eMedicine Specialties > Physical Medicine and Rehabilitation > Lumbar Spine Disorders
Spinal Stenosis and Neurogenic Claudication
Updated: Jun 16, 2009
Introduction
Background
Lumbar spinal stenosis (LSS) implies spinal canal narrowing with possible subsequent neural compression. LSS is classified by anatomy or etiology. Anatomic subclassifications include central canal and lateral recess stenosis. The classification of lumbar stenosis is important because of the implications of the underlying etiology and because it affects the therapeutic strategy, specifically the surgical approach.- 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
Disk desiccation and degenerative disk disease (DDD) with resulting loss of disk height may induce segmental instability. Such instability incites vertebral body and facet joint hypertrophy. Cephalad vertebral body IAP hypertrophy promotes central spinal canal stenosis. Further canal volume loss results from HNP, ligamentum flavum hypertrophy, and disk space narrowing.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.
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Further Reading
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)
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
