eMedicine Specialties > Physical Medicine and Rehabilitation > Lumbar Spine Disorders

Spinal Stenosis and Neurogenic Claudication

Michael B Furman, MD, MS, Physiatrist, Interventional Spine Care Specialist, Electrodiagnostics, Orthopedic and Spine Specialists
Kirk M Puttlitz, MD, Consulting Staff, Pain Management and Physical Medicine, Arizona Neurological Institute; Robert Pannullo, MD, Interventional Spinal Care Fellow, Department of Physical Medicine and Rehabilitation, KDV Orthopaedics and Rehabilitation Ltd; Jeremy Simon, MD, Attending Physician, Department of Physical Medicine, The Rothman Institute

Updated: Jun 16, 2009

Introduction

Background

• Central canal stenosis, commonly occurring at an intervertebral disk level, defines midline sagittal spinal canal diameter narrowing that may elicit neurogenic claudication (NC) or pain in the buttock, thigh, or leg. Such stenosis results from ligamentum flavum hypertrophy, inferior articulating process (IAP), facet hypertrophy of the cephalad vertebra, vertebral body osteophytosis, vertebral body compression fractures and herniated nucleus pulposus (HNP). Abnormalities of the disk usually do not cause symptoms of central stenosis in a normal-sized canal. In developmentally small canals, however, a prominent bulge or small herniation can cause symptomatic central stenosis. Large disk herniations can compress the dural sac and compromise its nerves, particularly at the more cephalad lumbar levels where the dural sac contains more nerves. (See images below and Images 1-3, 6.)

Lateral T2-weighted magnetic resonance imaging (MRI) scan demonstrating narrowing of the central spinal fluid signal (L4-L5), suggesting central canal stenosis.

Axial T2 magnetic resonance imaging (MRI) scan (L4-L5) in the same patient as in the above image, confirming central canal stenosis.

Trefoil appearance characteristic of central canal stenosis due to a combination of zygapophysial joint and ligamentum flavum hypertrophy.

Lumbar computed tomography (CT) myelogram scan demonstrates a normal central canal diameter.

• Lateral recess stenosis (ie, lateral gutter stenosis, subarticular stenosis, subpedicular stenosis, foraminal canal stenosis, intervertebral foramen stenosis) is defined as narrowing (less than 3-4 mm) between the facet superior articulating process (SAP) and posterior vertebral margin. Such narrowing may impinge the nerve root and subsequently elicit radicular pain. This lateral region is compartmentalized into entrance zone, mid zone, exit zone, and far-out stenosis. (See image below and Image 4.)
  • The entrance zone lies medial to the pedicle and SAP, and, consequently, arises from facet joint SAP hypertrophy. Other causes include developmentally short pedicle and facet joint morphology, as well as osteophytosis and HNP anterior to the nerve root. The lumbar nerve root compressed below SAP retains the same segmental number as the involved vertebral level (eg, L5 nerve root is impinged by L5 SAP).
  • The mid zone extends from the medial to the lateral pedicle edge. Mid-zone stenosis arises from osteophytosis under the pars interarticularis and bursal or fibrocartilaginous hypertrophy at a spondylolytic defect.
  • Exit-zone stenosis involves an area surrounding the foramen and arises from facet joint hypertrophy and subluxation, as well as superior disk margin osteophytosis. Such stenosis may impinge the exiting spinal nerve.
  • Far-out (extracanalicular) stenosis entails compression lateral to the exit zone. Such compression occurs with far lateral vertebral body endplate osteophytosis and when the sacral ala and L5 transverse process impinge on the L5 spinal nerve.

Lateral and axial magnetic resonance imaging (MRI) scan demonstrating right L4 lateral recess stenosis secondary to combination of far lateral disk protrusion and zygapophysial joint hypertrophy.

Amundsen and colleagues found concomitant lateral recess stenosis in all cases of central canal stenosis; consequently, in his study, pure central stenosis without lateral stenosis failed to exist.¹

Parenthetically, Keim and colleagues mention the following simplistic LSS anatomical classification scheme:²

• Lateral, secondary to SAP hypertrophy
• Medial, secondary to IAP hypertrophy
• Central, due to hypertrophic spurring, bony projection, or ligamentum flavum/laminar thickening
• Fleur de lis (clover leaf), from laminar thickening with subsequent posterolateral bulging

LSS arises from the following primary and secondary etiologies:

• Primary stenosis encompasses congenital malformations and developmental flaws. Congenital malformations include incomplete vertebral arch closure (spinal dysraphism), segmentation failure, achondroplasia, and osteopetrosis. Developmental flaws include early vertebral arch ossification, shortened pedicles, thoracolumbar kyphosis, apical vertebral wedging, anterior vertebral beaking (Morquio syndrome), and osseous exostosis. Primary stenosis is uncommon, occurring in only 9% of cases.
• Secondary (acquired) stenosis arises from degenerative changes, iatrogenic causes, systemic processes, and trauma. Degenerative changes include central canal and lateral recess stenosis from posterior disk protrusion, zygapophyseal joint and ligamentum flavum hypertrophy, and spondylolisthesis. Iatrogenic changes result following surgical procedures such as laminectomy, fusion, and diskectomy. Systemic processes that may be involved in secondary stenosis include Paget disease, fluorosis, acromegaly, neoplasm, and ankylosing spondylitis. (See image below and Image 7.)

Anterior view of a lumbar myelogram demonstrates stenosis related to Paget disease. Myelography is limited because of the superimposition of multiple spinal structures that contribute to the overall pattern of stenosis.

Pathophysiology

Alternatively, the caudal vertebral body SAP contributes to lateral recess and foraminal stenosis. Indeed, facet hypertrophy between L4 and L5 vertebrae may impinge the L4 nerve root in the foramen and the L5 proximal nerve root sheath in the lateral recess.

Jenis and An eloquently describe foraminal stenosis pathoanatomy, characterized by disk desiccation and DDD, which narrows disk height, permitting the caudad SAP to sublux anterosuperiorly.³ Such subluxation decreases foraminal space. Continued subluxation with resulting biomechanical disruption provokes osteophytosis and ligamentum flavum hypertrophy, further compromising foraminal volume. Anteroposterior (transverse) stenosis ultimately results from narrow disk height and hypertrophy anterior to the facet; specifically, the SAP and posterior vertebral body transversely trap the nerve root. Furthermore, in vertical (craniocaudal) stenosis, posterolateral vertebral endplate osteophytes and a lateral HNP may impinge the spinal nerve against the superior pedicle.

The 2 lower motion segments (L3-L4, L4-L5) are most commonly affected by degenerative stenosis. These segments are in a transition zone from the rigid sacrum to the mobile lumbar spine. Also, the posterior joints in this area have less of a sagittal orientation, which affords more rotation, and are therefore more vulnerable to rotatory strains.

