Review Article

Degenerative Lumbar Spinal

Stenosis: Evaluation and
Management
Abstract
Paul S. Issack, MD, PhD
Matthew E. Cunningham, MD,
PhD
Matthias Pumberger, MD
Alexander P. Hughes, MD
Frank P. Cammisa, Jr, MD

Degenerative lumbar spinal stenosis is caused by mechanical

factors and/or biochemical alterations within the intervertebral disk
that lead to disk space collapse, facet joint hypertrophy, soft-tissue
infolding, and osteophyte formation, which narrows the space
available for the thecal sac and exiting nerve roots. The clinical
consequence of this compression is neurogenic claudication and
varying degrees of leg and back pain. Degenerative lumbar spinal
stenosis is a major cause of pain and impaired quality of life in the
elderly. The natural history of this condition varies; however, it has
not been shown to worsen progressively. Nonsurgical management
consists of nonsteroidal anti-inflammatory drugs, physical therapy,
and epidural steroid injections. If nonsurgical management is
unsuccessful and neurologic decline persists or progresses,
surgical treatment, most commonly laminectomy, is indicated.
Recent prospective randomized studies have demonstrated that
surgery is superior to nonsurgical management in terms of
controlling pain and improving function in patients with lumbar
spinal stenosis.

From the Hospital for Special

Surgery, New York, NY.
J Am Acad Orthop Surg 2012;20:
527-535
http://dx.doi.org/10.5435/
JAAOS-20-08-527
Copyright 2012 by the American
Academy of Orthopaedic Surgeons.

August 2012, Vol 20, No 8

egenerative
lumbar
spinal
stenosis is a major cause of
pain and dysfunction in the elderly.
Most patients report leg and/or back
pain and have progressive symptoms
after walking or standing for even
short periods of time.1 Diagnosis is
typically made based on clinical history and physical examination and is
confirmed on imaging studies. In
most cases, treatment should begin
with nonsurgical management. In the
rare case of a progressive neurologic
deficit or cauda equina syndrome,
urgent surgical decompression is indicated. In most cases, the natural
history of degenerative lumbar stenosis is variable and does not follow a
progressively deteriorating course.
Recent prospective randomized tri-

als, particularly the Spine Patient

Outcomes Research Trial (SPORT)
study, have provided compelling evidence that decompressive surgery is
an effective treatment that provides
pain relief and functional improvement in patients with degenerative
lumbar spinal stenosis.2,3

Etiology
Lumbar spinal stenosis is a reduction
in the volume of the central spinal
canal, the lateral recesses, and/or
neuroforamina that decreases the
space available for the thecal sac
and/or exiting nerve roots.4,5 Approximately 20% of the time, this
condition is caused or exacerbated

527

Degenerative Lumbar Spinal Stenosis: Evaluation and Management

by congenital causes, such as failure

of the posterior elements to develop,
resulting in short pedicles and
laminae.4-6 More commonly, lumbar
stenosis is the result of degenerative
changes. The degenerative process is
thought to be initiated by disk dehydration, disk bulging, and collapse of
the disk space, which sets in motion
the sequence of events that result in
narrowing of the spinal canal. Disk
space narrowing and loss of the normal shock absorptive capacity of the
spinal segment results in an increased
transfer of stress to the facet joints,
which accelerates facet joint cartilage
degeneration and osteophyte formation.5,7 Facet joint hypertrophy, infolding of the ligamentum flavum,
and development of bulging disk osteophyte complexes all contribute to
circumferential narrowing of the central spinal canal and lateral recesses,
that is, the area of the spine bordered
by the superior articular facet posteriorly, the disk and vertebral body
anteriorly, the thecal sac medially,
and the pedicle laterally. These
stenotic changes cause neural compression that presents clinically as
variable degrees of leg and back
pain, as well as gait deterioration
and other neurologic deficits (eg,
numbness and weakness).

