JBJS | Instructional Course Lectures, The American Academy of Orthopaedic Surgeons

The Journal of Bone & Joint Surgery, Volume 81, Issue 4

Instructional Course Lecture | April 01, 1999

Instructional Course Lectures, The American Academy of Orthopaedic Surgeons - Spinal Stenosis*†

STEVEN R. GARFIN, M.D.‡, SAN DIEGO, CALIFORNIA; HARRY N. HERKOWITZ, M.D.§, ROYAL OAK, MICHIGAN; SRDJAN MIRKOVIC, M.D.#, CHICAGO, ILLINOIS

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An Instructional Course Lecture, American Academy of Orthopaedic Surgeons

The Journal of Bone & Joint Surgery. 1999; 81:572-86

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Introduction

Spinal stenosis is a narrowing or stricture of the spinal canal. Cauda equina and nerve-root compression are noted in many asymptomatic individuals⁸. Therefore, narrowing alone does not explain all of the symptoms and signs seen in patients who have the clinical syndrome of spinal stenosis, or neurogenic claudication.

The spinal degenerative process associated with aging leads to pathoanatomical and pathophysiological changes with occasional clinical consequences. Not only does narrowing occur, but abnormal spinal motion can further increase the degree of compression. With progressive degenerative changes and compression, spinal stenosis may become symptomatic, although the severity of the symptoms is not necessarily associated with the magnitude of the compression seen on imaging studies.

*Printed with permission of the American Academy of Orthopaedic Surgeons. This article will appear in Instructional Course Lectures, Volume 49, American Academy of Orthopaedic Surgeons, Rosemont, Illinois, March 2000.

†No benefits in any form have been received or will be received from a commercial party related directly or indirectly to the subject of this article. No funds were received in support of this study.

‡Department of Orthopaedics, University of California, San Diego, 200 West Arbor Drive, 8894, San Diego, California 92103.

§Department of Orthopaedics, William Beaumont Hospital, 3535 West 13 Mile Road, 604, Royal Oak, Michigan 48076.

‡Department of Orthopaedics, University of California, San Diego, 200 West Arbor Drive, 8894, San Diego, California 92103.

§Department of Orthopaedics, William Beaumont Hospital, 3535 West 13 Mile Road, 604, Royal Oak, Michigan 48076.

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Figs. 1-A and 1-B: Drawings showing neural organization within the thecal sac at the fourth and fifth lumbar and fifth lumbar and first sacral disc levels^18,153. M = motor components, and S = sensory components.

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TABLE I CLASSIFICATION OF STENOSIS OF THE SPINAL CANAL

I. Congenital or developmental

A. Idiopathic

B. Achondroplastic

C. Osteopetrosis

II. Acquired

A. Degenerative

1. Central

2. Lateral recess and foraminal

3. Degenerative spondylolisthesis

B. Iatrogenic

1. After laminectomy

2. After arthrodesis

3. After discectomy

C. Miscellaneous disorders

1. Acromegaly

2. Paget disease

3. Fluorosis

4. Ankylosing spondylitis

D. Traumatic

III. Combined: any combination of congenital, developmental, or acquired stenosis

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TABLE I CLASSIFICATION OF STENOSIS OF THE SPINAL CANAL

I. Congenital or developmental

A. Idiopathic

B. Achondroplastic

C. Osteopetrosis

II. Acquired

A. Degenerative

1. Central

2. Lateral recess and foraminal

3. Degenerative spondylolisthesis

B. Iatrogenic

1. After laminectomy

2. After arthrodesis

3. After discectomy

C. Miscellaneous disorders

1. Acromegaly

2. Paget disease

3. Fluorosis

4. Ankylosing spondylitis

D. Traumatic

III. Combined: any combination of congenital, developmental, or acquired stenosis

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TABLE II TOTAL MOTION OF THE FOURTH AND FIFTH LUMBAR AND THE FIRST SACRAL NERVE ROOTS AT THE DORSAL ROOT GANGLION¹³⁰

*The range is given in parentheses.

Nerve Root	Mean Total Motion* (mm)
L4	1.4 (0.0—2.5)
L5	2.1 (0.4—4.5)
S1	2.5 (1.0—5.0)

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TABLE II TOTAL MOTION OF THE FOURTH AND FIFTH LUMBAR AND THE FIRST SACRAL NERVE ROOTS AT THE DORSAL ROOT GANGLION¹³⁰

*The range is given in parentheses.

Nerve Root	Mean Total Motion* (mm)
L4	1.4 (0.0—2.5)
L5	2.1 (0.4—4.5)
S1	2.5 (1.0—5.0)

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TABLE III DIFFERENTIAL DIAGNOSIS OF SYMPTOMS

Findings	Neurogenic Claudication	Vascular Claudication	Lumbar Spondylosis
Pain
Type	Vague cramping, aching, sharp burning in lower extremities	Tightness, cramping (usually in calf)	Dull aching in low back
Location	Back, buttocks, lower extremities	Calf	Back
Radiation	Proximal to distal	Localized to lower extremities	Localized to back
Exacerbation	With standing, particularly with trunk extended; less with walking, rare with bicycling, unless trunk is extended	With walking and bicycling (activities involving lower extremities)	With general activity, bending, standing, twisting, and lifting
Improvement	With sitting, flexion, and squatting	With sitting and cessation of muscular activity	With decreased activity and rest
Time to relief	Prolonged	Rapid	Prolonged
Walking uphill	More or less pain	Pain	More or less pain
Walking downhill	Pain (with lumbar hyperextension)	Pain	More or less pain
Back pain	Common	Uncommon	Common
Limitation of spinal movement	Common	Uncommon	Common

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TABLE III DIFFERENTIAL DIAGNOSIS OF SYMPTOMS

Findings	Neurogenic Claudication	Vascular Claudication	Lumbar Spondylosis
Pain
Type	Vague cramping, aching, sharp burning in lower extremities	Tightness, cramping (usually in calf)	Dull aching in low back
Location	Back, buttocks, lower extremities	Calf	Back
Radiation	Proximal to distal	Localized to lower extremities	Localized to back
Exacerbation	With standing, particularly with trunk extended; less with walking, rare with bicycling, unless trunk is extended	With walking and bicycling (activities involving lower extremities)	With general activity, bending, standing, twisting, and lifting
Improvement	With sitting, flexion, and squatting	With sitting and cessation of muscular activity	With decreased activity and rest
Time to relief	Prolonged	Rapid	Prolonged
Walking uphill	More or less pain	Pain	More or less pain
Walking downhill	Pain (with lumbar hyperextension)	Pain	More or less pain
Back pain	Common	Uncommon	Common
Limitation of spinal movement	Common	Uncommon	Common

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TABLE IV DIFFERENTIAL DIAGNOSIS OF SIGNS

