Applied Radiology

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 after diskectomy.

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 stenosis.

Lumbar spine

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

Cervical spine

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 5).

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 phenomenon.7

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.

Thoracic spine

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 has occurred.9

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

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 7).

Spondylolisthesis

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 pattern.

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 (figure 9).

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 minimally positive.

Neuroforaminal stenosis

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 than pain.22

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.

Conclusion

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 symptoms.

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

References

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