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CHAPTER 47/MICROSCOPIC LUMBAR DISCECTOMY / 463
surgical versus standard lumbar discectomy. Br J Neurosurg 1996;10:
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21. Lagarrigue J, Chaynes P (1994). Comparative study of disk surgery
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22. Nachemson A, Jonsson E. Neck and back pain. Philadelphia: Lippincott Williams & Wilkins, 2000.
23. Postacchini F 1999.
24. Krämer J. The LIRCE principle: a risk value score for the spine. Eur
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25. Bernsmann 1997.
26. Dyke 1998.
27. Findlay G, Neurosurgeon in Liverpool UK. Personal communication,
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28. Yoshizawa 1998.
29. Bell G. Complications of lumbar spine surgery. In: Wiesel S, Weinstein
J, eds. The lumbar spine, 2nd ed. Philadelphia: WB Saunders, 1996.
30. Postacchini F. Lumbar disc herniation. Wien/New York: Springer-Verlag, 1998.
31. Wildförster 1991.
32. Bernsmann K, Krämer J, Ziozious I, et al. Lumbar microdisc surgery
with and without autologous fat graft. Arch Orthop Trauma Surg 2001;
121:476–480.
33. Lee A. Ischemic optic neuropathy following lumbar spine surgery. J
Neurosurg 1995;83:348–349.
34. Wolfe 1992.
35. Ahn V, et al. Meta-analysis of studies on cauda equina syndrome.
AAOS Abstracts 1999;Back letter 14.6.61.
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in the treatment of lumbar discitis. Eur Spine J 1997;6:98–101.
37. Rompe JD, Eysel P, Zoellner J, et al. Intra- und postoperativ e risikoanalyse
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38. Roberts MP. Complications of lumbar disc surgery. Spinal Surg 1988;
2:13–19.
CHAPTER 48
Classification, Natural History, and Clinical Evaluation
Yong Hai
Lumbar spinal stenosis is defined as the reduction in the
diameter of the spinal canal, lateral nerve canals, or
neural foramina. The stenosis may occur as a part of a
generalized disease process and involve multiple areas of
the canal and multiple levels or , conversely, may be localized or segmental. The reduction in the diameter of the
spinal canal or neural outlets may be attributable to bone
hypertrophy, ligamentous hypertrophy, disc protrusion,
spondylolisthesis, or any combination of these elements.
This clinical entity is used to describe a complex set of
symptoms, physical findings, and radiographic abnormalities caused by a narrowed spinal canal. Pain in the
back and leg(s) and, in particular, claudication caused by
compression and ischemia of nerve roots are the main
symptoms. Although it is one of the most common spinal
disorders in people older than 65 years, and frequently
causes significant functional impairment (1), there is still
some uncertainty in diagnosing and treating lumbar canal
stenosis, including:
1. Though nearly all people in this age group have radiographic evidence of degenerative disc and joint disease, the incidence of clinically symptomatic lumbar
canal stenosis is unknown.
2. The diagnosis is largely clinical. Although imaging
studies can confir m the diagnosis, they often show
abnormalities in people with no symptoms.
3. Treatment is mostly empiric. Although lumbar canal
stenosis is the most common reason for spinal
surgery in this older population group (2) and
accounts for inpatient expenses approaching $1 billion per year (3), no comparison of surgical versus
nonsurgical treatment has ever been done.
Lumbar spinal stenosis has been known for more than
100 years, but for a long time it was simply not
addressed. This occurred because the association between
herniated vertebral discs and sciatica received most of the
attention after it was discovered by Mixter (4) in 1934.
However, since the early 1950s, starting with the studies
of Verbiest (5), this has changed, and lumbar spinal stenosis now is an accepted clinical entity and a well-recognized spinal disorder.
Stenosis is most frequently a sequela of the aging
process, usually readily identifiable on imaging studies as
evidenced by the high incidence of positive radiographic
findings in asymptomatic patients (6–8). The presence of
a narrow canal on radiographic imaging studies does not
by itself define the syndrome. Rather, the syndrome is
defined by a complex set of symptoms and clinical f indings that must be supported by radiographic evidence.
