Degenerative Lumbar Spinal Stenosis Options for Aging Backs

The Physician and Sportsmedicine: Degenerative Lumbar Spinal Stenosis
Degenerative Lumbar Spinal Stenosis
Options for Aging Backs
Andrew L. Chen, MD, MS; Jeffrey M. Spivak, MD
THE PHYSICIAN AND SPORTSMEDICINE - VOL 31 - NO. 8 - AUGUST 2003
In Brief: Degenerative lumbar spinal stenosis commonly disables and functionally limits the aging
population. Degenerative changes may constrict the spinal canal, lateral recesses, and neural
foramina, compressing the neural elements. Clinicians can make an earlier, more accurate
diagnosis by using advanced imaging techniques. Nonoperative management is the mainstay of
treatment, although surgery is indicated in patients who have progressive neurologic decline or
when nonoperative measures have failed to adequately address symptoms.
In the 1980s, the median age of the US population increased by 1.4 years, with an additional 2
million people age 65 or older.1 More people are maintaining active lifestyles as they age;
consequently, symptomatic degenerative disease of the spine is often clinically significant and may
result in functional debilitation.
Lumbar spinal stenosis is characterized by narrowing of the spinal canal and/or the intervertebral
foramina that decreases space for the neural elements. The condition may be secondary to
congenital (developmental) or degenerative (acquired) causes.2
Congenital stenosis may occur as a result of developmentally narrow spinal canal dimensions or
bone dysplasias, such as dwarfism. Lumbar spinal stenosis may also arise from less common,
nondegenerative conditions (table 1) that must be ruled out, particularly in younger patients who
do not show radiographic evidence of degenerative changes.
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The Physician and Sportsmedicine: Degenerative Lumbar Spinal Stenosis
TABLE 1. Nondegenerative Conditions That May
Contribute to Lumbar Spinal Stenosis
Bone dysplasia
Calcium pyrophosphate deposition
Congenitally short pedicles
Achondroplastic dwarfism
Diffuse idiopathic skeletal hyperostosis
Infection
Metabolic bone disease
Hypoparathyroidism
Renal osteodystrophy
Ossification of the posterior longitudinal ligament
Paget's disease of bone
Previous lumbar surgery
Senile ankylosing hyperostosis of the spine
Tumors
Epidural lipoma
Intraspinal tumors or cysts
Vertebral osteomyelitis
Disk-space infection
Degenerative lumbar stenosis is primarily associated with spinal disease, but it may also result
from underlying spinal instability (spondylolisthesis), scoliosis, metabolic bone disorders, neoplastic
or infectious processes, or posttraumatic degenerative changes. Degenerative lumbar spinal
stenosis is seen primarily in patients older than 60, with an average age of 73 at presentation.3,4
Males are predominantly affected, with reported male-to-female ratios ranging from 3:1 to 12:1.2,3
Although the exact prevalence of degenerative spinal stenosis is unknown, advancements in
diagnostic imaging have increased recognition of this disorder.5
Basic Spinal Anatomy
Understanding spinal canal anatomy (figure 1) is fundamental to understanding the
pathophysiology of degenerative lumbar stenosis. The posterior edge of the vertebral bodies and
intervertebral disks form the anterior border of the spinal canal. The posterior bony arches
(laminae) and the ligamentum flavum form the posterior border of the spinal canal. The lateral
borders of the spinal canal are composed of the pedicles, the bony attachments of the posterior
arches to the vertebrae anteriorly. The spinal nerves exit segmentally through the neural foramina,
the spaces between the pedicles. Facet joints are located bilaterally at each level of the spine
posterolaterally at the disk space level. Degenerative enlargement of the facet joints may result in
central impingement on the spinal canal (central stenosis) or more laterally, where the nerve root
moves toward the foramen (lateral recess stenosis). Narrowing of the neural foramen may
compress the exiting nerve root (foraminal stenosis).
