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Degenerative Lumbar Spinal Stenosis

Options for Aging Backs

Andrew L. Chen, MD, MS; Jeffrey M. Spivak, MD


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.

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
Metabolic bone disease
   Renal osteodystrophy
Ossification of the posterior longitudinal ligament
Paget's disease of bone
Previous lumbar surgery
Senile ankylosing hyperostosis of the spine
   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).

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 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 SignNeurogenic ClaudicationVascular Claudication

Distal pulsesNormalDiminished or absent
Skin changesNoneMottled or atrophic
Loss of pretibial hair growth
Positional changePain improved with lumbar
flexion (eg, sitting, stooping)
Pain unaffected by lumbar posture
Walking distanceVariableIncreased pain with increased
distance ambulated
Relationship of pain to cessation
of ambulation
Prolonged time for pain resolutionPain typically subsides immediately

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 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.

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 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


Oral corticosteroids
Muscle relaxants
Tricyclic antidepressants
   (eg, nortriptyline hydrochloride)
Anticonvulsants (eg, gabapentin)
Calcitonin injections

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
Physical Therapy

   (eg, heat, ice, ultrasound,
   electrical stimulation)

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
Activity Modification
Riding stationary bicycle or
leaning forward on a treadmill

Promotes lumbosacral flexion; is usually well-tolerated
Lumbosacral corset (soft)
Lumbosacral orthosis (rigid)

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 1-week 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 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 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 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 activity-related 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.


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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; e-mail 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.