Cervical spinal stenosis can be congenital or acquired. In the less common congenital stenosis, a small spinal canal is produced by short pedicles and thick laminae (62). It commonly remains asymptomatic until degenerative changes are superimposed on the congenital stenosis later in life.
Acquired stenosis can be produced by a host of hyper- trophic degenerative changes often collectively referred to as cervical spondylosis. These include osteophytic lipping of the posterior margins of the vertebral body ends bordering the disc, hypertrophic degenerative changes involving Luschka’s joints or the facet joints, buckling or hypertrophy of the ligamenta flava, and OPLL. All these structures border the spinal canal; therefore, hypertrophic degenerative changes can produce spinal canal stenosis. Because Luschka’s joints, the facet joints, and the ligamenta flava also border the neural foramen, their involvement by degenerative processes can produce foraminal stenosis.
Although hypertrophic degenerative changes of any of the structures bordering the spinal canal or neural foramen can occur in isolation, they are commonly precipitated by intervertebral disc degeneration. As the disc degenerates and loses its normal load-dispersing ability, loads tend to become concentrated on the vertebral body margin toward which the spine is bent. This excessive loading can produce marginal osteophytes around the entire circumference of the vertebral body end plates. Those osteophytes developing on the posterior margin can encroach on the spinal canal to produce spinal stenosis (Fig. 6-54A,B). Luschka (i.e., uncovertebral) joints are situated between the uncinate processes that protrude from the lateral or posterolateral margins of the upper surface of the vertebral bodies and a reciprocal convexity on the lateral aspect of the inferior surface of the next higher vertebral body. Recent evidence indicates that they are not true joints (63). Rather, they are degenerative clefts within the lateral part of the intervertebral disc that begin in the second decade of life. The increased loading of Luschka joints produced by these degenerative changes produces bony spurs that can extend posteriorly into the lateral part of the spinal canal or posterolaterally into the neural foramen (Fig. 6-55A–C).
FIGURE 6-54. (A) Midplane sagittal and (B) right parasagittal T2-weighted images in a patient with congenital stenosis and superimposed degenerative spondylosis with central canal narrowing and cord compression. There is increased AP dimension to the C4, C5, and C6 vertebral bodies. Annular bulge and hypertrophy to the supporting ligamentous structures is responsible for compression to the cord. There is linear increased signal to the cord on the T2-weighted image (arrow ) compatible with early myelopathy.
FIGURE 6-55. Hypertrophic Luschka joints with associated bilateral foraminal stenosis. A: Axial image at the C5-6 segment shows the hypertrophic changes to the uncovertebral joints (arrow ) and associated foraminal stenosis. B: Coronal and C: sagittal oblique MPR images demonstrates to a better advantage the associated foraminal stenosis, the deformity at the uncovertebral joint and the subchondral bone sclerosis.
Disc degeneration is accompanied by dehydration and loss of disc height, with decreased space between vertebral bodies resulting in increased facet joint loads. The resultant facet joint degeneration involves cartilage erosion with joint space narrowing, subchondral bone sclerosis, and osteophyte formation. The osteophytes may encroach on the spinal canal or the neural foramen.
Loss of disc height results in decrease of the laminae inter- space, which causes the ligamentum flavum to buckle and bulge into the spinal canal, contributing to the spinal stenosis. Because the ligamentum flavum continues laterally into the facet joint capsule, buckling of this part of the ligamentum flavum can cause foraminal stenosis.
OPLL occurs more commonly at cervical than at other vertebral levels. It is best visualized via CT, where it appears as an ossification extending over several vertebral levels, separated from the posterior margin of the vertebral bodies by a thin radiolucent interval (Fig. 6-56A,B).
FIGURE 6-56. Ossification of the posterior longitudinal ligament OPLL. A: Axial CT at the level of C3 demonstrates the calcification to the fibers of the posterior longitudinal ligament. There is narrowing to the central canal by the mass effect exerted by the enlarged calcified ligament. B: Sagittal multi-planar reformatted image. The short arrows at the flowing calcifications within the anterior longitudinal ligament. The calcification extends from C2 up to C7. The OPLL (long arrow) extends from C2 up to the proximal border of C5.
When any of these potential causes of cervical stenosis sufficiently narrow the spinal canal, cord compression can produce myelopathic signs and symptoms. Spinal stenosis most frequently narrows the AP dimension of the spinal canal. Although the cross-sectional area of the spinal canal is smallest at the C4 and C7 levels, the smallest AP diameter is usually at the C3 through C5 levels (62). It has been stated that all spinal stenosis that reduces the AP dimension to less than 10 mm could produce quadriplegia (64).
Although the uppermost cervical cord segments are nearly round, at most cervical levels the cord has an elliptical outline with its major axis transversely oriented. With encroachment of the cord by spinal stenosis, it is usually first flattened anteriorly by an encroaching osteophyte. With progression, the anterior median fissure becomes indented and widened until the cord assumes a kidney bean shape (Fig. 6-57) (48). The lateral funiculi may become tapered anterolaterally because of tension on the denticulate ligaments. The cord may become notched dorsally because of posterior white column atrophy. It has been estimated that a 30% reduction in cord cross-sectional area may be required to produce signs of ascending and descending tract degeneration (65).