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The Physician and Sportsmedicine: Degenerative Lumbar Spinal Stenosis
Lumbar spinal stenosis may be localized to a single segment of the spine or may span multiple
segments. Each motion segment of the spine consists of two adjacent vertebrae and the
intervening intervertebral disk, facet joints, and supporting ligaments. Degeneration of this joint
complex commonly begins as disk desiccation. Mechanical failure of the disk then alters motion
segment kinematics with subsequent facet joint osteoarthritis and hypertrophy.6 Segmental
instability increases, the pedicles and laminae thicken,7 and the supporting ligamentous structures
undergo hypertrophy.8
Spinal canal impingement from disk space narrowing decreases the height and volume of the spinal
canal. Bulging of the disk in the anterior spinal canal and infolding of the ligamentum flavum
posteriorly also result from disk space narrowing. In most people who develop symptoms of spinal
stenosis, the cross-sectional area of the spinal canal begins in the low-to-normal range, with
limited capacity to accommodate the additional narrowing associated with degenerative changes.5
Moreover, foraminal stenosis may result from facet joint degeneration, lateral disk bulging, and
decreased disk height.3
Degenerative lumbar spinal deformity can be a major contributor to spinal stenosis. As asymmetric
disk space collapses and vertebral rotation causes segmental instability, degenerative lumbar
scoliosis may result.4 Spondylolisthesis (forward slippage or subluxation of one vertebra relative to
the one caudal to it) may lead to spinal instability and most commonly occurs at the L4-5
segment.7,9 Although forward translation is usually limited to 25% to 30%,9 associated disk
degeneration, posterior ligamentous thickening and infolding, and facet hypertrophy can cause
complete myelographic block with as little as 3 to 4 mm of subluxation.10
Clinical Presentation
Patients who have lumbar spinal stenosis may present with classic neurogenic claudication
characterized by activity-related intermittent pain, numbness, and paresthesias radiating down the
leg. Symptoms occur and may worsen with prolonged standing, activity, or positions involving
lumbar extension and are relieved by sitting, recumbency, or positions that reduce the degree of
lumbar lordosis, such as bending forward.4 Patients may have a long history of low-back pain with
a more recent onset of sciatic pain. This low-back pain is more vague than the radiculopathy
associated with a focal disk herniation. Patients may assume a simian posture, stooped with
flattening of normal lumbar lordosis. Progressive reduction in distances walked or standing time
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The Physician and Sportsmedicine: Degenerative Lumbar Spinal Stenosis
before symptom onset is often reported. The classic history is that of symptom relief when pushing
a grocery cart (upper-extremity weight-bearing with lumbosacral and hip flexion) as compared with
walking upright.
The history and physical exam can distinguish neurogenic claudication from vascular claudication
(table 2). Patients who have neurogenic claudication typically report the need to stop walking and
sit or stoop to relieve pain; standing worsens symptoms. These patients also report slow resolution
of acute symptoms and a variable walking distance before symptom onset. They show none of the
typical peripheral vascular changes (eg, diminution of distal pulses, skin atrophy and mottling, loss
of pretibial hair [on shins]) seen in vascular claudication.11
TABLE 2. A Comparison of Neurogenic and Vascular Claudication in Spinal Stenosis
Symptom or Sign
Neurogenic Claudication
Vascular Claudication
Distal pulses
Normal
Diminished or absent
Skin changes
None
Mottled or atrophic
Loss of pretibial hair growth
Positional change
Pain improved with lumbar
flexion (eg, sitting, stooping)
Pain unaffected by lumbar posture
Walking distance
Variable
Increased pain with increased
distance ambulated
Relationship of pain to cessation Prolonged time for pain resolution Pain typically subsides immediately
of ambulation
Unlike neurogenic claudication, pain associated with vascular claudication is unchanged with lumbar
postural changes. Riding a stationary exercise bicycle elicits pain in patients who have vascular
claudication, but not in patients who have neurogenic claudication as long as lumbar flexion is
maintained.
Other Causes of Pain
In addition to neurogenic claudication, spinal stenosis may contribute to other painful conditions.
Position-related radiculopathy. Patients who have degenerative lumbar spinal stenosis often present
with position-related radiculopathy rather than true neurogenic claudication.3 Extension of the lumbar
spine causes pain or paresthesias. Cadaver studies6,12 have demonstrated significant increases in dural
sac capacity with lumbar flexion as compared with extension, which buckles the ligamentum flavum,
increases disk protrusion, decreases interlaminar distance, and narrows the spinal canal by as much as
60% when compared with lumbar flexion.