Natural History
Prevalence of degenerative lumbar
spondylosis in the general population ranges from 20% to 25% and
increases with age >50 years.8 The
natural history of this disease re-

mains unclear given the lack of prospective studies with observational

cohorts. Johnsson et al9 followed 32
untreated patients with spinal stenosis over 49 months. Symptoms of
neurogenic claudication remained
unchanged in 22 patients (70%),
symptoms improved in 5 patients
(15%), and symptoms worsened in 5
patients (15%). None of the patients
had severe deterioration.
Cauda equina syndrome is a rare
condition caused by compression of
the lumbosacral nerve roots within
the spinal canal that produces varying degrees of motor weakness; saddle anesthesia; and bowel, bladder,
and gait dysfunction. Acute presentation frequently occurs in patients
with large central disk herniation,
whereas delayed presentation often
occurs in patients with chronic spinal
stenosis. Surgical decompression
should be performed as soon as possible to avoid progression of neurologic deficits.10

Diagnosis
Clinical Presentation
Patients with lumbar spondylotic
stenosis most commonly present
with neurogenic claudication and report discomfort while standing as
well as diminished walking capacity.
In a series of 68 patients with lumbar
spinal stenosis confirmed with myelography and surgery, neurogenic
claudication was observed in 94% of
patients, with primary symptoms of
pain (93%), numbness (63%), or

weakness (43%) reported.1 These

symptoms may be localized to the
buttocks and can radiate to the
lower extremities in a proximal to
distal fashion. Patients with lumbar
spondylotic stenosis have diminished
standing and walking tolerance;
however their ability to walk distances can be increased by ambulating with the spine in a flexedforward posture such as that used
when pushing a shopping cart.4 Typically, spinal extension narrows the
spinal canal and worsens neurogenic
symptoms, whereas spinal flexion
and sitting increases the diameter of
the spinal canal, partially alleviating
symptoms.4,5,11
On physical examination, back
pain or lower extremity symptoms
can be elicited with lumbar extension. Objective sensory findings such
as diminished sensation along a specific dermatome or motor weakness
suggest long-standing neural compression. Radicular symptoms are
most commonly seen in patients with
lateral recess or foraminal stenosis.
Patients with spondylotic stenosis
may also present with neurogenic or
vascular claudication. The orthopaedic surgeon must distinguish neurogenic claudication from vascular
claudication; patients with vascular
claudication may present with diminished walking capacity due to
cramping of lower extremity muscles
on exertion. Unlike patients with
neurogenic claudication, patients
with vascular claudication cannot
improve walking tolerance with postural changes. Patients with neuro-

Dr. Hughes or an immediate family member is a member of a speakers bureau or has made paid presentations on behalf of
NuVasive; serves as a paid consultant to BOSS Medical, Bovie Medical Corporation, Orthovita, and SpineView; and has received
research or institutional support from NuVasive. Dr. Cammisa or an immediate family member has received royalties from NuVasive;
serves as a paid consultant to Alphatec Spine, Centinel Spine, Disc Motion Technologies, HealthpointCapital Partners, IVY
Healthcare Partners, Mazor Surgical Technologies, NuVasive, Orthogem, Orthovita, Paradigm Spine, Spinal Kinetics, Spinal Partners
III, and Viscogliosi Brothers; and has stock or stock options held in Alphatec Spine, BI Members, Centinel Spine, Disc Motion
Technologies, HealthpointCapital Partners, IVY Healthcare Partners, Mazor Surgical Technologies, NuVasive, Orthovita, Orthopaedic
Investment Partners, Paradigm Spine, Small Bone Innovations, Spinal Kinetics, and Viscogliosi Brothers. None of the following
authors or any immediate family member has received anything of value from or owns stock in a commercial company or institution
related directly or indirectly to the subject of this article: Dr. Issack, Dr. Cunningham, and Dr. Pumberger.