Patients with spinal stenosis patients often present with
few objective physical findings. Up to 95% of patients
treated surgically have only subjective symptoms, mainly
pain (9,10). Accurate diagnosis and treatment decisions
must be based on a thorough knowledge of the clinical
syndrome and natural history (11–15). Vascular claudication in particular (16) must be considered in the differential diagnosis, in addition to lumbar spondylosis, peripheral vascular disease, and peripheral neuropathy.
CLASSIFICATION
The classification of lumbar stenosis is important
because of the implications of the underlying etiology of
the condition and when forming a therapeutic strategy,
specifically directing surgical approaches (17).
Spinal stenosis may be classified by either its etiology
or location. The classification of spinal stenosis proposed
by Arnoldi (18) in 1976 remains useful and is still the
most widely used classification. He divided lumbar
stenosis into two major groups: congenital or developmental stenosis, and acquired stenosis. Congenital stenosis (primary stenosis) is present at birth as part of a
malformation and is divided into idiopathic and achon-
464
CHAPTER 48/CLASSIFICATION, NATURAL HISTORY, AND CLINICAL EVALUATION / 465
droplastic etiologies. In contrary, acquired stenosis (secondary stenosis) is present in patients with symptoms and
signs of stenosis but with normal dimensions of the original vertebral canal and is further classified into degenerative, combined congenital and degenerative, spondylotic
and spondylolisthetic, iatrogenic posttraumatic, and
metabolic. Degenerative stenosis of the lumbar region is
the most common type of spinal stenosis. Symptomatic
lumbar stenosis typically occurs in patients in the fifth to
seventh decades of life with a reported incidence from
1.7% to 10%, and as the population ages, a greater number of patients will need to be treated for this condition
(19–23). Although there may be a structural predisposition to spinal stenosis (congenitally short pedicles),
symptomatic narrowing of the spinal canal usually is seen
in association with osteoarthritic changes of the lumbar
spine. Men and women seem to be affected equally with
spinal stenosis; however, women are afflicted with associated degenerative spondylolisthesis four times more
often than men (24).
Anatomic classification refers to central canal stenosis,
lateral recess stenosis, or neural foraminal stenosis.
Central stenosis refers to a narrowing of the spinal
canal across the anteroposterior diameter, the transverse
diameter, or both (17,25,26). The central canal is enclosed anteriorly by the posterior portion of the vertebral
body and the vertebral disc and posteriorly by the lamina
and the base of the spinous process. Central canal stenosis, commonly occurring at an intervertebral disc level,
defines midline sagittal spinal canal diameter nar rowing
that may elicit neurogenic claudication or pain in the buttock, thigh, or leg. Such stenosis results from ligamentum
flavum hypertrophy, inferior articulating process, facet
hypertrophy of the cephalad vertebra, vertebral body
osteophytosis, and herniated nucleus pulposus (27,28).
Stenosis at multiple levels is more common than strictly
segmental stenosis. In approximately 40% of cases, central stenosis is caused by soft tissue hypertroph y. On computed tomography (CT) scans, midsagittal lumbar canal
diameters less than 10 mm represent absolute stenosis
and midsagittal lumbar canal diameters less than 13 mm
represent relative stenosis (29).
Entrapment and compression of the nerve root in its
pathway through the spine, referred to as the nerve root
canal, is termed lateral stenosis (17,25,26,30,31). The
nerve root canal begins where the nerve root exits the
dura and ends where the nerve root leaves the interver tebral foramen. The nerve root canal is bordered by the
pedicle of the vertebra above and the pedicle of the vertebra below. The anterior side of the canal is formed by
the vertebral body and vertebral disc. The posterior side
of the canal is formed by the facet joint structures of the
vertebrae above and below. Lateral stenosis occurs when
the spinal nerve is compressed within the nerve root canal
or the vertebral foramina (32). As the disc narrows, the
pedicle may move in an inferior direction, narrowing the
lateral recess and pinching the spinal nerve (33,34). MacNab (35) originally described this entrapment and compression of the nerve root between a diffuse lateral bulge
of the disc and the pedicle above as pedicular kinking.
