Degenerative Disease

10.1055/b-0034-102687

Degenerative Disease

Degenerative Spinal Stenosis

Degenerative spinal stenosis can be central, subarticular (lateral recess) in location (the space between the posterior margin of vertebral body and the anterior margin of superior facet, bounded by the thecal sac medially and the pedicle laterally), or foraminal. Degenerative disease anteriorly (a disk bulge with or without accompanying osteophyte), posteriorly due to ligamentum flavum buckling or thickening, and posterolaterally due to facet joint hypertrophy can all contribute to spinal canal stenosis. In the lumbar spine, it is very common to have all three elements contributing ( Fig. 3.69 ).

The ligamenta flava are paired, thick ligaments (predominantly composed of elastic fibers) that connect the lamina of adjacent vertebral bodies. They extend from the anteroinferior aspect of the superior lamina to the posterosuperior aspect of the inferior lamina. The ligamenta flava increase in thickness normally from the cervical to the lumbar regions. They are situated posterolaterally in the canal, and anterolaterally are contiguous with the capsule of the facet joint. In degenerative disease, the ligamentum flavum becomes visibly thickened, and thus may cause narrowing of either the lateral recess or spinal canal. In regard to facet joint hypertrophy, hypertrophy of the superior articular facet is a primary cause of lateral recess stenosis, and resulting nerve compression. Epidural lipomatosis is simply excessive fat deposition in the epidural space. It is seen in chronic steroid use and in morbid obesity, and is usually thoracic and lumbar in distribution. It is reported that patients can become symptomatic, due to compression of the thecal sac.

The neural foramen is bounded by the pedicles superiorly and inferiorly, the vertebral body and disk anteriorly, and the facets posteriorly. Nerve roots exit from the thecal sac, pass through the lateral recess, and enter the neural foramen. Degenerative disease of the disk, endplates, and facets can all contribute to neural foraminal narrowing ( Fig. 3.70 ).

**Fig. 3.70** Degenerative neural foraminal narrowing, lumbar spine. On sagittal imaging at L5–S1, a disk osteophyte complex extends posteriorly and obliterates the inferior portion of the neural foramen, resulting in compression of the L5 nerve (*arrow*). Note the lack of normal fat (circumferential to the nerve), which is obliterated in both the anteroposterior or superoinferior dimensions. At L4–5, one level above, a similar process is seen, but less severe with only mild compromise of the neural foramen, with fat preserved both anteriorly and inferiorly to the nerve.

Imaging of the neural foramina, specifically for evaluation of narrowing, is best performed in the sagittal plane, but more specifically in the true cross-section to the foramen. In the lumbar spine, direct sagittal imaging approximates this plane. However, in the cervical spine, acquisition (or reconstruction) of planes that are oblique in two dimensions are necessary. This is required due to the course of the neural foramina in the cervical spine, which is both anterolateral and superoinferior. Neural foraminal narrowing in the lumbar spine, as viewed on the basis of sagittal MR, is specifically assessed by evaluation in both the craniocaudal and AP directions for perineural fat obliteration, and (for the most severe disease) by direct nerve root compression or morphologic change. Evaluation of foraminal stenosis should thus include a description of the specific fat planes that are obliterated, together with any changes in morphology of the nerve itself (due to compression). Although degenerative neural foraminal narrowing is commonly seen in patient exams, the correlation between clinical symptomatology and MR imaging appearance is generally poor.

