, whereas those
with lateral recess and foraminal stenosis present with radicular pain. Patients with significant symptoms that do not
respond to conservative treatment often elect surgical treatment. In fact, in adults older than 65, spinal stenosis is the
most common reason to undergo lumbar spine surgery.18,19

Anatomy
In order to understand how spinal stenosis causes symptoms,
we must first have a good understanding of the normal

anatomy of the lumbar spine. The spinal canals anterior

border is formed by the vertebral body, the disc, and the posterior longitudinal ligament. The lateral border is formed by
the pedicles, the lateral ligamentum flavum, and the neural
foramen. The posterior border is formed by the facet joints,
lamina, and ligamentum flavum. The shape of the spinal canal
may be circular, oval, or trefoil (Fig. 621). The circular and
oval canal shapes provide the most space for the neural elements centrally and in the lateral recess. The trefoil canal has
the smallest cross-sectional area.20 It is present in 15% of the
individuals and predisposes these individuals to lateral recess
stenosis.

Disc
Disc degeneration is believed to be the first step in degeneration of the spine. At birth, the nucleus pulposus and the
annulus occupy roughly 50% of the disc area. The nucleus is
gelatinous and there is a discrete boundary between the
nucleus and the annulus. Over time the collagen content
increases and the demarcation between the nucleus and the
annulus becomes less distinct. Other structures within the disc
also change with aging. The chondroitin sulfate concentration
decreases, and the ratio of keratin sulfate to chondroitin sulfate
increases. Because keratin sulfate has less hydrophilic potential, the disc dehydrates over time.
Hydration of the disc also changes due to an alteration in
the type of collagen within the disc over time. The annulus
contains 60% type II and 40% type I collagen, whereas the disc
contains mainly type II collagen. Type I collagen is associated
with decreased water content compared with type II collagen.
Thus as the type I collagen content increases with age, hydration of the disc decreases. The normal nucleus pulposus typically consists of 85% water, whereas the annulus consists of
78% water. With degeneration of the disc, the water content
drops to roughly 70%. A desiccated disc has a decreased ability
to handle mechanical load.
The Kirkaldy-Willis21 theory explains how these changes
progress over time. This theory is based on viewing the spine
as a tripod with the disc and the two facet joints making up
the three legs. This analogy makes it easier to understand how
alteration in one joint can alter the others. The initial stage in

1064
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62 Spinal Stenosis: Pathophysiology, Clinical Diagnosis, and Differential Diagnosis 1065

SECTION

FIGURE 621 The three typical shapes of the spinal canal:

Trefoil canals have the smallest cross-sectional area. (From
Hilibrand AS, Rand N: Degenerative lumbar stenosis: Diagnosis
and management. J Am Assoc Orthop Surg 7:239-248, 1999.)

IX
Round

Ovoid

Trefoil

the degenerative cascade is circumferential tearing of the

annulus, which progresses to radial tears. This, along with the
biochemical changes in the disc described previously, leads to
further degeneration of the disc and disc height loss. Altered
disc structure and disc height loss lead to bulging of the disc
and the posterior longitudinal ligament. This causes narrowing of the spinal canal and potential neural impingement. The
lost disc height also leads to buckling of the ligamentum
flavum and settling of the facet joints. The facet joints subsequently deteriorate and form osteophytes, which further
narrows the spinal canal. The altered structure, motion, and
biomechanics then lead to additional disc deterioration, which
propagates the cycle of degeneration.

Facet Joints
The lumbar facet joints are encapsulated structures that have a
uniform cartilaginous surface to produce a smooth gliding
motion. The superior articular process is concave and its articular surface faces medially and dorsally. The inferior articular
process is convex and its articular surface faces laterally and
ventrally. Lumbar facet joints are oriented 90 degrees in the
sagittal plane and 45 degrees anterior in the coronal plane.
Studies show that more sagittally oriented facet joints are associated with a degenerative spondylolisthesis. The two facet
joints are usually symmetric with respect to their joint angles
at each level. Facet tropism refers to an asymmetry between the
facet joints and has been theorized to lead to degeneration.
As the disc degenerates and narrows, the facet joints settle
and increased stress is placed across the facet joint. This leads
to facet joint degeneration, hypertrophy, and osteophyte formation. These osteophytes can cause impingement of the
thecal sac within the spinal canal or the nerve root in the
neural foramen.

Intervertebral Foramen
The anterior boundary of the intervertebral foramen is made
up of the posterior wall of the vertebral body and the disc. The

posterior boundary is made up of the lateral aspect of the facet

joint and the ligamentum flavum. Superior and inferior
boundaries are formed by the pedicles of the vertebral bodies
corresponding to that segment. The foramen is typically larger
than the ganglion and the nerve that it contains. The additional space is occupied by fat and loose areolar tissue that can
accommodate for motion. With degeneration, hypertrophy of
the facets can cause posterior compression of the neural elements (Fig. 622). Anterior compression of the neural elements usually arises from endplate osteophytes or foraminal
disc herniations. Decrease in disc height with degeneration
can cause a decrease in the foraminal height and neural compression. This type of vertical or up-down foraminal stenosis
is important to recognize because a posterior decompression
alone may not significantly improve the vertical compression
and may result in persistent symptoms after surgery.

NR

LF
O

S
O

D
S

FIGURE 622 Sagittal cross section demonstrating disc desiccation (D),

endplate sclerosis (S), osteophyte formation (O), hypertrophy and buckling
of the ligamentum flavum (LF), and nerve root (NR) compromise within the
foramen. (From Gallego J, Schnuerer AP, Manuel C: Basic Anatomy and
Pathology of the Spine, Memphis, Medtronic Sofamor Danek, 2001;
photograph by Wolfgang Rauschning, MD, PhD.)

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1066 SPINAL STENOSIS

L4-L5
Posterior

Cauda Equina
The thecal sac lies in the spinal canal and gives rise to nerve
roots at each segment. The nerve root initially courses along
the medial aspect of the pedicle and then progresses laterally,
inferior to the pedicle in the neural foramen. The nerve roots
within the cauda equina are arranged in a predictable pattern
within the thecal sac (Fig. 623). Cross section of the thecal
sac demonstrates the most caudal roots to be present in a
central and posterior position. The more cephalad roots are
located sequentially more lateral and anterior. At each level,
the motor fibers of a root are anterior and medial to the larger
sensory component. Dorsal root ganglia exist at every level
and can be intraspinal or intraforaminal. A variety of clinical
presentations arise on the basis of the anatomic location of
neural compression.

S2-5 S2-5
S
M

S
M

S1

S1
S

S
M

L5

L5
S
M

S
M
Anterior
L5-S1
Posterior
S5
S4
S2-3 S
M
S
S1
M
S
M

S
M

S4
S
M

S2-3
S
M

S1
S
M

Anterior
FIGURE 623 Drawings showing neural organization within the thecal sac
at the L4-L5 and L5-S1 disc levels. M, motor components; S, sensory
components. (From Garfin SR, Herkowitz HN, Mirkovic S: Spinal stenosis:
Instructional course lecture. J Bone Joint Surg Am 81:572-586, 1999.)