528

Journal of the American Academy of Orthopaedic Surgeons

Paul S. Issack, MD, PhD, et al

Figure 1

A, Parasagittal T2-weighted magnetic resonance image of the lumbar spine demonstrating multilevel lumbar
spondylosis, with disk dehydration (arrowhead), disk protrusion (arrow), and central canal narrowing at L2-S1.
Hypertrophic changes in the ligamentum flavum and facet joint are most prominent at L4-S1. B, Axial T2-weighted
magnetic resonance image of the L4-5 interspace showing hypertrophy of the facet joint (arrowhead) and ligamentum
flavum (arrow), causing severe central canal and lateral recess stenosis. C, Parasagittal T1-weighted magnetic
resonance image of the lumbar spine demonstrating loss of epidural fat (arrow) about the lower lumbar exiting nerve
roots (L3, L4, and L5) and neuroforaminal stenosis.

genic claudication typically cannot

alleviate symptoms simply by ceasing
to walk; these patients must sit or
adopt a flexed-foward posture to alleviate symptoms. Patients with vascular claudication have similar
symptoms whether ambulating or
riding a stationary bicycle, whereas
patients with neurogenic claudication have diminished symptoms of
claudication while in a seated position. In addition, patients with vascular claudication may have evidence
of vascular changes such as trophic
changes in the skin of the legs and
feet as well as diminished distal pulses; this is typically not observed in
patients with neurogenic claudication.12

Radiographic Evaluation
Clinical history and physical examination aid in diagnosis of degenerative lumbar spinal stenosis. Typically,
imaging studies are used to confirm
the diagnosis and identify the levels
August 2012, Vol 20, No 8

involved as well as any associated

pathology. Plain standing AP and lateral radiographs may demonstrate
spondylolisthesis, disk space narrowing, end plate sclerosis, osteophytes,
and facet hypertrophy.13 Lateral and
flexion and extension stress radiographs may be helpful in determining
whether spondylolisthesis is mobile
and may demonstrate a slip that is
not visible on the plain standing lateral view.
No consensus exists regarding the
definition of spinal stenosis in terms
of the diameter of the spinal canal or
area measurements. Often, the degree of soft-tissue compression that
can be caused by ligament infolding is underestimated when these
measurements are used to assess spinal stenosis on CT. Furthermore,
measurements of midsagittal and
anterior-posterior canal diameter
may appear normal in patients with
trefoil-shaped spinal canals who
have clinically relevant lateral recess

stenosis with compression of traversing nerve roots. The degree of spinal

stenosis is best evaluated on MRI because it can demonstrate disk degeneration or herniation, hypertrophy of
the ligamentum flavum and facet
capsule, and narrowing of the central
canal and lateral recess (Figure 1, A
and B). Parasagittal T1-weighted
magnetic resonance images may
demonstrate loss of epidural fat at
the exiting nerve root or frank nerve
root deformation, which suggests entrapment of the root in the foramina13 (Figure 1, C). Radiographic
findings that indicate likely instability include the presence of gapped
facets on axial CT scan and fluidfilled facets visible on axial T2weighted magnetic resonance images.14 In patients without lumbar
spinal stenosis, supine magnetic resonance images show sedimentation of
the lumbar nerve roots to the dorsal
part of the thecal sac as a result of
gravity. The absence of normal sedi-

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Degenerative Lumbar Spinal Stenosis: Evaluation and Management

mentation is a positive sign of lumbar spinal stenosis.15

When MRI cannot be obtained,
myelography followed by CT may be
used to assess the degree and location of stenosis; these imaging modalities are helpful for preoperative
identification of locations that require decompression. Radiographic
changes are often seen in patients
who are asymptomatic; therefore,
correlation of imaging results with
clinical findings is essential for identification of relevant pathology. In a
study of 67 asymptomatic patients
who had no reports of low back
pain, sciatica, or neurogenic claudication, Boden et al16 reported that
MRI findings in patients aged 60
years were abnormal on approximately 57% of the scans, with 21%
of scans demonstrating spinal stenosis.