Acute disk herniation. A more constant radicular pain resulting from severe nerve root compression
often occurs in addition to the more long-standing symptoms of activity-related numbness, weakness,
and pain in the lower extremities. As a result, spinal stenosis may mimic symptomatic lumbar disk
herniation.13 Sensory deficits are more common in patients who have spinal stenosis. Diminished motor
reflexes may represent normal aging, but, because degenerative spinal stenosis usually affects the
midlumbar spine, an abnormal patellar reflex associated with quadriceps atrophy and weakness may be
noted. Extensor hallucis longus weakness is seen with equal frequency in patients who have either
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The Physician and Sportsmedicine: Degenerative Lumbar Spinal Stenosis
lumbar spinal stenosis or a herniated lumbar disk, but a diminished patellar reflex is more common in
patients with spinal stenosis. Limited spinal mobility and nerve root tension signs, such as a positive
passive straight-leg raise or femoral stretch test, more commonly indicate a disk herniation than spinal
stenosis.13
Cauda equina syndrome. Acute cauda equina syndrome, characterized by extensive bilateral
neurologic symptoms (eg, saddle anesthesia, bilateral motor weakness, fecal or urinary incontinence,
sexual dysfunction), is uncommon with lumbar spinal stenosis. The rapid onset is more characteristic of
an acute lumbar disk herniation than the gradual onset of positional symptoms associated with lumbar
spinal stenosis. Nonetheless, these symptoms require a complete neurologic evaluation with rectal
examination of tone and sensation. Clinicians should maintain a high index of suspicion for all
progressive neurologic disturbances, because acute disk herniation may occur with long-standing
lumbar stenosis. Confirmed symptoms and signs should prompt urgent evaluation of the spinal canal
with magnetic resonance imaging (MRI) or computed tomography (CT) myelography. Urgent (within 48
hours of onset) surgical decompression may be necessary.
Chronic cauda equina syndrome may develop from gradually progressing spinal stenosis, and most
often results in bladder dysfunction and perineal pain. Because of the slowly progressive nature of the
neurologic decline, urgent decompression is not often necessary before full diagnostic evaluation.
Diagnostic Imaging
Clinicians have a choice of imaging techniques to help visualize bony elements, disks, and soft tissues
for diagnostic evaluation.
Plain radiography for suspected lumbar spinal stenosis should include anteroposterior (AP) and lateral
radiographs of the lumbosacral spine. Coned-down (close-up) views of L5-S1 should be obtained if this
is the suspected level of pathology. In most patients who have suspected degenerative lumbar spinal
stenosis, multilevel spondylosis is seen on x-rays. Degenerative spondylolisthesis usually occurs at L4-5
and typically causes less than 30% of anterior displacement.
Further evaluation of spondylolisthesis should include standing lateral flexion and extension views to
evaluate for translational and sagittal angular instability. Degenerative scoliosis, which may also
indicate underlying canal stenosis, should be fully evaluated by long-plate AP and lateral standing
radiographs of the entire spine. This is particularly important for surgical planning, because correction
of rotational and angular deformities may be necessary for operative success. Intrathecal injection of
contrast media (myelography) enhances visualization of stenotic segments.
CT is used to determine canal dimensions and configuration and to identify disk abnormalities and
herniation, facet degeneration and hypertrophy, ligamentous hypertrophy and redundancy, and
spondylosis or occult fractures.14 Advantages of this technique include excellent osseous detail,
especially of the lateral recess; ability to differentiate between disk, ligamentum flavum, and thecal sac
(within the dura mater); and visualization of far lateral disk abnormalities and the neural foraminal
architecture.
The addition of intrathecal, water-soluble contrast media (figures 2 and 3) with CT is more sensitive
than myelography alone and may improve the evaluation of patients who have persistent symptoms. A
better assessment of central spinal and lateral recess stenosis and improved visualization of foraminal
and far lateral disk abnormalities can be obtained. Because of its invasive nature, however, its use
should be limited to preoperative evaluation and planning after the initial diagnosis is made by either CT
or MRI. The combination of MRI and CT provides both bony and soft-tissue detail for preoperative
anatomic analysis and can obviate the need for myelography in most cases.
