DEGENERATIVE SPINE DISEASE
John R. Hesselink, MD, FACR
Degenerative spine disease is a major cause of chronic disability in the adult working population and a common reason for referral to an MR imaging center. Spinal degeneration is a normal part of aging, and neck and back pain are one of life's most common infirmities. There are many potential sources of pain, and finding the specific cause is often a confounding problem for both patient and doctor. Pain can originate from bone, joints, ligaments, muscles, nerves and intervertebral disks, as well as other paravertebral tissues. The landmark article by Mixter and Barr in 1934 on the ruptured intervertebral disk provided an anatomic basis for selected cases of back pain and neurologic dysfunction. Most neck and back pain responds to conservative therapy, but if the pain is unrelenting, severe, or associated with a radiculopathy or myelopathy, imaging is indicated to look for a treatable cause.
In the evaluation of degenerative spine disease, multiple anatomic sites need to be imaged, including the intervertebral disk, spinal canal, spinal cord, nerve roots, neuroforamina, facet joints, and the soft tissues within and surrounding the spine. Many pulse sequences are available, and specific protocols vary among different MR sites. There is general agreement that the spine needs to be imaged in at least two planes, and surface coils are used almost exclusively. In the cervical and thoracic regions a T2-weighted sequence is mandatory to assess damage to the spinal cord. Thin sections are required to visualize the neuroforamina, and pulse sequences must be tailored to counteract CSF flow and physiologic motion. The imaging requirements for the lumbar spine are less strenuous because the anatomical parts are larger. Most protocols include a T1-weighted sequence and some type of T2-weighted sequence to give a myelographic effect. Fast spin-echo (FSE) techniques allow enormous time savings, and if available, they have replaced conventional spin-echo for T2-weighted imaging of the spine. Three-dimensional gradient-echo (GRE) methods can achieve slice thicknesses less than one millimeter, an advantage for displaying cervical neuroforamina.
In the postoperative spine, gadolinium injection with T1-weighted imaging is essential to evaluate enhancing lesions. Fat-suppression is helpful to eliminate competing fat signal from bone marrow and other soft tissues.
INTERVERTEBRAL DISK DISEASE
The normal intervertebral disk consists of the nucleus pulposus surrounded by the anulus fibrosus. Both the anulus and the nucleus are composed of collagen and proteoglycans (chondroitin-6-sulfate, keratan sulfate, hyaluronic acid, and chondroitin-4-sulfate). The nucleus contains relatively more proteoglycans to give it a looser gelatinous texture. It blends in with the surrounding anulus without clear anatomic demarcation. The anulus has more collagen, and the collagen becomes progressively more compact and tougher at the periphery. The outer anulus is attached to the adjacent vertebral bodies at the site of the fused epiphyseal ring by Sharpey's fibers and to the anterior and posterior longitudinal ligaments. Normal disks are well hydrated, the nucleus containing 80 to 85% water and the anulus about 80%. Together with the cartilaginous end plates of the adjacent vertebral bodies, the intervertebral disk forms a disk complex that gives structural integrity to the interspace and cushions the mechanical forces applied to the spine.
With aging, certain biochemical and structural changes occur in the intervertebral disks. There is an increase in the ratio of keratan sulfate to chondroitin sulfate, and the proteoglycans lose their close association with the disk collagen. The disk also loses its water-binding capacity and the water content decreases down to 70%. These changes are reflected by a 6% decrease in MR signal intensity over a span of 79 years. The vertebral end plates also becomes thinner and more hyalinized. This degree of disk degeneration is considered a normal part of aging.
With more advanced degeneration, dense disorganized fibrous tissue replaces the normal fibrocartilaginous structure of the nucleus pulposus, leaving no distinction between the nucleus and anulus fibrosus. Development of anular tears weakens the anulus and allows nucleus to protrude into the defect. Tears that extend through the outer anulus induce ingrowth of granulation tissue and accelerate the degenerative process. Advanced degeneration can lead to gas formation or calcification within the disk. Also, fissures develop in the cartilaginous end plates, and regenerating chondrocytes and granulation tissue form in the area.