Findings	Neurogenic Claudication	Vascular Claudication	Lumbar Spondylosis
Neurological examination	Occasional findings, usually asymmetrical	Findings rare, symmetrical if present	Negative
Straight-leg-raising test	Usually negative	Negative	Negative
Femoral stretch test	Usually negative	Negative	Negative
Pulses	Present or symmetrically diminished	Diminished or absent, often asymmetrical	Symmetrical
Skin	Normal	Hair loss, atrophy	Normal
Bicycle test	Positive with lumbar hyperextension	Positive with the spine in any position	Negative

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TABLE IV DIFFERENTIAL DIAGNOSIS OF SIGNS

Findings	Neurogenic Claudication	Vascular Claudication	Lumbar Spondylosis
Neurological examination	Occasional findings, usually asymmetrical	Findings rare, symmetrical if present	Negative
Straight-leg-raising test	Usually negative	Negative	Negative
Femoral stretch test	Usually negative	Negative	Negative
Pulses	Present or symmetrically diminished	Diminished or absent, often asymmetrical	Symmetrical
Skin	Normal	Hair loss, atrophy	Normal
Bicycle test	Positive with lumbar hyperextension	Positive with the spine in any position	Negative

Classification

Spinal stenosis can be classified as either congenital or acquired³ (Table I). Congenital stenosis is commonly seen in individuals who have achondroplasia or another short-stature syndrome. The congenital classification also includes stenosis in individuals of normal stature who have congenitally short pedicles accompanied by bulging discs at multiple levels. The latter group frequently has symptoms when they are between the ages of thirty and forty years old.

Acquired degenerative stenosis tends to lead to symptoms in women at a mean age of seventy-three years and in men at a somewhat younger age⁸⁶. Degenerative spondylolisthesis, seen more often in women than in men, also may contribute to the symptoms of spinal stenosis^67,69,70,147.

Although there are many causes of spinal stenosis, this discussion will focus on the degenerative process. Degenerative changes and narrowing can occur (1) centrally; (2) in the lateral recess, leading to nerve-root impingement from an overhanging, hypertrophic facet joint; (3) within the nerve-root canal (foraminal stenosis); or (4) extraforaminally, frequently because of entrapment by osteophytes, discs, transverse processes, or the sacroiliac articulation for the fifth lumbar nerve root.

Anatomy

The cauda equina is bounded anteriorly by the discs, the posterior longitudinal ligament, and the vertebral bodies. The pedicles, along with the lateral extension of the ligamentum flavum, create the lateral margin. The posterior elements consist of the ligamentum flavum, the laminae, and the facet joints. The spinal nerve-root canals (neuroforamina) are bounded anteriorly by the discs and the vertebral bodies, posteriorly by the facet joints, and superiorly and inferiorly by the pedicles.

The mean anterior-posterior diameter of the spinal canal is twelve millimeters^27,28,109. A minimum cross-sectional area of at least 77 ± 13 square millimeters (mean and standard deviation) is necessary to accommodate average-size neural elements^{27,109,127,128}.

Within the cauda equina, the neural elements are organized in a well defined pattern (Figs. 1-A and 1-B). The most posterior neural elements within the thecal sac are the fifth sacral nerve roots, which progress anteriorly from the fourth through the first sacral vertebra, between the fifth lumbar and first sacral disc level. The most anterior element at the fifth lumbar and first sacral disc level is the first sacral nerve root. Between the fourth and fifth lumbar vertebrae, the fifth lumbar nerve root enters anterolaterally, displacing the first sacral nerve root more posteriorly. This arrangement progresses symmetrically and regularly, with one root being added in the cephalad direction at each disc level^18,152,153. The motor fiber components are anteromedial, and the larger sensory components are posterolateral. Root-specific sensory and motor fibers are contiguous and oriented in an oblique fashion. Within the neuroforamen lies the dorsal root ganglion, which consists of a small motor component anteriorly and a larger sensory component, containing neural fibers and cell bodies, posteriorly. The dorsal root ganglion is almost always within the confines of the neuroforamen and frequently is situated adjacent to the disc space at the level of the pedicles¹⁷.

Pathoanatomy: the Degenerative Process

The three primary biochemical components of the intervertebral disc are water, collagen, and proteoglycans. These constitute 90 to 95 percent of the normal disc volume^35,47,95. The collagen, arranged in laminae, allows extensibility of the disc and provides intervertebral attachment. Proteoglycans provide hydrodynamic and electrostatic properties and control tissue turgor by regulating fluid exchange within the disc matrix.

The water content of the disc varies with applied mechanical loads, but it normally accounts for a major portion of the weight of the disc. With age, the water content decreases^35,47,95. As the nucleus pulposus dehydrates, its ability to distribute stress diminishes, leading to fissures and tears within the annulus^24,96.

Collagen provides tensile properties to the disc. The nucleus consists exclusively of type-II collagen^33,55, which helps to provide higher levels of hydration by maintaining water, allowing the nucleus to resist compressive and deforming loads. The annulus consists of approximately equal amounts of type-II and type-I collagen. The type-I collagen content increases in the discs of individuals who are middle-aged and older^2,12,34.

Proteoglycans in the intervertebral disc are smaller than those in the articular cartilage, have a shorter core protein, and include different amounts of keratin sulfate and chondroitin sulfate chains^135,136. Disc compressibility is related to the proteoglycans, which are present in a higher concentration in the nucleus than in the annulus^2,140. With age and subsequent degeneration, the total proteoglycan content decreases^93,96,146. The rate of proteoglycan synthesis also decreases with age.

Electron-microscopic studies demonstrate that the biochemical constituents of the intervertebral disc have an architectural array that reflects their biomechanical properties. The annulus is composed of collagen fibrils, organized in lamellar layers that cross at angles of 40 to 70 degrees; these fibrils provide tensile strength. The tightly packed annular fibers become less dense and less organized at the nucleus-annulus border and form a loose network within the nucleus pulposus.

Degeneration of the Discs

Disc degeneration most often is the first step in the degenerative process of the spine^74-77,79. However, arthritis of the facet joints can precede any pathological evidence of disc degeneration¹⁵⁰.

During childhood and adolescence, the annulus of the disc is gelatinous. With time, it undergoes fibrocartilaginous metaplasia, and chondrocytes appear within the inner lamellae. The original sharp borders between the nucleus and the annulus gradually become indistinct. Cavitation, desiccation, and fibroblastic proliferation occur, and the nucleus eventually is replaced with fibrocartilaginous tissues^{20,21,30,40,53}.

The greatest increase in degeneration is observed between the ages of twenty-five and thirty-five years. By the age of fifty, most individuals have some degree of degeneration. The discs between the fifth lumbar and first sacral levels and between the fourth and fifth lumbar levels are the most commonly involved⁹².