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The Physician and Sportsmedicine: Degenerative Lumbar Spinal Stenosis
MRI is especially effective for the evaluation of the intervertebral disk, neural elements, and soft-tissue
elements of the spinal canal (figure 2). Despite its higher cost compared with CT and plain radiography,
its advantages include lack of radiation, direct multiplanar image reconstruction, and increased
sensitivity in detecting soft-tissue and disk pathology. Also, sagittal images help visualize the lower end
of the spinal cord, including the conus medullaris. MRI has been shown to be as accurate as CT
myelography, and diagnostically superior to either myelography or CT alone.15 Careful interpretation is
necessary, however, because overestimation of canal stenosis may occur if sclerotic osteophytes cause
regions of low signal intensity on T2-weighted images.
Electrophysiologic studies, such as electromyography, nerve-conduction velocities, and
somatosensory evoked potentials are not routinely used for establishing the diagnosis of degenerative
lumbar spinal stenosis. The clinical utility of such studies lies in their ability to help differentiate active
denervation from chronic, inactive changes in peripheral nerves, or to help rule out diffuse, peripheral
neuropathic abnormalities secondary to other conditions, such as diabetes mellitus. Normal
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The Physician and Sportsmedicine: Degenerative Lumbar Spinal Stenosis
neurophysiologic studies do not rule out symptomatic lumbar spinal stenosis, because the radiculopathy
may be intermittent and activity-related.
Clinical Correlation
Despite the increasing reliance on diagnostic tests, correlation of any radiographic abnormalities with
clinical signs and symptoms cannot be overemphasized. In a CT study of asymptomatic patients, 50%
of those older than 40 demonstrated findings that were consistent with spinal stenosis, disk herniation,
and facet joint degeneration.16 Similarly, in a separate study,17 MRI demonstrated lumbar spinal
stenosis in 3 of 14 asymptomatic subjects older than 60. Electrodiagnostic studies have been previously
shown to demonstrate the presence of abnormalities not evident on neurologic examination.3
Our diagnostic evaluation of lumbar spinal stenosis begins with AP and lateral views of the lumbosacral
spine, as well as coned-down views of L5-S1. If the history, physical examination, and radiographic
evaluation suggest spinal stenosis, we obtain MRIs with sagittal and coronal reconstructions to
characterize the level of stenosis and to further evaluate neurologic deficits, such as those caused by
herniated disks.
If a patient is considered a surgical candidate, we obtain CT scans to better delineate the osseous
architecture for preoperative planning. In postsurgical patients, MRI with gadolinium contrast is used to
differentiate pathology from scar tissue. When the pathology is unclear based on MRI findings, we
obtain CT myelograms to further characterize the stenosis. CT myelography is also useful in patients
who cannot undergo MRI (eg, patients with cardiac pacemakers) or in whom spinal instrumentation,
such as metal rods, would obscure or distort the images.
We do not routinely obtain electrophysiologic studies except in cases with mixed neurologic deficits with
multiple causes, such as patients with concomitant lumbar stenosis and peripheral neuropathy caused
by diabetes mellitus.
Nonoperative Management
Nonoperative treatment has been successful for patients who have lumbar spinal stenosis.18,19 Most
patients who have symptoms of degenerative lumbar stenosis will respond to nonoperative treatment
and not need surgery, at least initially. In the absence of acute focal neurologic deterioration or the
development of acute cauda equina syndrome, all patients should be treated with a trial of nonoperative
therapy (table 3) before consideration for surgical treatment.