Desiccation - loss of disk water
Disk bulge - circumferential enlargement of the disk contour in a symmetric fashion
Protrusion - a bulging disk that is eccentric to one side but < 3 mm beyond vertebral margin
Herniation - disk protrusion that extends more than 3 mm beyond the vertebral margin
Extruded disk - extension of nucleus pulposus through the anulus into the epidural space
Free fragment - epidural fragment of disk no longer attached to the parent disk
Patients with lumbar disk disease can present with back pain or a radicular pain syndrome. The classic sciatic syndrome consists of stiffness in the back and pain radiating down to the thighs, calves and feet, associated with paresthesias, weakness, and reflex changes. The pain from intervertebral disk disease is exacerbated by coughing, sneezing, or physical activity. Pain is usually worse when sitting, and with straightening or elevating the leg. Disk herniations occur most often at the lower lumbar levels - 90% at L4-5 and L5-S1, 7% at L3-4, and remaining 3% at the upper 2 levels.
One of the earliest signs of disk degeneration is loss of water content or desiccation, most noticeable in the nucleus pulposus. MR can detect early disk degeneration because, as the disks lose water, the MR signal decreases on gradient-echo and T2-weighted images. With more advanced degeneration, the disk collapses and gas may form within the disk. Calcification is not uncommon in chronic degenerative disk disease.
As a consequence of intervertebral disk degeneration, normal axial loading on the spine stretches and lengthens the anular fibers, resulting in rounded, symmetric bulging of the disk beyond the margins of the vertebral body. A bulging disk encroaches on the ventral spinal canal and inferior portions of the neuroforamina but does not displace or impinge the nerve roots. The combination of sagittal and axial views provides excellent visualization of the relationships of the disk to the spinal canal and neural foramina. When there is a generalized paucity of epidural fat, producing an MR "myelogram" with gradient-echo or T2-weighted images is helpful to show the relationship of the disk with the thecal sac.
In an anatomic and MR study of cadaveric spines, Yu and colleagues found three types of anular tears in degenerated disks. Concentric tears (Type I) are caused by rupture of the short transverse fibers connecting the lamellae of the anulus, and were seen as crescentic or oval spaces filled with fluid or mucoid material. In radial tears (Type II) the longitudinal fibers are disrupted through all layers of the anulus, from the surface of the anulus to the nucleus. Transverse tears (Type III) result from rupture of Sharpey's fibers near their attachments with the ring apophysis, and are imaged as irregular fluid-filled cavities at the periphery of the anulus.
Anular tears are depicted on MR scans as small focal areas of hyperintensity on sagittal T2- weighted images. Transverse tears are located at the periphery of the anulus adjacent to the vertebral margins. Radial tears tend to be more irregular and obliquely oriented. High-signal- intensity zones on T2-weighted MR images are commonly seen along the posterior margin of degenerated disks in asymptomatic patients. The high-signal-intensity does not imply acute disk disruption, and no association with trauma has been proven. They probably represent small transverse or concentric tears in the outer annular fibers
Complete disruption of the anulus exposes the nuclear material to the epidural tissues, inducing a focal inflammatory reaction. Vascular granulation tissue forms and grows into the disk through the anular tear. Enhanced MR images will detect more anular tears than T1 or T2-weighted images - mostly radial tears, but also a few transverse tears.
Degeneration of the intervertebral disk has secondary effects on the adjacent vertebral end plates and bone marrow. As discussed earlier in the section on pathophysiology, fissures develop in the cartilaginous end plates in concert with disk degeneration. Vascular granulation tissue grows into the fissures and induces an edematous reaction and vascular congestion in the adjacent bone marrow. Modic's group has classified the bone marrow changes according to the signal intensity on MR images. This first reaction of bone marrow edema and vascular congestion, called Type 1 change, is hypointense on T1 and hyperintense on T2-weighted images. Type 1 change routinely enhances with gadolinium and can simulate osteomyelitis. With time, the bone marrow converts to a predominantly fatty marrow (Type 2 change). Longitudinal studies have shown this fatty marrow replacement to be stable over a 2-3 year period. Type 2 change is hyperintense on T1 and isointense to hypointense on T2-weighted images, the exact signal intensity dependent on the degree of T2-weighting. Chronic disk disease leads to dense sclerosis of the vertebral end plates and adjacent vertebral bodies (Type 3 change). Conversion from Type 1 to Type 3 change generally requires a few years time. Type 3 change is reflected on the MR images as hypointensity on both T1 and T2-weighted images.
