Lumbar Spine Stenosis: A Common Cause of Back and Leg Pain

JAMIE A. ALVAREZ, M.D., and RUSSELL H. HARDY, JR., M.D.

University Hospitals of Cleveland/Case Western Reserve University,
Cleveland, Ohio

. Lumbar spine stenosis most commonly affects the middle-aged and elderly population.
Entrapment of the cauda equina roots by hypertrophy of the osseous and soft tissue structures
surrounding the lumbar spinal canal is often associated with incapacitating pain in the back and
lower extremities, difficulty ambulating, leg paresthesias and weakness and, in severe cases,
bowel or bladder disturbances. The characteristic syndrome associated with lumbar stenosis is
termed neurogenic intermittent claudication. This condition must be differentiated from true
claudication, which is caused by atherosclerosis of the pelvofemoral vessels. Although many
conditions may be associated with lumbar canal stenosis, most cases are idiopathic. Imaging of
the lumbar spine performed with computed tomography or magnetic resonance imaging often
demonstrates narrowing of the lumbar canal with compression of the cauda equina nerve roots by
thickened posterior vertebral elements, facet joints, marginal osteophytes or soft tissue structures
such as the ligamentum flavum or herniated discs. Treatment for symptomatic lumbar stenosis is
usually surgical decompression. Medical treatment alternatives, such as bed rest, pain
management and physical therapy, should be reserved for use in debilitated patients or patients
whose surgical risk is prohibitive as a result of concomitant medical conditions.

Low back pain resulting from degenerative disease of the

lumbosacral spine is a major cause of morbidity, disability and lost
productivity. Up to 90 percent of the U.S. population may have
significant low back pain at some point.1 In 1984, it was estimated
that over 5 million persons were incapacitated as a result of lower
back pain.2 The financial impact in terms of health care dollars and
lost work hours reaches billions of dollars each year in this country.3 With the increasing
longevity of our population and a continually climbing proportion of middle-aged and
elderly persons, the problem of lumbosacral pain is a significant health care issue. A
ubiquitous and potentially disabling cause of osteoarthritic pain of the lower back and
legs is stenosis of the lumbar spinal canal. This treatable condition is often a major cause
of inactivity, loss of productivity and, potentially, loss of independence in many persons,
particularly older persons.

Because of the slow progression of the disease, the diagnosis may be significantly
delayed. Given the potentially devastating effects of this condition, rapid diagnosis and
treatment are essential if patients are to be returned to their previous levels of activity.

Normal Anatomy

The lumbar vertebral canal is roughly triangular in shape and is narrowest in its
anteroposterior diameter in the axial plane. The average anteroposterior diameter of the
lumbar canal in adults, as determined by anatomic and radiographic studies, ranges from
15 to 23 mm.4 The canal is bounded anteriorly by the posterior edge of the vertebral body

1
including the posterior longitudinal ligament, which is closely apposed to the posterior
vertebral body surface, laterally by the pedicles, posterolaterally by the facet joints and
articular capsules, and posteriorly by the lamina and ligamenta flava (yellow ligaments).

As shown in Figures 1 and 2, entrapment of the cauda equina roots, which pass within
the dural sac, can occur as a result of progressive hypertrophy of any of the
osseocartilaginous and ligamentous elements surrounding the spinal canal. Moreover, the
intervertebral disc, which is composed of a gelatinous, centrally located nucleus pulposus
and a peripherally located annulus fibrosus, is prone to rupture or herniate posteriorly or
posterolaterally as a result of degenerative changes or trauma, producing neural element
compromise.

Figure 1. Normal anatomic structures of the lumbar spine at the third through the fifth
lumbar levels. Note the close association between the nerve roots and the dural tube, and
the ligamentum flavum, the facet joints, the pedicles and the lamina. The ligamentum
flavum (interlaminar ligament) attaches laterally to the facet capsules.

