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Vol 7, No 4, July/August 1999
239
The earliest description of lumbar
stenosis is attributed to Antoine
Portal, who in 1803 described Òtoo-
narrow vertebral canalsÓ in hunch-
backs with rickets. The concept of
acquired lumbar spinal stenosis
was popularized in the 1950s by
Verbiest. Since then, advances in
diagnostic and therapeutic modali-
ties, coupled with the extension of
life expectancy, have increased the
rate of detection and subsequent
operative intervention.
The general incidence of degen-
erative lumbar spinal stenosis
ranges from 1.7%
1
to 8%.
2
Symp-
toms typically develop in the fifth
or sixth decade of life in association
with osteoarthritic changes in the
lumbar spine. No sex predomi-
nance has been found, although
degenerative spondylolisthesis
associated with lumbar spinal
stenosis is four times more com-
mon among women.

3
No associa-
tion has been found with occupa-
tion or body habitus.
The goal of this article is to pro-
vide the reader with an under-
standing of lumbar stenosis as an
element of the degenerative pro-
cess of aging commonly seen in the
older population, as well as an
overview of treatment options
Basic Science
Anatomically, lumbar stenosis is
usually caused by a reduction in
the space available for the neural
elements due to variant osseous
anatomy or filling of the spinal
canal with hypertrophic tissue.
Three typical canal shapes have
been described: round, ovoid, and
trefoil (Fig. 1). Trefoil canals have
the smallest cross-sectional area
and are associated with the highest
incidence of symptomatic lumbar
stenosis.
4
Arnoldi et al
5
classified
lumbar stenosis as congenital, ac-

quired, or combined (Table 1). The
term Òcentral stenosisÓ is used
when compression of the dural sac
is the main component. ÒLateral
stenosisÓ refers to compression of
the nerve root in the lateral recess,
in the neural foramen, or lateral to
the neural foramen.
6,7
The pathophysiology of degener-
ative lumbar stenosis usually begins
with disk dehydration, resulting in
a loss of disk height and bulging of
the anulus fibrosus and ligamentum
flavum into the spinal canal. These
Dr. Hilibrand is Assistant Professor of
Orthopaedic Surgery, Rothman Institute at
Thomas Jefferson University, Philadelphia.
Dr. Rand is Adjunct Professor of Orthopaedic
Surgery and Spine Fellow, Vanderbilt Univer-
sity, Nashville, Tenn.
Reprint requests: Dr. Hilibrand, Rothman
Institute, 5th Floor, 925 Chestnut Street,
Philadelphia, PA 19107.
Copyright 1999 by the American Academy of
Orthopaedic Surgeons.
Abstract
Degenerative lumbar stenosis is a common cause of disabling back and lower
extremity pain among older persons. The process usually begins with degenera-
tion of the intervertebral disks and facet joints, resulting in narrowing of the

spinal canal and neural foramina. Associated factors may include a developmen-
tally narrow spinal canal and degenerative spinal instability. Nonoperative
management includes restriction of aggravating activities, physical therapy, and
anti-inflammatory medications. If nonoperative treatment has failed, surgical
treatment may be appropriate. Decompression should be performed so as to ad-
dress all clinically relevant neural elements while maintaining spinal stability. If
instability is present, autogenous intertransverse bone grafting is recommended.
There may be an advantage to augmenting some of these procedures with in-
ternal fixation. Surgical success rates as high as 85% have been reported, but
may be compromised by inadequate decompression, inadequate stabilization, or
medical comorbidities. Short-term follow-up data indicate that operative man-
agement provides more effective relief than nonoperative treatment, but prospec-
tive studies comparing the effects of nonoperative and operative interventions on
the long-term natural history of lumbar spinal stenosis are needed.
J Am Acad Orthop Surg 1999;7:239-249
Degenerative Lumbar Stenosis:
Diagnosis and Management
Alan S. Hilibrand, MD, and Nahshon Rand, MD
changes alter the loading of the
facet joints, which together with the
intervertebral disk form the three-
joint spinal motion segment.
Further degeneration leads to facet
arthrosis with sclerosis and osteo-
phytic overgrowth. The most com-
mon result is that as the nerve roots
traverse the lateral recesses, they
may be encroached on by hyper-
trophic facet joints, infolded liga-
mentum flavum, and a bulging anu-

lus. These degenerative changes
can also cause root stenosis in the
neural foramen. The anteroposteri-
or diameter of the foramen is
reduced by the bulging anulus ante-
riorly and the hypertrophic facets
posteriorly, while the foraminal
height is reduced by the loss of
intervertebral disk height and asso-
ciated facet subluxation.
8
The degenerative process is
sometimes accompanied by the
development of segmental instabil-
ity. Degenerative changes in the
supporting structures of the spinal
motion segment, including com-
promise of the facet joints and cap-
sular ligaments, may cause higher
mechanical stress across the degen-
erated anulus, leading to the devel-
opment of dynamic subluxation or
spondylolisthesis.
6
As abnormal
motion develops within a degener-
ated motion segment, it exacerbates
nerve root irritation in the stenotic
lateral recess and foramen.
The sequence of neuropatholog-

ic changes that result from stenosis
of the lumbar spinal canal have
been investigated in animal stud-
ies. Delamarter et al
9
employed a
dog model in which they created
varying degrees of stenosis and
demonstrated deleterious effects on
the neural elements by increasing
the degree of the stenosis. They
found that cortical evoked poten-
tials were highly sensitive to this
compression and were affected
long before any clinical signs oc-
curred. They also demonstrated
venous congestion and arterial con-
striction around compressed nerve
roots and dorsal root ganglia. The
result was blockage of axoplasmic
flow, with resulting edema, demye-
lination, and wallerian degenera-
tion of motor and sensory fibers.
Other authors have shown that
sensory fibers are more susceptible
to pressure and slower to recover
than motor fibers,
10
which may
explain the presence of subjective