Dynamic foraminal stenosis implies intermittent lumbar extension-provoked nerve root impingement from HNP, osteophytosis, and vertebral body slippage. Such dynamic stenosis with associated intermittent position-dependent symptoms may not manifest on imaging studies, thereby confounding diagnosis. Other factors promoting development of lumbar spinal stenosis(LSS) include shortened gestational age, and synovial facet joint cysts with resulting radicular compression. Adult degenerative scoliosis, secondary to DDD-induced instability with subsequent vertebral rotation and asymmetric disk space narrowing, promotes facet hypertrophy and subluxation in the curve concavity. Degenerative spondylolisthesis, when combined with facet hypertrophy, causes central canal and lateral recess stenosis.

Spinal canal size is not always predictive of clinical symptoms, and some evidence suggests that body mass may play a role in limitations of function in this population.⁴

Frequency

United States

Lumbar spinal stenosis (LSS) remains the leading preoperative diagnosis for adults older than 65 years who undergo spine surgery. The cost of more than 30,000 LSS surgeries performed in 1994 exceeds 1 billion dollars.

The incidence of lateral nerve entrapment is reportedly 8-11%. Some studies implicate lateral recess stenosis as the pain generator for 60% of patients with symptomatology of failed back surgery syndrome.

Incidence of foraminal stenosis increases in lower lumbar levels because of increased dorsal root ganglion (DRG) diameter with resulting decreased foramen (ie, nerve root area ratio). Jenis and An cite commonly involved roots as L5 (75%), L4 (15%), L3 (5.3%), and L2 (4%).³ The lower lumbar levels maintain greater obliquity of nerve root passage, as well as higher incidence of spondylosis and DDD, further predisposing patients to L4 and L5 nerve root impingement.

Mortality/Morbidity

In their review of lumbar spinal stenosis (LSS), Fritz and colleagues cited several studies suggesting that many patients show symptomatic and functional improvement or remain unchanged over time.⁵ For example, they mentioned Porter and colleagues' study in which 90% of 169 untreated patients with suspected lateral recess stenosis improved symptomatically after 2 years.⁶ Additionally, they reported Johnsson and colleagues' 4-year study of 32 patients treated conservatively for moderate stenosis, of whom only 16% worsened clinically and 30% reported diminished walking tolerance.⁷

Race

No known correlation exists between incidence of lumbar spinal stenosis and race.

Sex

Lumbar spinal stenosis occurs most frequently in males.

Age

Patients with lumbar spinal stenosis (LSS) due to degenerative causes generally are aged at least 50 years; however, LSS may be present at earlier ages in cases of congenital malformations.

Clinical

History

Lumbar spinal stenosis (LSS) classically presents as bilateral NC. Unilateral radicular symptoms may result from severe foraminal or lateral recess stenosis. Patients, typically aged more than 50 years, report insidious-onset NC manifesting as intermittent, crampy, diffuse radiating thigh or leg pain with associated paresthesias. Indeed, leg pain affects 90% of patients with LSS.

In a retrospective review of 75 patients with radiographically confirmed LSS, reports of weakness, numbness or tingling, radicular pain, and NC were in almost equal proportions. The most common symptom was numbness or tingling of the legs.⁸

NC pain is exacerbated by standing erect and downhill ambulation and is alleviated with lying supine more than prone, sitting, squatting, and lumbar flexion. Getty and colleagues documented 80% pain diminution with sitting and 75% with forward bending.⁹ Lumbar spinal canal and lateral recess cross-sectional area increases with spinal flexion and decreases with extension. Furthermore, cross-sectional area is reduced 9% with extension in the normal spine and 67% with severe stenosis. The Penning rule of progressive narrowing implies that the more narrowed the canal by stenosis, the more it narrows with spinal extension. Schonstrom and colleagues have shown that spinal compressive loading from weight bearing reduces spinal canal dimensions.¹⁰

NC, unlike vascular claudication, is not exacerbated with biking, uphill ambulation, and lumbar flexion and is not alleviated with standing. LSS patients compensate for symptoms by flexing forward, slowing their gait, leaning onto objects (eg, over a shopping cart) and limiting distance of ambulation. Unfortunately, such compensatory measures, particularly in elderly osteoporotic females, promote disease progression and vertebral fracture. Pain radiates downward in NC and, in contrast, upward in vascular claudication. Hall and colleagues note the presence of radiculopathy in 6% and NC in 94% of LSS patients.¹¹

Distinguishing between neurogenic and vascular claudication is important because the treatments, as well as the implications, are quite different. Vascular claudication is a manifestation of peripheral vascular disease and arteriosclerosis. Other vessels, including the coronary, vertebral, and carotid, are also often affected. Further complicating diagnosis and treatment in some patients, neurogenic and vascular claudication may occur together. This is because both conditions frequently occur in the elderly population.

Proposed mechanisms for development of NC include cauda equina microvascular ischemia, venous congestion, axonal injury, and intraneural fibrosis. Ooi and colleagues myeloscopically observed ambulation-provoked cauda equina blood vessel dilation with subsequent circulatory stagnation in LSS patients with NC.¹² They propose that ambulation dilates the epidural venous plexus, which, amidst narrow spinal canal diameter, increases epidural and intrathecal pressure. Such elevation of pressure ultimately compresses the cauda equina, compromises its microcirculation, and causes pain.

Another pain generator may be the DRG, which contains pain-mediating neuropeptides, such as substance P, that possibly increase with mechanical compression. The DRG varies spatially within the lumbosacral spine, with L4 and L5 DRG in an intraforaminal position and S1 DRG located intraspinally. Such foraminal placement may predispose to stenotic compression with subsequent radicular symptomology.

Lastly, severe radiologic stenosis in otherwise asymptomatic individuals suggests inflammation, not just mechanical nerve root compression. Specific inflammation generators may include HNP, ligamentum flavum, and facet joint capsule.

Katz and colleagues report that the historical findings most strongly associated with LSS include advanced age, severe lower extremity pain, and absence of pain when the patient is in a flexed position.¹³ Fritz and colleagues contend that the most important elements involve the postural nature of the patient's pain, stating that absence of pain or improvement of symptoms when seated assists in ruling in LSS.⁵ Conversely, LSS cannot be ruled out when sitting is the most comfortable position for the patient and standing/walking is the least comfortable.

Physical

Physical examination findings frequently are normal in patients with lumbar spinal stenosis (LSS). Nevertheless, review of the literature suggests diminished lumbar extension appears most consistently, varies less, and constitutes the most significant finding in LSS. Other positive findings include loss of lumbar lordosis and forward-flexed gait. Charcot joints may be present in long-standing disease. Radiculopathy may be noted with motor, sensory, and/or reflex abnormalities. Asymmetric muscle stretch reflexes and focal myotomal weakness with atrophy occur more with lateral recess than central canal stenosis. Some report objective neurologic deficits in approximately 50% of LSS cases. Provocative maneuvers include pain reproduction with ambulation and prone lumbar hyperextension. Pain alleviation occurs with stationary biking and lumbar flexion.

Patients may also have a positive result from the stoop test, which was described by Dyck in 1979.¹⁴ This is performed by having the patient walk with an exaggerated lumbar lordosis until NC symptoms appear or are worsened. The patient is then told to lean forward. Reduction of NC symptoms is a positive result and is suggestive of NC.

