The use of diagnostic imaging earlier in the course of a patient’s symptoms is supported by the following evidence: (1) patients with herniated discs treated surgically have better short-term outcomes than those treated conservatively ^10,¹¹; (2) the earlier the surgery the better the outcome¹²; and (3) surgery is cost-effective compared with conservative management (though this varies with the type of surgery).^13,¹⁴ However, the potential reduction in morbidity from early intervention requires the identification of accurate prognostic indicators, be they clinical or imaging based. Certainly, more than morphology is a factor. As has been suggested by Postacchini,¹⁵ two needs likely require consideration: (1) protracted conservative treatment may lengthen the time off from work and reduce the chances of successful surgical treatment; and (2) surgery should be avoided in patients with a herniated disc that may become asymptomatic or even disappear within a few months of onset. Thus, the possible benefits of imaging for degenerative diseases of the spine, other than as a presurgical tool, have never been carefully documented and quantified. Predicting which patients will benefit from imaging is a complicated and controversial subject. Its use as a preintervention planning tool is critical, but its employment for diagnostic information per se is less well accepted and the subject of much debate. Nevertheless, if imaging could be employed to prospectively determine which patients will not do well with surgery or other types of therapy, it would be of great value. Conversely, its use to identify patients undergoing prolonged conservative treatment who require more aggressive therapy (e.g., surgery) might be equally beneficial. This would save the cost of lost work, medical expenses, and personal discomfort. Clearly, there is little consensus, either within or among specialties, on the use of diagnostic tests for patients with back pain.¹⁶ The diagnostic evaluation depends heavily on individual physicians, their specialties, and patient socioeconomics, in addition to the patient’s symptoms.^16,¹⁷ On the other hand, patients with underlying risk factors (“red flags”), mainly, infection, trauma, and malignancy, warrant early imaging for timely intervention.

Imaging Considerations

The major benefit of imaging is its ability to depict the presence or absence of anatomic derangement and, in the former case, its effect on adjacent structures. The contrast sensitivity and multiplanar imaging capability of proton magnetic resonance (MR) provides a unique noninvasive means of imaging the intervertebral disc, adjacent osseous structures, and associated soft tissues. From an anatomic perspective, it is important to be able to demonstrate the osseous, fluid, and soft tissue interfaces within the three traditional compartments: the intramedullary, extramedullary intradural, and extradural spaces. The potential combinations of pulse sequence parameters, imaging planes, and postprocessing techniques available are almost limitless, and they can be used to highlight different aspects of the discovertebral complex and adjacent spaces. The methods include, but are not limited to, surface coil technology, cardiac gating, gradient refocusing, paramagnetic contrast agents, saturation pulses, gradient echo volume imaging, Turbo (fast) T2-weighted spin echo, fat suppression, magnetization transfer, short-tau inversion recovery (STIR), and diffusion techniques (including diffusion tensor imaging). Other modalities certainly do have a role based on the cost-effectiveness, accessibility, individual unique characteristics of some modalities, and, more importantly, contraindications to MRI. The technical aspects, advantages, and disadvantages of conventional and new modalities are briefly discussed in the following sections.

Counting Reference

The topic is discussed in detail in Chapter 175. It is extremely important that counting reference is clearly stated in the spine imaging report. This is to avoid wrong level surgeries with potential medico-legal implications. The two major factors responsible for discrepancy are (1) a transitional vertebra, which can be a sacralized L5 or lumbarized S1, and (2) variations in the number of rib-bearing vertebrae. Lumbosacral transitional vertebra (LSTV) is a common finding in the general population. Identification of LSTV on imaging is the essential first step in the interpretation of lumbar and thoracic imaging.¹⁸ The coronal MRI localizer image of the thoracic and lumbar spine can be useful because L4-5 is generally at the level of the iliac crest. Some prefer to use a vitamin E back-skin marker at an overlapping level in the thoracic spine, which, however, requires imaging of the entire spine. The iliolumbar ligament is easily identified on axial MRI and can be used as a marker of L5.¹⁹ There is a greater tendency of counting the lowest lumbar-type intervertebral disc space as L5-S1. Nevertheless, it is crucial that these approaches and variations be specified and clearly communicated in the report.

Plain Radiography

Plain radiography (PR) is still a very useful and cost-effective diagnostic tool by virtue of its availability and efficiency.²⁰ PR is generally used in trauma, for screening of degenerative disease, and for evaluation of sagittal translation using flexion-extension views. PR can aid MRI in characterization of disc disease by better demonstration of vacuum phenomena, disc calcification, bridging osteophytosis, and dorsal longitudinal calcification (though less common in the thoracolumbar spine). Conventional screen-film imaging has been nearly completely replaced by digital acquisition modalities, using either imaging plates (computed radiography, CR) or flat-panel detectors (direct radiography, DR).