Management
Nonsurgical
The goals of therapy in patients with
degenerative lumbar stenosis are to
alleviate pain and improve function. Nonsteroidal anti-inflammatory drugs (NSAIDS) may temporarily and partially alleviate pain. In
general, narcotic analgesics should
be avoided or used on a short-term
basis preoperatively and as needed in
the immediate postoperative period.
Both NSAIDs and narcotic analgesics
can be especially problematic in the
elderly patient population. NSAIDs
have been associated with an increased risk of bleeding, gastrointestinal, liver, renal, cardiovascular, and
central nervous system complications
in the elderly.17 Narcotic analgesics
are associated with significant alterations in normal mood and sleepwake cycle as well as gastrointestinal
complications and potential respiratory suppression; these symptoms are
magnified in the elderly population.

530

Physical therapy, with an emphasis

on abdominal flexion exercises and
core muscle strengthening, may help
to improve muscle strength, maintain
range of motion, and improve global
functioning.18 In a randomized clinical trial that compared two physical
therapy programs for patients with
lumbar spinal stenosis, 18 of 29 patients (62%) treated with a 6-week
regimen of manual physical therapy,
body weight supported treadmill
walking, and exercise demonstrated
improvement in disability, satisfaction, and treadmill walking tests at
1-year follow-up.19
Epidural steroid injections can also
be used to provide temporary relief
of radicular symptoms in select patients.20 In a prospective study of 34
patients with radicular pain caused
by degenerative lumbar spinal stenosis, Botwin et al21 treated patients
with fluoroscopy-guided lumbar
transforaminal epidural injections.
The authors reported that 75% of
patients noted at least a >50% reduction in pain scores, 64% had improved walking tolerance, and 57%
had improved standing tolerance at
1-year follow-up. Other studies have
reported temporary improvement in
pain and function following epidural
injection. Tran et al22 performed a
meta-analysis of randomized controlled trials to examine nonsurgical
management of lumbar spinal stenosis, including the use of lumbar epidural injection used to manage lumbar spondylotic stenosis. They
determined that there may be no
added benefit in adding steroids to
the anesthetic injection. Additionally,
concerns exist regarding the effects
on bone quality and blood glucose
levels with repetitive use of steroids.4,20 In patients with severe neurologic deficit, including limited
walking capacity or cauda equina
syndrome, epidural steroid injections
can exacerbate symptoms; case reports have described complications

such as vascular injury, hematoma

formation, and paralysis.23,24 Furthermore, clear evidence-based guidelines are lacking regarding the number and frequency of injections
needed to manage spinal stenosis.

Surgical
Surgery is indicated in patients with
clinical and radiographic evidence of
spinal stenosis who have intractable
pain, altered quality of life, or substantially diminished functional capacity and have either failed nonsurgical treatment or are not candidates
for nonsurgical treatment.25 Surgery
can predictably address positional
back pain and neurogenic claudication, but may not adequately address
pain secondary to degenerative disk
disease (eg, low back pain, referred
pain).2,3,25-27
The method of surgical intervention is based on the location and
character of stenosis. Spinal stenosis
usually occurs as the result of a
global degenerative process that involves the central canal, lateral recesses, neuroforamina, or a combination of these structures. Compression
may be isolated or may extend to
multiple levels and can involve the
central or lateral nerve roots, those
in the foramen, or a combination of
all three. Radicular symptoms or
motor weakness along specific nerve
root distributions require careful assessment of the lateral recess and foramen.4,6 Relative stability of the diseased segment should also be
assessed. Hypermobile segments (ie,
segments demonstrating spondylolisthesis, lateral listhesis, widened facets with fluid visible on MRI) adjacent to more normal segments may
require stabilization with in situ fusion techniques or instrumented arthrodesis and fusion. Neurogenic
claudication with central canal
stenosis may require laminectomy,
laminotomy, or indirect reduction

Journal of the American Academy of Orthopaedic Surgeons

Paul S. Issack, MD, PhD, et al

Figure 2

A, Illustration demonstrating resection of the spinous processes and

detachment of ligamentum flavum from the ventral aspect of the lamina with
a curet. B, Laminectomy and central decompression with a Kerrison rongeur.
C, Partial medial facetectomy and foraminotomy are performed with a 45
Kerrison rongeur. D, The superior tip of the superior facet is resected with a
45 Kerrison rongeur for decompression of the neuroforamen.

techniques for decompression of the

central canal. These techniques can
be performed via traditional open
approaches or minimally invasive
techniques.