Negative findings in the physical examination include skin color, turgor, and temperature; normal distal lower extremity pulses; and an absence of arterial bruits. Importantly, remember the 5 P s of vascular claudication in the assessment of these patients: pulselessness, paralysis, paraesthesia, pallor, and pain. The absence of these problems, excluding pain and paraesthesias, which are common to neurogenic and vascular claudication, should give the clinician confidence in the diagnosis of NC. Please refer to the excellent eMedicine article Peripheral Vascular Disease for more information on peripheral vascular disease and vascular claudication.

Dural tension signs should be unremarkable. Lumbar segment mobilization often fails to reproduce pain, and palpation locates no trigger points.

Katz and colleagues report physical examination findings most strongly associated with LSS include wide-based gait, abnormal Romberg test, thigh pain following 30 seconds of lumbar extension, and neuromuscular abnormalities;¹³ however, Fritz and colleagues state physical examination findings do not seem helpful in determining the presence or absence of LSS.⁵

Johnsson and colleagues' single study of the natural course of LSS reports unchanged symptoms in 70% of patients, improvement in 15%, and worsening in 15% after a 49-month observation period. Walking capacity improved in 37% of patients, remained unchanged in 33%, and worsened in 30%.⁷

Causes

See sections on Background and Pathophysiology.

Differential Diagnoses

Other Problems to Be Considered

Rheumatologic

Ankylosing spondylitis/spondyloarthropathy
Diffuse idiopathic skeletal hyperostosis (DISH)

Infectious

Epidural, subdural, intradural abscess
Diskitis
Pott's Disease

Metabolic

Osteomalacia
Parathyroid disease
Vitamin B-12 or folic acid deficiency

Traumatic

Lumbar strain

Developmental/Congenital

Scoliosis

Vascular

Peripheral vascular disease (with vascular claudication)
Abdominal aortic dissection

Psychogenic

Conversion disorder
Malingering

Workup

Laboratory Studies

• Lab studies are not necessary to support the diagnosis of lumbar spinal stenosis.

Imaging Studies

• Plain radiography
  • Nonspecific plain radiographic findings possibly implicating lumbar spinal stenosis (LSS) include the following:
    • Disk space narrowing
    • Facet hypertrophy and arthrosis
    • Spondylosis
    • Degenerative scoliosis and spondylolisthesis
    • Osteochondrosis
    • Transitional segmentation
    • Spinous process settling
    • Shortened interpedicular distance
  • Interpedicular distance, considered subnormal if less than 18 mm, commonly increases from upper to lower lumbar segments.
  • Some sources define pure absolute central canal stenosis as a mid-sagittal canal diameter of less than or equal to 10 mm, pure relative at 10-12 mm, and mixed as a combination thereof. Mid-sagittal canal diameter less than 15 mm and transverse diameter less than 20 mm usually are considered abnormal.
  • Posterior disk height of 4 mm or less and foraminal height of 15 mm or less may suggest foraminal stenosis; nevertheless, clinical correlation is required. No convincing correlation has been found between clinical symptoms and radiologic findings in a study of 100 symptomatic patients with LSS. Similarly, no correlation has been shown between physical function and radiologic findings.
• Computed tomography (CT) scanning
  • CT scan provides excellent central canal, lateral recess, and neuroforaminal visualization (see image below and Image 5). Additionally, CT scan offers contrasts between intervertebral disk, ligamentum flavum, and thecal sac. Unfortunately, CT scan, like magnetic resonance imaging (MRI), yields a high false-positive rate (35.4% when correlated with surgically proven LSS).
  • Parasagittal reconstructed CT scan findings suggesting stenosis include posterolateral vertebral body or facet osteophytosis extending into the foramen.

Axial lumbar computed tomography (CT) scan demonstrates marked right-sided spinal canal stenosis (black arrow) resulting from advanced right-sided facet hypertrophy. Note the vacuum disk sign within the intervertebral disc (yellow double arrow). The vacuum disk sign is further indication of degenerative changes and spinal instability.

• MRI
  • MRI remains the imaging modality of choice for LSS. Fritz and colleagues maintain that MRI effectively rules LSS in or out anatomically.^5,15
    • Advantages include nonionizing radiation and superior multiplanar soft-tissue visualization without osseous artifact. A trefoil-shaped central spinal canal may provoke more symptoms than a round or oval canal by depressing the lateral recess (see image below and Image 3).

Trefoil appearance characteristic of central canal stenosis due to a combination of zygapophysial joint and ligamentum flavum hypertrophy.

• Sagittal T1-imaged adipose tissue outlines neuroforaminal nerve root segments and dorsal root ganglia. Therefore, parasagittal MRI findings suggesting foraminal stenosis include paucity of T1-weighted perineural adipose tissue surrounding the nerve root and diminished foraminal size. Unfortunately, MRI abnormalities have been documented in 20% of asymptomatic subjects.¹⁶
• Myelography
  • This test effectively documents central canal stenosis and remains superior in evaluating lumbar disk herniation. Predictive value of myelography versus CT scan has been reported as 83% versus 72%, respectively, for lumbar disk herniation, and 93% versus 89% for LSS. Furthermore, myelography images the entire lumbar spinal canal, and enhances stenotic segments due to hyperextension during imaging; however, it may miss lateral stenosis and HNP because the dural sac terminates at the lateral mid zone, preventing contrast spread to the distal nerve root sheath.¹⁷ (See image below and Image 7.)
  • Myelography is less sensitive and specific than CT scan or MRI.¹⁸
  • Procedural complications include spinal headache, seizure, allergic reaction, and nausea.

Anterior view of a lumbar myelogram demonstrates stenosis related to Paget disease. Myelography is limited because of the superimposition of multiple spinal structures that contribute to the overall pattern of stenosis.

• If vascular claudication is suspected, referral to an internist for a workup is indicated. This includes a serum cholesterol level, arterial Doppler studies, ankle-brachial index values, and, in some cases, arteriography.