Any radial tear of the anulus is a potential site for herniation of the nucleus pulposus. On the sagittal view, dissection of nucleus pulposus through radial tears of the anulus is clearly depicted. Defects in the anulus with disk extending posteriorly are indicative of protrusion/herniation. In the sagittal plane, a herniated disk has an hourglass appearance along the posterior disk margin, which is described as a "squeezed toothpaste" effect. Axial scans show either asymmetry of the posterior disk margin or a soft-tissue mass displacing adjacent intraspinal structures.
Most disk herniations occur in a posterolateral direction into the spinal canal because the tough posterior longitudinal ligament is thicker and tougher in the middle and resists posterior extension near the midline. A herniated disk usually impinges on the nerve root as it courses inferiorly toward the foramen at the next lower level. For example, an L4-L5 herniated disk impinges on the L5 root. The L4 root is likely unaffected unless there is lateral and cephalad migration of a free fragment into the neural foramen.
The neural foramina are visualized on parasagittal images of the lumbar spine, and disk herniation can be detected by obliteration of foraminal fat. Nevertheless, axial MR is better for visualizing lateral disk herniations. Lateral disks compress the nerve root within the foramen or just beyond its lateral margin distal to the nerve root sheath.
In the lumbar region, Ross's group found marked enhancement, distinct from epidural venous plexus, surrounding disk herniations. Histology disclosed peridiskal scar tissue similar to the epidural scar observed in postoperative patients. The depth of penetration of the scar depends on how long the disk fragment has been in the epidural space. The vascular scar tissue is a part of the body's repair mechanism to resorb and remove the offending disk material. Over time, the entire disk fragment may be resorbed.
When an extruded disk loses its attachment to the parent disk, it becomes a free fragment or sequestration. If the disk fragment is near an interspace, sometimes it can be difficult to discern whether or not a pedicle of attachment remains. Free fragments can migrate some distance cephalad or rostral to the disk space, and it is important to alert the surgeon to their precise location. Rarely, a disk fragment may rupture through the thecal sac into the intradural compartment.
Most sequestered disks are higher signal than their disk of origin on T2-weighted images. The cause for this is unclear, but it may be due to increased water from granulation tissue, immune response, and inflammation. Chronic disk herniations tend to be hypointense due to loss of water content.
Subligamentous disk fragments are contained by the posterior longitudinal ligament (PLL). Schellinger and colleagues reviewed the anatomy of the PLL and anterior epidural space. Most contained disk fragments lateralize to either side of the anterior epidural space. An equal number migrate superiorly and inferiorly. The PLL has a high collagen content and is hypointense on MR. It can be seen as a thick dark line covering a contained herniated disk, usually seen best on sagittal images. The posterior margin of contained disk fragments usually maintain a smooth contour.
Non-contained disk fragments have gone through the PLL. Either interruption or absence of the peripheral dark line suggests disruption of the PLL. Once through the PLL, the disk fragments are not bounded by any membranes, and they tend to have more irregular contours.
Effect on Nerve Roots
The most direct effect on the nerve root is from compression by the herniated disk, but the disk need not compress the nerve root directly to cause radicular pain. Fragments of nucleus pulposus within the epidural space induce a focal inflammatory reaction that can secondarily irritate the adjacent nerve root.
In a study by Jinkins, nerve root enhancement was observed in 5% of patients scanned for back or leg pain. Of that group, 70% had disk protrusion and a radicular pain pattern in the distribution of the enhancing root. The other 30% without protruding disk had multiple enhancing roots, suggesting an idiopathic low-grade inflammation. Lane's group reported that multilevel nerve root enhancement, especially when continuous from the root sleeve cephalad toward the conus, is often asymptomatic and not associated with any nerve root compression. The continuous enhancement probably represents radicular veins.