L45

CE
F

F
LF

LF

FIGURE 624 Axial view cross section at the L4-5 disc level showing
advanced degenerative changes. Cauda equina (CE) compression is caused
by hypertrophic facets (F) and ligamentum flavum (LF) disc protrusion.
(From Gallego J, Schnuerer AP, Manuel C: Basic Anatomy and Pathology of
the Spine. Memphis, Medtronic Sofamor Danek, 2001; photograph by
Wolfgang Rauschning, MD, PhD.)

Classification
Stenosis can be anatomically classified as central, lateral recess,
and foraminal on the basis of the location of neural compression. With aging, central canal stenosis occurs as degenerative
changes progress. As the axial height of the disc and facet
joints decreases, the disc bulges into the spinal canal. The
central canal is further narrowed by posterior impingement
from enlarged facets and the hypertrophied ligamentum
flavum (Fig. 624). Hypertrophy of the soft tissues is responsible for 40% of spinal stenosis.22 With extension, the hypertrophied ligamentum buckles centrally into the canal and
worsens the central stenosis. This explains why patients with
stenosis typically report worsening of their symptoms in
extension.
Lateral recess stenosis typically results from posterior disc
protrusion in combination with some superior articular facet
hypertrophy. Lateral recess stenosis can present with lumbar
radiculopathy, and incidence of lateral recess stenosis ranges
from 8% to 11%.23-25 These patients present with pain or neurologic symptoms in a dermatomal distribution on the basis
of the nerve that is compressed in the lateral recess.
Foraminal stenosis causes compression of the exiting nerve
root and ganglion and also leads to lumbar radiculopathy.
Foraminal stenosis occurs most commonly in the lower
lumbar spine with the fifth lumbar nerve root being the most
commonly involved. Foraminal stenosis can occur from loss
of disc height, vertebral endplate osteophytes, facet osteophytes, spondylolisthesis, and disc herniations. Like central
canal stenosis, foraminal stenosis is worse in extension and
thus exacerbating and alleviating factors for symptoms from
foraminal compression are similar to those from central canal
stenosis.26
Spinal stenosis can also be classified on the basis of the
etiology, which can be congenital, acquired, or both.
Congenital stenosis is present as a normal variant in the population and is part of certain conditions such as dwarfism. In
these conditions, patients have short pedicles that are closer
together than the normal lumbar spine. In congenital stenosis,
few degenerative changes are sufficient to cause neural

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62 Spinal Stenosis: Pathophysiology, Clinical Diagnosis, and Differential Diagnosis 1067

BOX 621 Classification of spinal stenosis
I. Congenital/developmental
A. Idiopathic
B. Achondroplastic
C. Osteopetrosis

Deformity and Instability

The static changes that we discussed thus far can be worsened
by dynamic factors such as segmental instability. Instability
typically arises from degenerative changes and can be in the
form of translational or rotational abnormality. Translational
abnormality is found most commonly in women as a degenerative anterolisthesis of L4 on L5.27 The attachment of the
iliolumbar ligaments to the L5 level may act as a restraining
force and cause more relative motion at L4-5. The more sagittally oriented facet joints between the fourth and fifth lumbar
vertebrae can be an additional predisposing factor for instability at this level.28 Because the lamina and the spinous process
typically project inferior to the vertebral body, the amount of
room available between the inferior aspect of the L4 lamina
and the posterior superior aspect of L5 is substantially
decreased. This anterior translation of the L4 posterior elements, along with hypertrophy of the facets and the ligamentum flavum, leads to central and lateral recess stenosis.
Foraminal stenosis can also occur in this setting with collapse
of the disc space, disc herniation, endplate osteophytes, or
facet hypertrophy. With scoliosis, lateral subluxation and rotational instability can cause altered biomechanics that leads to
degeneration. The altered anatomy can also be a cause of narrowing of the central canal, lateral recess, and foraminal
regions. Degenerative changes superimposed on abnormal
anatomy lead to stenosis in these patients.

Pathophysiology
The term spinal stenosis describes the anatomic narrowing of
the spinal canal. How does spinal stenosis result in pain and
altered neurologic function? A number of cadaver and animal
studies have attempted to elucidate the mechanism of these
symptoms. Schonstorm evaluated the changes in nerve pressure that occur as the spinal canal narrows.29 In his human
cadaver study, the thecal sac constriction of 45% or more led
to an increased pressure in the nerve roots. As the degree of
compression increased, the pressure in the nerve roots
increased. Delamarter and colleagues30 also demonstrated the
importance of the magnitude of thecal sac compression in
alteration of neural function. They noted no alteration in neurologic function when the animals cauda equina was constricted by 25%, whereas more than 50% compression led to
motor or sensory deficits. Pedowitz and colleagues31 demonstrated that the duration of compression was also an important
factor in neural dysfunction.
Rydevik and colleagues32-37 demonstrated another effect of
compression of the thecal sac. They noted that once pressure
of more than 50mm Hg was achieved, capillary restriction

II. Acquired
A. Degenerative
1. Central
2. Lateral recess
3. Foraminal
B. Iatrogenic
1. Postlaminectomy
2. Adjacent to fusion
3. Malposition of hardware in the canal
4. Post-procedure epidural hematoma
C. Miscellaneous disorders
1. Acromegaly
2. Pagets
3. Fluorosis
4. Ankylosing spondylitis
D. Traumatic
III. Combined
Any combination of congenital/developmental or acquired stenosis

and electrophysiologic alteration occurred in the nerve roots.

Even at pressures as low as 5 to 10mm Hg, venous congestion
of the intraneural microcirculation occurred. Solute transport
decreased 45% across nerve root segments with the low pressure of 10mm Hg. This suggests that low-grade sustained
compression of the nerve roots could lead to vascular impairment and potential detrimental changes in the function of the
nerve roots. In addition to neural compression and altered
nutrition, inflammatory chemical mediators have also been
shown to be a cause of pain.38-43
The presence of stenosis increases with aging; however, it
often does not produce any symptoms. What causes pain in
some individual with mild spinal stenosis and no symptoms
in others with severe stenosis? The experimental evidence
reviewed earlier suggests that each individual may have an
innate ability to compensate for the accumulating pathologic
changes. Because the magnitude an individual can compensate for is different for different people, two individuals with
the same amount of stenosis may not exhibit the same symptoms. The rate at which these changes are occurring also
appears to be important. Individuals may become symptomatic with a lower magnitude of compression if it occurs rapidly.
This explains how a patient with stenosis can become symptomatic with an acute mild disc herniation.

Natural History
Patients with congenital stenosis typically become symptomatic earlier in life. Due to congenital narrowing of the canal in

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compression and symptoms. As one would expect, congenital

stenosis becomes symptomatic much earlier in life and patients
usually become symptomatic in the fourth decade. Acquired
stenosis can be caused by trauma, neoplasms, and infection,
along with other causes listed in Box 621.

