DEGENERATIVE SPINE DISEASE
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 
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Mixter WJ, Barr JS: Rupture of the intervertebral disk with involvement of the spinal canal. New Eng J Med211:210-215, 1934.
Close 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.
EXAMINATION TECHNIQUE
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. if( bInlineFloats ) { document.write( ” ); document.write( WPEndnote2 ); document.write( ‘
Close‘ ); document.write( ” ); } Georgy BA, Hesselink JR: MR imaging of the spine: recent advances in pulse sequences and specialtechniques. AJR 162:923-934, 1994.
Close 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
Pathophysiology
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%. if( bInlineFloats ) { document.write( ” ); document.write( WPEndnote4 ); document.write( ‘
Close‘ ); document.write( ” ); } Coventry MB. Anatomy of the intervertebral disk. Clin Orthop 67:9-15, 1969.
Close 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. if( bInlineFloats ) { document.write( ” ); document.write( WPEndnote5 ); document.write( ‘
Close‘ ); document.write( ” ); } Sether LA, Yu S, Haughton VM, Fischer ME: Intervertebral disk: normal age-related changes in MR signalintensity. Radiology 177:385-388, 1990.
Close 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
Lumbar Spine
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.
Disk Degeneration
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 if( bInlineFloats ) { document.write( ” ); document.write( WPEndnote7 ); document.write( ‘
Close‘ ); document.write( ” ); } 7. Yu S, Haughton VM, Sether LA, Wagner M. Anulus fibrosus in bulging intervertebral disks. Radiology169:761-763, 1988.
Close 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. if( bInlineFloats ) { document.write( ” ); document.write( WPEndnote8 ); document.write( ‘
Close‘ ); document.write( ” ); } Munter FM, Wasserman BA, Wu H-M, Yousem DM: Serial MR imaging of annular tears in lumbarintervertebral disks. AJNR 23:1105-09, 2002.
Close 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. if( bInlineFloats ) { document.write( ” ); document.write( WPEndnote9 ); document.write( ‘
Close‘ ); document.write( ” ); } Stadnik TW, Lee RR, Coen HL, et al: Annular tears and disk herniation: prevalence and contrast enhancementon MR images in the absence of low back pain or sciatica. Radiology 206:49-55, 1998.
Close 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. if( bInlineFloats ) { document.write( ” ); document.write( WPEndnote10 ); document.write( ‘
Close‘ ); document.write( ” ); } Ross JS, Modic MT, Masaryk TJ: Tears of the anulus fibrosus: Assessment with GD-DTPA-enhanced MRimaging. AJNR 10:1251-1254, 1989.
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 if( bInlineFloats ) { document.write( ” ); document.write( WPEndnote11 ); document.write( ‘
Close‘ ); document.write( ” ); } Modic MT, Steinberg PM, Ross JS, et al: Degenerative disk disease: assessment of changes in vertebral bodymarrow with MR imaging. Radiology 166:193-199, 1988.
Close 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.
Disk Protrusion/Herniation
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 if( bInlineFloats ) { document.write( ” ); document.write( WPEndnote12 ); document.write( ‘
Close‘ ); document.write( ” ); } Ross JS, Modic MT, Masaryk TJ, et al: Assessment of extradural degenerative disease with Gd-DTPA-enhanced MR imaging: correlation with surgical and pathologic findings. AJNR 10:1243-1249, 1989.
Close 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.
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, if( bInlineFloats ) { document.write( ” ); document.write( WPEndnote17 ); document.write( ‘
Close‘ ); document.write( ” ); } Jinkins JR: MR of enhancing nerve roots in the unoperated lumbosacral spine. AJNR 14:193-202, 1993.
Close 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 if( bInlineFloats ) { document.write( ” ); document.write( WPEndnote18 ); document.write( ‘
Close‘ ); document.write( ” ); } Lane JI, Koeller KK, Atkinson JLD: Enhanced lumbar nerve roots in the spine without prior surgery:radiculitis or radicular veins? AJNR 15:1317-1324, 1994.
Close 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.
SPINAL STENOSIS
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.
SPONDYLOSIS
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.
Lumbar Spine
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. if( bInlineFloats ) { document.write( ” ); document.write( WPEndnote30 ); document.write( ‘
Close‘ ); document.write( ” ); } Major NM, Helms CA: Central and foraminal stenosis of the lumbar spine. Neuroimag Clin North Am3:557-566, 1993.
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.
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