Significance and Natural History
The determination of clinically significant disk disease is an important radiologic and clinical decision because the possible consequences of back surgery are not insignificant. Identification of nerve root compression or severe effacement of the thecal sac, especially ventrolaterally, that correlates with radicular pain or a muscle weakness pattern supports the operative approach when conservative medical therapy has failed. But beyond that, things are less certain. Annular tears and focal disk protrusions are frequently found in asymptomatic populations. The annuloligamentous complex is richly innervated by the recurrent meningeal nerve. Annular tears involving this complex may be a source of diskogenic pain due to exposure of the nerve endings to the acid metabolites of the protruding nucleus pulposus.
Jensen and his group detected MR signs of intervertebral disk disease, consisting of bulge, protrusion, or extrusion, in 64% of asymptomatic adult subjects. Moreover, disk herniation does not relate directly to back pain or a radicular pain syndrome. In a study by Boden and colleagues, lumbar disk herniations were found in 28% of asymptomatic patients over 40 years of age.
Furthermore, patients with symptomatic disk herniations don't necessarily require surgery. Bozzao and colleagues followed 69 patients with herniated lumbar disks for 6 to 15 months while they were under conservatively medical therapy. On follow-up MR imaging, 63% showed a reduction in size of their herniated disk of more than 30%, 48% showed a reduction of more than 70%, and only 8% got worse or enlarged. Larger herniations were more likely to decrease, which they attributed to more vascularity or granulation tissue. The excellent depiction of abnormal morphology by MR imaging provides an opportunity to investigate further the natural history of intervertebral disk disease.
Cervical disk disease occurs most commonly at the levels of C5-6 and C6-7. A central disk herniation will most likely cause a myelopathy due to cord compression, along with neck pain and stiffness. If the disk extends laterally to compress nerve roots, the pain may radiate to the shoulder, arm, or hand.
A sagittal T1 study shows the margins of the spinal cord with respect to other structures within the spinal canal. Subtle scalloping of the cord may be present due to encroachment posteriorly by ligamentum flavum hypertrophy or anteriorly by disk or spondylosis. Because disk, ligaments, and bone have low or absent signal on T1-weighted images, it may not be possible to differentiate these structures from one another. The increased contrast between the CSF containing thecal sac and adjacent structures on T2-weighted FSE or GRE images improves visualization of extradural lesions that impinge on the thecal sac.
Degeneration of the intervertebral disk is accompanied by loss of water content and therefore signal intensity on MR images. Loss of disk signal is not a necessary prerequisite for disk herniation. On T1 images a herniated disk generally has the same signal characteristics as the parent disk and is seen as an extrusion of disk material into the spinal canal. Herniated disks can be midline or lateral, and it is important to clearly identify the location of the disk fragment for surgical planning. Midline extradural lesions can be identified on sagittal views by effacement of the thecal sac or cord, but when eccentric they may be seen better on the axial views. Normal signal intensity in the neural foramina may be diminished due to displacement of either epidural veins or foraminal fat.
High-signal above and below a herniated disk is frequently seen and most likely represents flow enhancement in engorged epidural veins containing slowly flowing blood. On parasagittal scans, flow enhancement in these veins may be the best indicator of an epidural abnormality when a central component is absent.
Indentation or compression of the cord is common with larger disks and is seen best on T2-weighted or gradient-echo sagittal images. When either herniated disks or osteophytes impinge on the spinal cord, cord injury can result, which points out the importance of prompt, accurate diagnosis and definitive therapy. As with any contusion, cord edema and swelling develop that may be seen as focal high-signal intensity on T2-weighted scans. There is also disruption of the blood-cord barrier, so enhancement may be observed with Gadolinium.
Symptomatic thoracic disks are uncommon, accounting for about 1% of all
disk herniations. The rib cage, small intervertebral disks, and coronal
orientation of the facets joints all contribute to limited mobility of the
thoracic spine, and consequently, a lower risk of disk herniation. The most
common level is T11-T12, where the spine is relatively less rigid. Sagittal
T2-weighted FSE sequences are excellent for displaying indentation of ventral
thecal sac and impingement of the spinal cord by thoracic disks. Axial images
help delineate lateralization to either side. Disk morphology is similar
to the cervical region. Calcification is more common in thoracic disk fragments
and parent disks than in cervical or lumbar region.