Dynamic Imaging and Upright Magnetic Resonance Imaging

Sagittal segmental lumbar motion is traditionally assessed with lateral flexion-extension radiographs. These dynamic studies often demonstrate a decrease in the slip percentage between the vertebral segments with extension and an increase with forward flexion. Ironically, the degree of spondylolisthesis can actually improve on the lateral film taken on the operating table in an anesthetized patient.²⁷ Somewhat analogous to the flexion-extension imaging, supine-prone imaging of the lumbar spine can also be more sensitive by showing a higher degree of listhesis in the prone position.²⁸ Position-dependent stenosis can be demonstrated on the lateral myelogram in flexion-extension postures, which would otherwise have been underestimated on the follow-up CT myelogram²⁹ (Fig. 172-1). Ben-Galim and Reitman in a study of a small group of patients showed position-dependent severe spinal canal stenosis on CT myelography with grade I or II spondylolisthesis. Additionally, they showed fluid-filled distended facet joints, a marker of positional translation.³⁰ Imaging findings on supine MRI may correlate poorly with clinical findings. This may be related to the positional dependence of spinal stenosis, which reflects dynamic changes in soft tissue structures. Therefore, it is potentially valuable to evaluate spinal disorders under mechanical loading. Hydraulic axial-loading devices have also been tried.³¹ Upright MRI in different postures can reproduce the positions that bring about their symptoms and may unmask findings that are not visible with routine supine imaging. Small disc herniations and ventral spondylolisthesis can be unmasked, and disc herniations can be increased in size on upright MRI compared with recumbent MRI.³² Assessment of the degree of spinal stability in the degenerative and postoperative lumbar spine can also be performed.^33,³⁴ Kinetic magnetic resonance images (kMRIs) in axially loaded, upright-neutral, flexion-extension positions can also accentuate the size of the disc herniations and play a potential problem-solving role in radiculopathy with negative supine static imaging.³⁵ Clearly, axial loading changes anatomic relations. The significance of the findings in terms of therapeutic decision making is not very clear.³⁶

FIGURE 172-1 Dynamic imaging. Erect lateral views of a lumbar myelogram in the extended (A) and flexed (B) positions showing a subtotal block to the contrast column at the L4-5 level in extension that is relieved in flexion. C, Routine supine CT myelogram shows mild diffuse disc bulge without significant compression of the thecal sac.

(From Saifuddin A: The imaging of lumbar spinal stenosis. Clin Radiol 55[8]:581–594, 2000, with permission.)

Morphologic Alterations on Imaging

Standardized reporting is a better means of communication and consistent reporting, as well as a useful source of database research. Given the complexity, inconsistency, and overlapping of terminology used to discuss the spine over the years, standardized report generation in spine imaging is needed the most to describe the morphologic alterations in the spine. A consensus-based terminology recommended by Millette et al.³⁷ is used in this chapter. It must be clearly understood that these terms are descriptive only and, in and of themselves, independent of the test. It cannot be overemphasized that these terms do not imply knowledge of etiology, symptoms, prognosis, or need for treatment. Recently, Carrinno et al.³⁸ showed moderate reliability in the interpretation of qualitative nondisc contour degenerative findings on lumbar MRI.

Degenerative morphologic changes are discussed in the following section as disc degeneration and end-plate bone marrow changes followed by facet joint degenerative alterations.

Disc Degeneration

The term disc degeneration is used for a variety of changes, including any or all of the following: real or apparent desiccation, fibrosis, narrowing of the disc space, bulging, fissuring or mucinous degeneration of the anulus, osteophytes of the vertebral apophyses, and end-plate/adjacent marrow changes. MRI and CT show disc space narrowing, T2-weighted signal intensity loss from the intervertebral disc, presence of fissures, fluid, vacuum changes and calcification within the intervertebral disc, ligamentous signal changes, marrow signal changes, and osteophytosis. These alterations result in disc herniation, malalignment, and spinal canal stenosis. Conventional theory suggests that aging and degeneration are very similar processes, albeit occurring at different rates. Historically, the two processes have been characterized morphologically and termed as spondylosis deformans and spondylosis osteochondrosis (deteriorated disc), respectively. The former affects the anulus fibrosus and adjacent apophyses, whereas the latter mainly affects the nucleus pulposus and the vertebral body end plates, particularly fissuring (numerous tears) of the anulus fibrosus. Scientific evidence suggests that spondylosis deformans is the consequence of normal aging, whereas intervertebral osteochondrosis represents a pathologic, though not necessarily symptomatic, process.³⁹ Anteriolateral osteophytosis is a reliable marker of spondylosis deformans, with a 100% incidence above 40 years.³⁹ Disc degeneration and aging are multifactorial processes that encompass a wide spectrum of changes and sequelae, of which the radial tear is but one. Disc degeneration may be explained primarily by genetic influences and complex unpredictable interactions of unidentified factors.

The nucleus pulposus is eccentrically located and more closely related to the dorsal surface of the intervertebral disc. With degeneration and aging, type II collagen increases outwardly in the anulus, and water loss from the nucleus pulposus is greater than from the anulus. This results in a loss of the hydrostatic properties of the disc, with an overall reduction of hydration in both areas to about 70%. In addition to water and collagen, the other important biochemical constituents of the intervertebral disc are the proteoglycans. It is not the individual composition but the relative composition of these constituents that in turn affects the hydrostatic properties and tensile strength of the intervertebral disc. The ratio of keratin sulfate to chondroitin sulfate increases. The disc becomes progressively more fibrous and disorganized, with the end stage represented by amorphous fibrocartilage and no clear distinction between nucleus and anulus. The degenerating disc manifests as diminishing T2 signal and loss of internal lamellation. T2 measurements also correlate with glycoaminoglycan concentration rather than absolute water content. So, it is not just the absolute concentration of water but also the state of water involved in the disc degeneration. The status of the proteoglycans is thus a major determinant of disc space T2 and T1 signal ³⁹^–⁴¹ (Fig. 172-2).