Other Tests

• Electrodiagnosis (EDX), including needle electromyography (EMG), nerve conduction studies (NCS), and somatosensory evoked potentials (SSEP), evaluates nerve root and peripheral nerve function.
  • Needle EMG diagnoses lumbosacral radiculopathy by detecting increased insertional activity, spontaneous potentials (eg, positive waves, fibrillations, fasciculations, chronic repetitive discharges), and decreased motor unit recruitment in paraspinal and lower extremity muscles innervated by the same nerve root. The presence of polyphasic motor unit potentials helps establish long-standing disease.
    • Limitations include inability to evaluate sensory and upper motor neurons.
    • Multisegmental muscle innervation may cause false negative results by preserving motor unit function despite nerve root compromise. Such innervation may elicit multilevel abnormalities in severe lumbar spinal stenosis (LSS).
    • Johnsson and colleagues have correlated myelographic LSS severity with multisegmental EMG abnormality.¹⁹
  • NCS differentiates LSS from other confounding neuropathic conditions such as lumbosacral plexopathy, generalized peripheral neuropathy, and mononeuropathy (eg, peroneal neuropathy at the fibular head, tarsal tunnel syndrome).
    • Canal stenosis may compress the cauda equina with resulting polyradicular insults. Such multiple lumbosacral radiculopathies involve lower lumbosacral (especially S1) nerve roots, are often bilateral and asymmetric, and frequently may manifest NCS abnormalities. Such abnormalities include decreased or unelicitable posterior tibial and peroneal compound motor action potentials (CMAPs) reflecting axon loss, and unobtainable H reflexes signifying bilateral S1 compression. Sensory nerve action potentials (SNAPs) remain unaffected (unless impingement occurs distal to the dorsal root ganglion), but may not be detectable in older persons. F waves may also be absent or prolonged in persons with LSS.²⁰
    • Wilbourn and Aminoff advocate measuring peroneal CMAP amplitude from tibialis anterior and M-wave amplitude during H-reflex testing to gauge the extent of L5 and S1 acute denervation, respectively.²¹
    • Overall, Wilbourn and Aminoff report variable EDX findings, including multiple, bilateral lumbosacral radiculopathies in 50% of LSS patients, with prominent chronic motor unit action potential (MUAP) changes, and fibrillations solely in distal musculature. The remaining 50% of patients demonstrate varied abnormalities, with some manifesting 2 radiculopathies commonly as a single radicular insult in each lower extremity, either symmetrically (eg, bilateral L5) or asymmetrically (eg, left S1 and right L5). Other patients display isolated L5 or S1 radiculopathy. Limited nondiagnostic findings may be elicited, including bilaterally absent H reflexes with normal lower extremity needle EMG and sural SNAPs, as well as fibrillations in a single S1-innervated limb muscle. Lastly, many patients demonstrate normal EDX tests.²¹
    • Diagnostically, EMG complements MRI in assessing radiculopathy. Specifically, EMG rarely presents false-positive results and carries high specificity (85%). Conversely, MRI carries high sensitivity and poor specificity (50%) and, consequently, demonstrates many false-positive asymptomatic abnormalities. Some advocate using highly specific EMG to determine whether structural abnormalities imaged on MRI carry functional and pathologic significance. Indeed, Robinson proposes that such use of needle EMG ultimately might prove helpful in avoiding costly and high-risk invasive interventions.²²
  • Somatosensory evoked potentials (SSEPs) are dispatched through large dorsal column myelinated fibers that are affected earlier than smaller fibers. Peripheral nerve lesions prolong SSEP latency and duration, while nerve root and spinal cord pathology induce further morphologic alterations.
    • Keim and colleagues have documented posterior tibial abnormalities in 95%, peroneal abnormalities in 90%, and sural abnormalities in 60% of LSS patients studied.² A high incidence of L4, L5, and S1 nerve root involvement existed, amidst a paucity of upper lumbar segment abnormality (measured by the saphenous nerve). Bilateral lower limb changes were documented in 7 of 20 patients, suggesting that bilateral lower limb SSEPs can uncover previously unsuspected lesions. SSEPs are useful intraoperatively during decompressive surgery to assist the physician in diagnosis of LSS amidst equivocal clinical and imaging studies. SSEPs also appear to be more sensitive than other EDX approaches in evaluating LSS-provoked nerve root compression.
    • Kraft contends the best EDX technique for assessing LSS is dermatomal somatosensory evoked potentials (DSEPs).²³ Insidious low-grade compression from LSS causes impaired nerve conduction, which is best appreciated by DSEPs (similar to nerve conduction study [NCS] slowing in carpal tunnel syndrome). Such pathology contrasts sharply with dramatic acute-onset HNP root compression, inducing axon loss with subsequent denervation best detected by needle EMG.
    • Using CT scan and MRI comparison standards, Kraft and colleagues demonstrated 78% sensitivity and 93% predictive value with DSEPs for an anatomical study positive for LSS when using multiple root disease (MRD) criteria. When criteria of multiple root disease and single root disease (SRD) were added, the sensitivity rose to 93%, with a positive predictive value of 94%. Kraft emphasized that the DSEP electrophysiologic signature of LSS is MRD, but SRD can suggest LSS, especially amidst applicable clinical history, physical examination, and positive EMG findings.²³ Conversely, Dumitru found DSEPs to be of low sensitivity when compared to needle EMG-proven radiculopathies.²⁴

Treatment

Rehabilitation Program

Physical Therapy

Two-stage treadmill testing has demonstrated longer walking times on an inclined treadmill, presumably due to promotion of spinal flexion. Conversely, level treadmill testing is thought to promote more spinal extension-induced NC and elicit earlier symptom onset and longer recovery time. Ancillary exercises to target weak gluteals, as well as shortened hip flexors and hamstrings, are indicated. Physical examination should be performed to assess for concurrent degenerative hip disease, which may mimic LSS. Traction harness-supported treadmill and aquatic ambulation to reduce compressive spine loading has been shown to improve lumbar range of motion (ROM), straight leg raising, gluteal and quadriceps femoris muscle force production, and maximal (up to 15 min) walking time.²⁰

Others advocate stationary cycling and abdominal muscle strengthening. Passive modalities such as heat, cold, transcutaneous electrical nerve stimulation (TENS), and ultrasound may provide transient analgesia and increased soft tissue flexibility in LSS patients.

The addition of a rolling walker is often necessary in many cases. The rolling walker provides some stability and promotes a flexed posture, which allows the afflicted patient to ambulate greater distances.

Medical Issues/Complications

In rare cases, central canal stenosis may provoke cauda equina syndrome with associated saddle anesthesia, bladder and/or bowel dysfunction and altered muscle reflexes. Additionally, patients with lateral recess stenosis – induced radiculopathy may manifest significant lower limb weakness or numbness. Lastly, intractable axial, radicular, or NC pain may result.

Surgical Intervention

Lumbar spinal stenosis (LSS) remains one of the most common conditions leading to lumbar spine surgery in adults aged 65 years and older. Increasing rates of LSS surgery among the Medicare population have been shown to be due possibly to imaging techniques that enable physicians to diagnose LSS more frequently. Other contributing factors may include improved surgical techniques that might allow patients previously managed conservatively to undergo surgery, as well as a philosophy that LSS surgery prevents future morbidity.

• Widely agreed upon indications for LSS surgery do not exist. Typically, patients undergo elective surgery to improve walking tolerance and disabling leg and back pain. Preoperatively, such disability infrequently is measured in objective quantitative terms. Some suggest preoperative treadmill testing to facilitate objective selection of potential surgical candidates.²⁵ Surgical emergencies (eg, cauda equina syndrome, rapid neurologic deterioration) rarely arise.
  • Surgical techniques include standard wide laminectomy and decompression, which first removes lamina and ligamentum flavum from the lateral borders of one lateral recess to the other and then decompresses entrapped nerve roots.²⁶
  • Foraminal enlargement surgery is used to address refractory foraminal stenosis-induced radicular pain. Other surgical decompressions include the following:
    • Laminotomy
    • Medial facetectomy
    • Medial or lateral foraminotomy.
  • Midline interlaminar approaches are used to address concurrent central and foraminal stenosis.
  • The Wiltse approach with foraminotomy is used for isolated foraminal stenosis by providing the following:
    • Widening the longissimus-multifidus muscle interval
    • Removing the lateral pars interarticularis and facet joint
    • Exposing the nerve root with subsequent decompression
  • In addition to decompression and foraminal enlargement, some patients with segmental instability from facet joint removal and pain secondary to DDD may require fusion. (See images below and Images 8-9.)
    • Fusion stabilizes the intervertebral segment while maintaining lordosis and foraminal size.
    • Additional options include arthrodesis and instrumentation.

