A series of biochemical changes takes place as an intervertebral disc ages. The disc gradually loses its waterbinding capacity, leading to dehydration of the nucleus pulposus. Concomitantly, the fibrocartilage content of the nucleus increases, which leads to a less pliable core. Eventually, the nucleus becomes virtually indistinguishable from the inner annulus and loses its ability to distribute forces correctly (3,6). These changes, in turn, require the annulus to assume unnatural forces that lead to tears in the annulus as well as traction spurs. These spurs form at the junction between the outer fibers of the annulus and their insertion into the vertebral bodies (6). These changes are associated with loss of disc height, causing axially directed compressive forces to be disproportionately distributed to the facet joints (6).
With these degenerative changes, the inner disc area of high signal intensity on T2-weighting slowly loses intensity (1). This corresponds to the loss of water from the nucleus and to the changes in biochemical consistency and structure as described in the preceding. In the later stages of degeneration, the signal intensity of the nucleus pulposus and inner annulus approximate that of the outer annulus, signifying the loss of water content and conversion to a dehydrated collagenous structure (1,3). Thus, differences between normal and degenerated discs are more easily appreciated on T2-weighted images, where water, or lack thereof, is more easily seen (1).
The hallmark in disc degeneration is the development of a radial tear of the annulus fibrosus, with resultant loss of fluid and fibrocartilage from the nucleus pulposus (4). Radial tears are almost always present in discs showing both early and severe degeneration and create a possible route for disc herniation (3,4,23). They are oriented perpendicularly to the lamellar fibers of the annulus (3). The most severely degenerated discs are associated with complete radial tears, those extending from the nucleus through the outer fibers of the annulus. In contradistinction, normal discs show an almost complete absence of radial tears.
Radial tears can be identified on MRI as a consequence of the pathologic changes (3). The substance of a tear has a greater degree of hydration than the surrounding annulus, accounting for the hyperintense signal on T2. Owing to collagen fibers replacing much of the substance of the nucleus pulposus, many degenerated discs with radial tears will demonstrate decreased signal intensity on T2-weighed images (12,23). Contrast-enhanced T1 images demonstrate foci of enhancement from neovascularity present as a part of the healing process (3,12) (Fig. 4).
As a disc suffers degenerative changes, a disc bulge may occur concomitantly with loss of height. This combination acts synergistically to narrow the intervertebral foramina. Loss of height causes a reduction in the craniocaudal dimension of a foramen, while the bulge may reduce its anteroposterior dimension. In addition, loss of height may lead to laxity and increased width of the ligaments about the spine (19).
As degeneration progresses, instability may lead to negative pressures inside of an intervertebral disc, caus-
ing gaseous conversion of interstitial nitrogen. This vacuum disc phenomenon is observed more frequently in the lumbar spine, and is seen as a signal void on MRI. These can often be visualized on plain films as gas pockets. On T2-weighted images, vacuum discs can paradoxically be seen as areas of high signal intensity consistent with fluid, because shifts in intradiscal pressures may cause fluid filling of the cleft when the patient is in the supine position (19,24).
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