Disk, Endplate, Foraminal, and Spinal Canal Disease

Cervical Spine

The cervical spine is most mobile at C4–5, 5–6, and 6–7, with most disk herniations occurring at these levels. The age of presentation is commonly the third to fourth decades. MR is the examination of choice. Thin section axial gradient echo T2-weighted scans are critical for diagnosis, supplemented by sagittal imaging. A very thin rim of low signal intensity can often be visualized on axial T2-weighted scans along the posterior aspect of the disk (in both normal patients and in the presence of a herniation), corresponding to the dura, volume averaged together with the posterior longitudinal ligament. Thin section post-contrast axial T1-weighted scans are usually not acquired in patients with radiculopathy; however, these do substantially improve visualization of foraminal disk herniations due to enhancement of the epidural venous plexus. In the cervical spine, the normal epidural venous plexus is prominent, and can be dilated adjacent to a disk herniation. Foraminal disk herniations in particular can be difficult to visualize, due to the relative isointensity of the disk to epidural venous plexus on axial gradient echo T2-weighted scans.

Symptoms from an acute cervical disk herniation can be radicular, due to a posterolateral or foraminal location ( Fig. 3.71 ), or myelopathic, with large central herniations. On high-resolution thin section axial gradient echo T2-weighted scans, the dorsal and ventral nerve roots, as they exit from the cervical cord, can be identified. Paired denticulate ligaments can also be commonly identified, interposed between the nerve roots. These consist of triangular ligament extensions with a broad base along the lateral margin of the cord and their apex attaching laterally to the dura.

**Fig. 3.71** Foraminal disk herniation, cervical spine (sagittal plane). Close inspection of sagittal images can substantially improve detection of foraminal herniations, which may otherwise go unrecognized. A C6–7 disk extrusion, foraminal in location, is easily identified in this patient both on T2- (*arrow*) and T1-weighted off-midline sagittal images. Oblique foraminal views offer a further improvement in depiction and detection of cervical foraminal disease, although unfortunately not performed by most sites.

As previously discussed, but worth repeating, there are seven cervical vertebrae and eight cervical nerves, C1–C8. The cervical nerves exit through the foramina above the corresponding numbered vertebrae, with C8 exiting in the foramen below the C7 vertebra. Thus, a posterolateral or foraminal disk herniation at C6–7 will cause compression of the C7 cervical nerve. Knowledge of the cervical dermatomes is important for correlation of clinical symptoms with anatomic findings, with pain diagrams distributed commonly to patients prior to the exam in many clinics. These are also very helpful in the thoracic and lumbar spine. The anatomic distribution of C6, C7, and C8 is easy to remember, with the C7 distribution including the middle finger, C6 including the thumb, and C8 including the fourth and fifth fingers.

An acute cervical disk herniation will be visualized as an anterior (or anterolateral or foraminal) epidural soft tissue mass ( Fig. 3.72 ). Close inspection of the cervical foramina is mandated, since a disk herniation in this position ( Fig. 3.73 ) is often much less evident than those that are central or paracentral in location. The abnormal soft tissue will be contiguous with the disk space, with the only exception being that of a free disk fragment. It should be noted, however, that the majority of free disk fragments will lie immediately adjacent to, and be inseparable from, the native disk. Disk herniations have signal intensity similar to, on both T1- and T2-weighted scans, the native disk. The focal nature of a disk herniation is used to differentiate this process from a disk bulge, with the latter often defined as a process involving 180 degrees or more of the disk circumference. In older patients, and those also involved long term in activities associated with marked motion of the cervical spine, asymptomatic chronic disk herniations are commonly observed ( Fig. 3.74 ).

**Fig. 3.72** Central and paracentral disk herniations, cervical spine. Sagittal and axial images reveal presumed acute (recent) disk herniations at C3–4 and C5–6. Note the relative absence of associated osteophytes on the sagittal images. The herniation at C3–4 is central in location, that at C5–6 paracentral with some extension into the foramen on the left. Both disk herniations are likely extrusions on the basis of the sagittal images.