In the lumbar regions, the cone-shaped terminus of the spinal cord (conus medullaris)
normally ends at about the L1 or L2 level in adults. Caudal to these levels, the roots of
the cauda equina are contained within the subarachnoid space of the dura-enclosed thecal
sac (Figure 3). Thus, canal stenosis at lumbar levels results in nerve root dysfunction
rather than spinal cord dysfunction.

Pathophysiology

2
Narrowing of the lumbar canal has many potential causes, and various classification
schemes have been devised in order to better describe the pathophysiology of this
condition. A classification system proposed by Verbiest5 categorizes the multiple causes
of lumbar stenosis into two types: conditions that lead to progressive bony encroachment
of the lumbar canal (including developmental, congenital, acquired and idiopathic causes)
or stenosis produced by nonosseous structures such as ligaments, intervertebral discs and
other soft tissue masses. For practical purposes, however, the etiologies of lumbar
stenosis can be divided into congenital or acquired forms.

Few causes of lumbar stenosis are truly congenital. Narrowed or "shallow" lumbar canals
may be a result of congenitally short pedicles, thickened lamina and facets, or excessive
scoliotic or lordotic curves. These anatomic changes may lead to clinically significant
stenosis if additional elements such as herniated intervertebral discs or other space-
occupying lesions further narrow the canal and contribute to the compression. Verbiest5,6
noted that lumbar canal diameters from 10 to 12 mm may be associated with claudication
if additional elements encroach on the
canal, and he referred to this type of
stenosis as "relative" canal stenosis.5-7

In most cases, stenosis of the lumbar

canal may be attributed to acquired
degenerative or arthritic changes of the
intervertebral discs, ligaments and facet
joints surrounding the lumbar canal.
These changes include cartilaginous
hypertrophy of the articulations
surrounding the canal, intervertebral disc
herniations or bulges, hypertrophy of the
ligamentum flavum and osteophyte
formation.

Some investigators have postulated that

the pathologic changes that result in
lumbar canal stenosis are the result of so-
called micro-instability at the articular
surfaces surrounding the canal.7 Micro-
instability refers to minute, abnormal Figure 3. Posterior view of the lumbar region of the
repetitive motion of the joints that link spinal canal, demonstrating the conus medullaris at
adjacent vertebra. These movements are the L1 to L2 level and the cauda equina nerve roots
clinically silent yet may result in inferiorly.
progressive loss of strength in the joint
capsules and lead to reactive bony and cartilaginous hypertrophy, thickening or
calcification of the ligamentum flavum, or subluxation of one vertebra on another
(spondylolisthesis), all of which may contribute to narrowing of the lumbar canal.

3
Compression of the microvasculature of the lumbar nerve roots, resulting in ischemia, is
believed to be a major contributing factor in the development of neurogenic claudication.
Wilson8 classified neurogenic claudication into two major types based on the putative
pathophysiologic mechanism: postural or ischemic. Postural neurogenic claudication is
induced when the lumbar spine is extended and lordosis is accentuated, whether at rest or
during exercise in the erect posture. With extension of the spine, degenerated
intervertebral discs and thickened ligamenta flava protrude posteriorly into the lumbar
canal, producing transient compression of the cauda equina. In the ischemic form, it is
theorized that transient ischemia occurs in compressed lumbosacral roots when increased
oxygen demand occurs during walking.

Other acquired conditions that can be associated with lumbar canal stenosis as a result of
osseous or fibrocartilaginous hypertrophy include fluorosis, hyperparathyroidism, Paget's
disease, ankylosing spondylitis, Cushing's disease and acromegaly.1,4

Clinical Presentation

Clinical History
Men are affected with slightly higher frequency than women. Although symptomatic
lumbar stenosis is usually a disease of the middle-aged and the elderly, younger patients
may also be affected. Typically, the earliest complaint is back pain, which is relatively
nonspecific and may result in delayed diagnosis. Patients then often experience leg
fatigue, pain, numbness and weakness, sometimes several months to years after the back
pain was first noticed. Patients may undergo minor trauma that can exacerbate symptoms,
which may lead to a more rapid diagnosis.