TABLE 3. Nonoperative Treatment for Degenerative Lumbar Spinal Stenosis
Method
Comments
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The Physician and Sportsmedicine: Degenerative Lumbar Spinal Stenosis
Medications
NSAIDs
Acetaminophen
Oral corticosteroids
Muscle relaxants
Narcotics
Tricyclic antidepressants
(eg, nortriptyline hydrochloride)
Anticonvulsants (eg, gabapentin)
Calcitonin injections
Physical Therapy
Conditioning
Stretching
Strengthening
Modalities
(eg, heat, ice, ultrasound,
electrical stimulation)
Activity Modification
Riding stationary bicycle or
leaning forward on a treadmill
Bracing
Lumbosacral corset (soft)
Lumbosacral orthosis (rigid)
Decrease inflammation, provide pain relief
Provides pain relief
Decrease inflammation; diminish radicular symptoms and pain
Decrease paravertebral muscle spasm
Not routinely used, but may help in acute flares
Decrease radicular symptoms
Decrease radicular symptoms
Decrease pain; increase ambulatory capacity in some patients
Encourages weight loss; improves aerobic conditioning
Promotes muscle relaxation and limberness, improves lumbosacral
motion,
and decreases muscle spasm
Improves muscle tone in back and abdominal muscles
May benefit some patients, but results are inconsistent
Promotes lumbosacral flexion; is usually well-tolerated
Supports weak musculature; provides minimal immobilization
Decreases symptoms by immobilization; should be prescribed in
slight flexion
NSAIDs = nonsteroidal anti-inflammatory drugs
In a study20 of nonoperative treatment, most patients who had mild-to-moderate lumbar
spinal stenosis remained unchanged after 4 years of follow-up, and no proof of severe
deterioration was found. This challenges the notion that early operative intervention is
necessary to prevent progression of stenosis and the development of profound neurologic
deficits.
Our approach to nonoperative treatment is multifaceted. The mainstays of nonoperative
management include anti-inflammatory drugs (NSAIDs), physical therapy with activity
modification, bracing, and epidural corticosteroid injection.
Oral medication. Treatment for lumbar spinal stenosis includes the use of mild analgesics
such as acetaminophen or nonsteroidal anti-inflammatory agents. Exacerbation of radicular
symptoms may be treated with a short course of oral steroids. Muscle relaxant medications
and narcotic analgesics are not used on a routine basis, but they may benefit patients who
have acute flares or muscle spasms. We routinely prescribe NSAIDs in conjunction with a 1week course of oral muscle relaxants if muscle spasms are present. If the patient reports
radicular symptoms, we often prescribe gabapentin or a short course of oral steroids for acute
exacerbations. Low-dose tricyclic antidepressants, such as nortriptyline hydrochloride, or
anticonvulsants, such as gabapentin, may be used to treat radicular symptoms.
In a double-blind, placebo-controlled, crossover study,21 patients who had symptomatic lumbar
spinal stenosis were given calcitonin injections. Pain decreased and ambulatory capacity
increased, although patients with severe pain at rest or ambulatory capacity limited to less
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than 300 m (328 yd) did not improve.
Physical therapy. Targeted regimens should include therapeutic stretching of the lumbosacral
spine, low-back and abdominal muscle strengthening, and general aerobic conditioning. We
advocate using a stationary bicycle or leaning forward while walking on a treadmill, because
these maintain relative flexion in the lumbosacral spine during exercise. Patients may also find
walking on an upward incline to be more comfortable than flat or downhill walking.
Physical modalities (eg, local heat or ice, electrical stimulation, massage, ultrasound, traction)
are commonly used but have not been proven effective for lumbosacral disorders.3,18
Therefore, these should be used only in conjunction with therapeutic exercises.
Bracing. Soft, corset-like braces can help control the symptoms of lumbar stenosis. Bracing
provides little immobilization, but it may help support the usually weak abdominal muscles
during activities. We have found that patients who experience muscle spasm often report
benefit from using a soft, lace-up lumbosacral corset. True immobilization with a rigid plastic
body jacket (lumbosacral orthosis) may help by limiting spinal motion and secondary
inflammation. Rigid braces should be fitted in slight flexion to provide relative opening of the
spinal canal.
Brace use should be temporary and should always be done in conjunction with physical therapy
to strengthen weak muscles and prevent further atrophy. We refer patients to physical therapy
for general conditioning, stretching, and strengthening exercises, and instruct patients to
modify their activities for symptomatic relief.
