Disc herniation is typically preceded by degenerative changes in the mucopolysaccharides of the nucleus pulposus, which produce fibrillation of the collagen (60). This eventually causes dehydration and loss of disc volume. As a result, the nucleus pulposus no longer serves as a normal load-dispersing mechanism, and excessive stress is borne by the annulus fibrosus. This produces annular fissuring and tears that can culminate in herniation of the nucleus pulposus. The loss of the load-diffusing function of the normal disc also causes facet joint degeneration and marginal osteophytosis of the vertebral body ends by virtue of the increased loads these joints must bear.
Cervical disc herniation occurs with less frequency than lumbar disc herniation. About 90% of cervical disc herniations occur, in order of decreasing frequency, at C5-6, C6-7, and C4-5 (61,62). On CT examination, a herniated cervical disc appears as a dense soft-tissue mass protruding from the disc space centrally or paracentrally into the spinal canal or posterolaterally into the neural foramen (Fig. 6-51).
FIGURE 6-51. CT evaluation of a herniated C5-6 nucleus pulposus. An axial CT myelogram shows a radiodense protrusion of the C5-6 disc (arrow ) that distorts the left anterior aspect of both the thecal sac and the spinal cord.
On T1-weighted MR images, the herniated cervical disc appears as a posterior extension of the moderate signal intensity of the disc into the low–signal-intensity region of the thecal sac (Fig. 6-52A,B). Because the spinal cord appears as a relatively high–signal-intensity structure outlined by the low–signal-intensity CSF, the relationship of the herniated disc to the spinal cord can be visualized directly by MRI. On T2-weighted MR images, the degenerated disc appears as a narrowed disc interval. The disc herniation appears as a moderate– to low– signal-intensity impingement on the now high–signal-intensity CSF. The posterior margin of the herniated disc may have a to determine its probability of causing a patient’s myelopathic very-low-signal-intensity margin interfacing with the CSF. This findings (Fig. 6-53A,B). It is sometimes difficult to differentiate may be a posterior longitudinal ligament elevated by the herni-lateral herniations of the disc into the neural foramen from osteoated disc, or it may be fragments of the posterior part of the phytic encroachments by MRI because they may both demon- annulus fibrosus (61). T2-weighted images also permit evalua-strate low signal intensity. In these circumstances, CT provides tion of the relationship of the herniated disc to the spinal cord good differentiation between bone and soft-tissue density.
FIGURE 6-52. A: T2*-weighted axial MRI of the cervical spine shows a left posterolateral herniated C6-7 nucleus pulposus (between arrow) indenting the thecal sac (arrowhead ) and extending into the ostium of the ipsilateral nerve root foramina. B: A T2-weighted left parasagittal MRI shows the disc fragment (arrow ) impinging upon the intermediate–signal-intensity thecal sac (arrowheads) and low–signal-intensity posterior longitudinal ligament.
FIGURE 6-53. A: Axial T2-weighted image at the C4-5 level demonstrates a bilobed protrusion contained in the midline by the posterior longitudinal ligament. Note complete obliteration of the normal CSF signal anterior to the cord, posterior displacement, and compression of the cord. B: The herniated disc elevates the posterior longitudinal ligament, compresses the cervical cord, which demonstrates increased signal intensity as a sign of myelopathy.
Source: Physical Medicine and Rehabilitation – Principles and Practice
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