Once the leg pain begins, it is most commonly bilateral, involving the buttocks and thighs
and spreading distally toward the feet, typically with the onset and progression of leg
exercise. In some patients, the pain, paresthesias and/or weakness are limited to the lower
legs and feet, remaining present until movement ceases. The lower extremity symptoms
are almost always described as burning, cramping, numbness, tingling or dull fatigue in
the thighs and legs. Disease onset is usually insidious; early symptoms may be mild and
progress to become extremely disabling. Symptom severity does not always correlate
with the degree of lumbar canal narrowing.

Classically, the symptoms of lumbar canal stenosis begin or worsen with the onset of
ambulation or by standing, and are promptly
relieved by sitting or lying down. Thigh or leg pain
Symptoms of lumbar stenosis
typically precedes the onset of numbness and motor
appear or worsen with the
weakness. Along with numbness and weakness,
onset of amublation or on
these symptoms and signs constitute the syndrome
standing, and are promptly
of neurogenic intermittent claudication. Patients
relieved by sitting or lying
commonly complain of difficulty walking even
short distances and do so with a characteristic
stooped or anthropoid posture in more advanced
cases. Although standing and walking exacerbate the extreme discomfort, bicycle riding

4
 can often be performed without much difficulty because of the theoretic widening of the
lumbar canal that occurs with flexion of the back. Some patients actually obtain transient
relief of pain by assuming a squatting position, which flexes the trunk. Conversely, lying
prone or in any position that extends the lumbar spine exacerbates the symptoms,
presumably because of ventral in-folding of the ligamentum flavum in a canal already
significantly narrowed by degenerative osseus changes.

Other common symptoms include stiffness of the thighs and legs, back pain (which may
be a constant symptom) and, in severe cases, visceral disturbances such as urinary
incontinence that may be a result of impingement of sacral roots. Back pain, a symptom
in nearly all patients with lumbar stenosis,5 may be present with or without claudication,
particularly in the earlier stages of the disorder.

Physical Examination Email This Link

Physical examination of patients with suspected lumbar stenosis should begin with Search AFP
examination of the back. The curvature of the spine should be noted, and the mobility and Browse by Topic
flexibility of the spine with any changes in neurologic symptoms during active flexion or
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presumably by stretching the compressed ipsilateral nerve root. Most patients with a true
positive straight leg raising sign complain of excruciating sciatica-like pain in the elevated
leg at 30 to 40 degrees of elevation. This sign is usually absent in patients with lumbar
stenosis.

It should be noted that herniation of disc material and subsequent reparative processes may
contribute to the overall picture of stenosis, but acute disc herniations generally produce a
clinical picture that differs from the more chronic symptoms of canal stenosis. Patrick's
sign, which reproduces leg pain with lateral rotation of the flexed knee, implies ipsilateral
degenerative hip joint disease. This is an important piece of the differential diagnosis in
patients with stenosis, some of whom may have both conditions.

Neurologic Examination
The neurologic examination in patients with idiopathic
A trefoil canal seen on CT is
degenerative lumbar stenosis may not reveal
virtually pathognomonic for
significant sensorimotor deficits at rest or in a neutral
lumbar stenosis.
position. Deep tendon reflexes may be decreased,
absent or normal, depending on the chronicity of the

5
caudal root compression. Upper motor neuron signs, such as hyperactive deep tendon
reflexes or the presence of pathologic reflexes, such as the Babinski's sign or Hoffmann's
sign, are typically absent unless there is injury to descending long tracts. With the onset of
walking, sensory deficits may appear, and motor weakness or reflex changes may be
elicited. Therefore, it is extremely important to perform a thorough neurologic examination
before and immediately after symptoms appear following a short period of ambulation.
Similarly, changes in the neurologic examination with variations in posture should also be
recorded.