Narrowing of the lateral recess can also be the result of
facet hypertrophy or enlargement and ossification of the
ligamentum flavum. Radiculopathy, or decreased function of a nerve root, is commonly observed with lateral
stenosis.
Lateral recess stenosis (i.e., lateral gutter stenosis, subarticular stenosis, subpedicular stenosis, foraminal canal
stenosis, intervertebral foramen stenosis) is defined as
narrowing (less than 3 to 4 mm) between the facet superior articulating process and posterior vertebral margin.
Such narrowing may impinge the nerve root and subsequently elicit radicular pain. This lateral region has been
compartmentalized by several authors into entrance zone,
mid-zone, exit zone, and far-out stenosis (30,31,36).
The entrance zone lies medial to the pedicle and supe-
rior articulating process, and, consequently, arises from
facet joint superior articulating process hypertrophy.
Other causes include developmentally short pedicle and
facet joint morphology, as well as osteophytosis and herniated nucleus pulposus anterior to the nerve root. The
lumbar nerve root compressed below superior articulating process retains the same segmental number as the
involved vertebral level (e.g., L5 nerve root is impinged
by L5 superior ar ticulating process).
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 disc margin osteophytosis.
Such stenosis may impinge the exiting spinal nerve.
Far-out (extraforaminal) stenosis entails compression
lateral to the exit zone. Such compression occurs with far
lateral vertebral body end-plate osteophytosis and when
the sacral ala and L5 transverse process impinge on the
L5 spinal nerve (8).
In order to correlate the classification of lumbar spinal
stenosis with surgical planning, Hansraj et al. (37,38)
introduced a classification of typical and complex lumbar
spinal stenosis. Typical lumbar spinal stenosis was classified in those patients:
•who did not undergo previous lumbar spine operations
•who did not have radiographic evidence of instability
•who had degenerative spondylolisthesis at most grade
1, with no instability, if present
•who had degenerative scoliosis with a curve less than
20°, if present.
In their study, patients with typical lumbar spinal
stenosis were treated with decompressive surgery. Complex lumbar spinal stenosis was classified in patients with
466 /SECTION V/SPECIFIC CLINICAL ENTITIES
• lumbar spine operations with evidence of radiographic
instability, if present
• radiographic evidence of postoperative junctional
stenosis, if present
•degenerative spondylolisthesis greater than grade 1
with instability, if present
•degenerative scoliosis with a curve greater than 20°, if
present.
These patients were treated with decompressive sur-
gery and also underwent surgical stabilization.
NATURAL HISTORY
The natural history of lumbar spinal stenosis is not
well understood. A slow progression appears to occur in
all affected individuals. Even with significant narrowing,
such persons are very unlikely to develop an acute cauda
equina syndrome in the absence of significant disc herniation. Anecdotally, the clinical course varies considerably. In most patients, the course is chronic and benign
(32,39,40).
Only one study has been concentrated on the natural
course of lumbar spinal stenosis. In 1992, Johnsson et al.
(40) reported on 32 patients followed up for an average of
49 months (range, 10–103 months). Fifteen percent of the
patients were improved, 70% were the same, and 15%
were worse. The patients received no specific nonoperative therapy. Two of the patients were not operated on
because of advanced cardiovascular disease, and the
remainder of the patients refused surgical treatment. No
proof of deterioration was found after 4 years, and the
authors concluded that the condition of the majority of
patients with lumbar stenosis who were treated conservativel y remained unchanged o ver a period of 4 y ears. Ho wever, the patients did not improve either, so surgical
decompression may be an option as decompression of the
symptomatic level yields a high rate of improvement.