IX

1068 SPINAL STENOSIS

these patients, significant stenosis is present at multiple levels

even with little degenerative change.44 Patients with degenerative stenosis present later in life during their 60s and have far
more advanced degeneration in their spine. Females are more
commonly affected with stenosis and the L4-5 level is the most
common segment involved.45
Multiple studies have looked at the short-term and longterm results of nonoperative treatment of patients with lumbar
stenosis.46-53 These studies show that a significant number of
patients respond favorably to nonoperative treatment. Some
patients, however, do not improve and some even worsen.
Johnsson and colleagues reviewed the results of 32 patients
who declined to have surgery at a 4-year follow-up period.54
They noted that 70% of patients were unchanged, while 15%
were the same and 15% worsened.
Recently, prospective studies have reported short-term and
long-term results of nonoperative and operative treatment.
The Maine Lumbar Spine prospective observational study
reported 8- to 10-year follow-up results on 97 patients.55 They
noted that a large number of patients (39%) that had initially
elected nonsurgical treatment subsequently elected to undergo
surgery. Of the patients who continued nonoperative treatment, most had stable symptoms. Miyamoto and colleagues
reported prospective results of nonsurgical treatment in 120
patients.56 Sixteen percent of the patients required surgical
treatment during the follow-up period of 5 years. Of the
nonsurgically treated patients, 53% of patients reported no
hindrance during the activities of daily living. No sudden
neurologic deterioration was reported. Roughly 23% of
patients had worsened but did not elect to undergo surgical
intervention.
The Finnish Lumbar Spinal Research Group reported the
results of a randomized controlled trial in 2007.57 They randomized 94 patients with mild to moderate stenosis into either
the surgical group or nonoperative group. At the 2-year
follow-up, patients noted improvement of symptoms in both
groups; however, the outcome of patients undergoing surgical
treatment was significantly better. The most recent prospective
study to evaluate patients with lumbar stenosis is the SPORT
study.58 This study reported prospective outcomes of 634
patients at 2-year follow-up. Patients undergoing surgical
treatment had better outcomes than those who underwent
nonsurgical treatment. Patients in the nonsurgical treatment
group showed small improvements in most outcome measures. It should be noted that no disastrous neurologic deterioration was noted with nonoperative treatment.
The recently published North American Spine Society
evidence-based guidelines for diagnosis and treatment of
lumbar stenosis provide some tangible conclusions from these
studies.59 They state that in one third to one half of patients
with mild to moderate stenosis, the natural history is favorable. Unfortunately, predicting which patients with stenosis
will worsen over time is impossible. In some studies symptomatic patients with severe stenosis did poorly over time, but
overall there is not sufficient evidence to draw any conclusions. What is known is that rapid or catastrophic deterioration is rare in patients with spinal stenosis. Knowing this can
be helpful in guiding treatment and evaluating these patients.

When a patient with spinal stenosis has rapidly worsening

neurologic status, other causes of neurologic dysfunction
should be investigated.

Clinical Presentation
Patients with lumbar spinal stenosis most commonly present
with leg pain.22 This leg pain presents as either neurogenic
claudication or radicular leg pain. Patients with neurogenic
claudication report a feeling of pain, heaviness, numbness,
cramping, burning, or weakness. The symptoms typically start
from the back or the buttocks and bilaterally radiate down
below the knees. One lower extremity may be worse than the
other; however, both legs are typically involved. Symptoms
usually do not follow a dermatomal pattern and are usually
related to activities. These abnormal sensations are typically
worse with extension of the lumbar spine during walking or
standing for a prolonged time. Some report worsening weakness if they keep walking. They may note ankle dorsiflexion
weakness that is typically described as feet slapping or even
falling as they attempt to keep walking. Walking downhill is
more challenging for these patients as the lumbar spine is
extended while going downhill. Most describe a set distance
they can walk before the symptoms become disabling. As the
stenosis worsens, this distance typically decreases, further disrupting the daily life and function of these patients. Relief of
symptoms typically comes from flexing the lumbar spine by
leaning forward, sitting, or lying down. As discussed earlier,
the degree of stenosis decreases as the lumbar spine is flexed
and patients naturally learn to position themselves in a posture
that minimizes discomfort and maximizes function. Keeping
this in mind, it is easy to understand why these patients typically lean forward on a grocery cart and have an easier time
riding a bike, walking uphill, or driving while sitting in a car.
In contrast to neurogenic claudication arising from compression of the thecal sac, radicular pain arises from compression of a particular nerve root in the lateral recess or the neural
foramen. Unlike claudication, radicular leg pain is described
by the patients in a specific dermatomal pattern corresponding to the compressed nerve root. The most common presentation of this is L5 radiculopathy from lateral recess stenosis
causing compression of the L5 nerve root. In addition to
numbness in the L5 distribution, weakness can be seen in
extensor hallucis longus and tibialis anterior muscle groups.
Low back pain is also a common complaint in patients with
stenosis. Although most patients note the radiation of this
pain into their legs, some present without leg pain or note
radiation of the pain only into their buttocks. Exacerbating
and alleviating factors for claudicatory low back pain are
similar to those for the leg pain. Spondylotic change with or
without spondylolisthesis is a common finding in this patient
population and often the cause for low back pain. Patients
with symptoms in both the low back and leg have a greater
disability than those who have symptoms only in one
location.60
Severe neurologic symptoms such as bowel and bladder
incontinence or profound weakness are uncommon in patients

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62 Spinal Stenosis: Pathophysiology, Clinical Diagnosis, and Differential Diagnosis 1069

Group, 22% of patients had an L5 motor weakness and 19%

had a sensory deficit. Straight leg raise test was positive in 3%
of the patients. In the recent SPORT study, asymmetric reflexes
were noted in 26%, motor weakness was noted in 28%, and
sensory deficit was noted in 29%.
An important part of the physical examination must be
identifying other common causes of similar symptoms. The
neurologic examination should focus on eliciting signs that
would suggest other neurologic causes of the patients symptoms. Hyper-reflexia, clonus, and upgoing toes, along with
other upper motor neuron findings, can suggest the presence
of myelopathy from cord compression. Sensory disturbance in
a stocking distribution suggests the presence of neuropathy. A
general musculoskeletal examination must include assessing
the irritability and limitation of motion in the hips to rule out
hip pathology. Palpation of the greater trochanter and iliotibial
band can help detect pathology in these easily treated structures. Diminished peripheral pulses along with diminished
skin hair are important clues that the symptoms may be
coming from vascular claudication.

Diagnostic Studies
Radiography

Physical Examination
A good physical examination of patients with lumbar spinal
stenosis should start with observation. Often these patients
will be sitting flexed forward on a chair in the examination
room. While standing and ambulating, stenosis patients still
often flex their trunk forward to decrease their symptoms.
This may also be noticed when checking their range of motion
as a decrease in the active lumbar extension. Reproduction of
the patients usual symptoms by prolonged lumbar extension
can also be helpful in confirming the diagnosis. Neurologic
examination is often normal in spite of long-standing debilitating symptoms. Lateral recess stenosis is more commonly
responsible for neurologic changes.65 When motor weakness
or sensory deficit is present, it is most often in the L5 distribution. A frequent neurologic finding is an asymmetrical deep
tendon reflex at the patellar or Achilles tendon. A symmetric
decrease in the reflexes is more indicative of age-related
changes. Nerve root tension signs are usually not present.
Changes in neurologic examination may become more obvious
after stressing the patients neurologic system. This can be
accomplished by asking the patient to walk until he or she
experiences significant symptoms. Re-examination at this
point may reveal changes in motor, sensory, or reflex examination that were not detected before the stress.
It is useful to review physical examination findings found
in some studies to get a better idea of their frequency. Amundsen and colleagues66 prospectively evaluated the clinical and
radiographic features of 100 patients with symptomatic spinal
stenosis. They reported a motor weakness in 23% and sensory
deficit in 51%. In the 2007 randomized controlled trial of 94
stenosis patients from the Finnish Lumbar Spinal Research