FIGURE 172-2 Degenerative disc changes. Anular disc bulges at L1-2 and L2-3. Disc space vacuum phenomena at L2-3 to L4-5, extending to the epidural space along the bulging disc at L2-3 (arrow). Mild degenerative spondylolisthesis, anterolisthesis at L4-5, and retrolisthesis at L2-3.

Anular Tears

Also called anular fissures, anular tears are separations between anular fibers, avulsion of fibers from their vertebral body insertions, or breaks through fibers that extend radially, transversely, or concentrically and involve one or many layers of the anular lamellae. The term tear, or fissure, describes the spectrum of such lesions and does not imply that the lesion is a consequence of trauma. Although it has certainly been verified that anular disruption is a sequela of degeneration and is often associated with it, its role as the causal agent of disc degeneration has certainly not been proved. Anular disruption initiates a reparative process as it is replaced by dense fibrous tissue and cystic spaces.⁴²^–⁴⁵ Fissuring, chondrocyte generation, and granulation tissue formation have been noted within the end plate, anulus fibrosus, and nucleus pulposus of degenerative discs, indicating attempts at healing.³⁹ Anular tears are commonly seen in the dorsal bulging discs as focal T2 hyperintensity on T2 and STIR imaging; there may be associated small disc protrusion. Anular tears consistently show focal contrast enhancement ⁴⁶ (Fig. 172-3).

FIGURE 172-3 Anular tears. Sagittal (A) and axial (B) T2 images show typical posterior anular tear with hyperintense T2 signal (arrows) and associated small disc protrusion.

Disc Gas “Vacuum Phenomenon”

Radiolucent foci on CT or plain films representing gas, principally nitrogen, occur at sites of negative pressure produced by the abnormal spaces. The vacuum phenomenon within a degenerated disc is represented on spin echo images as areas of signal void. Whereas the presence of gas within the disc is usually suggestive of degenerative disease, spinal infection may (rarely) be accompanied by intradiscal or intraosseous gas.⁴⁷ A protruding disc with a vacuum phenomenon can present as epidural gas foci on CT and hypointensities on MRI (see Fig. 172-2).

Disc Calcification and T1 Hyperintensity

Patchy, partial, or complete calcification of the disc space can be seen either as an isolated finding without degenerative stigmata or as a chronic dystrophic change in a degenerated disc. The clinical significance of a calcified disc is unknown. The disc space on CT and plain films can appears as fused, perhaps “autofused.” Calcification, depending on its biochemical status, can appear as hyperintense or hypointense on sagittal T1 imaging. Furthermore, the hyperintense T1 disc may represent an ossified disc, as can be proven by loss of signal on fat-suppressed MRIs due to lipid marrow. A calcified disc is easily demonstrable on CT (Fig. 172-4).

FIGURE 172-4 Disc space calcifications: Sagittal T1-, T2-, and fat-suppressed T1-weighted images of the upper lumbar spine. On the T1-weighted images, there is a focus of high signal (arrow). On the T2-weighted image, this same area has a decreased signal (arrow). On the fat-suppressed image, the region maintains its high signal, while areas which contain fat have a decreased signal (arrow). The high signal on T1, decreased signal on T2, and unaffected by fat suppression are indicative of calcification producing T1 shortening.

Degenerative Marrow Changes

The anulus fibrosus, vertebral end plate, and vertebral body have an interreactive relationship in the degenerative process, as is also evident from the model of chymopapain-treated discs.^48,⁴⁹ Paradiscal MR signal changes in the end plate and vertebral bodies take three forms.

Type I Changes

Type I changes demonstrate decreased signal intensity on T1-weighted images and increased signal intensity on T2-weighted images. Type I change is found in about 4% of nonsurgical lumbar spines, 8% in postdiscectomy discs, and 40% to 50% of chymopapain-treated discs.⁴⁸^–⁵⁰ The last group can be used as a model of acute disc degeneration. Histopathology of type I changes demonstrates disruption and fissuring of the end plate and vascularized fibrous tissues within the adjacent marrow, accounting for prolonged T1 and T2 MR signal. Enhancement of type I vertebral body marrow changes is seen with administration of IV gadolinium. The enhancement may involve a portion of the disc itself and is presumably related to the vascularized fibrous change. The type I signal is expectedly accentuated on STIR, mimicking bone marrow edema, and may be very difficult in some cases to differentiate from discitis osteomyelitis (discussed later under the differential diagnosis of vertebral osteomyelitis; Fig. 172-5).