Numerous other nonoperative outcome studies for
lumbar spinal stenosis have been published. In 1996,
Atlas et al. (41) assessed the outcomes of 81 patients who
were treated surgically and 67 patients who were treated
conservatively after 12 months. Although the conditions
of patients who underwent surgery were worse clinically
and radiographically at the start of the study, their results
were better after treatment than the results of the patients
who were treated conservati v el y. For 28% of patients who
were treated conservati vel y, pain was better to completely
gone, and for 15%, the pain was much w orse. In 2000, the
same authors (42) reported their results of 4 years’ follow-up in their perspective study of surgical or conservative treatment of lumbar spinal stenosis. Among 119
patients, 67 were treated surgically and 52 were treated
conservatively. After 4 years, 70% of the surgically
treated and 52% of the conservatively treated patients
reported that their predominant symptom, either leg or
back pain, was better. Satisfaction of patients with their
current state at 4 years was reported by 63% of the surgically treated and 42% of the conservatively treated
patients. Surgical treatment remained a significant determinant of 4-year satisfaction. For the conservatively
treated patients, there was no significant change in outcomes over 4 years, whereas the initial improvement seen
in the surgically treated patients modestly decreased over
the subsequent 4 years.
Swezey (43) reported on the outcomes of 47 patients
who had been evaluated 5 years earlier for lumbar spinal
stenosis. Patients had symptoms of neurogenic claudication, and CT or MRI findings of moderate to severe
stenosis (43 patients) or severe spondylosis b y plain radiographs (4 patients). Treatments included instruction of
ergonomics and flexion exercise, analgesic medications,
intermittent pelvic traction (11 patients), and epidural
steroids (13 patients). Eleven patients required laminectomy. Of the patients who were treated conservatively,
43% were improved. Symptoms of neurogenic claudication were unchanged in 30%.
Simotas et al. (44) reported 49 patients with lumbar
stenosis treated conservatively with an average follow-up
of 3 years. At 3 years following treatment, 9 of the 49
patients had undergone surgical intervention. Of the
remaining 40 unoperated patients, it is reported that two
suffered significant motor deterioration, one of whom
still reported overall symptoms as mild impro v ement, and
the other as definite worsening. Five of the 40 unoperated
patients reported feeling overall symptoms as probably or
definitely worse, 12 reported no change, 11 reported only
mild improvement, and 12 reported sustained improvement. Twelve of the 40 unoperated patients also had
no pain or only mild pain. The authors concluded that
aggressive nonoperative treatment for spinal stenosis
remains a reasonable option.
In a randomized study by Amundsen et al. (39), 100
patients with symptomatic lumbar spinal stenosis were
given surgical or conservative treatment and followed for
10 years. Nineteen patients with severe symptoms were
selected for surgical treatment and 50 patients with moderate symptoms for were chosen for conservative treatment, whereas 31 patients were randomized between the
conservative (18 patients) and surgical (13 patients) treatment groups. After a period of 3 months, relief of pain
had occurred in most patients. Some had relief earlier,
whereas for others it took 1 year. After a period of 4
years, excellent or fair results were found in half of the
patients selected for conservative treatment, and in fourfifths of the patients selected for surgery. Patients with an
unsatisfactory result from conservative treatment were
offered delayed surgery after 3 to 27 months (median, 3.5
months). The treatment result of delayed surgery was
essentially similar to that of the initial group. The treatment result for the patients randomized for surgical treatment was considerably better than for the patients ran-
CHAPTER 48/CLASSIFICATION, NATURAL HISTORY, AND CLINICAL EVALUATION / 467
domized for conservative treatment. Clinically significant deterioration of symptoms during the final 6 years of
the follow-up period was not observed. Patients with
multilevel af flictions that were either surgically treated or
not did not have a poorer outcome than those with singlelevel afflictions. Clinical or radiologic predictors for the
outcome were not found. The authors concluded that the
outcome was most favorable for surgical treatment, but
an initial conservative approach seems advisable for
many patients because those with an unsatisfactory result
can be treated surgically later, with a good outcome.
As the population becomes older, this condition is
encountered more frequently. The diagnosis accuracy has
improved and the number of cases detected is increasing.
Because of the relative unpredictability of surgical treatment, good knowledge of natural evolution and of the
predictive factors influencing the course of the disease is
crucial. Unfortunately, and in contrast with numerous
surgical series, few studies have dealt with natural evolution. Only one randomized study (39) has compared
short- and long-term results of medical versus surgical
treatment. Most of these studies are retrospective, with
methodologic flaws and are diff icult to compare. At the
present time no scientifically based recommendations
can be made to lumbar spinal stenosis patients at diagnosis. Similarly, predictors of success of medical and surgical treatment still need to be identified. However, results
of the studies published suggest that a substantial proportion of patients do not automatically deteriorate and will
remain unchanged or even improved by medical means.