**Fig. 3.73** Foraminal disk herniation, cervical spine (axial plane). Foraminal disk herniations in the cervical spine may be difficult to detect, due to isointensity with the venous plexus within the neural foramen on gradient echo T2-weighted scans. Careful image inspection, including all sequences and planes, is mandatory, together with a high sensitivity to abnormal soft tissue (disk material) within the foramen. In this instance, the disk herniation with high signal intensity (*arrow*) on the gradient echo T2-weighted scan and intermediate signal intensity on the corresponding T1-weighted scan is relatively well visualized. Although seldom used in this application, post-contrast scans allow exquisite visualization of cervical foraminal disk herniations, which appear as nonenhancing soft tissue easily differentiated from the intense enhancement of the abundant venous plexus.

**Fig. 3.74** Chronic central disk herniation, cervical spine. Asymptomatic small and large chronic cervical disk herniations are a common finding on screening MR examinations. Illustrated is one such small central disk herniation. Without inspection of axial images above and below, or the sagittal images for accompanying osteophytes, it is not possible to confirm such a herniation as either acute or chronic. There is mild associated cord flattening. Note that the central “H” of gray matter is well identified with higher signal intensity than more peripheral white matter on this axial gradient echo T2-weighted scan obtained at 3T.

Although often difficult in an individual patient to differentiate from an acute disk herniation, the presence of associated bony spurs extending from the vertebral body endplates can be used to identify a chronic disk herniation ( Fig. 3.75 ). These bony spurs occur due to bone remodeling, with elevation of the periosteum by a disk herniation and subsequent bone deposition. Myelopathic symptoms are more common with chronic disk herniations, with radicular symptoms common in acute disk herniations ( Fig. 3.76 ).

**Fig. 3.75** Disk herniation, chronic, cervical spine. The presence of an osteophyte just superior or inferior to a disk herniation, often visualized best on sagittal images, implies that the herniation is chronic. On the axial gradient echo T2-weighted scan, at C5–6, a left paracentral and foraminal herniation is visualized with high signal intensity disk material surrounded by a thin low signal intensity rim. This herniation is bordered superiorly by a prominent osteophyte (*small black arrow*), visualized both on the sagittal FSE T2-weighted scan and—as low signal intensity (*white arrow*)—on the axial gradient echo T2-weighted scan, covering the high signal intensity disk material immediately below.

**Fig. 3.76** Chronic cervical disk herniation with cord compression and signal abnormality. The chronic herniation seen on FSE (upper) and gradient recalled echo (GRE) (lower) T2-weighted images severely narrows the neural foramen on the right. There is moderate narrowing of the foramen on the left, degenerative in nature and unrelated to the disk herniation. The cord is deformed (compressed), with focal abnormal high signal intensity (*small white arrows*) consistent with gliosis seen on both scans.

Hypertrophic endplate spurs, also referred to as diskosteophyte complexes, are commonly seen on both MR and CT, and are typically asymptomatic. Given how frequent these are—most older patients have at least mild multilevel disease—it is not surprising that these do not correlate well with symptoms. Disk-osteophyte complexes are felt to be the end result of a disk bulge, which is defined as circumferential expansion of the disk, specifically greater than 180 degrees (and not focal, as with a chronic disk herniation). In many instances the chronic nature of this process can be identified on MR, due to the presence of associated broad based osteophytes (which manifest low signal intensity on all MR sequences) ( Fig. 3.77 ).

**Fig. 3.77** Mild cervical degenerative findings. There is reversal of the normal cervical lordosis. Minimal disk osteophyte complexes are noted at C4–5, C5–6, and C6–7. There is mild to moderate flattening of the cord (versus its normal elliptical appearance in cross-section), at the C4–5 level, a finding well seen on axial images.

These osteophytes are well identified on CT, albeit the associated disk bulge is often poorly visualized. One special area of note in the cervical spine involves the uncovertebral joints. These small synovial lined joints (also known as the joints of Luschka) lie between the uncinate processes of the lower cervical vertebrae posteriorly and laterally, and allow for flexion and extension, while limiting lateral flexion. Uncovertebral joints are present from C3 to C7, with encroachment upon the foramina anteriorly due to degenerative involvement occurring from C2–3 to C6–7. Hypertrophy of the uncovertebral joint is not uncommon in older patients, often asymmetric when comparing side to side and, together with facet osteoarthritis (posteriorly), causes foraminal narrowing in the AP dimension ( Fig. 3.78 ). Disk space narrowing is an additional cause of foraminal narrowing, decreasing the height of the neural foramen, with the end result of all these factors being nerve root compression.