FIGURE 172-5 A–C, Type I end-plate changes. T1 hypointense and T2 hyperintense end-plate changes at L3-4 (curved arrows); the end-plate signal is accentuated on short-tau inversion recovery (STIR) image due to suppression of the fat in the surrounding marrow. Note that the same bone marrow changes also surround a large Schmorl node at L3 (straight arrows). Note a small Schmorl node at L2; however, there is no surrounding reactive change or hypointense rim.

Type II Changes

Type II changes are represented by increased signal intensity on T1-weighted images and isointense or slightly hyperintense signal on T2-weighted images. Type II changes are identified in approximately 16% of patients on MRI.⁴⁸^–⁵⁰ Discs with type II changes, like type I, show evidence of end-plate disruption, with fat marrow in the end plate and adjacent vertebral body resulting in T1 hyperintensity due to T1 shortening (Fig. 172-6).

FIGURE 172-6 A–C, Type II end-plate changes. T1 and T2 hyperintense end-plate changes at L4-5 (arrows). Like the surrounding fatty marrow, the end-plate signal is suppressed on the short-tau inversion recovery (STIR) image.

Type III Changes

Type III changes are represented by a decreased signal intensity on both T1- and T2-weighted images due to extensive bony sclerosis, as evident on plain radiographs and CT. The first two types show no definite correlation with sclerosis seen at radiography, which is not surprising when one considers the histology. The sclerosis on plain radiographs is a reflection of dense woven bone within the vertebral body rather than of the marrow elements. The lack of signal in the type III change represents the relative absence of marrow in areas of advanced sclerosis (see Fig. 172-17B).

Facets, Pedicles, and Ligamentous Changes

The superior articulating process of one vertebra articulates with the inferior articulating process of the vertebra above by a synovium-lined articulation—the zygapophyseal joint. The lumbar facet joints are predisposed to arthropathy with alterations of the articular cartilage. Facet joint degeneration results in hypertrophic changes (osteophytosis), joint effusions, synovial cyst formation, and rostrocaudal subluxation. Mild to moderate facet joint osteophytosis is commonly seen in the lumbar spine at L4-5 and L5-S1 and is more suggestive of age-related change.^51,⁵² The important ligaments of the spine include the anterior longitudinal ligament, the posterior longitudinal ligament, the paired sets of ligamenta flava (connecting the laminae of adjacent vertebrae), the intertransverse ligaments (extending between transverse processes), and the unpaired supraspinous ligament (along the tips of the spinous processes). As these ligaments normally provide stability, any alteration in the vertebral articulations can lead to ligamentous laxity with subsequent deterioration. Loss of elastic tissue, calcification and ossification, and development of bone proliferation at sites of ligamentous attachment to bone are recognized manifestations of such degeneration.

Facet and Disc Degeneration

Generally, disc degeneration dominates facet arthropathy. Some degree of facet arthritic changes usually accompanies disc degeneration. Is facet disease a sequela of disc degeneration? The answer to this question is debatable, but at least it is clear that disc degeneration is more common and generally precedes facet joint arthropathy. Due to altered mechanics, disc degeneration probably accelerates facet joint arthropathy.⁵¹^–⁵⁴ A systemic component is hypothesized to account for facet arthrosis since there is a high incidence of concurrent lumbar and cervical facet arthrosis.⁵⁵ Osteophytosis of the facet joints is, to a degree, a counterpart of end-plate osteophytosis and specifically contributes to lateral recess and foraminal stenosis. Facet arthrosis may occur independently and be a source of symptoms on its own.⁵⁶ A smaller group of lumbar spines in our experience show dominant facet and ligamentous degenerative hypertrophic changes with absent to minimal degenerative disc changes.

Facet Joint Effusions

Pencil-thin homogeneous bilateral facet joint effusion is a common and normal finding in the lower lumbar spine. In an arthritic facet joint, synovial villi may become entrapped within the joint, with resulting joint effusions. STIR is the best method for demonstrating joint effusions. Large joint effusions (>1.5 mm) are highly predictive of degenerative spondylolisthesis on dynamic imaging, particularly at L4-5 ⁵⁷ (Fig. 172-7).

FIGURE 172-7 Facet effusions. Sagittal short-tau inversion recovery (A) and axial T2 (B) images showing facet joint effusions at L4-5 (arrows) and common associated finding of mild anterolisthesis at L4-5 (C).

Synovial Cysts

Herniation of the synovium through the facet joint capsule may result in synovial cysts. In a review of patients with degenerative facet disease, synovial cysts occurred at a ventral or intraspinal location in 2.3% of cases and dorsal or extraspinal location in 7.3%.⁵⁸ There is a more straightforward relationship of synovial cysts with osteoarthritis and the instability of the facet joints than degeneration of the intervertebral disc alone.⁵⁷ Intraspinal synovial cysts can be symptomatic, depending on their size. Typically, synovial cysts have T2 hyperintense cystic appearance, but signal intensity can vary due to debris, hemorrhage, gas, and superimposed infection. The cyst may exhibit rim enhancement (see Fig. 172-24). Distinguishing the synovial disc from the herniated disc is not usually difficult due to its location and MR characteristics. A dorsolateral extradural impression and associated juxtafacet asymmetrical soft tissue density on CT myelogram is a nonspecific finding; asymmetrical facet joint arthritis can be helpful in such cases.