Neurogenic vs. Vascular Claudication

The signs and symptoms of neurogenic intermittent claudication should be differentiated

from the leg claudication produced by atherosclerotic occlusive disease of the iliofemoral
vessels (vascular claudication). Vascular disease is commonly associated with other
problems such as impotence in men, dystrophic skin changes (nail atrophy, alopecia), foot
pallor or cyanosis, decreased or absent peripheral pulses and arterial bruits. Pain or
cramping in the buttocks associated with ambulation is often reported.

Patients with vascular claudication also obtain relief with rest and can very accurately
quantitate the distance that they can ambulate before symptoms reappear. However, in
contrast to claudication that is due to cauda equina compression, vaso-occlusive leg
claudication usually does not occur with changes in posture, and patients typically obtain
relief from the leg pain by simply resting the legs even while in the upright position (Table
1).

TABLE 1
Clinical Differentiation Between Neurogenic and Vascular
Claudication

Clinical Neurogenic
characteristics claudication Vascular claudication

Location of pain Thighs, calves, back Buttocks or calves

and, rarely, buttocks
Quality of pain Burning, cramping Cramping
Aggravating factors Erect posture, Any leg exercise
ambulation, extension of
the spine
Relieving factors Squatting, bending Rest
forward, sitting
Leg pulses and blood Usually normal Blood pressure decreased; pulses
pressure decreased or absent; bruits or
murmurs may be present
Skin/trophic changes Usually absent Often present (pallor, cyanosis, nail
dystrophy)

6
 Autonomic changes Bladder incontinence Impotence may coexist with other
(rare) symptoms of vascular claudication

Examination of the femoral, popliteal and pedal pulses, as well as inspection of the legs
and feet for trophic changes, is essential in order to differentiate vascular from neurogenic
claudication. Ankle/brachial indexes and bedside Doppler examinations should be
performed if any abnormality in the pulses is discovered or if vascular disease is suspected.
Significant symptomatic pelvofemoral atherosclerosis and lumbar stenosis occasionally
coexist in the same patient, and noninvasive circulation studies or arteriography may be
required to rule out vasculopathy.

Imaging/Diagnostic Studies

The diagnosis of lumbar stenosis depends largely on the clinical history and physical
examination. Radiographic confirmation of the diagnosis can be accomplished using
various imaging modalities. Plain films of the spine by themselves are not diagnostic but
may demonstrate degenerative changes in the vertebrae or disc spaces, disclose some forms
of occult spina bifida or reveal spondylolisthesis or scoliosis in some patients. The most
commonly involved levels are L3 through L5, although clinically significant stenosis can
exist at any or all lumbar levels in a given patient. In the past, lumbar myelography was the
usual method for establishing a diagnosis, but it is usually not necessary today. Modern
neuroimaging techniques such as computed tomographic (CT) scanning and magnetic
resonance imaging (MRI) have facilitated the diagnosis in recent years.

Computed Tomography
CT scans with or without intrathecal contrast injection define the bony anatomy in one or
two planes, are able to demonstrate the lumbar subarachnoid space well, may demonstrate
encroachment of the canal by hypertrophied lamina, osteophytes, facets or pedicles, and
can provide excellent visualization of the vertebral canal so that measurements of the canal
diameter can be made with improved accuracy and resolution compared with plain
myelograms. Three-dimensional reconstructions using CT also demonstrate the anatomy of
the vertebral canal.

Hypertrophy of the lamina, pedicles and apophyseal joints, along with a thickened
ligamentum flavum, impinge on the posterolateral aspects of the lumbar canal, giving it the
classic "cloverleaf" or "trefoil" appearance on axial CT scans (Figure 2). Although the
trefoil canal is considered to be virtually pathognomonic for lumbar stenosis, a normal
trefoil variant is occasionally encountered in an otherwise completely asymptomatic
patient.