Randomized studies with the necessary ethical precautions are needed to obtain clear-cut conclusions.
HISTORY AND CLINICAL EVALUATION
History
Spinal stenosis typically affects persons over 50 years of
age (45). It is uncommon in younger people unless they are
anatomically predisposed by a congenitall y narrow ed canal,
previous spine trauma or surgery, spondylolisthesis, or even
scoliosis. The classic symptom of central canal stenosis is
pseudoclaudication, also known as neuro genic claudication
(1–3,45–47). Patients typically complain of pain, paresthesia, weakness, or hea viness in the buttocks radiating into the
lower extremities with walking or prolonged standing,
relieved with flexion or sitting. Though many patients have
significant lumbar pain due to degenerative joint and disc
changes, most have more lower extremity discomfort rather
than spinal pain. The most important aspect of neurogenic
claudication is the relationship of symptoms to posture.
Symptoms occur with spinal extension and are relieved in
flexion. Patients usually have no symptoms or have minimal discomfort when seated or supine. They can walk
longer distances with less pain in a forward flex ed position,
such as when using a grocery cart while shopping (the “grocery cart sign”). They may be able to exercise using a stationary bicycle in the seated flexed position for a much
longer time than when walking in the erect position on a
treadmill. In a review of 68 patients with myelographically
proven, surgically conf irmed spinal stenosis (47), the most
common symptoms were pseudoclaudication and standing
discomfort (94%), followed by numbness (63%) and weakness (43%). Symptoms were bilateral in 68%. Discomfort
was felt both above and below the knee in 78%, in the buttocks or thigh in 15%, and below the knee in 7%. Historic
features correlating most strongly with a conf irmed diagnosis of spinal stenosis (likelihood ratio 3:2) include age
greater than 65 years, severe lower extremity pain, and
absence of pain when seated (13).
Recognition of spinal stenosis depends primarily on
the description of the leg symptoms. The history and
physical examination are an essential component in the
assessment of patients with lumbar spinal stenosis. Physical examination occasionally demonstrates neurologic
deficits or exacerbation of symptoms with spinal positioning. How e ver , man y patients with spinal stenosis ha v e
no abnormal findings on examination. Spinal imaging
confir ms the clinical impression. Because many people
who have no symptoms are found to have radiographic
abnormalities, clinical correlation is critical.
Patients with lumbar spinal stenosis usually undergo a
“staged” diagnosis (Fig. 48-1). The f irst diagnostic stage
is the physician visit, during which the patient receives a
physical examination. Results of the physical are combined with information from the patient history in a preliminary diagnosis. Lumbar spinal stenosis is not def initivel y diagnosed at this stage, so the diagnostic results are
described as “consistent with” spinal stenosis or not consistent with spinal stenosis.
Physical Examination
The most important features of the physical examination are the motor, reflex, and the palpatory examinations. The physical examination in patients with lumbar
canal stenosis is frequently normal or demonstrates only
nonspecific f indings. Many older people have reduced
spinal mobility, with or without spinal canal stenosis.
Extension is usually more limited than flexion (12,15).
Patients with stenosis often have lumbar, paraspinal, or
gluteal tenderness, probably related to underlying degenerative changes, muscle spasms, and poor posture. Some
assume a characteristic “simian stance”, with their hips
and knees slightly flexed and the trunk stooped forward
(45). This semiflexed posture allows patients to stand or
walk for longer distances. Hamstring tightness is often
present and may produce a false-positive straight legraise test. The neurolo gic e xamination typically is normal
or reveals only subtle abnormalities such as mild weakness, sensory changes, and reflex abnormalities. This is
468 /SECTION V/SPECIFIC CLINICAL ENTITIES
FIG. 48-1. Diagnosis and treatment of lumbar spinal stenosis. Clinical symptoms at the time of presentation to the physician. Patient may have one or all of the symptoms.
particularly true if the patient has rested in the seated
position before the physical examination begins. These
subtle findings may be unmasked if the patient is examined after walking until dev eloping leg and buttock symptoms similar to the presenting complaint (46).