**Fig. 3.78** Uncovertebral hypertrophy. Degeneration of the uncovertebral joint is common, leading to a broad osteophyte (*) in a characteristic position, as illustrated on axial CT. This process can lead both to foraminal narrowing and mild effacement of the thecal sac, the latter in a paracentral location.

Degenerative foraminal narrowing is common in older patients. The bony encroachment of the foramina is well visualized on CT, with sagittal reformatted images important in this regard. On CT it is readily evident that the osteophyte commonly extends into the mid-portion of the foramen, dividing the foramen into an upper and lower portion. Keeping this in mind, it is not surprising that, on thin section axial MR images, depiction of the foramen can be limited and misleading. With a large osteophyte lying in the mid-portion of the foramen, unless axial imaging is performed with very thin sections, partial volume imaging will lead to poor visualization of the encroachment. In the cervical spine, the standard MR sequences used for evaluation of the neural foramina include thin section T2*-weighted gradient echo imaging in the axial plane ( Fig. 3.79 ) and fast spin echo T1- and T2-weighted imaging in the sagittal plane. Due to the anterolateral, and slight inferior, course of the neural foramina, oblique sagittal images are, however, best for visualization of the foramina on MR, and should be routinely acquired.

**Fig. 3.79** Degenerative neural foraminal narrowing, cervical spine. On this gradient echo axial T2-weighted scan, the right neural foramen is widely patent, with moderate neural foraminal narrowing on the left. Mild facet osteoarthritis and disk degenerative disease (an osteophyte) contribute in this instance to the foraminal narrowing.

Ossification of the posterior longitudinal ligament is an uncommon cause of acquired cervical spinal stenosis. There is an increased incidence in Asian patients, in particular Japanese. Other, more common etiologies of cervical spinal stenosis include ligamentous infolding and facet joint hypertrophy. As with all cases of spinal stenosis, patients are at greater risk for traumatic spinal cord injury. The posterior longitudinal ligament is prominent, with low signal intensity on both T1- and T2-weighted scans ( Fig. 3.80 ), and in some instances with intermediate signal intensity centrally within focally prominent areas of ligamentous infolding. Involvement is multilevel and can be continuous or segmental. Spinal cord compression is seen with more prominent disease involvement.

**Fig. 3.80** Ossification of the posterior longitudinal ligament. There is multilevel effacement of the thecal sac, with cord compression, most prominent at C2–3 and C4–5. Axial imaging well depicts the densely ossified posterior longitudinal ligament (with low signal intensity on both T2- and T1-weighted scans), which at the level illustrated (C2–3) produces marked cord deformity and moderate to severe central spinal canal stenosis.

Degenerative (acquired) spinal stenosis, previously discussed in general terms, is caused by advanced degenerative disk disease, with the latter process also referred to by the term spondylosis ( Fig. 3.81 ). Contributing factors include decreased disk height with thickening and buckling of the intraspinal ligaments, prominence of the posterior longitudinal ligament and ligamentum flavum, disk bulges, herniations, and osteophytic spurs (anterior to the thecal sac), and hypertrophy of the facet joints (posterior to the thecal sac). Symptom onset is skewed toward the older population, and to some degree thus differentiated from acute disk herniations. Symptoms are myelopathic and include progressive/intermittent numbness, weakness of the upper extremities, pain, abnormal reflexes, muscle wasting (involving the interosseous muscles of the hand), and staggering gait. Although commonly not quantified, defined measurements are established for spinal stenosis, with evaluation best on axial images. Normal is defined as > 13 mm, borderline being 10 to 13 mm (these patients may experience symptoms), and < 10 mm diagnostic of cervical spinal canal stenosis. The most commonly affected levels are C4–5, 5–6, and 6–7, with multilevel involvement common. In mild spinal canal stenosis the ventral subarachnoid space will be effaced. With more severe disease there will be cord flattening. In advanced disease, myelomalacia, specifically edema, gliosis, and cystic changes can be present.