7
Magnetic Resonance Imaging
CT scans with intrathecal
contrast injection are able to
demonstrate the lumbar
subarachnoid space and nerve
roots with enhanced sensitivity,
but this is an invasive test with
potential morbidity. For this
reason, MRI scanning, with its Figures 4A and 4B . (Left) Unenhanced T1-weighted axial
magnetic resonance scan at a lumbar level showing severe stenosis.
multiplanar imaging capability, The combination of ligament and facet joint hypertrophy
is currently the preferred concentrically reduces the diameter of the lumbar canal. The
modality for establishing a significant reduction in the relative amount of epidural fat and
diagnosis and excluding other subarachnoid cerebral spinal fluid signal is further evidence of the
conditions. MRI depicts soft degree of canal stenosis. (Right) Unenhanced T1-weighted sagittal
magnetic resonance scan of the lumbosacral spine showing severe
tissues, including the cauda canal stenosis at the L4-5 level, produced by a combination of disc
equina, spinal cord, ligaments, herniation, spondyloarthritis and posterior element hypertrophy.
epidural fat, subarachnoid space Compare this stenosis with the moderate degree of stenosis
and intervertebral discs, with observed at levels above. Mild spondylolisthesis is also evident at
exquisite detail in most L5-S1.
instances. Loss of epidural fat on
T1-weighted images, loss of cerebrospinal fluid signal around the dural sac on T2-weighted
images and degenerative disc disease are common features of lumbar stenosis on MRI
(Figures 4a and 4b).

Electromyelography TABLE 2
Electromyelograms with nerve conduction Conditions That May Mimic
velocity studies may assist in confirming the Lumbar Stenosis
multiradicular involvement of cauda equina
compression. Electromyelography and nerve Conus medullaris and cauda equina
conduction velocity may also be helpful in neoplasms, and benign cystic lesions
(neurofibromas, ependymomas,
diagnosing demyelinating or inflammatory
hemangioblastomas, dermoids,
neuropathies and can be of great benefit in epidermoids, lipomas)
distinguishing vascular from neurogenic
claudication in situations where the clinical and Neural compression from metastatic
radiographic pictures are equivocal. Ultimately, disease to bone (lung, breast,
however, imaging studies are essential in the myeloma, lymphoma)
diagnosis of lumbar stenosis and, in most cases,
electromyelography and nerve conduction Centrally herniated discs
velocity studies will not be required.
Degenerative spondylolisthesis

Differential Diagnosis Trauma/fractures

As mentioned previously, compression of the Epidural abscess

lumbar root may have many causes. However,
few conditions produce the typical clinical picture Inflammatory arachnoiditis

8
of neurogenic claudication that occurs in lumbar
stenosis. Table 2 lists potential causes of cauda equina
compression that should be ruled out by appropriate
diagnostic studies before a diagnosis of lumbar
stenosis is made.

Cauda equina syndromes usually occur as a result of compression of the nerve roots in the
lumbosacral spine distal to the conus medullaris. Since the root supply to the lower
extremities and genitoperineal regions travels in very close apposition within the thecal
sac, external compression such as that occurring with lumbar canal stenosis is manifested
by dysfunction in multiple root distributions. For example, pain and other sensory deficits
may occur in several lumbar and/or sacral dermatomal territories, as well as weakness in
the various muscle groups supplied by these nerve roots.

Cauda equina syndromes also may occur secondary to neoplasms, trauma, and
inflammatory or infectious processes. An important reason to obtain MRI scans (as
opposed to CT scans) in patients with neurogenic claudication is that MRI aids in the
exclusion of more serious conditions, such as tumors of the conus medullaris or cauda
equina,9 or infectious processes.

It is rare for patients with tumors of the lumbosacral spine to present exclusively with
symptoms suggestive of neurogenic intermittent claudication. In contrast to the back and
leg pain associated with degenerative lumbar stenosis, the pain associated with a
lumbosacral spinal tumor typically worsens with recumbency, awakens the patient at night
and is relieved with walking.8

Lumbar epidural abscesses usually are associated with rapidly evolving neurologic deficits,
severe back pain and other clinical manifestations that facilitate the diagnosis. These
patients may or may not present with fever but almost always demonstrate back pain and
exquisite tenderness to palpation localized to the levels of suppuration.

