Nomenclature of Degenerative Disc Disease

Disc Degeneration

Overview . Describing morphology alterations seen in degenerative disc disease requires common terminology to standardize communication. A series of pathoanatomic terms and definitions proposed by an interdisciplinary committee and endorsed by multiple societies is summarized here. These general terms are descriptive and independent of imaging modality.

It cannot be overemphasized that the specific terms described below do not imply knowledge of etiology, symptoms, prognosis, or need for treatment.

MR signal intensity . Any or all of the following can occur with disc degeneration : Real or apparent desiccation, fibrosis, narrowed intervertebral disc space, bulging, fissuring/mucinous degeneration of the anulus, osteophytes of the vertebral apophyses, and endplate/adjacent marrow changes.

Severely degenerated discs with markedly decreased signal intensity may demonstrate linear areas of high signal intensity on T2-weighted images that may represent free fluid within cracks or fissures of the degenerated complex. Signal intensity changes in the intervertebral disc on T1-weighted images, while much less common than the loss of signal noted on T2-weighted images, can also be seen with degeneration.

Regions of decreased or absent signal within heavily calcified discs may occur. Signal loss has been attributed to a low mobile proton density as well as, in the case of gradient echo imaging, its sensitivity to the heterogeneous magnetic susceptibility found in calcified tissue.

Focal or diffuse areas of hyperintensity on T1-weighted spin-echo sequences may also be encountered in densely calcified intervertebral discs. These changes are related to T1 relaxation times secondary to a surface relaxation mechanism. These regions of high signal intensity on T1 are unaffected by fat suppression, suggesting that it is a T1 shortening effect rather than the presence of lipid. Hyperintensities within severely degenerated intervertebral discs that suppress on fat-saturation techniques presumably relate to areas of fatty marrow.

Separation between, or avulsion of, anular fibers from their vertebral body insertions, or breaks through fibers that extend transversely in a radial fashion, or concentrically through layers of the anular lamellae, are referred to as anular fissures . On MR, these changes are seen on T2-weighted images as high signal intensity within the outer anulus/posterior longitudinal ligament complex (the so-called “high-intensity zone”). These regions will also sometimes enhance following the administration of paramagnetic contrast, an effect thought to be secondary to reactive reparative tissue. The term “anular tear” should be avoided.

The role of anular disruption as the principle causal agent of disc degeneration has not been proven. In light of the continuing controversy surrounding the concept of “internal disc disruption,” it is probably unwarranted to imply that radial tears are more than a manifestation of advanced degeneration. While no data clearly support an unequivocal causal relationship between these degeneration changes and symptoms, anular disruption is important to consider because of a controversial concept of “discogenic pain” and its implications concerning the usefulness of discography for diagnosis. Back pain is thought to occur in some patients without morphological abnormalities, such as herniation or stenosis, which are thought to be related to leakage of nuclear material through the disrupted anulus into the epidural space.

Facet and ligament degenerative changes can occur with or without accompanying disc degeneration and can be readily identified on imaging studies. These changes are best described level by level, along with the presence of foraminal and canal narrowing, facet fluid, cysts, and other abnormalities.