Lateral view of a lumbar myelogram performed in a patient who has been fused across the L4-L5 and the L5-S1 vertebral interspaces using transpedicular screws. Treatment of lumbar spinal stenosis may include decompression laminectomies, followed by the placement of transpedicular screws (yellow arrows) with a posterior stabilization bar.

Sagittal view of a 3-dimensional volume image of the lumbar spine in a patient with a posterior fusion using transpedicular screws in L4 and L5. Note that an interposition graft has been placed between L4 and L5 to maintain satisfactory intervertebral distance.

• Surgical outcomes for patients with LSS vary.
  • Surgical outcome literature is difficult to assess due to observer bias, inadequate outcome data categorization, vaguely defined outcome measures, and study design.
  • Reports show widely varied outcomes (26-100% success and 31% dissatisfaction at 4.6 years), due to disparate research methodologies.
• Conservative versus surgical treatment for LSS remains controversial due to wide variations in outcome study type and quality.
  • Johnsson and colleagues document improvement in 60% of surgically treated patients with 25% worsened, compared with improvement in 30% of conservatively treated patients and no change in 60%.²⁷
  • Atlas and colleagues tracked 67 conservatively treated and 81 surgically treated patients over 12 months; surgically treated patients reported greater improvement in pain relief than those treated conservatively.²⁸
  • Treatment outcome predictors do not exist; specifically, severe spinal degenerative changes do not necessarily correlate with an unfavorable prognosis or mandate surgery.
• Simotas and colleagues cite that 12 of 49 patients treated conservatively with incorporation of analgesics, physical therapy, and epidural steroid injection, reported sustained improvement.²⁹ Conservative and surgical treatments have not been subjected to rigorous well-designed study.

Consultations

• Consultation with an internal medicine specialist or subspecialty may be indicated when low back pain (LBP) suggests an underlying systemic illness such as malignancy, infection, or metabolic bone disease. Also, if the diagnosis of vascular claudication is in question, referral to an internist is indicated.
• Consultation with a rheumatologist may be considered when back pain suggests a rheumatologic condition such as ankylosing spondylitis, rheumatoid arthritis, osteoporosis, or fibromyalgia.
• Consultation with a surgeon is warranted for deteriorating neurologic status (eg, cauda equina syndrome), segmental instability, and/or intractable radicular or NC pain.

Other Treatment

• Caudal ESI
  • Caudal ESI entails needle placement through the sacral hiatus into the sacral epidural space.
  • Advantages include ease of performance and low risk of dural puncture.
  • Disadvantages include large injectate volumes (6-10 mL) necessary to ensure adequate medication spread to more cephalad pathology (ie, above L4-L5). Furthermore, such large volumes potentially may dilute the effect of the corticosteroid.
• Interlaminar ESI
  • Interlaminar ESI entails needle passage through the interlaminar space, with subsequent injection directly into the epidural space. Consequently, delivery of medication occurs closer to the affected spinal segmental level than in caudal ESI.
  • Disadvantages include greater potential for dural puncture, and, like caudal ESI, limited spread of medication to the target site if a midline raphe or epidural scarring exists. Furthermore, interlaminar injection delivers medication to the posterior epidural space with possible limited ventral diffusion to nerve root impingement sites.
• Transforaminal ESI
  • Transforaminal ESI facilitates precise deposit of higher steroid concentrations closer to the involved spinal segment, and, consequently, might prove more efficacious in reducing pain.
  • Transforaminal ESI may be used for unilateral radicular pain provoked by lateral recess or foraminal stenosis.
  • Bilateral transforaminal ESI also may be used to treat bilateral central stenosis-induced NC pain when imaging studies demonstrate limited posterior epidural space, thereby precluding safe interlaminar ESI. Otherwise, interlaminar ESI may be used to treat bilateral or multilevel NC or radicular pain.
• Absolute contraindications to ESI include bleeding diathesis and anticoagulation therapy because of the increased risk of epidural hematoma. While the actual incidence of this complication is unknown, estimates in the literature suggest is occurs less than 1 in 150,000 outpatient epidural injections. Anticoagulation therapy (eg, warfarin, heparin) should be stopped a few days prior to injection. (Alternative methods of DVT prophylaxis, such as serial compression hose, should be instituted in the interim). In the case of patients taking Coumadin, PT/INR should be drawn the day of the procedure. Aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) should be discontinued before the procedure in accordance with their half-life and hematologic profile.
• Other absolute contraindications include systemic infection, injectate allergy, and pregnancy (because of the teratogenicity of fluoroscopy). Relative contraindications include diabetes mellitus (DM) and congestive heart failure, given the hyperglycemic and fluid retention properties of corticosteroids, respectively. Other relative contraindications include adrenal dysfunction and hypothalamic-pituitary axis suppression.
• Serious complications, although rare, include infection (eg, epidural or subdural abscess) and epidural hematoma. Epidural hematoma has been associated with traumatic needle insertions, but this is neither sensitive nor specific for predicting development. Vandermeulen and colleagues reported 61 case reports in the literature between 1904 and 1994 after central nervous blocks.³⁰ Dural puncture (in 5% of lumbar interlaminar ESIs and 0.6% of caudal injections) with possible subsequent subarachnoid anesthetic/corticosteroid deposition may provoke neurotoxicity, sympathetic blockade with hypotension, and/or spinal headache; however, contrast-enhanced fluoroscopic guidance minimizes the possibility of dural puncture and intravascular injection.
• Therapeutic epidural steroid injection (ESI) techniques are performed ideally using fluoroscopic guidance and radiologic contrast dye enhancement to ensure delivery of injectate to the target site. Studies document misplacement of 40% of caudal and 30% of interlaminar injections performed without fluoroscopy, even by experienced injectionists.
• Transient corticosteroid dose-related side effects include facial flushing, low-grade fever, insomnia, anxiety, agitation, hyperglycemia, and fluid retention. Steroids may suppress the hypothalamic-pituitary axis for 3 months following the injection. Lastly, vasovagal reaction, nerve root injury, injectate allergy, and temporary pain exacerbation can occur as well.
• Recent studies assessing efficacy of fluoroscopically guided, contrast-enhanced ESI, even for HNP-induced radicular pain, appear promising, suggesting that a significant inflammatory component amenable to corticosteroid treatment may accompany HNP-nerve root pathology.
• Studies of ESI for LSS treatment demonstrate mixed results due to varying injection and guidance techniques, patient populations, follow-up periods and protocols, ancillary treatments (eg, physical therapy, oral medication), and outcome measures. This lack of consistency limits the ability to assess ESI efficacy for LSS.
• Some studies, nevertheless, suggest that, unlike HNP-provoked radicular pain, NC may be more mechanical or ischemic than inflammatory in nature. Consequently, corticosteroid anti-inflammatory properties may fail to provide designed long-term symptom relief. Studies report that 50% of patients with LSS or HNP-provoked radicular pain received temporary relief and that such results were close to those associated with the placebo effect.
• Because of concomitant lateral recess stenosis from facet hypertrophy or lateral HNP, patients may fail transforaminal ESI therapy for HNP-induced radicular pain. ESI may do little to relieve chronic lateral recess stenosis-related radicular pain. Additionally, studies show patients with a preinjection duration of symptoms greater than 24 weeks may respond to ESI as favorably as those with symptoms of less than 24 weeks' duration. This finding, may suggest that chronic nerve compression could induce irreversible neurophysiologic change that ultimately renders the nerve root refractory to ESI.
• Future studies require controlled design, contrast-enhanced fluoroscopic guidance, and objective validated outcome measures before definitive conclusions can be drawn regarding efficacy of ESI treatment of LSS.

