Spinal stenois refers to constriction of the canals and various foramina of the spine. Plain radiography, computed tomography (CT), and magnetic resonance (MR) are all valuable assessment modalities. Here, the author reviews the MR features of stenosis.
Spinal stenosis refers to constriction of the canals and various
foramina of the spine. If sufficiently severe, the stenosis can
compress neural structures within the spine and cause neurological
symptoms. Spinal stenosis can involve the spinal canal, the lateral
recesses, or the neuroforamina. There are two varieties of spinal
stenosis: congenital and acquired.
Spondylosis and spinal stenosis are associated commonly with
intervertebral disk disease, particularly in patients over 50, and
they are significant sources of back pain, radiculopathy, and
myelopathy. Overlooking the patho-anatomic changes of spinal
stenosis is an important cause of the failed back surgery syndrome
Plain radiography, computed tomography (CT), and magnetic
resonance (MR) are all valuable imaging modalities for assessing
spinal stenosis. This review focuses on the MR features of spinal
Lumbar spinal stenosis is due to congenitally short pedicles, or
it may be acquired as a result of combined facet hypertrophy,
degenerated bulging disk, and hypertrophy of the ligamentum flavum.
Congenital spinal stenosis can be idiopathic (figure 1) or
associated with a developmental disorder, such as achondroplasia,
hypochondroplasia, Morquio's mucopolysaccharidosis, and Down's
syndrome. Spondylolisthesis, trauma, and surgical fusion are other
acquired causes of spinal stenosis.
Congenital spinal stenosis often is asymptomatic until middle
age, when secondary degenerative changes develop (figure 2).
Individuals with acquired degenerative stenosis become symptomatic
later in life, usually around the sixth through eighth decades. The
syndrome of neurogenic or spinal claudication includes bilateral
lower extremity pain, numbness, and weakness that is poorly
localized and usually associated with low back pain. The symptoms
are worse with standing or walking and relieved when the patient
lies down. The pain usually increases with extension and is
relieved with flexion.
The chronic compression of the thecal sac and cauda equina can
cause permanent nerve root damage.1 Symptomatic lumbar stenosis is
associated with central canal sagittal diameters of less than 12
mm; the normal range in adults is from 15 mm to 23 mm.2 Studies
have shown, however, that the dimensions of the bony spinal canal
correlate poorly with symptoms of degenerative spinal stenosis.
On the other hand, Schonstrom and colleagues3 showed that the
cross-sectional area of the dural (thecal) sac correlates extremely
well with surgically confirmed spinal stenosis. They determined
that a dural sac area of less than 100 mm2 was indicative of a
clinically significant lumbar spinal stenosis. Both the bone and
soft tissues of the spine contribute to the encroachment on the
cauda equina; thus, CT and/or MR imaging are required to evaluate
spinal stenosis fully.1
Spinal stenosis is displayed graphically in the sagittal plane
by gradient-echo or T2-weighted pulse sequences (figure 2). The
hyperintense thecal sac is effaced anteriorly by the bulging disk
and posteriorly by the ligamentum flavum, resulting in an hourglass
configuration. Acquired spinal stenosis usually is associated with
moderate to severe multilevel disk degeneration, consisting of loss
of normal signal, disk space narrowing, and intradiskal
calcification or air (figure 3). The calcification and air can be
difficult to discern within severely desiccated disks. On axial
views, the constricted canal often has a triangular or trefoil
shape, due to encroachment on the posterolateral aspects of the
canal by hypertrophied facets.4
Because the compression of the nerve roots within the thecal sac
is what causes the symptoms, assessment of the ratio of CSF to
nerve roots is important to make the diagnosis of spinal stenosis.
With progressive stenosis, the amount of CSF progressively
diminishes and the nerve roots become crowded together (figures 2C
and 3C). Constriction at the level of stenosis prevents the normal
superior and inferior movement of the nerve roots with flexion and
extension, resulting in a redundant serpiginous root pattern above
and below the stenosis (figure 3A).