The biomechanical and biochemical changes lead to a decrease in disc height. Annular bulging, disc herniation, and early osteophyte formation can be observed. As a sequela of these changes, increased biomechanical stresses are transmitted posteriorly to the facet joints. Arthritic changes and, occasionally, instability of the facet joints may develop. As the disc degenerates and the cephalocaudad foraminal space narrows, nerve-root entrapment can occur, resulting in stenosis both centrally and in the lateral recess.

Degeneration of the facet joints is similar to that of other synovial joints. With aging, the porosity of the bone increases, with concurrent erosion of cartilage and loss of joint space. Sclerosis, which may be observed at the joint, often decreases over time as alterations in stress distribution occur. As the degenerative process continues, the changes include hypertrophy of the facet joint, thickening of the overlying capsule, and the development of osteophytes.

In addition to the articular and osseous changes, the facet joints settle and erode^46,76,162. In the early stages, when the rate of disc degeneration exceeds that of alterations in the facet joints, there may be subtle retrolisthesis of the superior vertebral body on the inferior vertebral body, coupled with overriding facets and a bulging disc. However, if the rate of facet-joint alterations, including erosion of bone and cartilage and capsular laxity, exceeds that of the degenerative changes in the disc, anterior subluxation can occur. This is particularly true when the facet joints are in a sagittal plane⁵¹.

In many individuals, there is a gradual shift in alignment (kyphosis or lordosis). This, coupled with the broadening of the ligamentum flavum posteriorly and the bulging of the disc anteriorly, exacerbates the stenosis of the spinal canal, creating further compromise of the neural elements¹¹.

Segmental Instability

The tripod configuration of a spine with normal discs, facet joints, and ligaments allows smooth and symmetrical rotation and angulation of the spinal segments, with no appreciable change in the dimensions of the canal or the neuroforamen. As the degenerative cascade progresses, however, the central canal and the neuroforamen become less accommodating in rotation because of changes in the discs and facet joints as well as in the torsional stresses^75,143,144. This, coupled with altered motion, can produce inflammation of the neural elements of the cauda equina and can lead to pain^{32,36,41,45,97,116,137}.

The frequent presence of degenerative spondylolisthesis at the fourth and fifth lumbar levels is thought to be the result of the restraining effect of the iliolumbar ligaments on the fifth lumbar vertebral body and transverse processes, which allows subluxation and increased motion at the adjacent level⁸³.

The abnormal biomechanical stresses across the motion segment can be inferred radiographically by a collapsed disc space with end-plate sclerosis. Radiographically, this benign idiopathic vertebral sclerosis can resemble infection; however, the sclerosis is confined to the areas adjacent to the disc space, often in a trapezoidal fashion. Instability can be suspected on the basis of the presence of large osteophytes.

The degenerative process creates chemical, mechanical, and anatomical processes that eventually lead to nerve-root compression in all adults who are middle-aged or older. Degenerative changes are noted in most people who are more than sixty years old^40,92. However, most individuals who have evidence of mechanical compression of the nerve roots do not have pain⁸. In fact, neurological deterioration or other findings are rare, even in individuals who have enough pain to cause them to elect operative treatment. Sometimes symptoms decrease over time even when a decompression has not been performed and, therefore, compression of the cauda equina or the nerve roots has not been alleviated. Others have no change in the initial symptoms even though the degenerative process continues, and still others have a steady worsening of the symptoms^{65,67,69,70,94,147}. The symptoms and signs of neurogenic claudication are not solely related to the underlying compressive changes.

Pathophysiology

Nerve Compression

The pathophysiology of pain related to compression of spinal nerve roots, or the cauda equina, is not completely understood. Studies have demonstrated that compression is associated with symptoms and signs related to neurogenic claudication. However, compression alone does not independently cause pain^{8,44,61,118,121,159}. There must be inflammation and irritation of the nerve root in order for symptoms to develop in the lower extremities¹³¹. Compression of a normal nerve leads to paresthesias, sensory deficits, motor loss, and reflex abnormalities, but pain usually does not occur. However, if an inflamed nerve is compressed, then pain develops in addition to the objective signs^88,120,139.

Failure of a spinal nerve can be detected during in vitro mechanical testing with use of video dimension analysis, before there is any noticeable external evidence of disruption⁸⁰. Theoretically, this internal failure or disruption can also occur in vivo as the nerve is placed in tension or is tethered in an asymmetrical fashion. This disruption, coupled with increased intraneural tension, can lead to irritation and inflammation along the nerve. Irritation and inflammation can also occur during motion of the lower extremities or the spine, when the nerve is forced to elongate and deviate from its resting position^11,133. In an unobstructed, relatively nondegenerated spinal canal, the nerve moves as much as five millimeters within the neuroforamen with straight-leg-raising maneuvers¹³⁰ (Table II). If normal motion of the nerve is obstructed, the internal tension may increase and minor disruptions of the neural architecture may occur, leading to an inflammatory reaction.

Although imaging studies show the spine at one point in time and provide a static image, the effects of micromotion or macromotion on the nerve are progressive and dynamic. Lateral radiographs made with the spine in flexion and extension frequently demonstrate excessive motion. These alternating forces on the nerve root may lead to irritation and inflammation. This can be due to subluxation as well as to intermittent compression caused by ligament-buckling, disc protrusion, osteophyte impingement, or nerve and vascular tethering, all of which vary with changes in the position of the spine and in the alignment of the motion segments.

Compression

Compression can cause electrophysiological changes along the nerve root. This may stimulate pain fibers and result in pain. The effects of graded compressive pressure on the cauda equina were studied with use of a pig model^{43,85,98-104,108,123}. Application of pressure for two hours, followed by a one and one-half-hour recovery period, produced electrophysiological alterations in both afferent and efferent pathways. Two hours of compression at less than the diastolic blood pressure (the mean arterial pressure in pigs ranges from seventy to 100 millimeters of mercury [9.33 to 13.33 kilopascals]) led to no reproducible alterations in compound motor action potentials (efferent) or in compound nerve action potentials (afferent). Compression pressures between seventy-five and 100 millimeters of mercury (10.00 to 13.33 kilopascals), however, led to a gradual decrease in both efferent and afferent conduction. The change in afferent conduction was more rapid; however, recovery was more rapid and reliable in the efferent, or motor, pathways. Compression at 200 millimeters of mercury (26.66 kilopascals), which is greater than the mean arterial pressure, caused a rapid decrease in conduction with almost no recovery in the afferent fibers and only a 30 to 40 percent improvement in the efferent fibers after removal of the compression^{43,85,98-104,108,123}.

The duration of the compression is also important. Increasing the time from two to four hours has an effect on the nerve's ability to recover¹¹⁷. Although the initial deterioration is the same, the recovery is remarkably prolonged, particularly at 100 millimeters of mercury (13.33 kilopascals), when the duration of the compression is doubled. These changes are greater in the afferent than in the efferent pathways.