**Fig. 3.81** Moderate to severe cervical spondylosis. Osteophyte distribution within the cervical spine directly varies with spinal axis mobility. The more mobile lower cervical spine is affected initially with superior spread as disease worsens. Exams from two patients are illustrated, with the first demonstrating moderately advanced degenerative disease with disk osteophyte complexes at the C3–C7 levels. The osteophytes in this instance result in mild central spinal canal stenosis—note the lack of CSF surrounding the cord at the involved levels. In the second patient, there is severe central spinal canal stenosis at C4–5. An osteophyte compresses the thecal sac, obliterating the CSF space both anterior and posterior to the cord, and markedly flattens the cord. Additional common degenerative findings, present in this patient, include disk space height loss at the C4–5 and C5–6 levels and a slight anterolisthesis of C2 on C3.

Thoracic Spine

Disk herniations in the thoracic region are less common, as compared to their counterparts in the cervical and lumbar regions. Clinically, radicular symptoms with a dermatomal distribution may be seen ( Fig. 3.82 ). From published literature series, symptomatic thoracic disk herniations are most commonly present in the lower thoracic spine, from T9–10 to T11–12. Acute cord compression with myelopathy is rare.

**Fig. 3.82** Thoracic disk herniation, definitive vertebral body count, and level localization. Modern MR scanners can provide rapidly a sagittal scout of the entire spine, as illustrated. High-resolution images can also be fused from the cervical, thoracic, and lumbar regions, a process known as image composing. This has the advantage of definitive identification of vertebral body count. In the example shown, disk herniations are seen at T10–11 and T11–12, with a high-resolution axial image of the left paracentral disk herniation at T11–12 also presented. Note the mild deformity/flattening of the adjacent cord. Prior to the availability of these techniques, definitive vertebral body identification was often not possible on MR in the thoracic spine, due to the absence of a true count from C1, and in the lumbar spine due to the relatively high incidence of transitional vertebrae (and difficulty thus in defining the L5–S1 level).

The imaging evaluation of thoracic disk herniations is the province of MR. Diagnosis requires thin sections with high image quality, and specifically implementation of strategies to minimize motion artifacts due to the heart, respiration, and CSF pulsation ( Fig. 3.83 ). With excellent image quality, sensitivity is high even to very small disk herniations. In the past, specific level localization on MR was difficult; however, today, high-quality sagittal scout images of the cervicothoracic region can be acquired, with these mandatory for correct level identification (see Fig. 3.82).

**Fig. 3.83** Small central thoracic disk herniation, pitfalls of imaging technique. A small central disk herniation is seen in the midthoracic spine on thin section (3-mm) sagittal and axial T2-weighted FSE images, a standard imaging approach at both 1.5T and 3T. Such findings are commonly incidental, representing chronic small disk herniations without any clinical correlate, although in any one case it cannot be determined whether the lesion is acute or chronic. However, detection by the radiologist demands close attention to and inspection of the images, given that the lesion is small and that CSF pulsation artifact leads to an inhomogeneous appearance to adjacent CSF (CSF “flow voids”), in particular on axial scans.

There is a high incidence of chronic asymptomatic small thoracic disk herniations on routine MR imaging ( Fig. 3.84 ). Deformity of the cord contour is also common, often in the absence of any clinical symptoms and occurring even with very small herniations. In this regard it should be kept in mind that the MR evaluation is performed in only one position (supine), and is not physiologic, with disk herniations when the patient is upright, and particularly in flexion, likely causing impact upon nerves and the cord not seen by MR.