sensory changes in the absence of
objective physical findings.
The mechanism of pain produc-
tion in lumbar spinal stenosis re-
mains unclear. Although many
older patients have degenerative
changes in their lumbar spines, few
have any symptoms. Arnoldi et al
5
suggested that increased venous
pressure may explain the symp-
toms of neurogenic claudication.
Others have suggested that narrow-
ing of the spinal canal may lead to a
reduction in blood supply to the
cauda equina, resulting in ischemic
changes from the diffusion of
metabolites.
11
These changes may
stimulate the sinuvertebral nerve or
lead to secretion of pain mediators,
such as substance P, from the dor-
sal root ganglion. Perineural in-
flammation of unknown origin may
also result in pain generation.
Clinical Presentation
Symptomatic degenerative lumbar
stenosis usually has an insidious
onset and a slow rate of progres-

Degenerative Lumbar Stenosis
Journal of the American Academy of Orthopaedic Surgeons
240
Round
Trefoil
Ovoid
Fig. 1 The three typical shapes of the spinal canal. Trefoil canals have the smallest cross-
sectional area.
Table 1
Classification of Lumbar Spinal
Stenosis
Congenital (developmental) stenosis
Chondrodystrophy
Idiopathic
Acquired stenosis
Degenerative
Spondylolytic
Iatrogenic
Posttraumatic
Miscellaneous
Combined (degenerative changes
superimposed on a congenitally
narrow spinal canal)
sion. At initial presentation, most
patients have a long history of back
pain in the lumbar region with
recent development or progression
of lower-extremity pain. Discom-
fort in the back, buttocks, and/or
lower extremities is the most com-

mon complaint. Symptoms are
usually exacerbated by standing,
walking, and exercising in an erect
posture, which results in the devel-
opment of pain, tightness, heavi-
ness, and subjective weakness in
the legs.
12
This symptom complex,
referred to as Òneurogenic claudi-
cation,Ó is rapidly relieved by sit-
ting down or leaning forward.
Cycling, which involves forward
flexion, is usually tolerated by pa-
tients with lumbar stenosis. Pain-
less motor claudication, deficits in
proprioception leading to gait dis-
turbances, and bowel and bladder
dysfunction are relatively uncom-
mon.
Amundsen et al
12
reported that
the most common symptoms in pa-
tients with lumbar spinal stenosis
were back pain (prevalence of 95%),
claudication (91%), leg pain (71%),
weakness (33%), and voiding dis-
turbances (12%). In 70% of the
patients in their study, the pain

intensity was equally distributed
between the back and the lower
extremities; 25% had predominant-
ly leg pain. Radicular pain was
unilateral in 58% and bilateral in
42%. The radicular pattern corre-
sponded to the L5 root in 91%, S1 in
63%, L1-L4 in 28%, and S2-S5 in 5%.
In that study, 47% of the patients
had double-root involvement, 35%
had single-root involvement, 17%
had triple-root involvement, and
1% had quadruple-root involve-
ment.
Even in the presence of symp-
toms, there may be few associated
physical findings. A thorough
examination is required, however,
to rule out other conditions that
may cause referred pain to the lum-
bar region or lower extremities.
Abnormalities in gait may be related
to the lumbar stenosis, although
the possibility of cervical myelopa-
thy or an intracranial disorder
should also be considered, espe-
cially in patients with a positive
Romberg test. Patients frequently
assume a ÒsimianÓ posture, with
translation of the shoulders anterior

to the pelvis.
Tenderness, if present, is usually
noted on palpation of the sciatic
notches or the lumbosacral or
sacroiliac region. Lumbar lordosis
is generally reduced, and range of
motion is diminished. There are
usually no signs of nerve root ten-
sion, although lower-extremity
pain may be reproduced by forci-
ble lumbar extension. The straight-
leg-raising test may be positive if a
concurrent disk herniation or nerve
root entrapment is present. The
remainder of the neurologic exami-
nation is usually normal, at least
when the patient is at rest. If mus-
cle weakness is present, it is most
often in the L5 root distribution.
Postexercise examination may
reveal greater motor weakness and
help establish the diagnosis of lum-
bar stenosis.
Sensory examination should
include vibration and propriocep-
tion testing in addition to pin-prick
testing. Responses may be altered
by spinal stenosis or peripheral
neuropathy, as may be seen in dia-
betic patients. Deep tendon reflexes

may be diminished due to involve-
ment of the L3, L4, or S1 nerve
roots. Loss of deep tendon reflexes
is common among the elderly.
Evaluation of hip and knee
range of motion, joint irritability,
and peripheral pulses should be
documented. Amundsen et al
12
reported sensory changes in 51% of
patients with lumbar stenosis; re-
flex changes in 47%; lumbar ten-
derness in 40%; reduced spinal
mobility in 36%; positive straight-
leg-raising test in 24%; weakness in
23%; and perianal numbness in 6%.
Differential Diagnosis
It is essential to rule out other con-
ditions that may present with pain
in the low back and/or lower
extremity (Table 2). Peripheral vas-
cular claudication should be differ-
entiated from neurogenic claudica-
tion. Both conditions are most
prevalent in the older population
and may coexist. Symptoms of vas-
cular claudication are reproduced at
a consistent level of exertion (e.g.,
walking two blocks). These symp-
toms are most commonly described

as cramping or tightness in the large
muscle groups of the buttock, thigh,
and leg. Peripheral vascular disease
will result in diminished peripheral
pulses; therefore, in patients with
buttock, thigh, or leg pain, vascular
studies should be obtained, with
determination of ankle and brachial
indices. Aortic aneurysms are a less
common source of low back pain
but have serious consequences.
They may be palpable on examina-
tion, and can be assessed with
abdominal ultrasonography. The
Alan S. Hilibrand, MD, and Nahshon Rand, MD
Vol 7, No 4, July/August 1999
241
Table 2
Differential Diagnosis of Lumbar
Spinal Stenosis
Vascular conditions
Peripheral vascular disease
Aortic aneurysm
Musculoskeletal diseases
Degenerative arthritis of the hip
Degenerative arthritis of the knee
Pelvic and sacral disorders
Neurologic disorders
Diabetic neuropathy
Peripheral compressive neuropathy