Pathologic, traumatic or osteoporotic compression fractures of lumbar vertebrae also may

present with symptoms of cauda equina impingement. Healing of clinically silent fractures
may produce exuberant growth of bone, which may lead to canal stenosis and root
impingement. Therefore, a search for a history of treated malignancies, evidence of
concurrent malignancies or a history of falls or trauma to the spine may be important to the
diagnosis.
Epidural abscesses,
Degenerative subluxation of lumbar vertebrae
spondylolisthesis and
(spondylolisthesis) is another cause of acquired
compression fractures should
stenosis of the lumbar spinal canal, particularly at the
be considered in the differential
L4 and L5 levels, and may manifest clinically with
diagnosis of neurogenic
neurogenic intermittent claudication as well.5 Lumbar
claudication.
stenosis sometimes occurs following posterior lumbar
fusions, possibly as a result of reactive bony

9
hypertrophy at or adjacent to the fused segments.

Treatment

Since most patients who develop lumbar stenosis are middle-aged or elderly, it is important
to ascertain their relative surgical risks. Although decompressive lumbar laminectomy can
be an extensive procedure, most patients, even the elderly, are medically capable of
tolerating the procedure. In general, these patients are severely disabled by their symptoms
and are usually willing to accept a small degree of risk to obtain relief. Anticoagulation
therapy or severe cardiac or respiratory disease may be contraindications to surgery.

Risks and Complications of Decompressive Surgery

The risks of laminectomy depend on the number of levels to be decompressed,
concomitant medical problems, difficult anatomy as a result of scarring from previous
operations or a markedly stenotic canal that may require extensive bone removal and
dissection, as well as the overall risks imposed by general anesthesia. Potential
complications of the standard decompressive laminectomy include wound infection,
hematoma formation, dural tears with subsequent cerebrospinal fluid leaks and risk of
meningitis, nerve root damage and the potential for creating postoperative spinal
instability. Surgical blood loss is generally well tolerated, but transfusion may be required.
The overall surgical mortality associated with decompressive laminectomy is
approximately 1 percent.10

The standard decompressive lumbar laminectomy involves a midline incision over the
involved levels, dissection down to the spinous processes and progressive removal or
"unroofing" of the posterior elements of the lumbar canal (spinous processes, laminae and
pedicles), as well as removal of thickened ligamenta flava.

Typically, multilevel decompressive laminectomies are performed since canal stenosis

commonly occurs over several levels. Rarely is excision of herniated intervertebral discs
required. Removal of the medial portions of the articular facets is often performed,
particularly if there is evidence of osteophyte formation. This maneuver has the potential
of creating instability at the levels undergoing surgery if the bone resection is extended too
far laterally, particularly if bilateral facetectomies are performed.

An alternative technique7 spares the articular facets on one side and creates a unilateral
decompressive hemilaminectomy while undercutting the contralateral lamina, removing
the ligamentum flavum and performing unilateral bony fusion as well. Another type of
decompressive procedure that has been described with good postoperative success is
multilevel laminotomy, whereby "windows" or fenestrations are created by removing the
superior aspect of the inferior lamina and the inferior aspect of the superior lamina at
involved levels. Proponents of this approach believe that sparing the interspinous ligaments
and preserving spinous processes minimizes the risk of postoperative instability.

10
Recently, increasing attention has been paid to lateral Lumbar decompressive
recess stenosis syndrome as a cause of back pain and laminectomy provides relief to
claudication. The lateral recess is the space within the most patients, although those
spinal canal adjacent to the exit zone of the nerve with significant comorbidities
roots. are less likely to do well.
Some authors believe that, in select circumstances,
medial facetectomies, foraminotomies and decompression of the lateral recesses are
sufficient to relieve the symptoms of neurogenic claudication.11 Other procedures, such as
expansile laminoplasty, which involves the en-bloc removal and loose reattachment of the
posterior vertebral arches, have not been studied extensively. Overall, these various
procedures have met with mixed results, although some patients will undoubtedly benefit
from less extensive decompressive procedures depending on the morphology and anatomic
location of their nerve root impingement. Regardless of the surgical approach that is
chosen, if decompression is not adequate, relief of symptoms may be incomplete or the
problem may recur following a short period of clinical improvement.