Medication

First-line pharmacotherapy for lumbar spinal stenosis (LSS) includes NSAIDs, which provide analgesia at low doses and quell inflammation at high doses. An appropriate therapeutic NSAID plasma level is required to achieve anti-inflammatory benefit.

Aspirin, which binds irreversibly to cyclo-oxygenase and requires larger doses to control inflammation, may cause gastritis; consequently, it is not recommended. Additionally, it may induce multiorgan toxicity, including renal insufficiency, peptic ulcer disease, and hepatic dysfunction. Cyclo-oxygenase isomer type 2 (COX-2) NSAID inhibitors reduce such toxicity. NSAIDs retain a dose-related analgesic ceiling point, above which larger doses do not confer further pain control.

Muscle relaxants may be used to potentiate NSAID analgesia. Sedation results from muscle relaxation, promoting further patient relaxation. Such sedative side effects encourage evening dosing for patients who need to get sufficient sleep but may limit safe performance of some functional activities.

Membrane-stabilizing anticonvulsants, such as gabapentin and carbamazepine, may reduce neuropathic radicular pain from lateral recess stenosis.

Tricyclic antidepressants (TCAs) are often given for neuropathic pain, but their adverse effects limit their use in elderly persons. These include somnolence, dry mouth, dry eyes, and constipation. More concerning are the possible arrhythmias that may occur when used in combination with other medications.

Tramadol and acetaminophen confer analgesia but do not affect inflammation.

Oral opioids may be prescribed on a scheduled short-term basis. Consequently, cotreatment with a psychologist or other addiction specialist is recommended for patients with a history of substance abuse. Patients may be asked to sign a medication contract restricting them to 1 practitioner, 1 pharmacy, scheduled medication use, no unscheduled refills, and no sharing or selling of medication.

Matsudaira et al tested the effectiveness of limaprost, an oral prostaglandin E1 derivative, against that of etodolac, an NSAID, in improving the health-related quality of life in patients with symptomatic LSS.³¹ In a randomized, controlled trial, 66 patients suffering from central stenosis with acquired, degenerative LSS, along with neurogenic intermittent claudication and bilateral leg numbness related to the cauda equina, were administered a daily dose of limaprost (15 μg) or etodolac (400 mg) for 8 weeks. The results indicated that limaprost was more effective than etodolac in improving patients' physical functioning, vitality, and mental health, and in reducing pain and leg numbness.

Anticonvulsants

Use of certain antiepileptic drugs, such as the GABA analogue Neurontin (gabapentin), has proven helpful in some cases of neuropathic pain.³² These agents have central and peripheral anticholinergic effects, as well as sedative effects, and block the active reuptake of norepinephrine and serotonin. The multifactorial mechanism of analgesia could include improved sleep, altered perception of pain, and increase in pain threshold. Rarely should these drugs be used in treatment of acute pain, since a few weeks may be required for them to become effective.

Gabapentin (Neurontin)

Has anticonvulsant properties and antineuralgic effects; however, exact mechanism of action is unknown. Structurally related to GABA but does not interact with GABA receptors.

Dosing

Adult

900-1800 mg/d PO tid; may start 300 mg d 1, 300 mg bid d 2, and 300 mg tid d 3; may increase up to 1800 mg/d by adding 300 mg on following days

Pediatric

<12 years: Not established
>12 years: Administer as in adults

Interactions

Antacids may reduce bioavailability of gabapentin significantly (administer at least 2 h following antacids); may increase norethindrone levels significantly

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in renal or hepatic disease, breastfeeding women, and elderly patients

Carbamazepine (Tegretol)

Inhibits nerve impulses by decreasing cell membrane sodium ion influx.

Dosing

Adult

100 mg PO bid with meals; may increase 100 mg q12h until pain decreases; not to exceed 1.2 g/d; maintenance dose 200-400 mg bid

Pediatric

<12 years: Not established
>12 years: Administer as in adults

Interactions

Fatal reaction with MAOIs; toxicity with clarithromycin, verapamil, lithium, propoxyphene, isoniazid, diltiazem, cimetidine, erythromycin, and troleandomycin; decreased effects with thyroid hormones, theophylline, oral contraceptives, warfarin, primidone, phenytoin, and phenobarbital; increased effects of lithium, desmopressin, lypressin, and vasopressin

Contraindications

Documented hypersensitivity, bone marrow depression, and concomitant MAOI use

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Not to be used for relief of minor aches or pains; caution with increased intraocular pressure; obtain CBC counts (may cause aplastic anemia) and serum-iron baseline prior to treatment, during first 2 mo, and yearly or every other year thereafter; can cause drowsiness, dizziness, and blurred vision; caution while driving or performing other tasks requiring alertness; caution with breastfeeding, psychosis, cardiac disease, and renal or hepatic disease

Analgesics

Pain control is essential to quality patient care. Analgesics ensure patient comfort and have sedating properties, which are beneficial for patients who experience pain.

Acetaminophen (Tylenol, Feverall)

DOC for pain in patients with documented hypersensitivity to aspirin or NSAIDs, with upper GI disease, or who are taking oral anticoagulants.

Dosing

Adult

325-650 mg PO q4h prn; not to exceed 4 g/d

Pediatric

10-15 mg/kg PO q4h

Interactions

Decrease effects of chloramphenicol; caffeine and diflunisal may increase effects of acetaminophen; colestipol, anticholinergics, oral contraceptives, rifampin, and cholestyramine decrease effects of acetaminophen; severe hypothermia may occur with phenothiazines; coadministration with barbiturates, carbamazepine, hydantoins, and isoniazid may increase hepatotoxicity

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Hepatotoxicity possible in chronic alcoholics following various dose levels; severe or recurrent pain or high or continued fever may indicate a serious illness; APAP is contained in many OTC products and combined use with these products may result in cumulative APAP doses exceeding recommended maximum dose; caution in hepatic or renal disease

Tramadol (Ultram)

Mechanism not entirely known. Binds to opioid receptors; inhibits reuptake of serotonin, norepinephrine.