Dorsal Elements and Paraspinal Edema

Routine use of STIR and similar sequences has resulted in increased detection of dorsal elements and paraspinal soft tissue edema.^59,⁶⁰ Facet joint degenerative arthritis can result in para-articular and pedicular edema, joint effusion, and para-articular soft tissue edema. In patients at high risk, it may be difficult to differentiate from infected facet joints. The signal changes and sclerosis in the pedicles can be seen secondary to facet joint arthritis and underlying pedicle or pars fractures. The greatest mechanical stress is on the pars interarticularis, followed by pedicles as shown by Sairyo et al.⁶¹ These stresses can result in a spectrum of reactive bone marrow changes in the pars and pedicles. T2 hyperintense signal in the pedicles has been shown as an early marker of spondylolysis.⁶¹ There is evidence that categories of changes in MR signal intensity, similar to those described adjacent to degenerating discs, can be seen in lumbar pedicles adjacent to a spondylolytic defect of the pars interarticularis⁶² (Figs. 172-8 and 172-9).

FIGURE 172-8 Facet edema. A and B, Hypertrophic facet arthropathy at L2-3 (arrows). C, Associated marrow and soft tissue edema (arrows). Also note L2 and L3 pedicles edema (anterior arrows).

FIGURE 172-9 Pedicle edema. Hypointense T1 (A) and hyperintense T2 (B) pedicle signal (arrow) at L5. C, The T2 signal is accentuated on short-tau inversion recovery (STIR) image. D, CT shows pars interarticularis defect.

Morphologic and Functional Sequelae

Major sequelae of disc and dorsal elements degenerative changes are intervertebral disc displacement, malalignment, degenerative scoliosis, and spinal canal–foraminal stenosis. Disc displacement can be found as an isolated finding. Otherwise, there is usually a combination of the sequelae mentioned before.

Segmental Instability

Each level in the thoracolumbar spine consists of three joints: intervertebral disc space and bilateral facet joints. Degeneration of these joints results in segmental instability replacing the normal spinal motion, which can be irregular, excessive, restricted, translational, and/or angular. Segmental instability, which can cause static and dynamic stenosis, is considered a cause of LBP but is poorly defined.⁶³ On flexion-extension plain radiography, generally about 3 mm or more of sagittal translation is equated with instability. Spondylolisthesis is a term used in static imaging and refers to intervertebral displacement—anterolisthesis, retrolisthesis, or lateral listhesis. The different types, based on etiology, include congenital, degenerative, isthmic, iatrogenic, pathologic, and traumatic (Fig. 172-10).

FIGURE 172-10 A and B, Isthmic spondylolisthesis. Sagittal T2 imaging showing grade I anterolisthesis due to L5 spondylolysis (arrow).

Grading of Spondylolisthesis

Spondylolisthesis in the sagittal plane can be graded by one of two methods, independent of the imaging modality and type of spondylolisthesis.⁶⁴ The first is the method described by Meyerding.⁶⁵ The anteroposterior (AP) diameter of the superior surface of the lower vertebral body is divided into quarters, and a grade of I to IV is assigned to slips of one, two, three, or four quarters of the superior vertebra, respectively. The second method, first described by Taillard,⁶⁶ expresses the degree of slip as a percentage of the AP diameter of the top of the lower vertebra. Complete slip of L5 on S1 is termed spondyloptosis. The second method is favored by most authors as it is more accurately reproducible.⁶⁷ Measurement of the slip and its apparent progression, however, should be viewed with caution. Studies have shown that inter- and intraobserver error of up to 15% is possible. This variation can increase if an element of rotation is present. Therefore, only a progression of greater than 20% slip can be reliably assessed.^68,⁶⁹

Degenerative Spondylolisthesis

Degenerative spondylolisthesis (DS), which is usually seen with an intact pars interarticularis, is related to degenerative changes of the apophyseal joints and/or intervertebral discs and is most common at the L4-5 and L5-S1 vertebral levels. Lumbar DS is a major cause of spinal canal stenosis and is often related to low back and leg pain.⁷⁰ Long-standing DS is almost invariably accompanied by disc and facet degenerative changes, which obscure the origin of the process. Discogenic DS and facetic DS cause secondary stress and stretch on the facet joints and disc spaces, respectively. The degree of sagittal listhesis is generally mild in DS relative to other types, particularly isthmic spondylolisthesis. There may be associated degenerative scoliosis and listhesis in nonsagittal planes. Type I end-plate changes, which may be more extensive and quite prominent on a STIR sequence, even without spondylolisthesis on static imaging, may represent segmental instability⁷¹ and can mimic discitis osteomyelitis, as discussed later (Fig. 172-11).

FIGURE 172-11 Degenerative spondylolisthesis and scoliosis. A, Grade I anterolisthesis at L3-4 and L4-5. Note high-grade stenosis at L4-5 with redundant nerve roots (arrow). B, Typical degenerative scoliosis with lateral listhesis.

Pseudarthrosis

Pseudarthrosis is more common in a postoperative spine and can occur at the fusion level (nonunion) or adjacent levels (transitional). The latter can also have noniatrogenic causes.