Spondylosis can take the form of marginal end plate osteophytes, enlarged uncinate processes, or facet arthrosis. Degenerative joint disease itself, along with associated inflammatory reaction, can cause pain, or the symptoms can be derived from the osteophytes compressing neural structures. It is important to distinguish spondylosis from disk disease for therapeutic planning.
Vertebral Body Osteophytes
Marginal osteophytes form around the periphery of the vertebral body end plates of the lumbar spine. The larger ones generally project anteriorly or directly lateral and do not compress neural structures. Posterior and posterolateral osteophytes are more likely to cause problems.
Osteophytes are hypointense on all pulse sequences. Identification of central osteophytes requires gradient-echo or T2-weighted images to achieve good contrast between the osteophytes and the hyperintense CSF within the thecal sac. On T1-weighted scans, osteophytes may be silhouetted by the low-signal CSF Posterior ridging osteophytes produce broad ventral impressions on the thecal sac. In the cervical spine, if the posterior bony ridges are large, they can cause repeated trauma to the spinal cord with neck motion, eventually resulting in cord deformity, atrophy, and a myelopathy.
In the lumbar region, osteophytes encroaching on neural foramina are contrasted nicely by foraminal fat on T1-weighted scans. The lumbar neural foramen has the shape of an inverted teardrop, with the nerve root positioned in the superior aspect of the foramen. Fortunately, small osteophytes project first into the inferior aspect of the foramen and are unlikely to compress the nerve root until they get quite large.
Unco-Vertebral and Facet Joint Arthrosis
Some degree of spondylosis is invariably associated with degenerative disk disease. Decrease in height of the intervertebral disk places more stress on the facet joints and unco-vertebral joints, leading to degenerative joint disease. Moreover, with the loss of structural strength at the disk level, exaggerated motion occurs at these joints, accelerating the degenerative changes and placing stress upon the posterior supporting ligaments as well.
The unco-vertebral joints (uncinate processes) are unique to the cervical spine. With degeneration, osteophytes develop at these joints and project into the lateral spinal canal and foramina. Symptoms are caused by impingement of nerve roots as they exit the foramina.
Not all back pain or sciatica is due to intervertebral disk disease. Degeneration of the facet joint can cause a facet arthrosis syndrome, consisting of back pain aggravated by rest and relieved by repeated gentle motion. Facet joint hypertrophy, along with osteophyte formation along the posterior lateral margins of the vertebral body, can encroach upon the lateral recesses of the spinal canal and the neural foramina. Compression of the existing nerve roots results in a radicular pain syndrome, called the lateral recess syndrome.
MR shows the changes of facet sclerosis and the osteophytes but not the cartilage degeneration. Accurate assessment of mild foraminal narrowing requires high-quality images and is aided by careful patient positioning so that both foramina are sectioned together on the axial images. MR performs better in cases of moderate to severe foraminal disease. Volume acquisition methods with oblique image reformation are helpful for evaluating patients with cervical radiculopathy.
Juxtaarticular synovial cysts are associated with facet arthropathy, generally of fairly severe degree. They consist of a fibrous wall, often with a distinct synovial lining, and a cystic center that may or may not communicate with the facet joint. They are found most frequently at L4-5, the more mobile segment of the lumbar spine. Synovial cysts can compress the dorsal nerve roots and cause radicular symptoms.
On MR scans, synovial cysts appears as smooth, well-defined extradural masses in the posterolateral spinal canal. They are positioned adjacent to a facet joint and dorsal to or merges with a thickened ligamentum flavum. The cystic center has a highly variable MR signal pattern due to the spectrum of fluid components (serous, mucinous, or gelatinous), air, and hemorrhagic components. The hypointense perimeter reflects the fibrous capsule with calcium or hemosiderin from chronic hemorrhage, as well as the companion joint capsule and adjacent ligaments. The fibrous capsule may enhance with gadolinium. The combination of proton-density and T2-weighted axial images are best for detecting and delineating these lesions.