Cervical myelopathy
Amyotrophic lateral sclerosis
Demyelinating disease
Other
Renal disorder
Retroperitoneal tumors
Depression
Litigation-related issues
aorta can frequently be visualized
on axial spinal imaging.
Osteoarthritis of the hip may be
associated with buttock pain, a com-
mon complaint in patients with lum-
bar stenosis. These patients most
commonly relate their symptoms to
weight bearing on the affected limb,
although radiation therapy to the
groin or the anterior aspect of the
thigh may be a factor with both hip
arthritis and stenosis of the upper
lumbar spine. Hip irritability and
diminished range of motion, espe-
cially in internal rotation and abduc-
tion, are commonly seen with
degenerative arthritis of the hip.
Peripheral neuropathy, most
commonly the result of diabetes
mellitus, is another cause of lower-
extremity complaints in the elderly.
Generally, peripheral neuropathy

presents with dysesthesias and
paresthesias rather than activity-
and position-related claudication.
The anatomic distribution of symp-
toms may help distinguish these two
entities: in stenosis, sensation is
more likely to be diminished in a
dermatomal distribution; in contrast,
diabetic neuropathy is characterized
by a Òstocking/gloveÓ distribution.
Electromyography and nerve con-
duction studies are helpful in differ-
entiating the two entities.
Less common diagnoses, such as
renal infections and fevers, retro-
peritoneal tumors, and sacral or
presacral lesions should be consid-
ered as well. It should also be
borne in the mind that certain
nonorganic factors, such as depres-
sion and involvement in litigation,
may enhance the pain response.
Diagnostic Modalities
The primary role of imaging studies
is to confirm the clinical diagnosis
of lumbar stenosis, although ad-
vanced imaging studies are also
essential for preoperative planning.
Upright plain radiographs are nec-
essary to exclude pathologic condi-

tions of the spine, such as tumor,
infection, and fracture. The films
may demonstrate hypertrophic facet
joints narrowing the interlaminar
space, but these plain-radiographic
findings are not diagnostic of spinal
stenosis. Dynamic views should be
obtained to identify associated in-
stability, such as that due to spon-
dylolisthesis, scoliosis, or other
spinal deformity.
In patients with signs and symp-
toms consistent with spinal steno-
sis, magnetic resonance (MR) imag-
ing or postmyelographic computed
tomography (CT) is needed to con-
firm neural element compression.
Until the advent of MR imaging,
the most widely utilized radiologic
technique for evaluating spinal
stenosis was myelography in com-
bination with CT. On the myelo-
gram, nerve root entrapment in the
lateral recess or central canal steno-
sis is demonstrated by the level of
cutoff of contrast material. The
postmyelographic CT images can
then be used to identify the bone or
soft tissue at each level that must
be removed for decompression.

Using myelography and CT, Bolen-
der et al
4
correlated the degree of
symptomatic lumbar stenosis with
the anteroposterior diameter of the
dural sac. A sac narrower than 10
mm was usually associated with
clinical symptoms. Herno et al
13
also found that myelographic evi-
dence of complete cutoff of contrast
material and severe stenosis corre-
lated with better surgical outcome.
A disadvantage of myelography is
that it requires injection of contrast
medium into the spinal canal; post-
injection spinal headache is rela-
tively common.
Magnetic resonance imaging is a
noninvasive technique that can also
define neural element compression
through cross-sectional axial and
sagittal imaging. This very sensitive
method of evaluation should be
used to confirm a clinical diagnosis
of lumbar stenosis. In one study,
14
21% of asymptomatic individuals
aged 60 to 80 years had MR imaging

evidence of lumbar stenosis. Modic
et al
15
prospectively found 79%
agreement between the severity of
lumbar spinal stenosis noted at
surgery and the postmyelographic
CT findings, compared with 77%
agreement with MR findings. Two
advantages of plain myelography
over MR imaging include the ability
to evaluate dynamic neural element
compression on flexion-extension
views and the improved definition
of nerve root anatomy in scoliotic
patients.
Riew et al
16
recently compared
the relative contributions of MR
imaging and postmyelographic CT
in surgical planning for patients
with lumbar stenosis. The four
academic spine surgeons who par-
ticipated expressed a general pref-
erence for MR imaging over post-
myelographic CT for preoperative
planning. However, the surgical
plans derived from review of the
postmyelographic CT study alone

were much closer to those derived
from both studies together than
were the plans derived from a
review of the MR study alone.
Although the authors noted that
the two modalities provided com-
plementary information and were
both important, they concluded
that postmyelographic CT is supe-
rior to MR imaging as a single
study for the preoperative plan-
ning of decompression for lumbar
spinal stenosis.
Electrophysiologic studies are
rarely useful, except in identifying
the presence and source of a
peripheral neuropathy. About 80%
of patients with symptomatic lum-
bar stenosis will demonstrate elec-
tromyographic changes,
17
usually
consistent with single or multiple
radiculopathies. The presence of
these changes supports the diagno-
sis of lumbar spinal stenosis, al-
though their absence does not
Degenerative Lumbar Stenosis
Journal of the American Academy of Orthopaedic Surgeons
242

exclude the diagnosis. Somato-
sensory evoked potentials (SSEPs)
and dermatomal SSEPs may pro-
vide additional information by
identifying changes in the sensory
component of peripheral nerves or
in the dermatomes of the lower ex-
tremities.
10
Overview of Treatment
Options
The prevalence of lumbar spinal
stenosis is increasing with the aging
of the population. However, many
persons who have degenerative
changes consistent with lumbar
stenosis are asymptomatic. For
those with symptomatic lumbar
stenosis, the natural history has been
shown to be relatively stable in mild
to moderate cases. Johnsson et al
18
studied the progression of symp-
toms over 4 years in 32 patients with
lumbar stenosis who either refused
or were not medically cleared for
decompressive surgery. The symp-
toms of 70% of the patients were un-
changed at follow-up, with half of
the remainder better and half worse.