The rate of compression and its effect on nerve function may also be factors. Edema and nutritional deficits are related to the magnitude of the pressure and the rate of its onset. The higher the pressure and the more rapid the onset, the greater the edema and the loss of nutritional support^98-104.

A decrease in blood flow is another factor that may be related to the symptoms of spinal stenosis. With nerve compression in a pig model, there was progressive compression of the venules (ten millimeters of mercury [1.33 kilopascals]) followed by that of the capillaries (thirty millimeters of mercury [4.00 kilopascals]) and finally by that of the arterioles (sixty millimeters of mercury [8.00 kilopascals])^119,120. These pressures, perhaps more than coincidentally, are consistent with the electrophysiological changes observed in association with compression of the cauda equina. In the same pig model, induced hypotension led to a decrease in electrophysiological conduction, which started at fifty to seventy-five millimeters of mercury (6.67 to 10.00 kilopascals) as opposed to 100 millimeters of mercury (13.33 kilopascals). In contrast, hypertension, with a documented increase in the blood flow through the cauda equina, provided some protection of the electrophysiological function, with more resistance to deterioration in the compression phase and more rapid improvement during recovery compared with the levels in normotensive animals^119,120.

The blood supply to the cauda equina and the spinal nerve roots is from cephalad to caudad along the cauda equina and from caudad to cephalad as it traverses the neuroforamen across the dorsal root ganglia. Compression in any of these locations can interfere with the vascular supply and nutritional support to the nerve roots, the cauda equina, or the dorsal root ganglia or any combination of these structures^{6,106,107,154,164}.

In addition to ischemia, decreased nutritional support to the neural elements can occur as a result of compression of the thecal sac and the encased cerebrospinal fluid. The nutritional effects created by a decrease in the blood supply could be negated by continued nutritional support provided through the cerebrospinal fluid. However, if both are involved and the ability of the cerebrospinal fluid to percolate over the nerve tissues is impaired, functional deterioration can occur^{19,104,117,119,122,141}.

One other associated theory regarding the etiology of the pain is that venous congestion leads to vascular pooling and edema, either in the bone itself or in or along the nerve. This sequence of events can cause a compartment-type syndrome in the dorsal root ganglion or any of the neural elements. It probably occurs concurrently with the ischemia related to arterial compromise^{4,6,106,107,119,120,155,157}.

The Clinical Entity

History

Because spinal stenosis is a slow, relentless, degenerative process, the early symptoms are often insidious in onset. Vague complaints of low-back pain and stiffness are often the initial symptoms. These symptoms are exacerbated by activity and often are relieved by rest. The pain in the back and buttocks can continue for a prolonged period. Many individuals accept this discomfort, along with moderate limitations in activities of daily living imposed by pain and stiffness, as an inevitable part of the aging process.

The classic symptoms of spinal stenosis, or neurogenic claudication, involve the lower extremities and include pain, numbness, and tingling in the posterior or posterolateral aspect of the limb. Although the pain typically begins in the low back and radiates caudally, there may be skip areas or a sensation that the pain or numbness starts distally and progresses proximally. The symptoms may be asymmetrical and inconsistent: they may vary from side to side as well as from day to day. There may be cramping, a feeling of giving-way, a dull aching pain, and diffuse paresthesias^{31,42,48,52,126,134,148,161}.

A sudden onset of pain in the lower extremities, or a worsening of preexisting pain, is rare and may be associated with concomitant disc herniation or a more acute decrease in the vascular supply of the neural elements.

The classic clinical finding associated with spinal stenosis is exacerbation of the symptoms in the lower limbs when the spine is in extension and a decrease when the spine is in flexion. This is presumably related to the decrease in the capacity of the spinal canal with extension²⁹, and it explains why some individuals can walk well leaning on a shopping cart or a wheelchair and can ride a bicycle with the spine in the flexed position. However, walking in an upright (straight) posture, sitting with the spine in extension, or going up and down an incline may lead to marked dysfunction. The pain usually is rapidly relieved by a change in activity or position. However, because of concurrent degenerative spondylolisthesis, some individuals may have an increase in the symptoms in association with flexion of the spine, caused by exacerbation of the existing subluxation and possible nerve-root compression. Although the classic symptoms are in the lower limbs, they can also be localized to the back and buttocks.

Urinary dysfunction is uncommon in patients with stenosis⁶⁶. However, many patients report a feeling of urgency, frequent urination, or loss of control of the bladder. The confounding factor with this symptom is age, as it is not uncommon for many older individuals to have abnormalities in bladder control that are unrelated to stenosis.

The differential diagnosis includes vascular claudication, peripheral neuropathy, and lumbar spondylosis^26,54,142 (Table III). In patients with vascular disease, the lower-limb symptoms are primarily in the calf and are relieved fairly promptly by sitting. Unlike the pain associated with neurogenic claudication, the pain associated with vascular disease is less related to the position of the spine than it is to the activity and function of the lower limbs.

The peripheral neuropathies often are characterized by pain in both lower extremities, which occurs more often in a stocking-glove distribution than in a neurogenic, radicular pattern¹³. There may be bilateral symmetrical loss of reflexes and sensory neuropathy before motor loss. Vibratory sensation is also frequently diminished. Alternatively, motor weakness can occur without sensory findings. Pain is often not a limiting factor. The patient should be questioned regarding a history of diabetes, drug use, and alcoholism. Malignant tumors and renal dysfunction can also cause symptoms that are consistent with peripheral neuropathy. Electromyography and nerve-conduction studies are useful⁶³.

Physical Examination

Frequently, the findings on the neurological examination are normal (Table IV). Although many individuals report weakness of the lower extremities, a specific motor deficit is uncommon, particularly if the patient has rested for a period of time before the examination.

In many patients, however, some neurological abnormality or alteration is noted. Asymmetrical reflexes of the knee or ankle are consistent with this diagnosis. Symmetrically absent reflexes, particularly of the ankle, may be related more to alterations due to aging than to spinal stenosis. However, there may be attenuation of reflexes following repetitive stimulation. Abnormal reflexes, such as the Babinski and clonus signs, are negative (or absent) in patients with lumbar spinal stenosis. If these signs are present, the physician should look for concurrent cervical or thoracic stenosis or other spinal cord or neurological disorders.

The motor examination usually reveals some positive findings. Weakness of the muscles innervated by the fifth lumbar nerve root is the most common finding. Special attention should be paid to the great-toe extensor (the extensor hallucis longus muscle) and to the pelvic abductors (the gluteus medius and minimus as assessed with the Trendelenburg test). Weakness of the iliopsoas muscle is consistent with compression of the second lumbar nerve root. Alterations in extension of the knee suggest involvement of the third or fourth lumbar nerve root, both of which innervate the quadriceps. The tibialis anterior muscle, which is the primary dorsiflexor of the ankle, is supplied by the fourth and fifth lumbar nerve roots. Limitations in plantar flexion of the ankle, or in the ability to toe-walk, are related to the first sacral nerve root.