The diagnostic testing of patients with spinal stenosis often

starts with plain radiographs. In addition to the anteroposterior and lateral radiographs, flexion and extension lateral
views should be considered. Most patients suspected of stenosis are elderly and thus likely demonstrate a variety of
spondylotic changes on the radiographs. Particular attention
should be paid to diagnosing scoliosis and spondylolisthesis
in addition to any dynamic instability that can be detected on
the flexion-extension views. If scoliosis is noted, long cassette
scoliosis films would be helpful in evaluating the full extent of
the deformity in both the coronal and sagittal planes. Narrowing of the neural foramen and inferred narrowing of the
spinal canal from the location and extent of degenerated
structures should be evaluated. Ossification of ligamentous
structures, ankylosis of the spine, erosion of the disc space, or
any abnormal appearance of the bony structures should be
assessed (Fig. 625). It should be kept in mind that even
severe degenerative changes can be seen in asymptomatic
patients.67

Computed Tomography with

and Without Myelography
Prior to the common availability of magnetic resonance
imaging (MRI), a computed tomography (CT) scan was the
study of choice for visualizing pathologic anatomy in the axial
plane. Because a significant portion of the stenosis comes from
soft tissue pathology, visualization of the soft tissues is the top
priority in axial imaging. A CT scan is a poor modality for
detailed analysis of the soft tissue pathology (Fig. 626). A
meta-analysis demonstrated that the sensitivity of a CT scan
in detecting spinal stenosis ranges from 70% to 100%.68

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with stenosis. Urinary dysfunction is a common complaint in

this elderly population and can be present in 50% to 80% of
patients.61,62 Because various causes of urinary dysfunction
such as preexisting stress incontinence, urinary tract infections, and prostatic hypertrophy are common in this population, a careful history can help exclude these common causes.
The factors more commonly noted in patients with neurogenic
bladder dysfunction are perianal sensory disturbance, longer
duration of symptoms, and higher mean residual volumes on
urodynamic studies.63
In addition to obtaining a history specific to the patients
pain and neurologic symptoms, it is important to obtain a
comprehensive medical history. A patients report of preexisting peripheral arterial occlusive disease, hip arthritis, multiple
sclerosis, or neuropathy would substantially alter what symptoms are attributed to the stenosis. Similarly, obtaining an
overall picture of the medical comorbidities and physiologic
condition will also shed light on the ability of the patient to
safely undergo any invasive procedures. Knowing the patients
other medical conditions can also help identify patients who
may be at risk for inferior outcomes. Cardiovascular comorbidities, depression, and disorders influencing walking ability
have all been noted to be preoperative predictors of poor
postoperative outcomes.64

IX

1070 SPINAL STENOSIS

L4
L4

FIGURE 625 Anteroposterior (AP) (A) and lateral (B) radiograph of a patient with progressively worsening right
lumbar radiculopathy. * denotes the degenerative changes noted in the form of disc height collapse, endplate
sclerosis, and osteophytes. On the AP radiograph, the right side of the superior and lateral walls of the vertebral body
are indistinct with collapse of the height of L4 on the right compared with the left. On the lateral radiograph,
radiolucency is present in the L4 body along with an indistinct anterior wall. After additional workup, this patient was
diagnosed with multiple myeloma in the L4 vertebral body.

Diagnostic utility of the CT scan can be improved by combining it with myelography.69,70 The dye injected in the cerebrospinal fluid (CSF) during a myelogram provides good
contrast between the thecal sac and the surrounding soft tissue
and bony pathology. Preoperative complete contrast block on

a CT-myelogram has been correlated with an improved surgical outcome.71 The invasiveness of the myelogram and the
radiation associated with the CT are the two biggest drawbacks of this diagnostic modality. Given these limitations,
patients who are unable to have an MRI, who have scoliosis, or
who have previous spinal instrumentation are the most likely
to undergo this study (Figs. 627 and 628). In cases where
MRI findings are unclear, a CT or a CT-myelogram should be
considered to gain further information about the pathology.

Magnetic Resonance Imaging

FIGURE 626 Soft tissue window of a computed tomography scan

through the L4-5 level demonstrating stenosis. Please note the facet and
ligamentum hypertrophy better seen on the magnetic resonance imaging
of this patient in Figures 629 and 6210.

MRI is the diagnostic modality of choice in patients with

stenosis. It is noninvasive and provides images in axial,
coronal, and sagittal planes. MRI offers details of both the
bony and soft tissue anatomy. It provides improved visualization of the soft tissue elements of the spine (Figs. 629 and
6210). The degree of compression of the neural elements and
the offending pathology are both easily visualized. The central
canal, lateral recess, and neural foramen can all be visualized
along with the degree of stenosis that is present in each of
these regions. Facet arthropathy, ligamentum hypertrophy,
disc bulges or herniations, and other compressive pathology
such as synovial cysts are easily identified on MRI (Fig.
6211). Foraminal stenosis is best visualized on T1-weighted
sagittal images in which the nerve root and dorsal root ganglion are contrasted with the surrounding fat.

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62 Spinal Stenosis: Pathophysiology, Clinical Diagnosis, and Differential Diagnosis 1071

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IX

FIGURE 628 Postmyelogram computed tomography through the

adjacent-level stenosis of the patient in Figure 627.

FIGURE 627 Myelogram of a patient with neurogenic claudication who

had a history of a previous lumbar instrumented fusion. The arrows point
out the two levels of adjacent level stenosis.

FIGURE 629 T1-weighted (A) and T2-weighted (B) sagittal

MRI of a patient with L4-5 and L5-S1 stenosis. Please note the
disc bulges and ligamentum hypertrophy at the L4-5 and L5-S1
levels.

L4

L4

L5

L5

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1072 SPINAL STENOSIS

FIGURE 6210 Axial T2-weighted magnetic resonance imaging through

the L4-5 level demonstrating facet and ligamentum hypertrophy along with
a disc bulge causing stenosis. Note the increased T2 signal in the facet joint
corresponding to the instability this patient had on flexion-extension
radiographs at the L4-5 level.

Overall, the diagnostic accuracy of MRI is similar to that

of the CT-myelogram and does not have the drawbacks of
ionizing radiation and contrast injection in the CSF.72-75 The
reliability of MRI interpretation has also been investigated,
and there appears to be significant inter-reader variability in
assessing some anatomic locations.76-79 The measurement of
thecal sac area, as well as the ratings of the degree of central
and foraminal stenosis, show good reliability.80 The reading of
the degree of lateral recess stenosis, on the other hand, shows
significant variability. Although some have noted correlation

between the degree of stenosis and outcomes of treatments,

others have not been able to identify any such relationship.81-84
It has been theorized that supine MRIs may understate the
degree of stenosis because the patients may not be in the position of the worst compression during the study. Attempts have
been made to demonstrate pathology in MRI scans that is
obvious only under dynamic conditions.85-89 MRIs in flexion,
extension, axial loading, and upright positions have been
investigated without any conclusive evidence regarding their
utility. It is unclear what the results of invasive treatments will
be for those patients whose stenosis can only be detected
under dynamic conditions. What the existing studies do point
out is that the static images on the current MRIs should be
supplemented with the dynamic information available from
clinical presentation, as well as flexion and extension radiographs. One study noted that supine MRIs performed with the
lumbar spine extended (by having the hips and knees extended)
demonstrated more thecal sac compression than the images
obtained in the flexed position.90 This suggests that position
of the lower extremities during the MRI should be ascertained
as a routine part of the patients history.