Although the physical findings were
improved in almost half of the pa-
tients, 38% had progression of elec-
tromyographic changes. In the
shorter term, patients in the Maine
Lumbar Spine Study (Part III) who
were treated nonoperatively re-
mained symptomatically stable but
did not show any significant clinical
improvement.
19
Appropriate candidates who do
not improve with nonoperative in-
terventions are likely to realize
major benefits from decompressive
surgery if they have moderate to
severe lumbar stenosis. The litera-
ture supporting operative treatment
of lumbar stenosis has been shown
to have many methodologic flaws
with respect to indications for
surgery, surgical approaches, and
long-term outcome.
20
Recently,
however, the results in the Maine
Lumbar Spine Study (Part III) pro-
spectively demonstrated superior
outcomes at 1 year for operative
treatment of symptomatic lumbar

stenosis compared with continued
nonoperative management. The
preliminary results in the same co-
hort demonstrated that the opera-
tively treated patients maintained
their superior status compared with
nonoperatively treated patients
even at 3-year follow-up.
19
Longer
prospective follow-up is needed to
prove the long-term superiority of
operative treatment of lumbar ste-
nosis.
Nonoperative Management
Nonsteroidal anti-inflammatory
drugs (NSAIDs) should be part of
the initial management of sympto-
matic lumbar stenosis (Fig. 2). At
lower doses, the analgesic effect
reduces musculoskeletal pain; at
higher doses, NSAIDs provide an
anti-inflammatory effect on nerve
root and joint irritation. Unfortu-
nately, many elderly patients can-
not tolerate the gastrointestinal and
renal side effects. Another option is
enteric-coated aspirin, which may
be as effective, at lower cost and
with fewer gastrointestinal side

effects. Patients taking any of these
medicines should have their hepatic
and renal function monitored.
For patients with severe radicu-
lar complaints, corticosteroids are
potent anti-inflammatory agents
that may reduce nerve root irrita-
tion. However, their benefits must
be weighed against the potential
side effects, such as osteonecrosis
of the femoral head, hypergly-
cemia, and gastritis. In addition,
steroids may adversely affect the
mental status of elderly patients.
Many physicians continue to
prescribe narcotic analgesics for the
treatment of chronic back pain and
neurogenic claudication. These
medications are analgesic but not
anti-inflammatory. They are addic-
tive and have depressant effects on
mood and energy level. In the ab-
sence of an acute fracture or meta-
static cancer, they have a limited
role in the treatment of patients
with lumbar stenosis.
Other medications used to treat
stenotic symptoms include muscle
relaxants, antidepressants, and calci-
tonin. Muscle relaxants may pro-

vide short-term relief of muscle
spasm, but geriatric patients may
have adverse reactions. Tricyclic
antidepressants are useful in the
treatment of chronic numbness and
dysesthetic leg pain, and help estab-
lish an effective sleep pattern.
Salmon calcitonin has been reported
as a medical treatment for neuro-
genic symptoms of stenosis. Al-
though it may be indicated in the
management of spinal stenosis re-
lated to Paget disease, its efficacy has
not been demonstrated in double-
blinded studies.
21
Physical therapy is another com-
mon nonoperative intervention for
symptomatic lumbar stenosis. A
modification of the standard low-
back-pain exercise program may be
used, wherein postural exercises in
flexion are combined with pelvic
stabilization and aerobic condition-
ing. The stabilization exercises are
utilized to strengthen the abdomi-
nal and lumbodorsal muscle groups
and unload the spinal elements. A
program of aerobic conditioning
can improve overall muscle tone

and truncal balance as well as assist
in weight loss, which is important
in the treatment of lumbar stenosis
in obese individuals. Patients with
lumbar stenosis are ideally suited to
the exercise bicycle. We also en-
courage walking, if tolerated by the
patient. Aquatic therapy can be
beneficial for some patients limited
by medical comorbidities.
Brace or elastic-corset immobi-
lization for low back pain due to
spinal stenosis is another available
treatment. The support from a
Alan S. Hilibrand, MD, and Nahshon Rand, MD
Vol 7, No 4, July/August 1999
243
brace may provide short-term relief
when back pain is related to seg-
mental instability or spondylolisthe-
sis, although it can prevent lumbar
flexion, which may limit its regular
use. An elastic corset may also
assist the posterior musculature by
providing a counterforce to contrac-
tions, reducing strain. Long-term
brace wear leads to truncal decondi-
tioning, however, and has therefore
fallen out of favor.
Epidural steroid injection (ESI)

is an invasive modality that may be
used to treat patients with lumbar
stenosis. It involves delivery of a
corticosteroid preparation, such as
methylprednisolone, around the
stenotic cauda equina and nerve
roots in order to relieve lower-
extremity pain and neurogenic
claudication. Numerous articles
have been written regarding the
efficacy of ESI in the treatment of
lumbar radicular syndromes; how-
ever, only a few of these studies
included patients with degenera-
tive lumbar stenosis.
Cuckler et al
22
performed a pro-
spective, randomized, double-blind
study of epidural steroids in pa-
tients with lumbar radicular syn-
dromes, approximately half of
whom had diagnoses of lumbar
spinal stenosis. In the patients with
spinal stenosis, no statistically sig-
nificant difference was seen in
symptomatic improvement be-
tween steroid and placebo injec-
tions at 24-hour and 1-year follow-
up. However, a similar study in