Corticosteroid injection. Using epidural steroid injections to treat lumbar spine disorders,
including stenosis, remains controversial. Many studies fail to demonstrate a therapeutic
benefit of steroid injection over placebo, although most available studies are limited by poor
study design or the lack of radiographic guidance of the steroid injections.22,23 Moreover,
serious complications have been reported with epidural steroid injections into the lumbar
region, including transient paresis and paralysis, epidural hematoma, infection, and chemical
meningitis.24
Patients who have diabetes mellitus should be counseled that the locally injected steroid might
cause transient elevation of serum glucose. These patients should, therefore, monitor blood
sugar closely in the first few days following an injection, because they may require temporary
alteration of their insulin therapy.
We believe that the indication for epidural steroid injection is the treatment of an acute flare
with radicular symptoms. Steroid injections should not be given simply because other
nonoperative therapies have failed to provide pain relief; under these circumstances, injections
are likely to be unsuccessful. In our experience, rigid adherence to this indication and having
the epidural injection performed by an interventional radiologist who uses imaging guidance
has yielded successful results. Therefore, although the issue remains controversial, we consider
radiographically guided epidural steroid injection to be a potentially efficacious pain
management alternative for lumbar spinal stenosis.
Alternative treatments. Patients frequently inquire about nonallopathic treatments for back
pain. Many patients seek osteopathic or chiropractic consultation in addition to allopathic
evaluation. Nutritional supplements, such as glucosamine and chondroitin sulfate, have gained
popularity as potentially beneficial for the treatment of musculoskeletal ailments in general.
Traditional practices, such as acupuncture, have also been used to treat back pain. Although
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The Physician and Sportsmedicine: Degenerative Lumbar Spinal Stenosis
the orthopedic literature lacks prospective randomized controlled trials, many patients report
subjective relief of symptoms. Rigorous scientific inquiry is needed to establish the efficacy of
such measures so that informed decisions can be made about the use of alternative
treatments.
Operative Management
Because degenerative spinal stenosis is not life-threatening and catastrophic neurologic
deterioration is very rare, operative treatment should be considered only when nonoperative
treatment has failed to improve function or provide adequate pain relief to allow daily
activities. Much less commonly, urgent surgery is indicated to address progressive neurologic
deficits or the development of the cauda equina syndrome.
The main goal in the operative treatment of lumbar spinal stenosis is to decompress the
affected neural elements throughout their entire course from the central canal to their exit
through the neural foramina. The secondary goal of surgery is to maintain spinal stability or to
restore stability in cases of preoperative degenerative instability.
Many operative techniques for decompression of the degenerative lumbar spine have been
described.
Laminectomy. The standard decompression procedure, called laminectomy, involves removal
of the spinous processes and central portion of the laminae overlying the affected stenotic
segments (figure 4). Hypertrophic arthritic facet joints are shaved to relieve compression along
the central spinal canal, lateral recess, and neural foramen as needed.
Postoperative spondylolisthesis is a potential complication of lumbar decompression without
fusion of the operative segments.25 An increased risk of instability is associated with total
facetectomy and preexisting degenerative spondylolisthesis at the operative level. To minimize
the risk of postoperative instability, some surgeons advocate multiple laminotomies (partial
removal of lamina) to decompress the lateral recesses and neural foramina and to maintain the
central posterior elements for stability. Maintaining the integrity of these structures is believed
to improve postoperative structural stability, but this has not been confirmed in any
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prospective randomized studies.
The results of standard operative decompression for lumbar spinal stenosis are encouraging.