Electromyography, Nerve Condition Studies,

and Somatosensory Evoked Potentials
Electromyography (EMG), nerve conduction studies (NCSs),
and somatosensory evoked potentials (SSEPs) are not part of
the routine workup of patients with spinal stenosis. EMG identifies the effect of nerve function through recording the electrical activity of muscle at rest and with stimulation. EMG
identifies lower motor neuron dysfunction and does not evaluate any sensory dysfunction. Electromyographic changes have
been documented in up to 80% of patients with spinal stenosis.84,91-94 EMG can be useful in differentiating chronic changes

Figure 6211 T2-weighted sagittal (A) and axial (B) magnetic resonance imaging of a patient with a right L5-S1
synovial cyst causing a right lumbar radiculopathy. * denotes the synovial cyst on the sagittal view. In the axial view
the cyst is noted to arise from the right facet joint and causes neural compression.

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62 Spinal Stenosis: Pathophysiology, Clinical Diagnosis, and Differential Diagnosis 1073

Differential Diagnosis
Neurogenic claudication is the hallmark of spinal stenosis.
Patients describe a variety of abnormal sensations that radiate
down their legs with ambulation. Symptoms are typically
relieved by forward flexion of the lumbar spine and are worse
with extension. Sudden onset or severe motor weakness and
bowel and bladder dysfunction in these patients should
prompt evaluation of other etiologies of these symptoms such
as cord compression. In spite of various attempts to create a
single validated method of consistently diagnosing spinal stenosis, no single test or algorithm is available to accurately
diagnose all patients with symptomatic spinal stenosis.59,98-100
The differential diagnosis of spinal stenosis includes vascular claudication, lumbar spondylosis, lower extremity arthritis,
cord compression, neurologic disorders, peripheral neuropathy, infection, tumors, and lumbosacral plexus lesions. Symptoms from neurogenic claudication start proximally and
progress distally, whereas symptoms from vascular claudication start distally and progress proximally. Vascular claudication causes symptoms with a constant level of exertion
regardless of the position of the lumbar spine. Thus leaning
forward on a grocery cart or going uphill does not allow these
patients to walk longer. Similarly, patients with vascular claudication continue to be limited on a bike, while the patients
with neurogenic claudication have better endurance on a bike.
On physical examination, painless full extension of the lumbar
spine; shiny, hairless legs; and weak peripheral pulses are all
hallmarks of vascular claudication.
Lumbar spondylosis typically causes pain in the low back
without significant pain or abnormal sensation in the legs.
Peripheral neuropathy typically causes burning pain and paresthesias that are unrelated to activity. A history of diabetes,
vitamin deficiencies, alcoholism, chemotherapy, drug abuse,
and exposure to toxins should be elicited in these patients.
Physical examination in neuropathy patients will typically
demonstrate hypoesthesia or dysesthesia in a glove and stocking distribution. Ankle reflexes will often be absent bilaterally.
NCSs are helpful in establishing a diagnosis in these patients.

A history of isolated joint pain with ambulation will help

identify patients with lower-extremity arthritis. Hip arthritis
typically presents with groin pain radiating into the anterior
thigh but can also be a cause of buttock pain. Physical examination demonstrating hip irritability and limitation in internal
rotation suggests hip pathology is symptomatic. A thorough
history and physical examination can thus help eliminate the
majority of common conditions that mimic lumbar spinal
stenosis. Presence of constitutional symptoms and intense
nighttime pain suggest a possible infection or malignancy.
These symptoms should trigger an MRI and laboratory studies,
which would help eliminate these more rare conditions.

Summary
Lumbar spinal stenosis is a common finding in the elderly. With
the aging population in the United States, the number of patients
with spinal stenosis seeking treatment will dramatically increase
over the next 20 to 30 years. Because pathologic changes can
be present in asymptomatic patients, abnormalities found on
imaging modalities are not a good method of diagnosing symptomatic spinal stenosis. Findings from a thorough history and
physical examination should be correlated with corresponding
pathologic abnormalities on MRI or a CT-myelogram. This is
especially important if any invasive treatment will be recommended. Plain radiographs complement the other imaging
modalities to create a full clinical picture that includes the
detection of any dynamic instability. EMG, NCSs, and SSEPs
are typically not helpful in confirming the diagnosis of stenosis.
Despite our long history of treating patients with spinal stenosis, there is no single diagnostic test that can help identify
patients with symptomatic spinal stenosis.
PEARLS
1. In patients with mild to moderate lumbar spinal stenosis,
rapid or catastrophic neurologic deterioration is rare.
2. Magnetic resonance imaging (MRI) is the noninvasive study of
choice in patients suspected of having spinal stenosis.
3. Imaging studies should be correlated with specific findings on
history and physical examination that would be expected on
the basis of the specific neural elements that are compressed.
4. No single diagnostic test can confirm the presence of
symptomatic spinal stenosis.
PITFALLS
1. Abnormal imaging is not a reliable method of diagnosing
symptomatic lumbar spinal stenosis. The incidence of clinically
silent lumbar degenerative disease is high.
2. Electrodiagnostic studies are not typically helpful in the
diagnosis of spinal stenosis.
3. Most patients with spinal stenosis have a normal neurologic
examination.
4. In evaluating patients with stenosis, do not forget to examine
the hip joints and lower extremity vascularity.

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SECTION

from active ongoing denervation. However, it should be kept

in mind that there is a significant incidence of false-negative
electromyograms in patients with spinal stenosis. This can be
attributed to the fact that EMG does not measure sensory dysfunction and thus does not catch the more common abnormality in patients with neurogenic claudication. EMG also does not
help differentiate symptomatic from asymptomatic patients.
NCS measures the speed with which impulses travel down
an axon. NCS is useful in differentiating changes that are
occurring from neuropathy versus radiculopathy. SSEPs
measure the electrical transmission of sensory stimulation
starting from the peripheral nerves and going through the
spinal cord and brain. A lesion in the peripheral nerve will
prolong the latency response, whereas lesions of the root and
cord will cause changes in the waveform. SSEP is more sensitive and specific compared with an EMG, although there continue to be false negatives and false positives.95-97

IX

1074 SPINAL STENOSIS

REFERENCES

KEY POINTS
1. Lumbar disc degeneration is a nearly universal finding in the
aging population.
2. Degeneration alone does not imply a pathologic entity. A
disease may be said to exist relative to the symptoms with
which the patient presents.

1. Verbiest H: A radicular syndrome from developmental narrowing of the lumbar vertebral canal. J Bone Joint Surg Br 36:230237, 1954.
2. Verbiest H: Further experiences on pathologic influence of a
developmental stenosis of the lumbar vertebral canal. J Bone
Joint Surg Br 38:576-583, 1956.