Spinal stenosis refers to constriction of the canals and various foramina of the spine. If sufficiently severe, the stenosis can compress neural structures within the spine and cause neurological symptoms. Spinal stenosis can involve the spinal canal, the lateral recesses, or the neuroforamina. Spondylosis and spinal stenosis are commonly associated with intervertebral disk disease, particularly in patients over 50, and they are significant sources of neck and back pain and radiculopathy. Overlooking the patho-anatomic changes of spinal stenosis is an important cause of the failed back surgery syndrome after diskectomy.
Spinal stenosis is due to congenitally short pedicles, or it may be acquired as a result of combined facet hypertrophy, degenerated bulging disk, and hypertrophy of the ligamentum flavum. Congenital spinal stenosis can be idiopathic or associated with a developmental disorder, such as achondroplasia, hypochondroplasia, Morquio's mucopoly-saccharidosis, and Down's syndrome. Spondylolisthesis, trauma, and surgical fusion are other causes of spinal stenosis.
Congenital spinal stenosis is often asymptomatic until middle age, when secondary degenerative changes develop. The acquired type is a disease of primarily adult men with moderate to severe degenerative spine disease. The syndrome of neurogenic or spinal claudication includes bilateral lower extremity pain, numbness, and weakness that is poorly localized and usually associated with low back pain. The symptoms are worse with standing or walking and relieved when the patient lies down.
Spinal stenosis is graphically displayed in the sagittal plane by gradient-echo or T2- weighted pulse sequences. The hyperintense thecal sac is effaced anteriorly by the bulging disk and posteriorly by the ligamentum flavum, resulting in an hourglass configuration. Acquired spinal stenosis is usually associated with moderate to severe multilevel disk degeneration, consisting of loss of normal signal, disk space narrowing, and intradiskal calcification or air. The calcification and air can be difficult to discern within severely desiccated disks. On axial views the constricted canal often has a triangular or trefoil shape due to encroachment on the posterolateral aspects of the canal by hypertrophied facets.
Since compression of the nerve roots within the thecal sac causes the symptoms, assessment of the ratio of CSF to nerve roots is important to make the diagnosis of spinal stenosis. With progressive stenosis, the amount of CSF progressively diminishes and the nerve roots become crowded together. Constriction at the level of stenosis prevents the normal superior and inferior movement of the nerve roots with flexion and extension, resulting in a redundant serpiginous root pattern above and below the stenosis. Nerve root enhancement may also be seen, due to either breakdown of the blood-nerve barrier from mechanical injury, inflammatory response, and Wallerian degeneration/regeneration of axons, or engorgement of intrathecal veins and perineural vascular plexus. As a result of epidural compression, prominent enhancement of retrovertebral venous plexus is common.
When bulging disks, spondylosis, and ligamentum flavum hypertrophy progress to constrict the spinal canal and cord, a spinal stenosis develops. These changes are depicted on sagittal gradient-echo or T2-weighted images as hourglass narrowing of the thecal sac, usually involving multiple levels in the mid- and lower cervical region. In patients with a congenitally borderline or narrow canal, relatively mild degenerative changes are sufficient to cause spinal stenosis. On T1-weighted scans, canal stenosis results in scalloping of the normally smooth dorsal and ventral margins of the cord. As learned from myelography, the degree of canal stenosis and cord scalloping shown on the images is greater when the neck is in a hyperextended position, due to buckling of the ligamentum flava. Imaging in a neutral position may show less severe stenosis. Nonetheless, the hyperextended view illustrates what happens to the cord with acute hyperextension. The spinal cord is more susceptible to traumatic injury in patients with spinal stenosis.
Spondylolysis refers to a cleft or break in the pars interarticularis of the vertebra. It is found in about 6% of adults, mostly in males, 93-95% occur at L5, and most are bilateral. The etiology is uncertain, but the current theory is that it represents a stress fracture from repeated trauma to the spine. The pars defect is demonstrated best in parasagittal images and is easier to see if the bone has a generous component of marrow or if soft tissue is interposed between the bone fragments. With subluxation, there is often a step-off at the pars defect. On axial views, the key observation is a horizontal line (an extra joint) between adjacent facets joints on consecutive images.