Nerve root enhancement also may be seen, due to either breakdown
of the blood-nerve barrier from mechanical injury, inflammatory
response, and wallerian degeneration/regeneration of axons, or
engorgement of intrathecal veins and perineural vascular plexus.
Since nerve root enhancement suggests some neural injury, it may
indicate a more severe or significant stenosis. The thecal sac also
may enhance from repetitive trauma at the stenotic level. As a
result of epidural compression, prominent enhancement of
retrovertebral venous plexus is common.5
In older adults, cervical myelopathy most often is secondary to
cervical spinal stenosis. Direct compression of the cervical spinal
cord with vascular compromise is likely the causative mechanism for
the myelopathy. A relationship has been observed between the
cross-sectional area of the cord and the severity of the
myelopathy. Older male patients tend to be affected and the
spondylotic changes involve more than one nerve root level. This is
in contradistinction to cervical disk protrusion, which tends to
impinge upon a single nerve root.6
In patients with myelopathy secondary to spondylosis and spinal
stenosis, defining the extent of anterior, lateral, and posterior
impingement is necessary to plan the surgical approach. Sagittal
gradient-echo or T2-weighted images disclose hourglass narrowing of
the thecal sac, usually involving multiple levels in the mid- and
lower cervical region (figure 4). In patients with a congenitally
borderline or narrow canal, relatively mild degenerative changes
are sufficient to cause a spinal stenosis.
On T1-weighted scans, canal stenosis results in scalloping of
the normally smooth dorsal and ventral margins of the cord. As
learned from myelography, the degree of canal stenosis and cord
scalloping shown on the images is greater when the neck is in a
hyperextended position, due to buckling of the ligamentum flava.
Imaging in a neutral position may show less severe stenosis.
Nonetheless, the hyperextended view illustrates what happens to the
cord with acute hyperextension. The spinal cord is more susceptible
to traumatic injury in patients with a spinal stenosis (figure
MRI depicts cervical spinal stenosis as accurately as CT
myelography, particularly on axial T2-weighted images.5 Other
investigators have determined that MRI can overestimate the degree
of stenosis in the cervical region; this was more likely in cases
of severe narrowing. The anteroposterior diameter of the canal was
underestimated, especially on the sagittal images. Truncation
artifact and CSF pulsations were thought to be responsible for this
A much less common cause of spinal stenosis is ossification of
the posterior longitudinal ligament (OPLL), which occurs most often
in the cervical region and almost exclusively in Orientals.
Degenerative disk disease is associated commonly with OPLL. It
appears as a segmental or continuous thick band of hypointensity
along the posterior aspects of the vertebral bodies. A high
percentage of continuous OPLL contains bone marrow. A thick dark
band with some central increased signal is quite characteristic of
this entity.8 Otherwise, MR can have difficulty distinguishing
hypertrophy from ossification. T2-weighted sagittal images are best
for showing the widening of the ventral epidural space with
effacement of the thecal sac. Other things to consider in
differential diagnosis would be epidural hemorrhage
(deoxyhemoglobin or hemosiderin) or air.
Nontraumatic spinal stenosis of the thoracic spine is rare, but
one entity that has a predilection for the thoracic region is
ossification of the ligamentum flavum. In the Far East, it is one
of the most common causes of compression of the posterior thoracic
spinal cord. The ossified ligament is hypointense on T1- and
T2-weighted images, unless infiltration by fatty marrow elements
Another cause of enlargement of the ligamentum flavum is
deposition of calcium pyrophosphate dihydrate crystals. It can
occur at any level of the spine. The calcified ligament is
hypointense on all pulse sequences, and it can cause focal cord
compression or spinal stenosis.10,11
Epidural lipomatosis is another rare cause of spinal stenosis
that is more frequent in the thoracic spine. It is caused by
excessive deposition of fat in the epidural space, usually
secondary to Cushing's disease or corticosteroid therapy.12
Spondylolysis refers to a cleft or break in the pars
interarticularis of the vertebra. It is found in about 6% of
adults, mostly in males; 93% to 95% occur at L5, and most are
bilateral. The etiology is uncertain, but the current theory is
that it represents a stress fracture.13 Fetal cadavers do not have
pars defects, so it is not congenital. A study of 6- to 7-year-old
children showed a 6% incidence, the same as for adults. This
evidence suggests that the pars fracture occurs during early
childhood. Animals do not have pars defects, so it is likely
related to the upright posture and lumbar lordosis of humans. Only
one-half of patients with spondylolysis alone are symptomatic. It
appears that associated changes, such as degenerative disease and
spondylolisthesis, are required to produce symptoms.