One meta-analysis showed an average of 64% of patients had a good or excellent outcome
after surgery.26 Operatively managed patients have significantly better outcomes at 1-year
evaluation when compared with nonoperatively treated patients, despite the fact that operative
candidates tended to have increased symptoms before surgery. Risk factors associated with a
worse outcome after operative management include diabetes mellitus, osteoarthritis of the hip,
preoperative degenerative scoliosis, and preoperative lumbar fracture.27,28
Fusion. The role of spinal fusion following decompressive laminectomy of degenerative lumbar
spinal stenosis remains controversial.29-31 Spinal fusion has no proven additional benefit after
routine decompressive laminectomy in the absence of spinal deformity or instability, and the
procedure has a higher complication rate than laminectomy alone.29 Patients who have
preoperative spinal instability (eg, degenerative spondylolisthesis or scoliosis) benefit from
concomitant spinal fusion of the unstable segments.30,31
The role of spinal fusion with instrumentation (constructs of rods and hooks, wires, or screws
to stabilize the fusion) remains controversial. Advocates for instrumentation report early
postoperative relief of symptoms provided by immediate stabilization, decreased progression of
spondylolisthesis, improved rates of fusion, and improved overall clinical outcome. Opponents
have reported increased complication rates with instrumentation as compared to
noninstrumented fusion without significant improvement in clinical outcome.26-31 Current
instrumentation techniques use pedicle screw fixation. Hook or wire fixation requires an intact
laminae and necessitates extending fusion to normal motion segments. Pedicle screw
instrumentation was recently approved by the US Food and Drug Administration for use in
degenerative spondylolisthesis.
Backbone of Information
Degenerative lumbar spinal stenosis is a common cause of low-back pain, radiculopathy, and
disability among older patients. Classic symptoms of neurogenic claudication include activityrelated pain, numbness, and paresthesias that are improved with lumbosacral flexion and
worsened by extension. When the diagnosis of degenerative lumbar spinal stenosis is
suspected, radiographic studies including plain radiographs, MRI, or CT should be obtained.
Nonoperative treatment continues to be the mainstay of treatment for patients who have
degenerative lumbar spinal stenosis, although surgical decompression is warranted in patients
with unremitting or progressive symptoms and neurologic deficit. Spinal fusion may be
necessary for operative success in patients with instability or deformity, but a definitive role for
fusion with instrumentation has yet to be elucidated for this group.
References
1. Statistical Abstract of the United States, ed 114. Washington, DC, United States Bureau
of the Census, 1994
2. Arnoldi CC, Brodsky AE, Cauchoix J, et al: Lumbar spinal stenosis and nerve entrapment
syndromes: definition and classification. Clin Orthop 1976;115(Mar-Apr):4-5
3. Spivak JM: Degenerative lumbar spinal stenosis. J Bone Joint Surg Am 1998;80(7):10531066
4. Grubb SA, Lipscomb HJ, Conrad RW: Degenerative adult onset scoliosis. Spine 1988;13
http://www.physsportsmed.com/issues/2003/0803/chen.htm (11 of 13)2/17/2005 9:56:54 AM
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5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
18.
19.
20.
21.
22.
23.
24.
25.
26.
27.
(3):241-245
Jones RA, Thomson JL: The narrow lumbar canal: a clinical and radiological review. J
Bone Joint Surg Br 1968;50(3):595-605
Kirkaldy-Willis WH, Wedge JH, Yong-Hing K, et al: Pathology and pathogenesis of lumbar
spondylosis and stenosis. Spine 1978;3(4):319-328
Rauschning W: Pathoanatomy of lumbar disc degeneration and stenosis. Acta Orthop
Scand Suppl 1993;251:3-12
Coventry MB, Ghormley RK, Kernohan JW: The intervertebral disc: its microscopic
anatomy and pathology. J Bone Joint Surg 1945;27:105-112, 233-247
Grobler LJ, Robertson PA, Novotny JE, et al: Etiology of spondylolisthesis: assessment of
the role played by lumbar facet joint morphology. Spine 1993;18(1):80-91
Schnitker MT, Curtzwiler FC: Hypertrophic osteosclerosis (bony spur) of the lumbar
spine: producing the syndrome of protruded intervertebral disc wth sciatic pain. J
Neurosurg 1957;14(2):121-128
Hawkes CH, Roberts GM: Neurogenic and vascular claudication. J Neurol Sci 1978;38
(3):337-345
Dai LY, Xu YK, Zhang WM, et al: The effect of flexion-extension motion of the lumbar
spine on the capacity of the spinal canal: an experimental study. Spine 1989;14(5):523525
Jonsson B, Stromqvist B: Symptoms and signs in degeneration of the lumbar spine: a
prospective, consecutive study of 300 operated patients. J Bone Joint Surg Br 1993;75
(3):381-385
Bolender NF, Schonstrom NS, Spengler DM: Role of computed tomography and
myelography in the diagnosis of central spinal stenosis. J Bone Joint Surg Am 1985;67
(2):240-246
Bischoff RJ, Rodriguez RP, Gupta K, et al: A comparison of computed tomographymyelography, magnetic resonance imaging, and myelography in the diagnosis of
herniated nucleus pulposus and spinal stenosis. J Spinal Disord 1993;6(4):289-295
Wiesel SW, Tsourmas N, Feffer HL, et al: A study of computer-assisted tomography: I.