Ankle reflexes are diminished in 43% to 65% of
patients, while knee reflex es are abnormal in 18% to 42%
(13,15). The straight leg-raising test and other nerve root
tension signs are usually negative unless there is concomitant disc herniation. A careful motor examination
should be done. Leg weakness is generall y mild and overwhelmingly in the distribution of the L4, L5, or S1 nerve
roots. Objective evidence of subtle weakness can usually
be demonstrated in about 50% of persons with spinal
stenosis (2). Weakness of the muscles inner vated by the
L5 nerve root is the most common finding (46), and
weakness of great toe extensors (extensor hallucis
longus) and hip abductors should be sought, the latter by
the Trendelenburg test (46).
The Trendelenburg test is performed by having the
patient stand on one leg; if the gluteus medius is not functional or is denervated, the pelvis drops on the side opposite the damaged muscle. This is shown clinically by an
abnormal, waddling gait called the “Trendelenburg gait”,
caused by trying to compensate for a drooping pelvis.
The gait should be carefully observed. Difficulty in walking on the toes suggests S1 root involvement. Diff iculty
with heel walking suggests L4 or L5 nerve dysfunction.
Sensory abnormalities may be present in 46% to 51% of
preoperative spinal stenosis patients (2,12).
CHAPTER 48/CLASSIFICATION, NATURAL HISTORY, AND CLINICAL EVALUATION / 469
Katz et al. (13) found a positive lumbar extension test
to be strongly predictive of imaging confirmed spinal
stenosis. This test is performed by asking the standing
patient to hyperextend the lumbar spine for 30 to 60 seconds. A positive test is defined by reproduction of the
buttock or leg pain. Katz et al. (13) examined the value of
the history and physical examination in the diagnosis of
degenerative lumbar spinal stenosis. In this study, 93
patients over 40 years of age with symptoms of low back
pain were examined by attending physicians who were
then asked the extent to which they were certain the
patient had lumbar spinal stenosis. The diagnostic
impressions of expert clinicians and imaging, when av ailable, were used as a reference standard to evaluate the
attending physician’s diagnosis. Severe lower extremity
pain, absence of pain when seated, a wide-based gait,
thigh pain following 30 seconds of lumbar extension, and
neuromuscular deficits were all strongly associated with
patients with lumbar spinal stenosis. No pain when seated
and wide-based gait had the highest specificity, 93% and
97%, respectively. The highest sensitivity came from age
greater than 65 (77%), pain below buttocks (88%), and
no pain with flexion (79%).
Fritz (48) has developed a treadmill test as a clinical
diagnostic tool for the differentiation of neurogenic claudication due to lumbar spinal stenosis from other
pathologies that may produce similar symptoms. Spinal
extension and weight bearing that occur during walking
narrow the spinal canal and exacerbate the symptoms of
lumbar spinal stenosis. Spinal flexion or nonweight-bearing postures that occur while sitting increase the dimensions of the spinal canal and reduce symptoms. The treadmill test involves having the patient walk on a level
surface and an inclined surface. The time until onset of
symptoms, total walking time, and time until symptoms
return to baseline are recorded for each surface. Walking
on an inclined plane produces spinal flexion and may be
better tolerated by patients with lumbar spinal stenosis.
The treadmill test was evaluated using 45 subjects with
low back pain of v arying etiologies and self-reported limitations in walking. Diagnostic images with MRI or CT
were used as the gold standard for diagnosis. Twenty-six
of the subjects were diagnosed by imaging as being
stenotic. Self-reported sitting to relieve symptoms was
significantly related to diagnosis. The sensitivity of this
self-reported measure was 88.5% [95% confidence interval (CI) of 76.2 to 100], but specificity was 38.9% (95%
CI of 16.4 to 61.4). For the treadmill test, earlier onset of
symptoms with level walking, greater total walking time
during inclined walking, and prolonged recovery after
level walking were signif icantly related to a diagnosis of
lumbar spinal stenosis. The sensitivity and specificity for
earlier onset of symptoms with level w alking were 68.0%
(95% CI of 49.7 to 86.3) and 83.3% (95% CI of 66.1 to
100), respectively; for larger total walking time during
inclined walking they were 50.0% (95% CI of 37.5 to
62.5) and 92.3% (95% CI of 77.8 to 100), respectively;
and for prolonged recovery after level walking they were
81.8% (95% CI of 5.7 to 97.9) and 68.4% (95% CI of
47.5 to 89.3), respectively. The authors concluded that a
two-stage treadmill test might be more useful in the differential diagnosis of lumbar spinal stenosis compared to
patients’ self-reports of posture.