The pars defect is demonstrated best in parasagittal images
(figure 6) and is easier to see if the bone has a generous
component of marrow or if soft tissue is interposed between the
bone fragments.14 With subluxation, there is often a step-off at
the pars defect. Visualization of the pars can be difficult on MR
because degenerative facet disease often is associated with loss of
marrow signal and sclerosis of the pars interarticularis.15 On
axial views, the key observation is a horizontal line (an extra
joint) between adjacent facets joints on consecutive images (figure
Spondylolisthesis refers to forward displacement of one vertebra
over another, usually of the fifth lumbar over the body of the
sacrum, or of the fourth lumbar over the fifth. It is estimated
that spondylotic spondylolisthesis occurs in about 4% of the
general population of adults.16 Spondylolisthesis is graded
according to how far the vertebral body moves forward on the one
below (grade 1 = 25%, grade 2 = 50%, grade 3 = 75%). There are two
types of spondylolisthesis: isthmic (open-arch type), associated
with spondylolysis, and degenerative (closed-arch type).
With isthmic spondylolisthesis, the pars defect divides the
vertebra into an anterior part (vertebral body, pedicles,
transverse processes, and superior articular facet) and a posterior
part (inferior facet, laminae, and spinous process). The anterior
part slips forward, leaving the posterior part behind. As a result,
the spinal canal elongates in its anterior-posterior dimension, so
that spinal canal stenosis is uncommon with isthmic
spondylolisthesis (figure 7). Grade-1 spondylolisthesis often is
asymptomatic, but with progressive anterior subluxation, the
intervertebral disk and the posterior-superior aspect of the
vertebral body below encroach on the superior portion of the neural
foramen.17 The foramen also is elongated in a horizontal direction
and may have a bilobed configuration (figure 6B). Exuberant
fibrocartilage at the pars pseudarthrosis can compromise the neural
foramen further and cause nerve root compression.
Degenerative spondylolisthesis occurs in an older age group,
usually those over 60 years old, and it is more common in women at
the level of L4-L5. It develops when there are severe degenerative
changes and excess motion of the facet joints. Subluxation at the
facet joints allows forward or posterior movement of one vertebra
over another. A degenerative spondylolisthesis narrows the spinal
canal, and symptoms of spinal stenosis are common. Hypertrophic
facet arthrosis is a frequent cause of foraminal narrowing (figures
3 and 8).
The sagittal plane is best for displaying the abnormal anatomy
of spondylolisthesis: T2-weighted images for the canal and
T1-weighted images for the pars interarticularis and neural
foramina. The sagittal view clearly shows the degree of subluxation
and the relationship of the intervertebral disk to the adjacent
vertebral bodies and the spinal canal. Parasagittal images are good
for showing encroachment on the foramina by disk or hypertrophic
bone (figure 8B). Loss of the normal fat signal cushioning the
nerve root is a sign of significant foraminal stenosis (figure 7D).
In addition, coronal or oblique views effectively display the
course of the nerve roots.18
Ulmer and colleagues19 proposed the "wide canal sign" to
distinguish between isthmic and degenerative spondylolisthesis.
Using a midline sagittal section, they noted that the sagittal
canal ratio (maximum anteroposterior diameter at any level divided
by the diameter of the canal at L1) did not exceed 1.25 in normal
controls and in subjects with degenerative spondylolisthesis. In
patients with spondylolysis, the measurement always exceeded 1.25.