A stress neurological examination involves repeating the nerve-root-specific examinations (that is, the motor examinations and the assessments of the reflexes) after the patient has walked rapidly in the hall until symptoms occurred. This examination is useful if the initial examination revealed normal findings because objective findings may become observable after the patient has walked. There is no defined time or rate of walking; rather, the individual walks until pain similar to that reported on physical examination occurs.

The straight-leg-raising test is characteristically negative, even for patients who have radicular pain.

The evaluation also should include an assessment for evidence of tumor, infection, osteoporotic compression fractures, and vascular insufficiency. The assessments for the first three possible diagnoses include evaluation of pain in the spine, particularly during percussion and palpation in the midline over the spinal column (spinous processes) and pelvis. The range of motion of the hips and the FABER (flexion, abduction, and external rotation) test should also be performed during the examination, particularly if the symptoms are localized to the hip and groin. Bursitis of the greater trochanter is a frequent concurrent finding, and it may be the primary cause of hip pain. Degenerative joint disease commonly occurs in the same age-group (and, often, in the same individuals) as do radicular pain and spinal stenosis. The vascular examination should include palpation of distal pulses and, if necessary, of the abdomen to assess the possibility that there is an abdominal aortic aneurysm.

Imaging Studies

Radiography should not be ignored in the initial evaluation of a patient who has symptoms of spinal stenosis. Anteroposterior radiographs and lateral radiographs made with the spine in flexion and extension provide useful information with regard to instability and deformity. The latter radiographs should be evaluated for any subtle suggestion of degenerative spondylolisthesis, or gross motion between flexion and extension. Additionally, both the anteroposterior radiographs and the lateral radiographs should be assessed for the presence of deformity (scoliosis) or for the possibility that a tumor or osteoporotic fractures are causing some of the symptoms.

Magnetic resonance imaging has rapidly become the imaging study of choice for the diagnosis of spinal stenosis and the planning of the operation. In general, however, the diagnosis can be made on the basis of the history, the physical examination, and plain radiographs. Magnetic resonance imaging should be reserved for planning the operation, assessing the number of levels involved, and evaluating the spine for the presence of a tumor or an infection if either is suspected. Central stenosis and stenosis of the lateral recesses can be seen well on magnetic resonance images. Abnormalities of the facets, osteophytes, disc herniations or protrusions, and ligamentous changes leading to nerve compression also can be seen⁹⁴.

Computerized tomography without use of contrast medium in the spinal canal is not recommended for routine use in the workup of patients with spinal stenosis as the disorder frequently involves more than one level and a large number of cuts would be necessary to assess the entire lumbar spine. Additionally, and perhaps more importantly, computerized tomography without enhancement does not depict the neural elements well, so an intraspinal tumor could be missed.

Myelographically enhanced computerized tomography is useful, particularly in patients who have scoliosis or instrumentation. The myelogram outlines the neural elements and can be used to assess central stenosis. Computerized tomography performed after myelography provides useful information regarding the lateral recesses, hypertrophy of the facet joints, and osteophytes.

Treatment

Indications for Treatment

There have been few studies of the natural history of lumbar spinal stenosis, and these have been based on small numbers of patients^7,65,110.

Existing information suggests that severe debilitating neurological deterioration in patients who have been managed nonoperatively is rare. It also appears that complete resolution of the symptoms is unusual although it can occur. However, a similar percentage of patients have worsening of the symptoms. These observations suggest that operative treatment of spinal stenosis often can be deferred. The decision to operate on a patient who has this condition should be based on a decrease in the patient's quality of life and an increase in the symptoms rather than on relatively subtle neurological findings and a positive magnetic resonance imaging scan. Additionally, it is reasonable to recommend operative treatment in an effort to decrease the neurological signs and to improve the quality of life. Operative intervention, however, cannot routinely be expected to reverse neurological deficits in every patient.

Nonoperative Treatment

Any patient who is seen because of pain in the back and the lower extremities related to spinal stenosis most likely is requesting some form of treatment. In general, nonoperative treatment will help many individuals. The primary modalities include education, reassurance, analgesics (often those available over the counter, such as acetaminophen), nonsteroidal anti-inflammatory medications^64,149,151, and narcotics if necessary. Exercise is important^49,62 and should include aerobic conditioning with or without light impact, as tolerated. Exercise on a stationary bicycle, with the patient riding in a semistanding, slightly forward-flexed position, is often well tolerated and helps to improve cardiopulmonary function. Physical therapists are helpful in that they prescribe exercises as well as provide education and instructions on self-treatment. The efficacy of physical therapy modalities^90,91 may not be scientifically proved, but they are safe and can provide symptomatic relief in certain individuals. Corset-type braces^5,160 may provide limited truncal support and relief of pain; however, they should be worn only for short periods of time in order to avoid additional muscle-deconditioning.

Another treatment alternative for the relief of pain in the lower extremities is the epidural injection of steroids. We are not aware of any randomized, controlled studies of such injections performed exclusively in patients who had spinal stenosis. However, observational studies have suggested that epidural administration of steroids provides some relief of symptoms. Epidurally injected steroids are relatively safe and are tolerated by most individuals^{14,25,78,84,114,115,132}. They have few side effects, although it may be difficult to insert the needle safely and correctly in the epidural space of a patient who has degenerative arthritis of the spine. Not infrequently, because of an underlying spinal deformity and stenosis, an intrathecal injection leads to spinal headaches, nausea, and vomiting when the patient assumes an upright position. These symptoms frequently subside with short-term bed rest, but if they persist they may be alleviated with use of an epidural blood patch.

Caution should be exercised when treatment is prescribed for older individuals. Acetaminophen can affect hepatic and renal function. Nonsteroidal anti-inflammatory medications can lead to duodenal or gastric ulcers. They also can adversely affect hepatic and renal function, which, coupled with sodium retention, can cause increased hypertension. Exercise and physical therapy have few disadvantages other than aggravating pain or delaying more definitive operative treatment in some individuals. In general, however, exercise will improve the patient's overall condition and will allow the operative procedure to be better tolerated even if it does not decrease the symptoms.

Operative Treatment

Operative treatment is indicated when the patient's quality of life has deteriorated to the point that the pain is no longer tolerable. In such patients, pain, numbness, or weakness in one or both lower extremities restricts activities of daily living to a severe degree. If the history and the findings on the physical examination are consistent and magnetic resonance imaging demonstrates stenosis, operative treatment is a realistic option.