1973 by Dilke et al
23
demonstrated a
significant (P<0.05) improvement in
short-term pain and functional
measures.
In a study restricted to patients
with symptomatic lumbar stenosis,
Hoogmartens and Morelle
24
found
that 48% of patients treated with
ESI demonstrated functional im-
provement from their preinjection
status approximately 2 years after
treatment. However, the patients
were evaluated retrospectively and
were not compared with a control
group. Furthermore, the authors
conceded that the improvement
rate was close to that of the placebo
effect. Nevertheless, they suggested
that ESI is a good alternative to sur-
gical treatment in older patients
with medical comorbidities.
At our center, we reserve ESI for
patients with mild to moderate
stenosis and major medical comor-
bidities for whom medical treat-
ments and physical therapy have

not been efficacious. If the first in-
jection provides symptomatic relief,
one or two additional injections are
prescribed. We use ESI to facilitate
a return to more aggressive truncal
strengthening and aerobic condi-
tioning, which may provide longer-
term relief of symptoms. There are,
however, potential complications of
ESI, including meningitis, para-
paresis, arachnoiditis, and epidural
hematoma.
25
Other invasive modalities con-
tinue to be widely used despite a
lack of scientific support. Facet-
joint injections may provide tempo-
rary relief in select patients with
Degenerative Lumbar Stenosis
Journal of the American Academy of Orthopaedic Surgeons
244
No symptoms Symptoms
Successful
Unsuccessful Successful
No further
workup
No further
workup
Referrals
No further workup

Advanced
imaging studies
Severe
stenosis
Mild to moderate
stenosis
Minimal
stenosis
Unsuccessful at
6-12 weeks
Patient with
lumbar stenosis
NSAIDs
Physical therapy
Weight loss
NSAIDs
Physical therapy
Weight loss
Operative
intervention
Operative
intervention
Epidural
steroids
Reevaluate
for other
causes
Fig. 2 Algorithm for nonoperative management of degenerative lumbar stenosis.
low back pain, although their effi-
cacy in lumbar stenosis has not

been shown.
26
Manipulation is
another common treatment modali-
ty for back pain that has not been
proved efficacious in treating
patients with degenerative lumbar
stenosis.
Operative Treatment
Not all patients for whom nonopera-
tive treatment has failed will be sur-
gical candidates. However, when
nonoperative intervention cannot
restore the patient to a tolerable
quality of life, operative treatment
can be considered (Fig. 3). A thor-
ough workup should identify any
associated degenerative pathologic
changes, such as spondylolisthesis,
segmental instability, or scoliosis,
that might require stabilization in
addition to decompression. Decom-
pressive surgery is clearly indicated
in cases of progressive neurologic
deficit, cauda equina syndrome, and
disabling lower-extremity weakness.
In addition, decompressive treat-
ment is appropriate for patients with
neurogenic claudication and/or
pain that significantly affects the

patientÕs quality of life.
Previous reviews have suggest-
ed that surgical treatment of lum-
bar stenosis is successful (defined
as significant pain relief with a
return to activities of daily living)
in 80% to 85% of cases.
17,27
How-
ever, other authors have found a
much lower rate of successful
results, perhaps attributable to dif-
fering definitions of a Òsuccessful
result.Ó In a retrospective review 4
years after lumbar decompression,
Katz et al
28
found Òsuccessful out-
comesÓ (defined as relief of pain
and no reoperation) in only 57% of
cases. Factors associated with un-
successful outcomes were multiple
comorbidities, single-level decom-
pressions, and a 5% annual inci-
dence of degeneration at levels ad-
jacent to the decompression. In
another shorter-term follow-up
study of patients who underwent
surgery for lumbar stenosis, the
authors identified predominating

low back pain as another factor
associated with poor outcomes
after surgical treatment of lumbar
stenosis.
29
Katz et al
28
have suggested that
surgical results deteriorate with
time. However, Herno et al
30
ob-
served 67% and 69% successful
outcomes in their patients at 7 and
13 years after lumbar decompres-
sion, respectively.
Preoperative planning for lum-
bar decompression begins with a
review of the clinical findings and
evaluation with MR imaging or
postmyelographic CT to precisely
identify areas of neural element
compression by articular processes,
capsular tissue, bulging anulus, and
ligamentum flavum in the lateral
recesses and foramina. Patients
will sometimes present with multi-
level disease despite well-defined
neurologic deficits referable to one
or two motor roots (Fig. 4). Several

authors have suggested that pro-
duction of symptomatic disease
may require compression of the
cauda equina at more than one
level.
11,31,32
As a result, in some
centers it is routine to address all
levels of moderate or severe steno-
sis visualized with postmyelo-
graphic CT at the time of surgical
decompression.
For surgical decompression, the
patient is placed in the prone knee-
chest position, although the more
lordotic position of the Jackson
spinal table may be preferred when
internal fixation is planned. The
lumbar spine is exposed through a
midline incision of skin, subcuta-
neous tissue, and thoracolumbar
fascia. Subperiosteal exposure is
carried out laterally to the facet
joint capsules, which are preserved,
and the lateral extent of the pars
interarticularis is identified.
Compressive elements are re-
moved by undercutting the facet
joints and pars interarticularis, tak-
ing care to preserve at least 50% of

the facet joint surface area and
approximately 1 cm of the dorsal
Alan S. Hilibrand, MD, and Nahshon Rand, MD
Vol 7, No 4, July/August 1999
245
No spondylolisthesis Spondylolisthesis
Stable
Fusion ±
instrumentation
Fusion ±
instrumentation
Fusion ±
instrumentation
No or minimal
scoliosis
Significant
scoliosis
Lumbar
decompression
only
Fusion
in situ
Surgical
candidate
Unstable
(>3 mm on
dynamic films)
StableUnstable (grade II or
higher or >3 mm on
dynamic films)