Dosing

Adult

50-100 mg PO q4-6h prn; not to exceed 400 mg/d

Pediatric

Not established

Interactions

Decreased tramadol levels with carbamazepine; increased CNS depression with opiates, hypnotics, sedatives, and alcohol; norepinephrine and serotonin reuptake inhibition (use together with MAOIs with caution)

Contraindications

Documented hypersensitivity; opioid-dependent patients; concurrent use of MAOI or within 14 d; use of SSRIs, TCAs, opioids, and acute alcohol intoxication

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Can cause dizziness, nausea, constipation, sweating, pruritus; additive sedation with alcohol and TCAs; abrupt discontinuation can precipitate opioid withdrawal symptoms; adjust dose in liver disease, myxedema, hypothyroidism, hypoadrenalism; caution in elderly patients, pregnancy, and breastfeeding; seizures; development of tolerance or dependency with extended use

Tricyclic antidepressants

A complex group of drugs that have central and peripheral anticholinergic effects and sedative effects. They have central effects on pain transmission. They block the active reupdate of norepinephrine and serotonin.

Amitriptyline (Elavil)

Analgesic for certain chronic and neuropathic pain. Blocks reuptake of norepinephrine and serotonin, which increases concentration in the CNS. Decreases pain by inhibiting spinal neurons involved in pain perception. Highly anticholinergic. Often discontinued because of somnolence and dry mouth.
Cardiac arrhythmia, especially in overdose, has been described; monitoring the QTc interval after reaching the target level is advised. Up to 1 mo may be needed to obtain clinical effects.

Dosing

Adult

30-100 mg PO qhs

Pediatric

Children: 0.1 mg/kg PO qhs; increase, as tolerated, over 2-3 wk to 0.5-2 mg/d qhs
Adolescents: 25-50 mg/d PO initially; increase gradually to 100 mg/d in divided doses

Interactions

Phenobarbital may decrease effects; coadministration with CYP2D6 enzyme system inhibitors (eg, cimetidine, quinidine) may increase levels; inhibits hypotensive effects of guanethidine; may interact with thyroid medications, alcohol, CNS depressants, barbiturates, and disulfiram

Contraindications

Documented hypersensitivity; use of MAOIs within 14 d of initiating therapy; history of seizures, cardiac arrhythmias, glaucoma, or urinary retention

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in cardiac conduction disturbances and history of hyperthyroidism, renal impairment, or hepatic impairment; avoid use in elderly persons

Follow-up

Further Inpatient Care

• Inpatient care is necessary for patients with lumbar spinal stenosis who elect to undergo surgery. The length of stay in the hospital is dependent on the type of procedure performed, but, on average, the patient is released 2-5 days following surgery. Following the operation, it is important that these patients resume basic mobility, activities of daily living (ADL), and ambulation as soon as possible and become educated on proper body mechanics and back safety techniques prior to their dismissal. A short course of active physical therapy may be recommended after surgery for these patients to strengthen the lower back and abdominal muscles to speed recovery time. Ideally, an appropriate exercise program can be initiated before surgery and continued thereafter.

Further Outpatient Care

• Many patients with lumbar spinal stenosis choose to receive conservative treatment for back and leg pain. An active physical therapy program often is beneficial for these patients to improve flexibility and strength to maintain or improve their current activity levels. Other forms of treatment (eg, ESI) may be administered on an outpatient basis and used in conjunction with other medications and physical therapy. Please see the Physical Therapy and Other Treatment sections for further discussion of these treatments.

Deterrence

• No prevention exists for lumbar spinal stenosis.

Complications

• Complications that may develop in patients with lumbar spinal stenosis (LSS) include the following:
  • Cauda equina syndrome (in rare cases)
  • Lower extremity weakness and numbness
  • Intractable axial, radicular, or NC pain
  • Disability and loss of productivity
• Complications that may develop in patients after surgery include the following:
  • Sustained axial and radicular pain
  • Progressive spinal deformity
  • Cerebrospinal fluid leak
  • Epidural hematoma
  • Pulmonary embolism (PE)
• Some authors report spondylolisthesis as a complication of lumbar decompression without arthrodesis, especially after total facetectomy. Preoperative risk factors for postoperative development or progression of L4 or L5 spondylolisthesis include the following:
  • Absence of degenerative osteophytosis
  • Small and sagittally oriented facets
  • Well-maintained disk height
• Ciol and colleagues report a substantial reoperation rate following LSS surgery in the Medicare population, for reasons that remain unclear.³³
  • Possible explanations may include the following:
    • Failure of implanted devices
    • Changed patient expectations
    • Aggressive surgical philosophy

Patient Education

• Patients with lumbar spinal stenosis should be educated to avoid aggravating factors, such as excessive lumbar extension and downhill ambulation. Additionally, patients should be instructed on correct posture and should also receive instructions concerning a home exercise program (eg, flexion-biased lumbar stabilization, flexibility training, gluteal strengthening, aerobic conditioning).
• For excellent patient education resources, visit eMedicine's Back, Ribs, Neck, and Head Center and Muscle Disorders Center. Also, see eMedicine's patient education articles, Back Pain, Lumbar Laminectomy, and Chronic Pain.

Miscellaneous

Medicolegal Pitfalls

• The clinician may fail to diagnose LBP as a manifestation of serious systemic illness such as malignancy or infection. Consequently, LBP evaluation demands a careful history with review of systems, thorough physical examination, and judicious use of imaging.
• Additionally, the physician may fail to make timely diagnosis of serious sequelae of lumbar spinal stenosis, such as cauda equina syndrome or radiculopathy with profound lower limb neurologic deficit.
• Interventional lumbar spine procedures (eg, epidural injections) carry potential for complications, including epidural hematoma, infection, and dural puncture. Competency in such procedures, proper patient monitoring, and preparation to manage such complications are essential.

Multimedia

Media file 1: Lateral T2-weighted magnetic resonance imaging (MRI) scan demonstrating narrowing of the central spinal fluid signal (L4-L5), suggesting central canal stenosis.

Media file 2: Axial T2 magnetic resonance imaging (MRI) scan (L4-L5) in the same patient as in the above image, confirming central canal stenosis.

Media file 3: Trefoil appearance characteristic of central canal stenosis due to a combination of zygapophysial joint and ligamentum flavum hypertrophy.

Media file 4: Lateral and axial magnetic resonance imaging (MRI) scan demonstrating right L4 lateral recess stenosis secondary to combination of far lateral disk protrusion and zygapophysial joint hypertrophy.

Media file 5: Axial lumbar computed tomography (CT) scan demonstrates marked right-sided spinal canal stenosis (black arrow) resulting from advanced right-sided facet hypertrophy. Note the vacuum disk sign within the intervertebral disc (yellow double arrow). The vacuum disk sign is further indication of degenerative changes and spinal instability.

Media file 6: Lumbar computed tomography (CT) myelogram scan demonstrates a normal central canal diameter.