Decompressive laminectomy with nerve-root decompression is the standard procedure for the relief of symptoms in the lower extremities that are associated with spinal stenosis⁵⁷. It must be emphasized that operative treatment is most often performed to relieve symptoms in the lower extremities and not low-back pain, although the latter often decreases as well after the operation. In addition to the decompression of the central canal, laminectomy should also relieve the compression of the spinal nerve roots at each level of involvement. A tight lateral process can be evaluated intraoperatively by assessing the ease of passage of an elevator out the nerve-root canal. At the completion of the decompression, the elevator should easily pass out along the nerve root.

An alternative to decompression with use of a standard, complete laminectomy is a limited laminotomy with a foraminotomy. This may be accomplished with sparing of the spinous processes, the interspinous ligaments, and most of the lamina. The laminotomy is performed at the level of the facet joints, with undercutting of one-quarter to one-half of the facet along with removal of the lateral portion of the ligamentum flavum.

Because spinal stenosis is a global and often a multilevel disorder, the decompression should include all levels that were determined to be compressed on the preoperative imaging study, although the symptoms may be clinically suggestive of only single-level unilateral nerve-root compression.

If there is any deformity, particularly degenerative spondylolisthesis or supple scoliosis, an arthrodesis with or without instrumentation should be considered^50,57. However, the addition of an arthrodesis makes the operation more complex and of a longer duration, increases the blood loss and the risk of medical complications, and prolongs the period of rehabilitation for these often elderly and perhaps also medically debilitated individuals^16,145.

Perhaps the most controversial aspect of operative treatment for spinal stenosis centers on the indications for the addition of a spinal arthrodesis to the decompressive laminectomy. Factors to consider can be classified as either preoperative structural alterations or intraoperatively induced alterations.

Preoperative Structural Alterations

Degenerative Spondylolisthesis

Numerous articles advocating no arthrodesis have appeared in the literature^39,59,60, while others have recommended arthrodesis at the time of the decompressive laminectomy^{15,22,37,57,87,134}. However, the role of arthrodesis in patients who have an associated spondylolisthesis and are managed with a decompressive laminectomy appears to have been resolved. Herkowitz and Kurz performed a prospective study comparing decompressive laminectomy alone with decompressive laminectomy combined with an intertransverse-process arthrodesis in fifty patients who had single-level spinal stenosis associated with a degenerative spondylolisthesis⁵⁷. Twenty-four of twenty-five patients who had a concomitant arthrodesis had good-to-excellent results. Those authors recommended arthrodesis for all patients with an associated degenerative spondylolisthesis who are managed with a decompressive laminectomy. Several subsequent reports have supported the addition of an arthrodesis when the stenotic segment is associated with a degenerative spondylolisthesis^{15,37,72,113,125}.

Caputy and Luessenhop reported on ninety-six patients who had decompression alone for the treatment of spinal stenosis¹⁵. Five years postoperatively, twenty-six patients were considered to have had failure of the treatment. Of these twenty-six patients, sixteen had recurrent pain in the lower extremities, and five of the sixteen had a preexisting degenerative spondylolisthesis at the stenotic level. Those authors recommended the addition of an arthrodesis for all patients who have a laminectomy for the treatment of spinal stenosis and also have a degenerative spondylolisthesis.

Postacchini et al. reported on the occurrence of laminar regrowth following decompressive laminectomy for spinal stenosis¹¹². Of forty patients who had been followed for a mean of 8.6 years, sixteen had had degenerative spondylolisthesis preoperatively. Six of the sixteen patients had a decompression only, and ten also had an arthrodesis. The patients who did not have an arthrodesis had more bone regrowth and a poorer clinical outcome than did those who had an arthrodesis.

In summary, the data regarding spondylolisthesis in association with spinal stenosis strongly support the addition of an arthrodesis at the time of a decompressive laminectomy.

Scoliosis and Kyphosis

The operative management of patients who have spinal stenosis in association with preexisting idiopathic or degenerative lumbar scoliosis is not as clear-cut as is that of patients who have an associated degenerative spondylolisthesis. Previous studies have been primarily retrospective analyses of operative techniques and have not included comparisons of the various operative options^129,163.

Not all patients who are managed with decompression for spinal stenosis within an area of scoliosis or kyphosis need a concomitant arthrodesis. The decision as to whether a concomitant arthrodesis should be performed should be based on several factors. The first factor to consider is the flexibility of the curve. If the curve demonstrates partial correctability on side-bending radiographs, a decompressive laminectomy alone would most likely increase the risk of curve progression. The second factor is a documented history of curve progression, which, by itself, may be an indication for arthrodesis. The third factor is scoliosis with a predominant radiculopathy within the concavity of the curve; in this situation, a decompressive laminectomy with a partial facetectomy may not be sufficient to alleviate nerve-root compression in the concavity. The fourth factor is lateral spondylolisthesis. A segmental level with a lateral slip that also demonstrates motion on side-bending radiographs suggests hypermobility, and the segment may become more unstable following a decompressive laminectomy. The fifth factor to consider is loss of lumbar lordosis such that the patient is not in sagittal balance. This can be assessed on a lateral radiograph, made with the patient standing, that includes the entire spine from the base of the skull to the sacrum. On this radiograph, a plumb line drawn inferiorly from the odontoid process should pass through the posterior half of the fifth lumbar vertebral body of a normally aligned spine. Laminectomy may lead to increased kyphosis, resulting in increased low-back pain.

Recurrent Spinal Stenosis at the Same Segment

Patients who have a second decompressive laminectomy at the same segment are candidates for an arthrodesis⁵⁸. Additional removal of a facet joint or facet joints is usually necessary to adequately decompress the central canal and the lateral recesses. Removal of more than 50 percent of each facet joint may lead to segmental instability, especially when the facet joints lie in a sagittal orientation^1,9,81. Segmental instability may be detected on flexion-extension radiographs. Excessive movement of the motion segment is defined as more than four millimeters of translational movement or more than 10 degrees of angular change as measured at the end plate compared with the motion of the adjacent segments cephalad and caudad.

Patients who have recurrent stenosis in conjunction with an iatrogenic spondylolisthesis also benefit from a concomitant arthrodesis, as additional instability often occurs following the second decompression⁷².

With the increasing rate of lumbar spinal arthrodesis over the last fifteen years, the development of spinal stenosis adjacent to the site of the arthrodesis is becoming common⁸². The options for operative treatment of this condition are decompression alone or decompression with an arthrodesis, with or without instrumentation. Detailed prospective studies of large numbers of patients are lacking, and evidence-based recommendations are therefore difficult to make¹⁵⁸. However, it seems reasonable to recommend decompression alone for patients who have stenosis cephalad to the site of an arthrodesis, if there is no instability and no excessive removal of the facet joints during the operative procedure; otherwise, instrumentation should be added to the arthrodesis.