Fig. 3 Algorithm for operative management of degenerative lumbar stenosis.
surface of the pars.
33
The effective-
ness of the decompression is
checked by carefully mobilizing the
compressed root with a No. 4
Penfield elevator and probing the
neural foramen with an angled
dural elevator. Foraminotomy is
usually necessary in patients with
significant degenerative stenosis.
This may require removal of por-
tions of the superior articular pro-
cess of the caudal vertebra, a portion
of the pars interarticularis, the anu-
lus fibrosus, or the pedicle of the
superior vertebra. This aspect of the
decompression may be accom-
plished with a Kerrison rongeur,
small curettes, or a high-speed burr.
When the root can be easily mobi-
lized from the pedicle and an angled
dural elevator can be easily passed
out the foramen around the root, the
decompression is adequate. In the
absence of instability, posterolateral
grafting has not been shown to
improve outcome.
34

Degenerative spondylolisthesis
is a radiographic finding often
associated with spinal stenosis at
the L4-5 level, especially in women
(Fig. 5). In 1991, Herkowitz and
Kurz
35
published a controlled
prospective study of patients with
lumbar stenosis and degenerative
spondylolisthesis who were ran-
domized to either decompression
alone or decompression with in
situ intertransverse autogenous
bone grafting. The authors demon-
strated significantly better out-
comes in patients who underwent
decompression and grafting proce-
dures (P = 0.0001).
In another study, the same
group studied patients with steno-
sis and degenerative spondylolis-
thesis treated by decompression
and grafting, prospectively com-
paring outcomes with and without
internal fixation.
36
Although radio-
graphic evidence of arthrodesis
was significantly more likely with

internal fixation (P = 0.0015), the
clinical outcome was not improved.
The authors concluded that even in
the absence of a solid fusion, the
intertransverse bone grafting pro-
cedure stiffened the spine suffi-
ciently to relieve nerve root irrita-
tion.
In some patients with spinal
stenosis, dynamic lateral radio-
graphs may indicate segmental
instability, defined as more than 3
mm of motion between vertebrae on
dynamic views.
37
We routinely
obtain preoperative prone and
supine lateral radiographs of all
lumbar stenosis patients. If the films
document segmental instability,
decompression with intertransverse
bone grafting is recommended. The
use of internal fixation in this group
of patients remains controversial;
some surgeons include fixation in
the physically active patient with at
least 5 mm of motion and localized
mechanical complaints.
Degenerative Lumbar Stenosis
Journal of the American Academy of Orthopaedic Surgeons

246
Fig. 4 Images of a patient who presented with chronic neurogenic claudication, bilateral lower-extremity numbness, and significant
weakness of the L4 and L5 muscle groups preventing ambulation. A, Lateral radiograph demonstrates anterolisthesis at L4-5 and retrolis-
thesis at L3-4. Note obliteration of L3-4 disk space and narrowing of neural foramen (arrow). B, Myelogram shows cutoff of contrast
material from the L2-3 level through the L4-5 level. C, Postmyelographic CT at L3-4 level shows absence of contrast material secondary to
proximal cutoff, with hypertrophy of the ligamentum flavum, degenerated facets, and congenitally narrow (trefoil-shaped) spinal canal.
D, Anteroposterior radiograph obtained 6 weeks postoperatively demonstrates wide decompression from L2 through L5, with complete
resection of the right L3 pars region (arrows) due to severe foraminal stenosis. Note early consolidation of autogenous iliac-crest bone
graft in intertransverse gutters.
A B C D
2
3
4
5
2
3
4
5
2
3
4
5
Patients undergoing revision lum-
bar decompression should receive
special attention. Frequently, there is
persistent lateral recess and/or
foraminal stenosis not addressed at
the index procedure, which should
be widely decompressed at the revi-
sion operation. Some patients may

have iatrogenic spondylolisthesis,
scoliosis, or postlaminectomy insta-
bility. This can lead to significant
coronal and/or sagittal decompensa-
tion, which must be addressed at
reoperation. We routinely evaluate
candidates for revision lumbar
decompression with 3-ft-long stand-
ing radiographs. If patients have
coronal decompensation or loss of
lumbar lordosis, intertransverse
bone grafting and internal fixation
may be helpful to restore anatomic
sagittal coronal alignment.
Whether operative treatment of
recurrent lumbar stenosis can be as
successful as primary procedures
continues to be controversial.
Herno et al
38
found that revision
procedures were as successful as
primary procedures when patients
presented at least 18 months after
the index procedure with few
comorbidities. Overall, however,
outcomes were significantly worse
for revision procedures than for pri-
mary procedures in the study pop-
ulation (P<0.0017). Stewart and

Sachs
39
reported that at an average
follow-up of 4 years, 72% of their
patients who had undergone repeat
decompression were able to return
to their preinjury work status, 83%
of those treated with grafting went
on to a solid arthrodesis, and none
of the 39 patients required another
procedure. In general, better out-
comes are associated with a pain-
free interval after the initial proce-
dure, and worse outcomes are asso-
ciated with periradicular fibrosis.
Complications
Although operative treatment can
improve the quality of life of
patients with lumbar stenosis, it
can also be associated with major
complications, which should be
discussed with the patient. Postop-
erative complications may include
epidural hematoma, instability fol-
lowing wide decompression in the
absence of bone grafting, nonunion
of the graft with failure of any con-
comitant instrumentation, and the
need for future surgery due to the
development of new disease at

adjacent levels.
Any lengthy procedure in an
elderly patient under general anes-
thesia poses risks to the cardiovascu-
lar and respiratory systems. These
procedures are often associated with
major blood loss, which may require
transfusion and invasive cardiac
monitoring.
Despite antibiotic prophylaxis
and strict observation of sterile
technique, infection and sepsis re-
main a risk, especially when inter-
nal fixation is applied. A recent
historical cohort study of patients
undergoing lumbar decompression
and arthrodesis, with or without
internal fixation, revealed an infec-
tion rate of 2% to 3% for degenera-
tive spondylolisthesis.
40
In the same study,
40
the incidence
of nerve root injury from placement
of bone screws in the pedicle for
degenerative spondylolisthesis was
0.4%. Nerve root injury can occur as
a result of manipulation of a severely
Alan S. Hilibrand, MD, and Nahshon Rand, MD