Laminectomy
Laminectomy is performed with the
patient positioned prone on a supportive frame that allows the abdomen to hang free to decrease epidural venous pressure and surgical
site bleeding. Exposure of the posteAugust 2012, Vol 20, No 8

rior elements is performed from the

midline to the lateral pars interarticularis and facets with great care
taken to avoid damage to the facet
joint or pars interarticularis. After
resection of the spinous processes
and superficial dorsal lamina, central
decompression is performed with removal of the midline laminae and
underlying ligamentum flavum (Figure 2, A-C). Partial medial facetectomies can then be performed to decompress the lateral recess and

expose the neuroforamina and exiting nerve roots, which may be decompressed using Kerrison rongeurs
(Figure 2, D). A ball-tipped probe,
Woodson elevator, or angled dural
separator should be used to assess
the anteroposterior and proximaldistal volume of the neuroforamina.6
Several studies have evaluated outcomes of decompressive laminectomy for spinal stenosis. Some of
these studies reported on outcomes
of decompressive laminectomy and
nonsurgical treatment in a cohort of
148 patients with symptomatic lumbar stenosis who were followed for
10 years.26-28 Eighty-one patients underwent laminectomy, and 67 received nonsurgical treatment, with
both groups assessed at 1, 4, and 8
to 10 years following treatment.26
Leg or back pain was substantially
improved in 55% of patients in the
surgical group and 28% in the nonsurgical group at 1-year follow-up.26
However, these differences became
less substantial over time; at 8- to
10-year follow-up, leg or back pain
was significantly improved in 54%
of surgically treated patients compared with 42% of nonsurgically
treated patients.28 These studies were
limited by their nonrandomized design in which potential confounders
cannot be excluded, the high rate of
loss to follow-up, and various degrees of decompression; these issues
make it difficult to assess the value
of decompression surgery.26-28
More recently, prospective randomized studies have rigorously
evaluated surgical management of
spinal stenosis.3,29,30 Amundsen et al29
reported on the results of 100 patients with symptomatic lumbar spinal stenosis who were assigned to
either surgical or nonsurgical treatment. A partial randomization was
done, with 31 patients assigned to either nonsurgical or surgical treatment groups. At 4-year follow-up,
excellent or fair results were ob-

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Degenerative Lumbar Spinal Stenosis: Evaluation and Management

served in 9 of 18 patients in the nonsurgical group and 10 of 13 patients

in the surgical group. Malmivaara
et al30 evaluated 94 patients with
lumbar spinal stenosis treated either
surgically (50 patients) or nonsurgically (44 patients) in randomized
multicenter trial. The surgical group
included 10 patients treated with instrumented posterolateral fusion. At
2-year follow-up, disability, leg pain,
and back pain were improved to a
greater degree in the surgical group
than in the nonsurgical group. Walking ability did not differ between the
two treatment groups. A drawback
of the study is that inclusion of patients treated with fusion makes it
difficult to attribute good outcomes
to decompression alone. Crossover
of the patient population is another
limitation of this study; 9% of the
nonsurgical group underwent surgical intervention due to exacerbation
of symptoms, and 8% of the decompressive surgery group did not undergo surgery due to relief of symptoms, thereby further confounding
the researchers ability to detect differences between the groups.
Effectiveness of surgical management of lumbar spinal stenosis was
evaluated in the SPORT study. This
prospective randomized multicenter
trial had three study arms based on
diagnosis: lumbar disk herniation,
degenerative spondylolisthesis or spinal stenosis.2,3 Patients with spinal
stenosis without spondylolisthesis
who had symptoms for at least 12
weeks and failed nonsurgical treatment were enrolled in the spinal
stenosis arm of the study. These patients were assigned to either a randomized or an observational cohort
and underwent decompressive surgery or nonsurgical care, respectively. Nonsurgical care consisted of
physical therapy, education and/or
counseling with home exercise instruction, and NSAIDs. Initially, 365
patients were assigned to the obser-