Nonunion of Bone Fusion

Nonunion is the result of failed spinal fusion. The failed fusion typically manifests with axial or radicular pain months to years after surgery. The common causes of this complication are inadequate surgical technique, excessive stresses across the fusion site, insufficient internal or external stabilization, and unrecognized metabolic abnormalities.⁷² Diagnosis is based on clinical presentation and imaging studies, after other causes of persistent pain are excluded.⁷³ The degree of fusion and associated motion seen on flexion-extension radiographs that is indicative of solid or failed fusion remains a point of controversy due to significant interobserver variations.⁷⁴ The choice of bone graft material can affect the radiographic assessment of interbody fusion. CT has higher contrast resolution and is therefore better than radiography for assessment of bone fusion. One of the main reasons for CT’s superiority is that premineralized osteoid may be functionally fused but radiographically lucent, therefore leading to underestimation on plain radiography. Bony arthrodesis is usually evident by 6 months, with evidence of bridging trabecular bone. Bridging bone is usually seen lateral to the implant and may also be noted within the implant itself. Mature solid fusion is generally present at between 12 and 24 months^75,⁷⁶ (Fig. 172-12).

FIGURE 172-12 Pseudarthrosis. A, Postoperative spine with well-formed L4-5 interbody fusion (black arrows) but pseudarthrosis at L5-S1 interbody fusion (white arrow). Note anti-kickout screw at L4-5 (curved arrow). B, Posterolateral fusion mass at L5-S1 with gross defect due to pseudarthrosis (arrow). C, Segmental pseudarthrosis through anterior and dorsal columns at a level just above the L2-3 and L3-4 interbody fusion (arrows). D, Similar segmental pseudarthrosis due to neuroarthropathy (Charcot spine, arrows).

Disc Space Failed Fusion

Failed fusion at the disc space manifests as lucency at the device margins or lucent lines through the fusion mass by about 18 to 24 months. Lucency around the fusion devices (e.g., cage or pedicular screws) represents abnormal motion and predicts delayed or failed fusion. Cystic change at the end plates adjacent to the implant is a reliable marker of failed fusion. Other signs include malpositioning and subsidence of the fusion devices ⁷⁴^–⁷⁶ (see Fig. 172-12).

Posterolateral Failed Fusion

Posterolateral failed fusion is divided into three types: Type I shows atrophy and resorption of the grafted bone; type II shows a lack in trabecular continuity of the fusion mass; and type III shows a gap either cranially or caudally between the fusion mass and lumbar matrix (which includes the transverse process and superior facet). CT is better than PR for diagnosing all types of posterolateral failed fusion, particularly type III ⁷⁷ (see Fig. 172-12).

Transitional or Segmental Pseudarthrosis

Segmental pseudarthrosis is usually secondary to transition of the mechanical loading to the adjacent level above the surgical fusion or fusion due to ankylosing spondyloarthropathies and advanced degenerative processes. Neuropathic spine (Charcot spine) can also result in segmental pseudarthrosis. The typical CT imaging pattern is lucency through the ventral and dorsal pillars in a transverse plane with or without associated spondylolisthesis. MRI shows corresponding hyperintense T2 (fluid) signal in the transverse plane defects and variable end-plate signal changes (see Fig. 172-12).

Intervertebral Disc Displacement (Disc Herniation)

Degeneration allows the disc to displace focally or diffusely in any direction beyond the end-plate margins of the disc space. The anulus fibrosus in a displaced disc tries to contain or limit the herniating nucleus pulposus. A variety of terms are used to describe disc displacement. See Figure 172-13 for diagrammatic representation of disc displacements.

FIGURE 172-13 Schematics of disc herniations. Diagrammatic representation of disc herniations. A, Sagittal illustration of normal disc, anular tear, and herniation of the nucleus pulposus. B, Focal disc herniation (<25% of the disc margin) and broad-based herniation (>25% of the disc margin). C, Difference between protrusion and extrusion in the axial plane. Note that the base of the protrusion is broader than the extent of the disc herniation beyond the margins of the disc. The extrusion, on the other hand, shows a greater extension beyond the disc margins than the width of the base.

Anular Disc Bulge

An anular bulge is a generalized extension, greater than 50% of the circumference of the disc tissues to a short distance (<3 mm) beyond the edges of the apophyses. A bulge is not a herniation; it is generally diffuse and may be asymmetrical. The latter usually occurs when associated lateral listhesis and scoliosis are present. The nucleus pulposus is contained by the anulus fibrosus. Grading of the disc bulging is subjective. Associated end-plate hypertrophy (spondylosis) may be present but is less prominent than in the cervical spine. Disc bulging may show crescentic calcification along its dorsal margin on sagittal CT (see Fig. 172-11A).

Intra-Anular Disc Displacement

Intra-anular disc displacement is the peripheral displacement of nuclear tissue into a fissure of the anulus. This is distinguished from disc herniation in that it does not extend beyond the disc space itself.