Finally, if a spondylolisthesis is seen at L5-S1 in a patient under
45 years of age, it very likely is of the isthmic type.
Lateral recess stenosis
The lateral recess is an open canal bounded by the vertebral
body anteriorly, the pedicle laterally, and the superior articular
facet posterolaterally. The nerve root courses through the lateral
recess on its way to the exiting neuroforamen. Short pedicles
associated with congenital spinal stenosis reduce the dimensions of
the lateral recesses (figures 2B and 3C). Hypertrophic changes of
the vertebral end plates, uncovertebral joints (cervical spine),
and the superior facets can constrict the lateral recess.
Impingement of the nerve root can produce a radicular pain
In the cervical spine, the most common cause of lateral recess
stenosis is hypertrophy of the uncovertebral joints. These changes
are depicted best on axial views, either with CT or MR imaging
In the lumbar region, facet arthrosis and hypertrophy of the
superior facet are invariably involved (figure 10). The first
change noted in facet arthrosis is bony sclerosis that appears
hypointense on MR images. These changes are associated with
subchondral cysts, narrowing and irregularity of the articular
surfaces, and bony hypertrophy of the facets. Facet joint
hypertrophy, along with osteophyte formation along the posterior
lateral margins of the vertebral body, can encroach upon the
lateral recesses of the spinal canal.20 Compression of the existing
nerve roots results in a radicular pain syndrome, called the
lateral recess syndrome. The pain is worse with standing or walking
and is relieved with squatting or sitting. Neurologic signs may be
minimal. The straight leg raising test often is negative or
The neuroforamen is bounded by the vertebral body, uncovertebral
joint (cervical), and intervertebral disk anteriorly, the superior
facet of the lower vertebra posteriorly, and above and below by the
pedicles of the adjacent vertebrae. The nerve root is positioned in
the superior aspect of the foramen, just below the pedicle. The
foramen contains abundant fat and also serves as a conduit for
radicular arteries and venous plexus. The normal dimensions of the
neural foramen in the cervical spine are 9 mm in height, 4 mm in
width, and 4 mm to 6 mm in length.21 In the sagittal plane, the
lumbar foramen has the shape of an inverted teardrop.
Compression of the nerve root within a neuroforamen results in a
radicular pain syndrome. Since the nerve root lies in the superior
recess of the neural foramen, it occupies only a small portion of
the canal, and marked stenosis might not produce nerve root
compression or symptoms. For symptoms of sciatica to occur, some
degree of nerve root inflammation must be present; acute
compression does not lead to acute pain in the absence of such
irritation. When a noninflamed nerve is compressed, paresthesias,
reflex abnormalities, and motor and sensory losses occur rather
The anatomic source of foraminal stenosis is similar to that of
lateral recess stenosis: primarily the uncinate processes in the
cervical region (figures 4B and 4C) and the superior facets in the
lumbar spine (figures 10 and 11). A bulging degenerated disk
projects into the inferior aspect of the foramen and does not cause
nerve root compression. On the other hand, an extruded disk
fragment can migrate into the superior aspect of the foramen and
impinge on the nerve root.
The central canal, lateral recesses, and the neural foramen are
the three sites in the spine that can be responsible for the
clinical presentation of spinal stenosis. Pure central canal
stenosis is rarely seen in the absence of narrowing of the lateral
recesses or nerve root canal. Only radiographic examination can
determine reliably the anatomic site primarily responsible for the
It is difficult to define the criteria for central and lateral
recess stenosis. Agreement is lacking about the lower limit of
normal for the dimensions of the relevant spinal structures. Also,
studies have shown that there is a relative lack of correlation
between severity of symptoms and the degree of spinal stenosis.
Frequently, radiologic abnormalities are more severe than the
symptoms would suggest.23
In spite of these difficulties, the severity of spinal stenosis
in symptomatic patients (as seen on preoperative radiologic
evaluations) is related to the probability of a favorable outcome
after surgery; those with more severe stenosis are more likely to
benefit from surgical intervention.24 AR
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