Intraoperative Structural Alterations

Removal of the Facet Joints

Abumi et al. demonstrated the importance of the lumbar facet joint for the structural stability of the motion segments in cadaver specimens¹. After the specimens had been subjected to cyclical loading in a mechanical testing device, those authors concluded that removal of more than 50 percent of each facet joint led to unacceptable movement of the motion segment.

Similar results were reported by Boden et al. with use of a cadaver model⁹. Those authors demonstrated that stability of the motion segment was not impaired after a decompressive lumbar laminectomy if the medial one-half of each facet joint had been preserved. When there has been excessive excision (removal of more than 50 percent of each facet joint) during a decompression, a posterolateral arthrodesis should be considered to prevent postoperative instability.

Disc Excision

Disc herniation in conjunction with spinal stenosis is relatively infrequent, but it does occur^42,57. Most true disc herniations in patients with spinal stenosis represent extrusions or free fragments of disc, often at the level of the foramen. In this situation, removal of the disc fragment at the time of the decompressive laminectomy is necessary to reduce symptoms. So-called radical disc excision (removal of as much disc material as possible) may lead to an iatrogenic spondylolisthesis because it destabilizes the anterior column after the posterior column has been weakened by the decompressive laminectomy²²; therefore, this procedure is not recommended.

Spinal Instrumentation

The goals of internal fixation are to correct deformity, stabilize the spine, protect the neural elements, improve the rate of fusion, reduce the number of segments that must be included in the arthrodesis, and decrease the rehabilitation time.

Fixation extending into the caudad portion of the lumbar spine and the sacrum presents problems, especially in older patients. It is not possible to place hooks in segments that have been treated with laminectomy. In addition, traditional posterior hook-based distraction systems often lead to a loss of lumbar lordosis. Maintenance of lumbar lordosis is an important factor in the long-term success of an arthrodesis. Failure to maintain lumbar lordosis may lead to postural (flatback) deformity and potentially to disabling back pain.

Pedicle-based fixation appears to solve the technical problems associated with traditional implant systems when use of a spinal instrumentation system is indicated after a decompressive lumbar laminectomy. Pedicle fixation places the fixation points through the strongest part of the osteopenic vertebra. It allows segmental fixation, which improves torsional stability and helps to maintain lumbar lordosis. Segmental fixation also may reduce the number of motion segments that must be included in the arthrodesis, thus preserving some lumbar motion. Pedicle-screw systems are better able to achieve sacral fixation than are conventional hook-and-rod systems. Additionally, spinal deformity is reduced more efficiently with use of pedicle-based segmental fixation.

Pedicle fixation has some disadvantages. There is a substantial learning curve, even for experienced spine surgeons^156,165. Failure to place the pedicle screw in the correct location may lead to neurological damage and loss of fixation²³. In addition, the longevity of pedicle-fixation systems is not known¹⁰.

A surgeon who is contemplating an arthrodesis must balance the benefits and risks of adding instrumentation. In most instances, instrumentation is added to supplement the arthrodesis in order to improve the chance for a solid fusion as well as to correct a preexisting deformity. Fischgrund et al. compared the results of decompressive laminectomy that was performed in combination with posterolateral arthrodesis in sixty-eight patients who had spinal stenosis and degenerative spondylolisthesis with those in another group that had the same procedure with the addition of internal fixation³⁸. Those authors found a higher rate of fusion in the group that had instrumentation, but the clinical outcomes in the two groups were similar.

The prevalence of pseudarthrosis following posterolateral arthrodesis without instrumentation increases with the number of levels included in the arthrodesis. The rate of pseudarthrosis also increases if translational or angular instability is present. Instrumentation decreases the rate of nonunion¹⁶⁵.

The indications for the addition of instrumentation after decompression and arthrodesis in patients who have spinal stenosis include: (1) correction or stabilization of scoliosis or kyphosis, (2) arthrodesis, with an associated decompressive laminectomy, of two or more motion segments, (3) recurrent spinal stenosis with iatrogenic spondylolisthesis, and (4) translational motion of more than four millimeters and angular motion of more than 10 degrees with the spine in flexion and extension compared with the amounts of motion at the adjacent levels. The addition of instrumentation to a one-level arthrodesis after a decompressive laminectomy in patients who have degenerative spondylolisthesis improves the rate of fusion compared with that in patients who are not managed with instrumentation, but it does not appear to markedly improve the long-term clinical outcome³⁸.

Much needs to be clarified regarding arthrodesis and instrumentation for the treatment of lumbar degenerative disorders. Additional prospective, controlled studies will help to answer these questions so that operative treatment can provide the most effective and long-lasting results.

Complications

Operative treatment is directed toward alleviating radiculopathy or neurogenic claudication in the lower extremities. Individuals who have isolated low-back pain without deformity are usually best managed nonoperatively. The results of operative treatment are also affected by medical comorbidities such as cardiopulmonary disease, diabetes, kidney disease, and a poor nutritional status. Patients with these comorbidities often have a long period of functional disability, which causes additional deconditioning and may impair the ability to recover rapidly. An older age is not in itself a contraindication to operative treatment, especially in light of the longer life expectancy and improved health that now characterize the older population.

In general, operative treatment has led to a high rate of clinical success with regard to the relief of pain in the lower extremities of patients who have spinal stenosis^{42,50,57,89,105,124}. The outcome is affected by the patient's premorbid condition: the more comorbidities, the greater the risk of postoperative complications^16,71,73.

It is important for patients with spinal stenosis to have a thorough evaluation along with an assessment of their nutritional status before operative treatment. The goals of operative treatment are to relieve pain and to improve the patient's quality of life, and these goals usually are achieved after appropriate treatment.

Because degenerative spinal stenosis affects an elderly population, the rate of complications related to operative intervention is higher than that associated with spinal procedures in younger individuals.

Analyses of complications of operative treatment require a large population base in order to generate data. The most commonly used databases (although they are not ideal or necessarily accurate) are those of Medicare and the National Hospital Discharge Survey. Data from these types of sources are not as accurate as those from a well controlled study, but they do provide estimates of the rates of complications for large patient populations. Ciol et al. analyzed data on 30,000 patients who had had operative treatment of spinal stenosis in 1985 or 1989¹⁶. The complications were divided into four groups: infections, vascular, cardiopulmonary, and death. Mortality rates were related to age and the presence of comorbidities. Patients who were less than seventy-five years old had a mortality rate of less than 1 percent, whereas those who were more than eighty years old had a 2.3 percent mortality rate. Complications were twice as frequent in patients who were more than eighty years old than in those who were less than seventy years old. The prevalence of complications increased almost twofold when three or more comorbidities were present and when an arthrodesis had been performed in conjunction with decompression.