3. In the absence of pathognomonic findings, the diagnosis of

spinal stenosis rests on a Venn diagram approach in which
historical elements overlap with physical examination and
imaging findings.

3. Verbiest H: Spondylolisthesis: The value of radicular signs and

symptoms. J Intern Coll Surg 39:461-481, 1963.

4. Once symptomatic, most patients will continue to have

symptoms on at least an intermittent basis until surgically
decompressed.

5. Verbiest H: Unilateral lumbo-sacral radicular symptoms due to

sequestrated disc material in the spinal canal. Cesk Neurol 31:
93-101, 1968.

5. On the other hand, rarely does stenosis progress rapidly.

Therefore a trial of nonoperative management is indicated in
most cases.

6. Verbiest H: Neurogenic intermittent claudication in cases with

absolute and relative stenosis of the lumbar vertebral canal
(ASLC and RSLC), in cases with narrow lumbar intervertebral
foramina, and in cases with both entities. Clin Neurosurg
20:204-214, 1973.

6. Patients with symptomatic stenosis may present with one or

more of a combination of axial pain, radiculopathy, and
neurogenic claudication. Each of these is associated with
different historical and examination findings.

4. Verbiest H: Pathomorphic aspects of developmental lumbar

stenosis. Orthop Clin North Am 6:177-196, 1966.

7. Verbiest H: Results of surgical treatment of idiopathic developmental stenosis of the lumbar vertebral canal. J Bone Joint Surg
Br 59:181-188, 1977.
8. Verbiest H: The treatment of lumbar spondyloptosis or impending lumbar spondyloptosis accompanied by neurologic deficit
and/or neurogenic intermittent claudication. Spine 4:68-77,
1979.

KEY REFERENCES
1. Weinstein JN, Tosteson TD, Lurie JD, et al: Surgical versus
nonsurgical therapy for lumbar spinal stenosis. N Engl J Med
358:794-810, 2008.
A large prospective study evaluating outcomes of lumbar
spinal stenosis patients treated with surgical versus
nonsurgical treatment.
2. Watters WC III, Baisden J, Gilbert TJ, et al: Degenerative
lumbar spinal stenosis: an evidence based clinical guideline
for the diagnosis and treatment of degenerative lumbar
spinal stenosis. Spine J 8:305-310, 2008.
Evidence-based guidelines produced by North American
Spine Society regarding diagnosis and treatment of patients
with lumbar spinal stenosis.
3. Atlas SJ, Keller RB, Wu YA, et al: Long-term outcomes of
surgical and nonsurgical management of lumbar spinal
stenosis: 8 to 10 year results from the Maine Lumbar Spine
Study. Spine 30:936-943, 2005.
A prospective observational cohort study evaluating
outcomes of surgical and nonsurgical treatment after 8 to 10
years.
4. Kirkaldy-Willis WH, Wedge JH, Yong-Hing K, et al: Pathology
and pathogenesis of lumbar spondylosis and stenosis. Spine
3:319-328, 1978.
A classic article describing the pathogenesis of lumbar
stenosis.
5. Verbiest H: A radicular syndrome from developmental
narrowing of the lumbar vertebral canal. J Bone Joint Surg Br
36:230-237, 1954.
A historical perspective on diagnosis and treatment of
lumbar spinal stenosis.

9. Verbiest H: Stenosis of the lumbar vertebral canal and sciatica.

Neurosurg Rev 3:75-89, 1980.
10. Verbiest H: Developmental stenosis of the bony lumbar vertebral canal. Acta Orthop Belg 53:373-387, 1987.
11. Kirkaldy-Willis WH, Paine KWE, Cauchoix J, et al: Lumbar
spinal stenosis. Clin Orthop 99:30-50, 1974.
12. Kirkaldy-Willis WH, Wedge JH, Yong-Hing K, et al: Pathology
and pathogenesis of lumbar spondylosis and stenosis. Spine
3:319-328, 1978.
13. Kirkaldy-Willis WH: Lumbar spinal nerve entrapment. Clin
Orthop 169:171-178, 1982.
14. Kirkaldy-Willis WH: The relationship of structural pathology
to the nerve root. Spine 9:49, 1984.
15. Kirkaldy-Willis WH: Presidential symposium on instability of
the lumbar spine. Spine 10:254-291, 1985.
16. Boden SD, Davis DO, Dina TS, et al: Abnormal magneticimaging scans of the lumbar spine in asymptomatic subjects: A
prospective investigation. J Bone Joint Surg Am 72:403-408,
1990.
17. Jensen MC, Brant-Zawadzki MN, Obuchowski N, et al: Magnetic resonance imaging of the lumbar spine in people without
back pain. N Engl J Med 331:69-73, 1994.
18. Deyo RA, Ciol MA, Cherkin DC, et al: Lumbar spinal fusion:
a cohort study of complications, reoperations, and resource use
in the Medicare population. Spine 18:1463-1470, 1993.
19. Deyo RA, Gray DT, Kreuter W, et al: United States trends in
lumbar fusion surgery for degenerative conditions. Spine
30:1441-1445, 2005.
20. Hillabrand AS, Rand N: Degenerative lumbar stenosis:
Diagnosis and management. J Am Assoc Orthop Surg 7:239248, 1999.

Downloaded from ClinicalKey.com at ClinicalKey Global Flex Package Trial June 07, 2016.
For personal use only. No other uses without permission. Copyright 2016. Elsevier Inc. All rights reserved.

62 Spinal Stenosis: Pathophysiology, Clinical Diagnosis, and Differential Diagnosis 1075

21. Yong-Hing K, Kirkaldy-Willis WH. The pathophysiology of
disc degeneration of the lumbar spine. Ortho Clin North Am
14(3):59-64, 1983.

40. Olemarker K, Nordborg C, Larsson K, et al: Ultrastructural

changes in spinal nerve roots induced by autologous nucleus
pulposus. Spine 21:411-414, 1996.

22. Arbit E, Pannullo S: Lumbar stenosis: A clinical review. Clin

Orthop Rel Res 384:137-143, 2001.

41. Muramoto T, Atsuta Y, Iwahara T, et al: The action of prostaglandin E2 and triamcinolone acetonide on the firing activity
of lumbar nerve roots. Orthopedics 21:172-175, 1997.

SECTION

42. Hashizume H, Kawakami M, Nishi H, et al: Histochemical

demonstration of nitric oxide in herniated lumbar discs: A
clinical and animal model study. Spine 22:1080-1084, 1997.

IX

23. Vanderlinden R: Subarticular entrapment of the dorsal root

ganglion as a cause of sciatic pain. Spine 9:19-22, 1984.
24. Kunogi J, Hasue M: Diagnosis, operative treatment of intraforaminal, extraforaminal nerve root compression. Spine 16:13121330, 1991.
25. Porter R, Hibbert C, Evans C: The natural history of root
entrapment syndrome. Spine 9:418-421, 1984.
26. Morishita Y, Hida S, Naito M, et al: Measurement of the local
pressure in the intervertebral foramen and the electrophysiologic values of the spinal nerve roots in the vertebral foramen.
Spine 31:3076-3080, 2006.
27. Rosenburg NJ: Degenerative spondylolisthesis: Predisposing
factors. J Bone Joint Surg Am 67:240-246, 1975.
28. Spivak JM: Degenerative lumbar spinal stenosis: Current concepts review. J Bone Joint Surg Am 80:1053-1066, 1998.
29. Schonstorm N, Bolender NF, Spengler DM, et al: Pressure
changes within the cauda equine following constriction of the
dural sac. An in vitro experimental study. Spine 9:604-607,
1984.
30. Delamarter RB, Bohlmann HH, Dodge LD, et al: Experimental
lumbar spinal stenosis: Analysis of the cortical evoked potentials, microvasculature, and histopathology. J Bone Joint Surg
Am 72:110-120, 1990.

