Spinal Stenosis

Spinal stenosis refers to impingement upon neural tissue in the central spinal canal, intervertebral foramina, or lateral recesses. These conditions may result from developmental anomalies, one or any combination of the degenerative changes detailed in the preceding, or a number of other conditions (19). The term stenosis, however, should be reserved for patients with clinical findings consistent with such a diagnosis. Findings on imaging without clinical correlation should be referred to as narrowed (30,31).

Developmental stenosis accounts for a minority of cases in roughly a 1:10 ratio with respect to degenerative causes, and can be grouped into those due to hereditary-idiopathic spinal stenosis and those related to disorders of skeletal growth, such as the mucopolysaccharidoses, Down's syndrome, and achondroplasia, among others (30). These stenoses result from a hypoplastic vertebral arch with short, thick pedicles. In addition, the distance between pedicles at a given level may also be reduced, resulting in a horizontally narrowed central spinal canal (32). These patients are usually asymptomatic until degenerative changes act synergistically to produce symptoms (26).

Dural sac encroachment comprises the principal lesion in central stenosis and is distinguished by elimination of bordering epidural fat or impingement upon the thecal sac (22) (Fig. 8). This can lead to compressive myelomalacia, which gives an array of MRI findings. In the early stages, myelomalacia is seen as an area of high signal on T2-weighted imaging that is believed to represent edema and microvascular stasis. Unenhanced Tl-weighted images are essentially normal. Post-contrast images, however, may demonstrate enhancement due to disruption of the blood-brain barrier. With progression, T2-weighting continues to show high signal, while Tl-weighted images begin to lose signal intensity. These finding represent gliosis and cystic necrosis. Ultimately, atrophy and syrinx formation can be observed if the insult is not removed (19).

Lateral recess stenosis often occurs in conjunction with central stenosis but may be seen alone. As the nerve root descends at an angle through the lateral recess, it is critical to remember that lateral recess pathology at a given lumbar level often affects a nerve root that will exit more

Lateral Recess Stenosis

Fig. 8. Central canal and lateral recess narrowing. Axial T2-weighted image shows significant narrowing of the central canal (arrowhead) and lateral recesses which is in part due to ligamentum flavum hypertrophy (stars) and in part due to facet hypertrophy with additional fluid present in the facets (arrows).

Fig. 8. Central canal and lateral recess narrowing. Axial T2-weighted image shows significant narrowing of the central canal (arrowhead) and lateral recesses which is in part due to ligamentum flavum hypertrophy (stars) and in part due to facet hypertrophy with additional fluid present in the facets (arrows).

inferiorly. Axial cuts with both T2-weighting and post-contrast T1 images can demonstrate the stenosis (26).

Degenerative changes may result in stenosis of the intervertebral foramina by the mechanisms described in the preceding. These effects are best visualized on parasagittal images that demonstrate the foramina in cross-section. Findings consistent with foraminal stenosis include differing amounts of displacement and/or obliteration of the hyperintense fat within the foramen (26). However, axial images should also be obtained.

Nonspecific degenerative changes may cause intervertebral foramen narrowing. With loss of disc height, there is reduction in the craniocaudal dimension of the foramen. This forces the superior articular process of the inferior vertebral body into the inferior aspect of the notch of the superior pedicle, resulting in osteophyte formation. The situation is exacerbated further by laxity in the annu-lus fibrosus and ligamentum flavum and additional osteophytosis of the vertebral bodies. These factors act in concert to cause a stenotic intervertebral foramen (26).

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