Use of the treadmill-bicycle test for the differential
diagnosis of neurogenic claudication was also examined
by Tenhula et al. (49). In their study, 32 patients with documented lumbar spinal stenosis were evaluated before
and after surgery. Patients were found to have a signif icant increase in their symptoms from the start to the end
of the treadmill test but fewer patients were found to have
significant symptoms on bicycle testing. Two years after
surgery, patients had an improvement in their walking
ability on treadmill testing, but showed no improvement
in their ability to bicycle. The authors believe the treadmill-bicycle test may be a useful tool for the differential
diagnosis of neurogenic claudication.
CENTRAL CANAL STENOSIS VERSUS
LATERAL STENOSIS
Symptoms of pseudoclaudication are associated primarily with central lumbar stenosis. In contrast, patients
with purely lateral recess stenosis:
• usually do not develop symptoms of neurogenic claudi-
cation (15)
• typically have radicular symptoms in a specific der-
matomal pattern (30)
• often have pain at rest, at night, and with the Valsalva
maneuver (30)
• tend to be younger (mean age 41 years) than patients
with central canal stenosis (mean age 65 years) (15).
DIFFERENTIAL DIAGNOSIS
The differential diagnosis is broad, and many conditions may be ruled out with a thorough evaluation (Fig.
48-2). Peripheral neuropathy, ar teriovascular disease, and
hip arthritis are common entities with similar symptoms.
In older patients with back or leg pain, diagnostic possibilities differ from those in younger patients; nonmechanical causes of back pain such as malignancy, infection, or abdominal aortic aneurysm are more common in
older patients than in younger patients (11,14).
Malignancy
Red flags that should raise the suspicion of underlying
malignancy include significant weight loss, intractable
night pain unrelieved by change in posture or pain medicine, or history of malignancy (50).
470 /SECTION V/SPECIFIC CLINICAL ENTITIES
FIG. 48-2. Differential diagnosis of lumbar spinal stenosis. Arrows indicate the possible or most likely
condition associated with the described symptoms. Many of these symptoms overlap, and an individual
may need additional testing to determine the exact cause of low back pain.
Infection
Fever with localized back tenderness, recent systemic
infection, or history of an invasive spinal procedure
should raise the possibility of a spinal infection (11).
eral neuropathy usually have a stocking-glove distribution of pain or paresthesia. There may be a bilateral
symmetric reflex loss. Vibratory sensation is frequently
diminished (46). Numbness is typically constant with
peripheral neuropathy.
Vascular Claudication
Hip Disease
When evaluating leg pain in older adults, neurogenic
claudication must be distinguished from vascular claudication (Table 48-1).
Hip disease may produce gait difficulty and leg symptoms. A careful examination of the hips and sur rounding
soft tissue should be done to exclude significant hip
Peripheral Neuropathy
Peripheral neuropathy may also superficially mimic
features of spinal stenosis. How e ver , patients with periph-
TABLE 48-1. Findings in neurogenic claudication and vascular claudication
Finding Neurogenic claudication Vascular claudication
Symptoms with walking Yes Yes
Symptoms with standing Yes No
Variable walking distance before symptoms Yes No
Relief with flexion Yes No
Relief with sitting Yes Yes
Peripheral pulses diminished No Yes
arthritis and gluteal or trochanteric bursitis.