532

vational cohort; however, many patients in the nonsurgical group opted

to have surgery. At 2-year follow-up,
193 of 289 patients (67%) in the
randomized cohort had undergone
surgery, whereas 157 patients (43%)
in the observational cohort received
nonsurgical care and underwent surgery. As-treated analysis, which combined both cohorts, showed that surgery had a marked advantage over
nonsurgical treatment, with substantial decreases in pain and improvement in physical function as measured by the Medical Outcomes
Study 36-item Short-Form General
Health Survey and the modified Oswestry Disability Index (ODI). These
differences remained significant at 2
and 4 years.2,3
Complications associated with
laminectomy include infection, dural
tear, epidural hematoma, and instability. One study reported that, following laminectomy, 2 of 103 patients (2%) with lumbar stenosis
developed deep infection, requiring
irrigation and dbridement.31 Recently, a 10.5% incidence of durotomy was reported in 389 patients
who underwent laminectomy for
lumbar degenerative spondylolisthesis. No significant differences in pain
or physical function based on Medical Outcomes Study 36-item Short
Form scores or ODI were observed
at 1, 2, 3, and 4 years in patients
with or without durotomy, which
suggests that incidental durotomy
does not significantly affect outcome.32 Epidural hematoma following laminectomy is rare and requires
urgent surgical decompression to
avoid neurologic deficit.33 In a study
of 27 patients treated with posterior
spinal decompression procedures,
the incidence of postlaminectomy instability was 3.7%; this complication
can be avoided by preserving the
pars interarticularis and at least 50%
of the facet joints.34

Minimally Invasive Surgical

Approaches
Compared with traditional open
techniques, minimally invasive surgery (MIS) for management of spinal
stenosis results in better preservation
of posterior musculature, diminished
intraoperative bleeding, and requires
less recovery time.35,36 MIS approaches for stenosis include laminotomy, microendoscopic laminotomy
with tubular retractors, and laminoplasty. Although MIS approaches
have some advantages over open
procedures, the economic value and
cost-effectiveness of MIS requires
further investigation.37
Laminotomy
Laminotomy involves removal of a
small portion of one side of the lamina. Resection of the distal half of
the superior hemilamina is often necessary to identify and remove the insertion site of the ligamentum flavum. Contralateral decompression
can be performed with preservation
of the spinous processes and supraspinous and interspinous ligaments
by tilting the operating table away
from the surgeon. Using an operating
microscope, the contralateral ligamentum can be visualized and resected and then the lamina can be
undercut38,39 (Figure 3). Toyoda
et al38 reported on 57 patients who
underwent bilateral decompression
via unilateral laminotomies. Of these
patients, 27 had lumbar spinal stenosis without instability, 20 had degenerative lumbar spondylolisthesis, and
10 had degenerative lumbar scoliosis. At a mean 6-year follow-up, the
average Japanese Orthopaedic Association (JOA) score improved from
13.8 3.6 points preoperatively to
22.6 4.7 points at final follow-up.
At final follow-up, no significant differences in JOA score or percentage
of slippage were noted among patients with these three diagnoses.
This technique is limited because of

Journal of the American Academy of Orthopaedic Surgeons

Paul S. Issack, MD, PhD, et al

compared with 36% of control patients. Tuschel et al44 recently reported on 46 patients with spinal
stenosis who underwent implantation of the X-STOP device. At a
mean 40-month follow-up, no improvement was noted, and the revision rate was approximately 30%.
Most revisions occurred within the
first year. In addition, there is evidence that implantation of these devices may not improve outcomes and
in fact may worsen neural compression in severely stenotic patients.45,46
Indications for the use of these implants are not well defined, and longterm studies are lacking at this time.