Vol 7, No 4, July/August 1999
247
Fig. 5 Images of a patient who presented with lower-back and bilateral lower-extremity numbness with ambulation. A, Lateral radio-
graph shows grade I degenerative spondylolisthesis at L4-5. B, Myelogram shows truncation of the column of contrast material and bilat-
eral fifth-root cutoff (arrows) at the level of the spondylolisthesis. C, Postmyelographic CT scan demonstrates severe spinal stenosis at the
level of the spondylolisthesis. D, Anteroposterior radiograph obtained 6 weeks postoperatively demonstrates L4 decompressive laminec-
tomy and intertransverse bone grafting (arrows). The patient was asymptomatic.
A B C D
4
5
4
4-5
5
4
5
compressed nerve root or the use of
internal fixation. Although there are
no large clinical studies that specifi-
cally assess the neurologic complica-
tions of decompressive lumbar
surgery, a recent review by Wang et
al
41
of the data on 641 patients
revealed an incidence of dural tears
of 13.7%; however, half of the opera-
tions in that series were revisions.
Summary
Degenerative lumbar stenosis is a
common cause of back and leg pain

in older patients. It usually results
from degeneration of the lumbar
motion segments, which causes
insidious compression of the neural
elements. Only a small proportion
of the elderly population will have
symptoms that merit referral to an
orthopaedic surgeon. Most patients
will obtain symptomatic improve-
ment with medication and physical
therapy and not require operative
intervention. However, it has not
been shown that any nonoperative
treatment can alter the relatively
stable natural history of the disease.
The findings from the Maine
Lumbar Spine Study
19
suggest that
surgical treatment can improve on
the natural history of lumbar steno-
sis at short- to intermediate-term
follow-up. If nonoperative treat-
ment has failed and operative man-
agement is elected, it is crucial that
all pathologic changes be addressed
at surgery. An intertransverse
grafting (fusion) procedure should
be included if there is any preoper-
ative or intraoperative evidence of

instability. Although the applica-
tion of internal fixation increases
the likelihood of successful ar-
throdesis, further study is needed
to determine which patients will
benefit. Questions regarding the
long-term clinical outcome of surgi-
cal treatment of lumbar spinal
stenosis require prospective studies
for clarification.
Degenerative Lumbar Stenosis
Journal of the American Academy of Orthopaedic Surgeons
248
References
1.Roberson GH, Llewellyn HJ, Taveras
JM: The narrow lumbar spinal canal
syndrome. Radiology1973;107:89-97.
2.De Villiers PD, Booysen EL: Fibrous
spinal stenosis: A report on 850 myelo-
grams with a water-soluble contrast
medium. Clin Orthop1976;115:140-144.
3.Rosenberg NJ: Degenerative spondy-
lolisthesis: Predisposing factors. J Bone
Joint Surg Am1975;57:467-474.
4.Bolender NF, Schšnstršm NS, Speng-
ler DM: Role of computed tomogra-
phy and myelography in the diagnosis
of central spinal stenosis. J Bone Joint
Surg Am1985;67:240-246.
5.Arnoldi CC, Brodsky AE, Cauchoix J,

et al: Lumbar spinal stenosis and
nerve root entrapment syndromes:
Definition and classification. Clin
Orthop1976;115:4-5.
6.Wiltse LL, Guyer RD, Spencer CW,
Glenn WV, Porter IS: Alar transverse
process impingement of the L5 spinal
nerve: The far-out syndrome. Spine
1984;9:31-41.
7.Kirkaldy-Willis WH, Wedge JH, Yong-
Hing K, Reilly J: Pathology and patho-
genesis of lumbar spondylosis and
stenosis. Spine1978;3:319-328.
8.Zinreich SJ, Heithoff KB, Herzog RJ:
Computed tomography of the spine,
in Frymoyer JW, Ducker TB, Hadler
NM, Kostuik JP, Weinstein JN,
Whitecloud TS III (eds): The Adult
Spine: Principles and Practice, 2nd ed.
Philadelphia: Lippincott-Raven, 1997,
vol 1, pp 467-522.
9.Delamarter RB, Bohlman HH, Dodge
LD, Biro C: Experimental lumbar
spinal stenosis: Analysis of the cortical
evoked potentials, microvasculature,
and histopathology. J Bone Joint Surg
Am1990;72:110-120.
10.Garfin SR, Rydevik BL, Lipson SJ:
Spinal stenosis: Pathophysiology, in
Rothman RH, Simeone FA (eds): The