Protrusions

Protrusions are disc displacements in which the greatest distance in any plane between the edges of disc material beyond the disc space is less than the distance between the edges of the base in the same plane (neck is broader than dome). Protrusion is still contained by the anulus fibrosus fibers and therefore is not a true herniation. There may be an associated anular tear, which is usually evident on MRI as T2 hyperintensity, typically in the dorsal or dorsolateral disc protrusions. If the protrusion is less than 25% of the disc circumference, it is referred to as focal, and if between 25% and 50%, it is referred to as broad-based (Fig. 172-14).

FIGURE 172-14 Disc protrusion. Mild broad-based disc protrusion at L2-3 with moderate thecal sac compression; there is underlying developmental shortened pedicles (arrows, A and C). Right foraminal L3-4 disc protrusion (arrows, B and D).

Extrusions

Extrusions are disc displacements that are true herniations in which in at least one plane, any one distance between the edges of the disc material beyond the disc space, is greater than the distance between the edges of the base in the same plane (dome is broader than neck). Extrusions usually extend above or below into the suprapedicular or infrapedicular zone, resulting in further narrowing of the neck but still abutting the native disc. The signal intensity of the extruded portion may be increased on T2-weighted images. There may be associated curvilinear areas of decreased signal intensity on the T2-weighted images, which are related to torn portions of the anulus and posterior longitudinal ligament (Fig. 172-15).

FIGURE 172-15 Disc extrusion. Sagittal (A) and axial (B) T2 imaging showing small left central disc extrusion (arrows) with compression of left S1 nerve root, which cannot be discretely identified (grade III compression). Note intact right S1 nerve root and its sheath (arrow on the right in B).

Sequestration

Sequestration is displaced disc material that has completely lost any continuity with the parent disc. The extrusion is referred to as “migrated” if it has displaced from the site of extrusion, regardless of whether it is sequestrated. Sequestrated fragments can lie ventral to the posterior longitudinal ligament (especially if they have migrated behind the vertebral bodies where the posterior longitudinal ligament is not in direct opposition), dorsal to the ligament, rarely in the intradural or intraradicular space, and even in the dorsal extradural space.⁷⁸ Nevertheless, penetration almost invariably occurs through the posterior longitudinal ligament; either dorsal, where it is fused with the anulus, or rostrally or caudally, where it fuses with the vertebral body margin. In the majority of patients in whom sequestrated fragments migrate behind the vertebral body, the sequestration usually lateralizes, with disc material pushing across the midline and the leading edge being smoothly capped. It has been postulated that this shape is imposed by a midline septum in the ventral epidural space. This space is largest in the lower lumbar region and is delineated dorsally by the posterior longitudinal ligament and laterally attached membranes and ventrally by the vertebral body. It is divided into two compartments by a sagittally aligned septum. Sequestrated fragments within the lateral recess and the neural foramen have been shown to produce eroded cortical bone and expansion of those spaces and, thus, should be considered in the differential diagnosis of a mass arising and expanding the neural foramen and lateral recess. Intradural disc herniation is very rare, with few cases reported.^79,⁸⁰ It is most frequent in the lower lumbar spine. The mechanism is thought to be the development of chronic inflammation leading to adhesions between the dura mater and posterior longitudinal ligament. The appearance on axial MRI is described as a “hawk-beak sign.”⁸¹ As the herniated disc penetrates, the ligament extends through the dura instead of pushing it away. Other possible causes are congenital connections between the ligament and the dura or previous surgery (Fig. 172-16).

FIGURE 172-16 Sequestered disc. Sagittal T1 (A) and T2 (B) imaging shows left-sided sequestered disc with mild thecal sac compression. Note that extruded disc has lost contact with the bulging disc at L4-5 (arrows). C, Also note increased T2 signal in the herniated disc resulting in lesser conspicuity on axial T2 slice due to adjacent hyperintense fat (arrows).

FIGURE 172-17 A, Calcified herniated disc. Large disc extrusion at L2-3 with severe central spinal canal stenosis. Note isointense T1 and T2 signal to the native disc and expected mild rim enhancement. Surgery revealed a calcified rocklike herniated disc material. MRI was not helpful in predicting the calcified nature of the herniated disc. B, Calcified herniated disc and type III end-plate change. Advanced disc degeneration at L5-S1 with type III end-plate changes, shown as hypointense T1 and T2 signal and sclerosis on CT (anterior arrows). CT also shows a calcified extruded disc as also predicted on MRI due to T1 hyperintense signal (posterior arrow). Surgery revealed an epidural perineural mass–like structure. Biopsy was negative for neoplasm.

Imaging Characterization of a Disc Herniation

Disc herniation is not always clear-cut on imaging, and it may appear as a protrusion in one plane and an extrusion in another. If there is displacement away from the disc space in craniocaudal plane, it should be referred to as an extrusion. In the transverse plane, the disc abnormality is usually described as central, right, or left central, lateral recess, foraminal, or extraforaminal (lateral and far lateral). In the sagittal plane, the terms discal, infrapedicular, and suprapedicular are most commonly employed.