Media file 7: Anterior view of a lumbar myelogram demonstrates stenosis related to Paget disease. Myelography is limited because of the superimposition of multiple spinal structures that contribute to the overall pattern of stenosis.

Media file 8: Lateral view of a lumbar myelogram performed in a patient who has been fused across the L4-L5 and the L5-S1 vertebral interspaces using transpedicular screws. Treatment of lumbar spinal stenosis may include decompression laminectomies, followed by the placement of transpedicular screws (yellow arrows) with a posterior stabilization bar.

Media file 9: Sagittal view of a 3-dimensional volume image of the lumbar spine in a patient with a posterior fusion using transpedicular screws in L4 and L5. Note that an interposition graft has been placed between L4 and L5 to maintain satisfactory intervertebral distance.

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Keywords

spinal stenosis, neurogenic claudication, stenosis, stenosis lumbar, lumbar spinal stenosis, laminectomy, spine surgery, disk surgery, disc surgery, foraminal stenosis, stenosis surgery, spinal stenosis surgery, spinal stenosis treatment, central stenosis, central canal stenosis, claudication, intervertebral foramen stenosis, lateral gutter stenosis, lateral recess stenosis, subarticular stenosis, subpedicular stenosis, neural compression, spinal canal narrowing, ligamentum flavum hypertrophy, facet hypertrophy of cephalad vertebra, vertebral body osteophytosis, herniated nucleus pulposus, HNP, foraminal canal stenosis, incomplete vertebral arch closure, spinal dysraphism, segmentation failure, achondroplasia, osteopetrosis

early vertebral arch ossification, osseous exostosis, shortened pedicles, thoracolumbar kyphosis, apical vertebral wedging, anterior vertebral beaking, Morquio syndrome, posterior disc protrusion, zygapophyseal joint hypertrophy, spondylolisthesis, diskectomy, discectomy, Paget disease, fluorosis, acromegaly, ankylosing spondylitis, disc desiccation, degenerative disk disease, degenerative disc disease, failed back surgery syndrome, bilateral neurogenic claudication, cauda equina microvascular ischemia, intraneural fibrosis, radiculopathy

Contributor Information and Disclosures

Author

Michael B Furman, MD, MS, Physiatrist, Interventional Spine Care Specialist, Electrodiagnostics, Orthopedic and Spine Specialists
Michael B Furman, MD, MS is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, American Medical Association, International Spine Intervention Society, North American Spine Society, Pennsylvania Medical Society, and Physiatric Association of Spine, Sports and Occupational Rehabilitation
Disclosure: pfizer Honoraria Speaking and teaching

Coauthor(s)

Kirk M Puttlitz, MD, Consulting Staff, Pain Management and Physical Medicine, Arizona Neurological Institute
Kirk M Puttlitz, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation and Phi Beta Kappa
Disclosure: Nothing to disclose.

Robert Pannullo, MD, Interventional Spinal Care Fellow, Department of Physical Medicine and Rehabilitation, KDV Orthopaedics and Rehabilitation Ltd
Robert Pannullo, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation and Phi Beta Kappa
Disclosure: Nothing to disclose.

Jeremy Simon, MD, Attending Physician, Department of Physical Medicine, The Rothman Institute
Jeremy Simon, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, International Spine Intervention Society, North American Spine Society, and Physiatric Association of Spine, Sports and Occupational Rehabilitation
Disclosure: Nothing to disclose.

Medical Editor

J Michael Wieting, DO, MEd, Professor of Physical Medicine and Rehabilitation, Professor of Osteopathic Principles and Practices, Director of Sports Medicine, Associate Director of Physician Assistant Training Program, Department of Osteopathic Principles and Practice, Lincoln Memorial University-DeBusk College of Osteopathic Medicine
J Michael Wieting, DO, MEd is a member of the following medical societies: American Academy of Osteopathy, American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, American College of Forensic Examiners, American College of Sports Medicine, American Osteopathic Association, American Osteopathic College of Physical Medicine and Rehabilitation, Association of Academic Physiatrists, and International Society of Physical and Rehabilitation Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Patrick M Foye, MD, FAAPMR, FAAEM, Associate Professor of Physical Medicine and Rehabilitation, Co-Director of Musculoskeletal Fellowship, Co-Director of Back Pain Clinic, Director of Coccyx Pain Service (Tailbone Pain Service: www.TailboneDoctor.com), University of Medicine and Dentistry of New Jersey, New Jersey Medical School
Patrick M Foye, MD, FAAPMR, FAAEM is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, Association of Academic Physiatrists, and International Spine Intervention Society
Disclosure: Nothing to disclose.

CME Editor

Kelly L Allen, MD, Regional Medical Director, IMX-Medical Management Services
Disclosure: Nothing to disclose.

Chief Editor

Rene Cailliet, MD, Professor-Chairman Emeritus, Department of Rehabilitation Medicine, University of Southern California School of Medicine; Former Director, Department of Rehabilitation Medicine, Santa Monica Hospital Medical Center
Rene Cailliet, MD is a member of the following medical societies: American Academy of Pain Medicine, American Academy of Physical Medicine and Rehabilitation, American Pain Society, Association of American Medical Colleges, International Association for the Study of Pain, and Pan American Medical Association
Disclosure: Nothing to disclose.

Related eMedicine topics:
Cauda Equina
Cauda Equina and Conus Medullaris Syndromes
Cauda Equina Syndrome [Emergency Medicine]
Cauda Equina Syndrome [Orthopedic Surgery]
Degenerative Disk Disease
Degenerative Lumbar Disc Disease in the Mature Athlete
Lumbar Degenerative Disk Disease
Spinal Stenosis [Neurosurgery]
Spinal Stenosis [Orthopedic Surgery]
Spinal Stenosis [Radiology]

Clinical guidelines:
Diagnosis and treatment of degenerative lumbar spinal stenosis. North American Spine Society - Medical Specialty Society.  2002 (revised 2007 Jan).  262 pages.  NGC:005896 

Guidelines for the performance of fusion procedures for degenerative disease of the lumbar spine. Part 9: fusion in patients with stenosis and spondylolisthesis. American Association of Neurological Surgeons - Medical Specialty Society
Congress of Neurological Surgeons - Professional Association.  2005 Jun.  7 pages.  NGC:005370

Guidelines for the performance of fusion procedures for degenerative disease of the lumbar spine. Part 10: fusion following decompression in patients with stenosis without spondylolisthesis. American Association of Neurological Surgeons - Medical Specialty Society
Congress of Neurological Surgeons - Professional Association.  2005 Jun.  6 pages.  NGC:005371

Clinical trials:
A Pivotal Study of a Facet Replacement System to Treat Spinal Stenosis

Dynamic Stabilization for Lumbar Spinal Stenosis With Stabilimax NZ® Dynamic Spine Stabilization System

IDE Clinical Trial Comparing Coflex vs. Fusion to Treat Lumbar Spinal Stenosis (coflex)

Investigating Superion™ In Spinal Stenosis [ISISS]

Lumbar Stenosis Outcomes Research (LUSTOR)

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