Although clinicians consider a combination of results of
the history and physical examination and imaging findings
to be the most effectiv e means of diagnosing lumbar spinal
CHAPTER 48/CLASSIFICATION, NATURAL HISTORY, AND CLINICAL EVALUATION / 471
stenosis, no objective criteria for using the history and
physical examination ha ve been reported. In addition, there
are no reported clinical trials of the effectiveness of such a
composite diagnosis. The onl y quantitati ve e vidence correlating diagnostic information with outcomes is for the
imaging findings. Clinical decision making should be
based on a collection of data, including the history and
physical findings, functional status, imaging and electrodiagnostic studies, and other adjunctive studies.
REFERENCES
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1053–1066.
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CHAPTER 49
Imaging of Spinal Stenosis and Degenerative Lumbar Spondylolisthesis with Stenosis
Donald L. Renfrew and Kenneth B. Heithoff
There is no universally accepted def inition of the term
spinal stenosis. Gunzburg et al. (1), in an article correlating computed tomography (CT) findings with decompression surgery, state, “Lumbar spinal stenosis is . . . a
clinical condition and not a radiologic finding or diagnosis.” Nonetheless, the same authors also aff irm, “CT or
MRI [magnetic resonance imaging] combined with myelography has become the standard tool for iconographic
evaluation of (spinal stenosis).” In an article on conser vative treatment of spinal stenosis published in 2000,
Simotas et al. (2) state, “No validated system for radiographic rating of stenosis exists.” Although we recognize that this controversy exists, we offer this chapter to
explain and illustrate our approach to the imaging of
spinal stenosis.
Many authors (3–5) use the term stenosis to signify
any reduction of size of the spinal canal or neural foramina, whether from chronic bone, cartilage, or degenerative changes or from acute disc herniation, tumor, or
epidural abscess. Others (6,7) reserve use of the term
stenosis for bony reductions in canal size. Most clinical
cases of spinal stenosis follow from degenerati v e changes
of the intervertebral discs and facet joints. Although
osteophytes along the disc and facet joints contribute to
narrowing, degenerative soft-tissue abnormalities usually
account for more of the narrowing than do bony abnormalities (5). Degenerative soft-tissue abnormalities include thickening of the ligamentum flavum (8), bulging
of the disc, and capsular swelling of the facet joints.
Therefore, we use the term stenosis for fixed bony or relatively f ixed soft-tissue reductions in canal size. Used in
this manner, the term is descriptive and does not name a
disease process. Most cases of stenosis defined in this
way result from degenerative disc bulging, osteophytic
spurring, and facet arthropathy (Fig. 49-1), but stenosis
may be caused by any of several other processes. Exam-
ples include foraminal stenosis from scoliosis (Fig. 49-2)
or lytic spondylolisthesis (Fig. 49-3), and spinal canal
stenosis from closed arch spondylolisthesis (Fig. 49-4) or
after surgery (Fig. 49-5).
CLASSIFICA TION AND NOMENCLATURE
Classification systems of stenosis may use cause (e.g.,
congenital, degenerative, or combined) or location (e.g.,
spinal canal, subarticular recess, and foramen) (Fig. 49-6).
Another method of classification is by severity (mild,
moderate, or severe). When reporting an imaging study,
we grade spinal canal, subarticular, and foraminal stenosis
not only relative to other levels in the same patient (and,
when necessary because of an inherently small canal, an
idealized norm from other patients), but also taking into
account the degree of neural compression (Table 49-1;
Figs. 49-1 to 49-5, 49-7) (9). Reliance solely on percentages of narrowing overrates the severity of stenosis in
patients with inherently large spaces (canals, subarticular
recesses, and foramina) while underrating the severity of
stenosis in patients with small spaces (Tables 49-2 to 49-
4). In addition to grading the degree of stenosis, note may
be made in appropriate cases that the spinal canal has a
trefoil configuration, a characteristic of congenital or developmental (short pedicle) spinal stenosis (Fig. 49-8).
Grading spinal canal stenosis and lumbar foraminal
stenosis and neural compression may be done relatively
easily on most scans. Grading lumbar subarticular recess
stenosis is more difficult because of either scan quality
(for technical or patient related reasons) or crowding of
neural structures. As an alternative to grading subarticular stenosis using a mild–moderate–severe scale, it may
be preferable to note simply that narrowing is present,
and estimate whether compression of the associated neural structure is likely or not.
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