Figure 3

A, Illustration demonstrating microdecompression. The shaded area shows

the ipsilateral decompression. The dashed lines represent the contralateral
area to be decompressed under the midline structures. B, Axial view of the
contralateral decompression. The contralateral exiting nerve root is protected
during the procedure.

the difficulty in accessing stenosis in

the lateral canal and foramen.

access without extensive facetectomy.42

Microendoscopic Laminotomy
In a prospective study of 53 patients
with spinal stenosis, Pao et al40 performed microendoscopic laminotomy using a tubular retractor and a
fiberoptic endoscopic system. Of
these patients, 45 (85%) were satisfied with treatment at an average 16month follow-up. Significant improvement in ODI and JOA scores
was noted, and 40 patients (80%)
had good to excellent results. Complication rates were high and included dural tears in five patients
and transient neuralgia in four
patients. Khoo and Fessler41 compared microendoscopic decompressive laminotomy with open decompression in patients with lumbar
spinal stenosis and noted that the microendoscopic procedure was associated with reduced blood loss, shorter
postoperative hospital stay, and diminished use of narcotics. A drawback of this technique is that the ipsilateral lateral recess is difficult to

Interspinous Process Devices

Recently, interspinous process devices have been used to manage lumbar spinal stenosis. These implants
block spinal extension at the level of
the facet joint and limit canal narrowing associated with spinal extension. In a prospective randomized
controlled multicenter trial, Zucherman et al43 analyzed outcomes of
191 patients with symptomatic spinal stenosis. Ninety-one patients
were treated nonsurgically and 100
were treated with the X-STOP interspinous implant (Medtronic, Memphis, TN). At 2-year follow-up,
symptom scores improved by 45%
over baseline in patients treated with
the X-STOP implant compared with
7% improvement in the control
group. The X-STOP group had a
44% mean improvement in function
compared with no improvement in
the control group. In addition, 73%
of patients treated with the X-STOP
device were satisfied with surgery

August 2012, Vol 20, No 8

Economics
A cost analysis performed using a
subset of patients with spinal stenosis from the SPORT study showed
that surgical management of spinal
stenosis improved health to a greater
extent than nonsurgical care (quality
adjusted life year [QALY] gained,
0.17) at a cost of $77,600 per QALY
gained at 2-year follow-up.47 At 4-year
follow-up, QALY gains were maintained (0.22) and costs per QALY
gained decreased to $59,400.48 The
authors concluded that the economic
value of surgery for spinal stenosis
compares favorably with many
health interventions.47,48

Summary
Degenerative lumbar spinal stenosis
is a major cause of impaired quality
of life and diminished functional capacity in the elderly. Patients commonly present with neurogenic claudication and diminished standing
and walking tolerance; however,
their ability to walk distances can be
increased by ambulating with the
spine in a flexed-forward posture.
On physical examination, back pain
or lower extremity symptoms can often be elicited with lumbar exten-

533

Degenerative Lumbar Spinal Stenosis: Evaluation and Management

sion. Radicular symptoms may be

seen in patients with lateral recess or
foraminal stenosis.
Plain AP and lateral radiographs
may demonstrate spondylolisthesis,
disk space narrowing, end plate sclerosis, osteophytes, and facet hypertrophy. MRI can best demonstrate
the degree of narrowing in the central canal and lateral recess. Because
the natural history of spinal stenosis
is generally benign but progressive,
initial treatment with NSAIDs; physical therapy, with an emphasis on
core strengthening; and epidural steroid injections may be beneficial.
Surgical management is indicated
following failure of nonsurgical measures. Recent prospective randomized controlled studies have demonstrated a definite advantage of
surgery over nonsurgical treatment
in decreasing pain and improving
function in patients with degenerative spinal stenosis. Decompressive
laminectomy is the most commonly
performed procedure used to address
global stenosis. MIS approaches include laminotomy, microendoscopic
laminotomy, and laminoplasty. Fusion is not indicated except in the
setting of concomitant spondylolisthesis, scoliosis, or iatrogenic instability. In well-selected patients, surgical decompression can provide
marked pain relief and restore physical function and quality of life.

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