Results of Surgical Treatment

Most patients benefit from wide decompression of the lumbar canal. Some reports place
the percentage of patients benefiting from surgery at 95 percent, with greater than 90
percent of patients returning to their previous activity levels, regardless of age.12 However,
recent reports2,12 dismiss these figures as optimistic, instead claiming long-term neurologic
improvement in approximately 65 percent of patients. It is fairly clear, however, that in
most patients with clear radiographic and clinical evidence of stenosis, decompressive
surgery provides significant relief.

In a recent analysis, comorbid conditions and psychologic factors were found to play a
significant role in patients' individual perceptions of outcome following either
laminectomy or laminotomy. Patients with significant comorbid illnesses reported less
relief of pain and less functional recovery than expected following decompression.13 In
patients with chronic, severe symptoms, decompression of the neural elements may not
result in immediate pain resolution, nor are longstanding preoperative motor deficits likely
to resolve immediately. Nonetheless, following cauda equina decompression, the relentless
progression of neurologic dysfunction may be slowed or halted.

Nonsurgical Treatment for Lumbar Stenosis

Conservative treatment for lumbar stenosis, such as lumbar bracing, bed rest, physical
therapy and pain management, has few proven benefits in the long term. Unless
debilitating medical conditions prohibit surgery under general anesthesia, medical or
nonsurgical management of lumbar stenosis is not a practical option if symptoms are
incapacitating. Nonsurgical management of this condition may be attempted initially in
patients with mild symptoms of short duration.

Morbidly obese patients with symptoms of neurogenic claudication may improve

following institution of a weight loss program. Back strengthening exercises, strict physical

11
therapy regimens and symptomatic management with nonsteroidal analgesics also may
benefit some patients initially but, in contrast to patients with herniated intervertebral discs
(who often respond favorably to nonsurgical management), patients with lumbar stenosis
often show no improvement on long-term follow-up. Their symptoms rapidly return with
the resumption of activity. Since many of these persons are severely limited by pain, early
surgery is the best way to return them to full activity and independent living.

This article was prepared under the auspices of the Joint Committee on Medical Education and
Subcommittee for Continuing Medical Education for Non-Neurosurgeons of the American
Association of Neurological Surgeons and the Congress of Neurological Surgeons.

The Authors

JAMIE A. ALVAREZ, M.D.,

is chief resident of neurosurgery at University Hospitals of Cleveland/MetroHealth
Medical Center at Case Western Reserve University School of Medicine, Cleveland. A
graduate of the State University of New York Health Science Center at Syracuse College
of Medicine, he served an internship in general surgery and a residency in neurologic
surgery at University Hospitals of Cleveland.

RUSSELL W. HARDY, JR., M.D.,

is a professor of neurologic surgery at Case Western Reserve University School of
Medicine. He graduated from Harvard Medical School, Boston, and served an internship in
general surgery at Boston City Hospital (Harvard Surgical Service) and a residency in
neurologic surgery at University Hospitals of Cleveland.

Address correspondence to Russell H. Hardy, Jr., M.D., University Hospitals of Cleveland/Case

Western Reserve University, Department of Neurological Surgery, 11100 Euclid Ave., Cleveland,
OH 44106-5042. Reprints are not available from the authors.

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3. Roberts MP. Complications of lumbar disc surgery. In: Hardy RW Jr, ed. Lumbar disc disease. 2d
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 7. Jane JA Sr, Jane JA Jr, Helm GA, Kallmes DF, Shaffrey CI, Chadduck JB, et al. Acquired lumbar
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