Spine, 3rd ed. Philadelphia: WB Saun-
ders, 1992, vol 1, pp 791-826.
11.Parke WW, Watanabe R: The intrinsic
vasculature of the lumbosacral spinal
nerve roots. Spine1985;10:508-515.
12.Amundsen T, Weber H, LilleŒs F,
Nordal HJ, Abdelnoor M, Magnaes B:
Lumbar spinal stenosis: Clinical and
radiologic features. Spine1995;20:
1178-1186.
13.Herno A, Airaksinen O, Saari T,
Miettinen H: The predictive value of
preoperative myelography in lumbar
spinal stenosis. Spine1994;19:1335-
1338.
14.Boden SD, Davis DO, Dina TS,
Patronas NJ, Wiesel SW: Abnormal
magnetic-resonance scans of the lum-
bar spine in asymptomatic subjects: A
prospective investigation. J Bone Joint
Surg Am1990;72:403-408.
15.Modic MT, Masaryk T, Boumphrey F,
Goormastic M, Bell G: Lumbar herni-
ated disk disease and canal stenosis:
Prospective evaluation by surface coil
MR, CT, and myelography. AJR Am J
Roentgenol1986;147:757-765.
16.Riew KD, Hilibrand AS, Bridwell KH,
et al: MR versus CT-myelography:
Surgical decision-making for lumbar

stenosis, in Proceedings of the 13th Annual
Meeting of the North American Spine
Society. Rosemont, Ill: North American
Spine Society, 1998, pp 117-118.
17.Spengler DM: Degenerative stenosis
of the lumbar spine. J Bone Joint Surg
Am1987;69:305-308.
18.Johnsson KE, RosŽn I, UdŽn A: The
natural course of lumbar spinal steno-
sis. Clin Orthop1992;279:82-86.
19.Atlas SJ, Deyo RA, Keller RB, et al: The
Maine Lumbar Spine Study, Part III: 1-
Year outcomes of surgical and nonsur-
gical management of lumbar spinal
stenosis. Spine1996;21:1787-1795.
20.Turner JA, Ersek M, Herron L, Deyo R:
Surgery for lumbar spinal stenosis:
Attempted meta-analysis of the litera-
ture. Spine1992;17:1-8.
21.Porter RW, Miller CG: Neurogenic
claudication and root claudication
treated with calcitonin: A double-blind
trial. Spine1988;13:1061-1064.
22.Cuckler JM, Bernini PA, Wiesel SW,
Booth RE Jr, Rothman RH, Pickens GT:
The use of epidural steroids in the
treatment of lumbar radicular pain: A
prospective, randomized, double-
blind study. J Bone Joint Surg Am
1985;67:63-66.

23.Dilke TFW, Burry HC, Grahame R:
Extradural corticosteroid injection in
the management of lumbar nerve root
compression. BMJ1973;2:635-637.
24.Hoogmartens M, Morelle P: Epidural
injection in the treatment of spinal
stenosis. Acta Orthop Belg1987;53:
409-411.
25.Dougherty JH Jr, Fraser RAR: Compli-
cations following intraspinal injections
of steroids: Report of two cases. J
Neurosurg1978;48:1023-1025.
26.Jackson RP, Jacobs RR, Montesano PX:
Facet joint injection in low-back pain:
A prospective statistical study. Spine
1988;13:966-971.
27.Lipson SJ: Spinal stenosis. Rheum Dis
Clin North Am1988;14:613-618.
28.Katz JN, Lipson SJ, Larson MG,
McInnes JM, Fossel AH, Liang MH:
The outcome of decompressive lami-
nectomy for degenerative lumbar
stenosis. J Bone Joint Surg Am1991;73:
809-816.
29.Katz JN, Lipson SJ, Brick GW, et al:
Clinical correlates of patient satisfac-
tion after laminectomy for degenera-
tive lumbar spinal stenosis. Spine
1995;20:1155-1160.
30.Herno A, Airaksinen O, Saari T: Long-

term results of surgical treatment of
lumbar spinal stenosis. Spine1993;18:
1471-1474.
31.Porter RW: Spinal stenosis and neuro-
genic claudication. Spine1996;21:2046-
2052.
32.Olmarker K, Rydevik B: Single- versus
double-level nerve root compression:
An experimental study on the porcine
cauda equina with analyses of nerve
impulse conduction properties. Clin
Orthop1992;279:35-39.
33.Abumi K, Panjabi MM, Kramer KM,
Duranceau J, Oxland T, Crisco JJ:
Biomechanical evaluation of lumbar
spinal stability after graded facetec-
tomies. Spine1990;15:1142-1147.
34.Grob D, Humke T, Dvorak J: Degen-
erative lumbar spinal stenosis: Decom-
pression with and without arthrodesis.
J Bone Joint Surg Am1995;77:1036-1041.
35.Herkowitz HN, Kurz LT: Degenera-
tive lumbar spondylolisthesis with
spinal stenosis: A prospective study
comparing decompression with
decompression and intertransverse
process arthrodesis. J Bone Joint Surg
Am1991;73:802-808.
36.Fischgrund JS, MacKay M, Herkowitz
H, Brower R, Montgomery DM, Kurz

LT: Degenerative lumbar spondylolis-
thesis with spinal stenosis: A prospec-
tive, randomized study comparing
decompressive laminectomy and arth-
rodesis with and without spinal instru-
mentation. Spine1997;22:2807-2812.
37.Boden SD, Wiesel SW: Lumbosacral
segmental motion in normal individu-
als: Have we been measuring instabili-
ty properly? Spine1990;15:571-576.
38.Herno A, Airaksinen O, Saari T,
Sihvonen T: Surgical results of lumbar
spinal stenosis: A comparison of
patients with or without previous back
surgery. Spine1995;20:964-969.
39.Stewart G, Sachs BL: Patient outcomes
after reoperation on the lumbar spine.
J Bone Joint Surg Am1996;78:706-711.
40.Yuan HA, Garfin SR, Dickman CA,
Mardjetko SM: A historical cohort
study of pedicle screw fixation in tho-
racic, lumbar, and sacral spinal fusions.
Spine1994;19(suppl 20):2279S-2296S.
41.Wang JC, Bohlman HH, Riew KD:
Dural tears secondary to operations on
the lumbar spine: Management and
results after a two-year-minimum fol-
low-up of eighty-eight patients. J Bone
Joint Surg Am1998;80:1728-1732.
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