Reoperation was reported in fifteen of eighty-eight patients in the study by Katz et al.⁶⁸. The need for reoperation after operative treatment for spinal stenosis is related to several factors^56,68. First, spinal stenosis may develop at other levels as it can be a progressive degenerative condition. Second, the index operation may not have been adequate; the procedure may not have addressed the stenosis sufficiently, or the appropriate procedure may not have been done. Third, the index operation may have failed because of the development of instability, failure of fusion, or failure of the hardware. Fourth, stenosis may develop again because of laminar regrowth¹¹¹.

Outcomes

As with any intervention, a satisfactory outcome often depends on the selection of patients and the performance of a technically correct and appropriate operative procedure¹³⁸. Katz et al. reported the results of a six-month follow-up of 194 patients who had had decompression for spinal stenosis⁷¹. Forty patients were not satisfied with the outcome. Patient dissatisfaction was related to a poor preoperative functional status, the presence of multiple comorbidities, and the predominance of back pain compared with symptoms in the lower extremities. In general, however, long-term follow-up has demonstrated a high rate of satisfactory outcomes after operative treatment^56,68,72.

Although patients may continue to have back pain, most are satisfied with the results of the operation and would consent to have it again if circumstances were similar. Operative treatment appears to be more beneficial than continued nonoperative treatment when the clinical picture and the findings on imaging studies warrant this approach⁶⁵.

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TABLE I CLASSIFICATION OF STENOSIS OF THE SPINAL CANAL

I. Congenital or developmental

A. Idiopathic

B. Achondroplastic

C. Osteopetrosis

II. Acquired

A. Degenerative

1. Central

2. Lateral recess and foraminal

3. Degenerative spondylolisthesis

B. Iatrogenic

1. After laminectomy

2. After arthrodesis

3. After discectomy

C. Miscellaneous disorders

1. Acromegaly

2. Paget disease

3. Fluorosis

4. Ankylosing spondylitis

D. Traumatic

III. Combined: any combination of congenital, developmental, or acquired stenosis

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TABLE I CLASSIFICATION OF STENOSIS OF THE SPINAL CANAL

I. Congenital or developmental

A. Idiopathic

B. Achondroplastic

C. Osteopetrosis

II. Acquired

A. Degenerative

1. Central

2. Lateral recess and foraminal

3. Degenerative spondylolisthesis

B. Iatrogenic

1. After laminectomy

2. After arthrodesis

3. After discectomy

C. Miscellaneous disorders

1. Acromegaly

2. Paget disease

3. Fluorosis

4. Ankylosing spondylitis

D. Traumatic

III. Combined: any combination of congenital, developmental, or acquired stenosis

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TABLE II TOTAL MOTION OF THE FOURTH AND FIFTH LUMBAR AND THE FIRST SACRAL NERVE ROOTS AT THE DORSAL ROOT GANGLION¹³⁰

*The range is given in parentheses.

Nerve Root	Mean Total Motion* (mm)
L4	1.4 (0.0—2.5)
L5	2.1 (0.4—4.5)
S1	2.5 (1.0—5.0)

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TABLE II TOTAL MOTION OF THE FOURTH AND FIFTH LUMBAR AND THE FIRST SACRAL NERVE ROOTS AT THE DORSAL ROOT GANGLION¹³⁰

*The range is given in parentheses.

Nerve Root	Mean Total Motion* (mm)
L4	1.4 (0.0—2.5)
L5	2.1 (0.4—4.5)
S1	2.5 (1.0—5.0)

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TABLE III DIFFERENTIAL DIAGNOSIS OF SYMPTOMS

Findings	Neurogenic Claudication	Vascular Claudication	Lumbar Spondylosis
Pain
Type	Vague cramping, aching, sharp burning in lower extremities	Tightness, cramping (usually in calf)	Dull aching in low back
Location	Back, buttocks, lower extremities	Calf	Back
Radiation	Proximal to distal	Localized to lower extremities	Localized to back
Exacerbation	With standing, particularly with trunk extended; less with walking, rare with bicycling, unless trunk is extended	With walking and bicycling (activities involving lower extremities)	With general activity, bending, standing, twisting, and lifting
Improvement	With sitting, flexion, and squatting	With sitting and cessation of muscular activity	With decreased activity and rest
Time to relief	Prolonged	Rapid	Prolonged
Walking uphill	More or less pain	Pain	More or less pain
Walking downhill	Pain (with lumbar hyperextension)	Pain	More or less pain
Back pain	Common	Uncommon	Common
Limitation of spinal movement	Common	Uncommon	Common

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TABLE III DIFFERENTIAL DIAGNOSIS OF SYMPTOMS

Findings	Neurogenic Claudication	Vascular Claudication	Lumbar Spondylosis
Pain
Type	Vague cramping, aching, sharp burning in lower extremities	Tightness, cramping (usually in calf)	Dull aching in low back
Location	Back, buttocks, lower extremities	Calf	Back
Radiation	Proximal to distal	Localized to lower extremities	Localized to back
Exacerbation	With standing, particularly with trunk extended; less with walking, rare with bicycling, unless trunk is extended	With walking and bicycling (activities involving lower extremities)	With general activity, bending, standing, twisting, and lifting
Improvement	With sitting, flexion, and squatting	With sitting and cessation of muscular activity	With decreased activity and rest
Time to relief	Prolonged	Rapid	Prolonged
Walking uphill	More or less pain	Pain	More or less pain
Walking downhill	Pain (with lumbar hyperextension)	Pain	More or less pain
Back pain	Common	Uncommon	Common
Limitation of spinal movement	Common	Uncommon	Common

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TABLE IV DIFFERENTIAL DIAGNOSIS OF SIGNS

Findings	Neurogenic Claudication	Vascular Claudication	Lumbar Spondylosis
Neurological examination	Occasional findings, usually asymmetrical	Findings rare, symmetrical if present	Negative
Straight-leg-raising test	Usually negative	Negative	Negative
Femoral stretch test	Usually negative	Negative	Negative
Pulses	Present or symmetrically diminished	Diminished or absent, often asymmetrical	Symmetrical
Skin	Normal	Hair loss, atrophy	Normal
Bicycle test	Positive with lumbar hyperextension	Positive with the spine in any position	Negative

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TABLE IV DIFFERENTIAL DIAGNOSIS OF SIGNS

Findings	Neurogenic Claudication	Vascular Claudication	Lumbar Spondylosis
Neurological examination	Occasional findings, usually asymmetrical	Findings rare, symmetrical if present	Negative
Straight-leg-raising test	Usually negative	Negative	Negative
Femoral stretch test	Usually negative	Negative	Negative
Pulses	Present or symmetrically diminished	Diminished or absent, often asymmetrical	Symmetrical
Skin	Normal	Hair loss, atrophy	Normal
Bicycle test	Positive with lumbar hyperextension	Positive with the spine in any position	Negative