43. Yabuki S, Kikuchi S, Olemarker K, et al: Acute effects of nucleus

pulposus on blood flow and endoneurial fluid pressure in rat
dorsal root ganglia. Spine 23:2517-2523, 1998.
44. Singh K, Samartzis D, Vacarro AR, et al: Congenital lumbar
spinal stenosis: A prospective, control-matched, cohort radiographic analysis. Spine J 5:615-622, 2005.
45. Hall S, Bartleson JD, Onofrio BM, et al: Lumbar spinal
stenosis: Clinical features, diagnostic procedures, and results of
surgical treatment in 68 patients. Ann Intern Med 103:271-275,
1985.
46. Jones RA, Thomson JL: The narrow lumbar canal: A clinical and
radiological review. J Bone Joint Surg Br 50:595-605, 1968.
47. Tile M, McNeil SR, Zarins RK, et al: Spinal stenosis: Results of
treatment. Clin Orthop 115:104-108, 1976.
48. Blau JN, Logue V: The natural history of intermittent claudication of the cauda equina: A long term follow-up study. Brain
101:211-222, 1978.
49. Rosomoff HL, Rosomoff RS: Nonsurgical aggressive treatment
of lumbar spinal stenosis. Spine 1:383, 1987.

31. Pedowitz R, Garfin S, Massie J, et al: Effects of magnitude and

duration of compression on spinal nerve root conduction. Spine
17:194-199, 1992.

50. Postacchini F, Cinotti G, Gumina S, Perugia D: Long-term

results of surgery in lumbar stenosis: 8-year review of 64
patients. Acta Orthop Scand Suppl 251:78-80, 1993.

32. Rydevick B, Lundborg G: Permeability of intraneural microvessels and perineurium following acute, graded experimental
nerve compression. Scand J Plast Reconstr Surg 11:179-187,
1977.

51. Herno A, Airaksinen O, Saari T, Luukkonen M: Lumbar spinal

stenosis: A matched-pair study of operated and non-operated
patients. Br J Neurosurg 10:461-465, 1996.

33. Rydevick B, Lundborg G, Bagge U: Effects of graded compression on intraneural blood flow. An in vivo study on rabbit tibial
nerve. J Hand Surg 6:3-12, 1981.
34. Rydevick B, Nordborg G: Changes in nerve function and nerve
fiber structure induced by acute, graded compression. J Neurol
Neurosurg Psychiatry 43:1070-1082, 1981.
35. Rydevick B, Brown M, Lundborg G: Pathoanatomy and
pathophysiology of nerve root compression. Spine 9:7-15,
1984.
36. Rydevick B, Holm S, Brown MD, et al: Diffusion from the cerebrospinal fluid as a nutritional pathway for spinal nerve roots.
Acta Physiol Scand 138:247-248, 1990.
37. Rydevick B, Pedowitz RA, Hargens AR, et al: Effects of acute,
graded compression on spinal nerve root function and structure. An experimental study of the pig cauda equina. Spine
16:487-493, 1991.
38. Kang JD, Georgescu HI, Larkin L, et al: Herniated lumbar intervertebral discs spontaneously produce matrix metalloproteinases, nitric oxide, interleukin-6, and prostaglandin E2. Spine
21:271-277, 1996.
39. ODonnel JL, ODonnel AL: Prostaglandin E2 content in herniated lumbar disc disease. Spine 21:1653-1656, 1996.

52. Benoist M: The natural history of lumbar degenerative spinal

stenosis. Joint Bone Spine 69:450-457, 2002.
53. Atlas SJ, Keller RB, Robson D, et al: Surgical and nonsurgical
management of lumbar spinal stenosis. Spine 25:556-562,
2000.
54. Johnsson KE, Rosen I, Uden A: The natural course of lumbar
spinal stenosis. Clin Orthop 82-86, 1992.
55. Atlas SJ, Keller RB, Wu YA, et al: Long-term outcomes of surgical and nonsurgical management of lumbar spinal stenosis: 8
to 10 year results from the Maine Lumbar Spine Study. Spine
30:936-943, 2005.
56. Miyamoto H, Sumi M, Uno K, et al: Clinical outcome of nonoperative treatment for lumbar spinal stenosis, and predictive
factors relating to prognosis, in a 5-year minimum follow-up. J
Spinal Disord Tech 21:563-568, 2008.
57. Malmivaara A, Slatis P, Heliovaara M, et al: Surgical or nonoperative treatment of lumbar spinal stenosis? Spine 32:1-8,
2007.
58. Weinstein JN, Tosteson TD, Lurie JD, et al: Surgical versus
nonsurgical therapy for lumbar spinal stenosis. N Engl J Med
358:794-810, 2008.
59. Waters WC, Baisden J, Gilbert TJ, et al: Degenerative lumbar
spinal stenosis: An evidence based clinical guideline for the

Downloaded from ClinicalKey.com at ClinicalKey Global Flex Package Trial June 07, 2016.
For personal use only. No other uses without permission. Copyright 2016. Elsevier Inc. All rights reserved.

1076 SPINAL STENOSIS

diagnosis and treatment of degenerative lumbar spinal stenosis.
Spine J 8:305-310, 2008.
60. Lin S-I, Lin R-M, Huang L-W: Disability in patients with degenerative lumbar spinal stenosis. Arch Phys Med Rehabil 87:12501256, 2006.
61. Hellstrom PA, Tammela TL, Niinimaki TJ: Voiding dysfunction
and urodynamic findings in patients with lumbar spinal stenosis and the effect of decompressive laminectomy. Scand J Urol
Nephrol 29:167-171, 1995.
62. Johnsson KE: Lumbar spinal stenosis: A retrospective study of
163 cases in southern Sweden. Acta Orthop Scand 66:403-405,
1995.
63. Kawaguchi Y, Kanamori M, Ishihara H, et al: Clinical symptoms
and surgical outcome in lumbar spinal stenosis patients with
neuropathic bladder. J Spinal Disord 14:404-410, 2001.
64. Aalto TJ, Malmivaara A, Kovacs F, et al: Preoperative predictors
of postoperative clinical outcome in lumbar spinal stenosis.
Spine 31:E648-63, 2006.
65. Ciric I, Mikhael M, Tarkington J, et al: The lateral recess syndrome. J Neurosurg 53:433-443, 1980.
66. Amundsen T, Weber H, Lilleas F, et al: Lumbar spinal stenosis:
Clinical and radiologic features. Spine 20:1178-1186, 1995.
67. Frymoyer JW, Newberg A, Pope MH, et al: Spine radiographs
in patients with low-back pain: An epidemiological study in
men. J Bone Joint Surg Am 66:1048-1055, 1984.
68. Kent DL, Haynor DR, Larson EB: Diagnosis of lumbar spinal
stenosis in adults: A meta-analysis of the accuracy of CT, MR,
and myelography. AJR Am J Roentgenol 158:1135-1144, 1992.