Containment refers to the integrity of the outer anulus covering the disc herniation. Imaging is not accurate in delineating containment of the nucleus pulposus. One may view the continuum of herniated disc disease as starting with anular disruption, proceeding on to small focal herniation that is not broken completely through the anulus-ligamentous complex to frank herniation (extrusion), which has dissected through the anulus and dorsal ligamentous complex completely. Disc herniations may show variable degrees of containment, and a line of decreased signal intensity has been reported around sequestrated fragments and large extruded discs where disruption of the anulus and ligament is clearly evident. This is thought to be secondary to anular and ligamentous fibers, which are carried away with the disc herniation. The anulus fibrosus and posterior longitudinal ligament are so intertwined at the level of the disc that a distinction between the two structures may be impossible or, for that matter, irrelevant. Technical limitations of CT and MRI usually preclude the distinction of a contained from an uncontained disc herniation.

Contrast enhancement is commonly seen as rim enhancement along the dorsal margin of disc herniation. Rarely, the disc herniation is diffusely enhanced, and it may be difficult to differentiate from epidural scarring in a postoperative spine.

Hyperintense zone (HIZ) in a disc has been used in correlative studies of MR and provocative discography. This nonstandard term generally represents anular tears.^82,⁸³

Compression of the nerve root within its sleeve may not correlate with patient symptoms. A grading system by Pfirrmann et al.⁸⁴ had significant reliability and surgical correlation:

Grade 0 (normal): No contact of disc material with the nerve root.

Grade 1 (contact): Visible contact of disc material with the nerve root and loss of the epidural fat layer between the two.

Grade 2 (deviation): The nerve root is displaced dorsally by disc material.

Grade 3 (compression): The nerve root is compressed between disc material and the wall of the spinal canal; it may appear flattened or be indistinguishable from disc material (see Fig. 172-15B).

A herniated disc may be densely calcified, which may not be easily predictable on preoperative MRI. An isointense to hyperintense T1 signal can be helpful in such cases. CT clearly demonstrates calcification of disc herniation and ossification of the posterior longitudinal ligament (Fig. 172-17).

Intravertebral Disc Herniations (Also Known as Schmorl Nodes)

Nonacute Schmorl node (SN) intrabody herniations are common spinal abnormalities regarded as incidental observations. They have been reported in 38% to 75% of the population.^85,⁸⁶ Most intrabody herniations probably form after axial loading trauma, with extrusion of nuclear material through the vertebral end plate, resulting in reactive bone marrow edema. Another theory is that Schmorl nodes are the end result of ischemic necrosis beneath the cartilaginous end plate, with secondary herniation into the body of the vertebra.⁸⁷ SNs are mostly well defined and have an isointense intrinsic T1/T2 signal to the disc.⁸⁸ SNs have been traced to episodes of significant, sudden-onset, localized, nonradiating back pain and tenderness. Wagner et al.⁸⁹ showed in symptomatic patients that 57% of cases on MRI had SNs surrounded by vertebral body marrow edema. The remaining nodes (43%) were not immediately apparent as SNs and manifested only as vertebral body edema, suggesting end-plate fracture, but did evolve into classical chronic SNs as revealed on follow-up imaging.⁸⁹ Contrast enhancement demonstrated vascularized SNs, with a higher incidence of surrounding edema. They are more common in symptomatic patients.^90,⁹¹ A concentric hypointense ring appearance has a high negative predictive value for the absence of underlying fracture, infection, or malignancy.⁸⁸ Giant cystic SNs have been described by Hauger et al.⁹² as a clinicoimaging entity in a small series of six cases (Fig. 172-18; and see also Fig. 172-5).

FIGURE 172-18 Schmorl node. Ill-defined hypointense T1 (A) and hyperintense T2 (B) reactive marrow changes (arrows) around Schmorl node at L4 inferior end plate. The signal alteration is similar to type I end-plate change. C, Note sclerosis along the margin of the Schmorl node. Also note hypointense rim of the node (B). D, Another patient with well-defined hyperintense T2 signal around the Schmorl node (arrow).

Although consistent terminology is important for communication, it is not at all clear whether or not these categories of descriptive findings of disc herniations are clinically relevant. Although it has been proposed that it is critical to differentiate between various degrees of herniation, the reality is that disc herniation most likely represents a spectrum or continuum rather than discrete entities with specific clinical relationships. Therefore, the term herniation has been interchangeably used in the literature with protrusion, extrusion, and sequestration.

Spinal Canal and Foraminal Stenosis

Spinal stenosis refers to any type of narrowing of the spinal canal, nerve root canals, or intervertebral foramina.⁹³ Two broad groups have been defined: (1) acquired (usually related to degenerative changes) and (2) congenital or developmental. Developmental stenosis can be exacerbated by superimposed acquired degenerative changes. In the acquired type, there has been no association between the severity of pain and the degree of stenosis. The most common symptoms are sensory disturbances in the legs, LBP, neurogenic claudication, weakness, and relief of pain by bending forward. Clinical stenosis is perhaps a better term than spinal stenosis (as diagnosed on imaging studies). The imaging changes are in general more severe than expected from the clinical findings.⁹⁴ Although there does appear to be a correlation between cross-sectional area and midsagittal measurements in patients with symptomatic spinal stenosis, measurement of canal stenosis is not generally used.³⁹