The incidence of positive CAT scans in an asymptomatic group of patients. Spine 1984;9
(6):549-551
Boden SD, Davis DO, Dina TS, et al: Abnormal magnetic-resonance scans of the lumbar
spine in asymptomatic subjects: a prospective investigation. J Bone Joint Surg Am
1990;72(3):403-408
Fast A: Low back disorders: conservative management. Arch Phys Med Rehabil 1988;69
(10):880-891
Moreland LW, Lopez-Mendez A, Alarcon GS: Spinal stenosis: a comprehensive review of
the literature. Semin Arthritis Rheum 1989;19(2):127-149
Johnsson KE, Rosen I, Uden A: The natural course of lumbar spinal stenosis. Clin Orthop
1992;279(June):82-86
Eskola A, Pohjolainen T, Alaranta H, et al: Calcitonin treatment in lumbar spinal
stenosis: a randomized, placebo-controlled, double-blind, cross-over study with oneyear follow-up. Calcif Tissue Int 1992;50(5):400-403
Rydevik BL, Cohen DB, Kostuik JP: Spine epidural steroids for patients with lumbar
spinal stenosis. Spine 1997;22(19):2313-2317
Cuckler JM, Bernini PA, Wiesel SW, et al: 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(1):63-66
McLain RF, Fry M, Hecht ST: Transient paralysis associated with epidural steroid
injection. J Spinal Disord 1997;10(5):441-444
Robertson PA, Grobler LJ, Novotny JE, et al: Postoperative spondylolisthesis at L4-5: the
role of facet joint morphology. Spine 1993;18(11):1483-1490
Turner JA, Ersek M, Herron L, et al: Surgery for lumbar spinal stenosis: attempted metaanalysis of the literature. Spine 1992;17(1):1-8
Herno A, Airaksinen O, Saari T, et al: Lumbar spinal stenosis: a matched-pair study of
http://www.physsportsmed.com/issues/2003/0803/chen.htm (12 of 13)2/17/2005 9:56:54 AM
The Physician and Sportsmedicine: Degenerative Lumbar Spinal Stenosis
operated and non-operated patients. Br J Neurosurg 1996;10(5):461-465
28. Atlas SJ, Deyo RA, Keller RB, et al: The Maine Lumbar Spine Study, Part III: 1-year
outcomes of surgical and nonsurgical management of lumbar spinal stenosis. Spine
1996;21(15):1787-1795
29. Laus M, Tigani D, Alfonso C, et al: Degenerative spondylolisthesis: lumbar stenosis and
instability [in English and Italian]. Chir Organi Mov 1992;77(1):39-49
30. Herkowitz HN, Kurz LT: Degenerative lumbar spondylolisthesis with spinal stenosis: a
prospective study comparing decompression with decompression and intertransverse
process arthrodesis. J Bone Joint Surg Am 1991;73(6):802-808
31. Zdeblick TA: A prospective, randomized study of lumbar fusion: preliminary results.
Spine 1993;18(8):983-991
Dr Chen and Dr Spivak are orthopedic surgeons in the department of orthopedic surgery at
NYU-Hospital for Joint Diseases in New York City. Address correspondence to Andrew L.
Chen, MD, MS, 14th floor, Hospital for Joint Diseases, 301 E 17th St, New York, NY, 10003; email correspondence to [email protected].
Disclosure information: Drs Chen and Spivak disclose no significant relationship with any
manufacturer of any commercial product mentioned in this article. No drug is mentioned in this
article for an unlabeled use.
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