77. Speciale AC, Pietrobon R, Urban CW, et al: Observer variability

in assessing lumbar spinal stenosis severity on magnetic resonance imaging and its relation to cross-sectional spinal canal
area. Spine 27:1082-1086, 2002.
78. Weiner BK, Patel NM, Walker MA: Outcomes of decompression for lumbar spinal canal stenosis based upon pre-operative
radiographic severity. J Orthop Surg 2:3, 2007.
79. Song, K, Jang E, Jung H, et al: Observer variability in the evaluation of multiple lumbar stenosis by routing MR-myelography
and MRI. J Spinal Disord Tech 21:569-574, 2008.
80. Lurie JD, Tosteson AN, Tosteson TD, et al: Reliability of readings of magnetic resonance imaging features of lumbar spinal
stenosis. Spine 33:1605-1610, 2008.
81. Uden A, Johnsson KE, Johnsson K, et al: Myelography in the
elderly and the diagnosis of spinal stenosis. Spine 10:171-174,
1985.
82. Ogikubo O, Forsberg L, Hansson T: The relationship between
the cross-sectional area of the cauda equine and the preoperative symptoms in central lumbar spinal stenosis. Spine
13:1423-1428, 2007.
83. Geisser ME, Haig AJ, Tong HC, et al: Spinal canal size and
clinical symptoms among persons diagnosed with lumbar
spinal stenosis. Clin J Pain 23:780-785, 2007.
84. Haig AJ, Geisser ME, Tong HC, et al: Electromyography and
magnetic resonance imaging to predict lumbar stenosis, low
back pain, and no back symptoms. J Bone Joint Surg 89:358-366
2007.

69. Herkowitz HN, Garfin SR, Bell GR, et al: The use of computed
tomography in evaluating non-visualized vertebral levels
caudad to a complete block on a lumbar myelogram: A review
of 32 cases. J Bone Joint Surg Am 69:218-224, 1987.

85. Schmid MR, Strucki G, Duewell S, et al: Changes in crosssectional measurements of the spinal canal and intervertebral
foramina as a function of body position: in vivo studies
on an open-configuration MR system. Am J Radiol 172:1095,
1999.

70. Bell GR, Rothman RH, Booth RE, et al: A study of computer
assisted tomography: II. Comparison of metrizamide myelography and computed tomography in the diagnosis of herniated
lumbar disc and spinal stenosis. Spine 9:552-556, 1984.

86. Zamani AA, Moriarty T, Hsu L, et al: Functional MRI of the

lumbar spine in erect position in a superconducting openconfiguration MR system: Preliminary results. J Magn Reson
Imaging 8:1329-1333, 1998.

71. Herno A, Airaksinen O, Saari T, et al: The predictive value of

preoperative myelography in lumbar spinal stenosis. Spine
19:1335-1338, 1994.

87. Vitzthum HE, Konig A, Seifert V: Dynamic examination of the

lumbar spine by using vertical, open magnetic resonance
imaging. J Neurosurg 93:58-64, 2000.

72. Modic MT, Masaryk T, Boumphrey F, et al: Lumbar herniated

disk disease and canal stenosis: Prospective evaluation by
surface coil MR, CT, and myelography. AJR Am J Roentgenol
147:757-765, 1986.
73. Schnebel B, Kingston S, Watkins R, et al: Comparison of MRI
to contrast CT in diagnosis of spinal stenosis. Spine 14:332-337,
1989.
74. Postacchini F, Amatruda A, Morace GB, et al: Magnetic resonance imaging in the diagnosis of lumbar spinal canal stenosis.
Ital J Orthop Trauma 17:327-337, 1991.
75. Bischoff RJ, Rodriguez RP, Gupta K, et al: A comparison of
computed tomography-myelography, magnetic resonance
imaging, and myelography in the diagnosis of herniated nucleus
pulposus and spinal stenosis. J Spinal Disord 6:289-295, 1993.
76. Hamanishi C, Matukura N, Fujita M, et al: Cross-sectional area
of the stenotic lumbar dural tube measured from the transverse
views of magnetic resonance imaging. J Spinal Disord 7:388393, 1994.

88. Weishaupt D, Schmid MR, Zanetti M, et al: Positional MR

imaging of the lumbar spine: Does it demonstrate nerve root
compromise not visible at conventional MR imaging? Radiology 215:247-253, 2000.
89. Willen J, Wessberg PJ, Danielsson B: Surgical results in hidden
lumbar spinal stenosis detected by axial loaded computed
tomography and magnetic resonance imaging. Spine 33:E109115, 2008.
90. Madsen R, Jensen TS, Ope M, et al: The effect of body position
and axial load on spinal canal morphology. Spine 33:61-67,
2008.
91. Jacobsen RE: Lumbar stenosis: An electromyographic evaluation. Clin Orthop 115:68-72, 1976.
92. Spengler DM: Degenerative stenosis of the lumbar spine. J Bone
Joint Surg Am 69:305-308, 1987.
93. Johnsson KE, Rosen I, Uden A: Neurophysiologic investigation
of patients with spinal stenosis. Spine 12:483-487, 1987.

Downloaded from ClinicalKey.com at ClinicalKey Global Flex Package Trial June 07, 2016.
For personal use only. No other uses without permission. Copyright 2016. Elsevier Inc. All rights reserved.

62 Spinal Stenosis: Pathophysiology, Clinical Diagnosis, and Differential Diagnosis 1077

95. Dvonch V, Scoff T, Bunch WH, et al: Dermatomal somatosensory evoked potentials: Their use in lumbar radiculopathy.
Spine 9:291-293, 1984.
96. Keim HA, Hajdu M, Gonzales EG, et al: Somatosensory evoked
potentials as an aid in diangnosis and intraoperative management of spinal stenosis. Spine 10:338-388, 1985.
97. Kondo M, Matsuda H, Kureya S, et al: Electrophysiological
studies of intermittent claudication in lumbar stenosis. Spine
14:862-866, 1989.

98. Tenhula J, Lenke LJ, Bridwell KH, et al: Prospective functional

evaluation of the surgical treatment of neurogenic claudication
in patients with lumbar spinal stenosis. J Spinal Disord 13:276282, 2000.
99. Graff ID, Park A, Bierma-Zeinstra S, et al: Diagnosis of lumbar
spinal stenosis: A systematic review of the accuracy of the diagnostic tests. Spine 31:1168-1176, 2006.
100. Konno S, Hayashino Y, Fukuhara S, et al: Development of a
clinical diagnosis support tool to identify patients with lumbar
spinal stenosis. Eur Spine J 16:1951-1957, 2007.

Downloaded from ClinicalKey.com at ClinicalKey Global Flex Package Trial June 07, 2016.
For personal use only. No other uses without permission. Copyright 2016. Elsevier Inc. All rights reserved.

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94. Chiodod A, Haig AJ, Yamakawa KSJ, et al: Magnetic resonance

imaging vs electrodiagnostic root compromise in lumbar spinal
stenosis. Am J Phys Med Rehabil 87:789-797 2008.

IX