Spondylolisthesis refers to forward displacement of one vertebra over another, usually of the fifth lumbar over the body of the sacrum, or of the fourth lumbar over the fifth. Spondylolisthesis is graded according to how far the vertebral body moves forward on the one below (Grade 1 = 25%, Grade 2 = 50%, Grade 3 = 75%). There are two types of spondylolisthesis, isthmic (open-arch type), associated with spondylolysis, and degenerative (closed-arch type).
With isthmic spondylolisthesis, the pars defect divides the vertebra into an anterior part (vertebral body, pedicles, transverse processes, and superior articular facet) and a posterior part (inferior facet, laminae, and spinous process). The anterior part slips forward, leaving the posterior part behind. As a result, the spinal canal elongates in its anteroposterior dimension, so that spinal canal stenosis is uncommon with isthmic spondylolisthesis. Grade I spondylolisthesis is often asymptomatic, but with progressive anterior subluxation, the intervertebral disk and the posterior-superior aspect of the vertebral body below encroach on the superior portion of the neural foramen. The foramen is also elongated in a horizontal direction and may have a bilobed configuration. Exuberant fibrocartilage at the pars pseudarthrosis can further compromise the neural foramen and cause nerve root compression.
Degenerative spondylolisthesis occurs in an older age group, usually over 60 years old, and it is more common in women at the level of L4-L5. It develops when there are severe degenerative changes and excess motion of the facet joints. Subluxation at the facet joints allows forward or posterior movement of one vertebra over another. A degenerative spondylolisthesis narrows the spinal canal, and symptoms of spinal stenosis are common. Hypertrophic facet arthrosis is a frequent cause of foraminal narrowing.
The sagittal plane is best for displaying the abnormal anatomy of spondylo-listhesis, T2-weighted images for the canal and T1-weighted images for the pars interarticularis and neural foramina. The sagittal view clearly shows the degree of subluxation and the relationship of the intervertebral disk to the adjacent vertebral bodies and the spinal canal. Parasagittal images are good for showing encroachment on the foramina by disk or hypertrophic bone. Loss of the normal fat signal cushioning the nerve root is a sign for significant foraminal stenosis.
Ulmer and colleagues proposed the "wide canal sign" to distinguish between isthmic and degenerative spondylolisthesis. Using a midline sagittal section, they noted that the sagittal canal ratio (maximum anteroposterior diameter at any level divided by the diameter of the canal at L1) did not exceed 1.25 in normal controls and in subjects with degenerative spondylolisthesis. In patients with spondylolysis, the measurement always exceeded 1.25.
In the early postoperative period, interpretation of the MR images is extremely difficult. The presence of fat graft, hematoma, gas, and inflammation complicates the observed signal intensities. Moreover, recurrent disk and epidural scar exhibit similar topographical and signal characteristics. After about one month, the acute postoperative changes resolve, making it easier to distinguish scar from disk. As before surgery, recurrent disk is often in continuity with the parent disk. Discontinuity in the anulus fibrosus is not entirely reliable because it can result from the surgical incision as well as from disk rupture. Unless the disk material has become separated as a free fragment or sequestration, it remains similar in signal characteristics to the parent disk on both T1- and T2-weighted images. In general, herniated disks are relatively well-defined and, in some cases, have a hypointense rim.
On the other hand, epidural scar has poorly defined margins and is either isointense or hypointense on short TR/TE sequences compared to the adjacent disk. With more T2-weighting, scar generally increases in signal, but to a lesser degree many months or years after surgery. In addition, if the soft-tissue abnormality can be followed posteriorly along the lateral margin of the spinal canal to the region of the laminectomy, it is probably scar. Retraction of the thecal sac to the side of the soft tissue is another sign favoring postoperative scar.
Gadolinium should be used routinely in the postoperative back because it is a valuable aid for differentiating the various postoperative tissues. Epidural scar enhances to a much greater degree on MR than on contrast-enhanced CT. The enhancing scar clearly identifies nerve roots trapped within the scar and outlines any retained or recurrent disk fragments. A disk fragment induces a local inflammatory reaction, and vascular granulation tissue often forms about its perimeter. As a result, the perimeter of a herniated disk may enhance with gadolinium, but the central part will not, thus distinguishing it from epidural scar.