Spine and Spinal Cord Imaging

Spine and Spinal Cord Imaging (8)

It is clear, after multiple research studies to assess the usefulness of imaging in low back pain, that uncomplicated acute low back pain is a benign, self-limited condition that does not warrant any imaging studies. The vast majority of patients are back to their usual activities within 30 days. Radiographic evaluation of the lumbar spine includes frontal and lateral radiographs. These are indicated in the evaluation of back pain and weight loss, after mild trauma in patients older than 50 y/o, in patients with unexplained fever, immunosuppression, history of cancer, prolonged use of steroids and focal neurologic, or disabling symptoms. Oblique views are useful for the assessment of defects to the pars interarticularis when suspecting spondylolysis and for the evaluation of the nerve root foramina. The relative radiation dose level for a routine radiographic examination of the lumbar spine is between 1 and 10 mSv (56). Although plain radiographs remain valuable for detecting many types of spine fractures and degenerative changes, the high resolution of osseous and soft-tissue structures provided by CT and MRI has made these modalities invaluable for the diagnosis of degenerative, traumatic, neoplastic, and infectious diseases of the spinal column and spinal cord. 


Although much spinal trauma is well visualized on plain films, CT has a number of advantages over this modality. These include the demonstration of fractures not seen in plain films, an accurate determination of the amount of spinal canal encroachment by fracture fragments (Fig. 6-66A,B), the identification of neural foramen impingement by fractures involving its boundaries, and a more precise evaluation of facet disruption.

MR can display impingement on the dural sac or the spinal cord by bone fragments, as well as any resultant cord contusion (Fig. 6-66C). It can demonstrate acute cord enlargement as a sign of cord edema or hemorrhage and cord atrophy. CT myelography can be used to diagnose post- traumatic cystic myelopathy because the cyst will take up the contrast and be displayed as a well-marginated, homogeneous, high-density region within the cord. When MRI is not available or contraindicated, CT myelograpy can be used to assess the degree of spinal canal stenosis and cord compression.

FIGURE 6-66. MDCT visualization of spinal trauma. A: CT of a burst fracture of L1 shows displacement of a fracture fragment into the spinal canal (arrow ). There is significant comminution to the superior articular surface of the vertebral body. B: Sagittal MPR reconstruction demonstrates the large fragment (arrow ) extending into the spinal canal. There is mild compression of the superior end plate of L2. C: Sagittal T2-weighted MR image demonstrates increased signal intensity to the bone marrow of the L1 and L2 vertebral bodies due to the presence of edema and hemorrhage. There is posterior displacement of the conus and proximal cauda equina in the spinal canal. Increased signal to the conus (arrow) is compatible with a cord contusion.

CT also can augment the interpretation of the signs of vertebral instability seen on plain radiographs (Fig. 6-67A–C) (71). These signs include the following:

  • Vertebral displacements involving the whole vertebra or fracture fragments.
  • Widening of the interspinous interval, which implies injury to the posterior spinal ligaments secondary to hyperflexion injury.
  • Increased dimensions of the vertebral canal in the sagittal or coronal plane often evaluated by an increased interpedicle distance, which implies a complete disruption of the vertebral body in the sagittal plane.
  • Widening of the facet joint interval, which implies ligamentous disruption.
  • Disruption of the alignment of the posterior aspect of the vertebral bodies, such as occurs in burst fractures or lap-seatbelt fractures (Fig. 6-68).

FIGURE 6-67. A: Axial image at the C5 cervical segment. There is a burst comminuted fracture to the vertebral body. A fracture through the posterior arch is present as well. B: Sagittal MPR reconstruction demonstrates anterior collapse and posterior subluxation in relationship to the adjacent vertebral bodies. C: Sagittal T2-weighted MR shows increased signal to the vertebral body compatible with edema, prevertebral soft-tissue swelling (arrow ) and edema (arrow ) within the interspinous spaces as a secondary sign of ligamentous injury to the posterior supporting ligaments.

FIGURE 6-68. Sagittal T2-weighted image of the thoracic spine. There is a fracture dislocation (Chance fracture) at the C7-T1 inter- space. There is bone marrow edema to the C7, T1, and T2 vertebral bodies and extensive prevertebral soft-tissue swelling. Edema is also appreciated within the posterior supporting structures. There is compression and edema (white arrow ) to the cord extending from C6 up to the T2 segment.

T1-weighted sagittal and axial MR images provide the best evaluation of vertebral alignment and the bony and ligamentous boundaries of the spinal canal. They also allow the best delineation of the low signal intensity of a traumatic syringomyelia against the higher signal intensity of the surrounding spinal cord. T2-weighted sagittal MR images that produce a high– signal-intensity CSF provide the best estimate of the degree of encroachment of a bony fragment on the thecal sac or the spinal cord.

MRI has a number of advantages over other modalities for imaging spinal trauma. First, it permits evaluation of vertebral alignment at the cervicothoracic junction of the spine,

which is relatively inaccessible by other modalities. Second, it provides a means to evaluate adjacent soft-tissue damage. For example, hemorrhage in the prevertebral space that can occur with hyperextension injuries is identified on T2-weighted images as a high–signal-intensity area. MRI also identifies high–signal-intensity hemorrhage in the posterior paravertebral muscles that can occur secondary to hyperflexion injuries. In addition, MRI is the most sensitive modality for the assessment of ligamentous injuries as it detects edema within the supporting ligaments, a finding not assessed by any other imaging modality (Figs. 6-66 and 6-67C). Of importance is the fact that MRI provides a noninvasive means of evaluating the relationship of retropulsed vertebral body fragments or anteriorly displaced neural arch fragments to the spinal cord (Fig. 6-66C). In most centers, MRI has replaced myelography as the procedure of choice for evaluating the effects of vertebral trauma on the spinal cord. Most important, MRI can evaluate the extent and type of spinal cord injury (71,72).

An acutely injured spinal cord tends to enlarge, thereby filling the spinal canal and displacing the epidural fat. This can be visualized by both CT and MRI. However, MRI provides the best means of evaluating the type of spinal cord trauma and its evolution. MRI is valuable in the early stages of spinal cord injury in determining the type of spinal cord injury and the prognosis for recovery. It can identify the level and completeness of cord transection by direct visualization of the transection site. In the nontransected cord, it can discriminate cord hemorrhage from cord contusion with edema. Spinal cord contusion with edema causes high signal intensity on T2-weighted images within the first 24 hours of injury. Acute hemorrhage of less than 24 hours’ duration appears as a low– signal-intensity area on T2-weighted images. Within a few days of the trauma, the subacute hemorrhage site becomes hyper- intense on T2-weighted images as a result of the accumulation of paramagnetic methemoglobin (Fig. 6-69). Kulkarni et al. found that the type of injury visualized by MRI correlated with the patient’s recovery of neurologic function (73). Those patients with cord contusion and edema exhibited significant functional recovery, whereas those with hemorrhage made little functional progress. Therefore, the MRI characteristics of the injury may provide the clinician with important prognostic data.

MRI is also invaluable for identifying late sequelae of spinal cord trauma, including myelomalacia and post-traumatic spinal cord cysts or syringomyelia. Myelomalacia is thought to develop within an injured segment of the spinal cord as a result of ischemia or the release of enzymes from damaged spinal cord tissues, or both (74). The myelomalacic area is made up of the products of neuronal degeneration, scar tissue, and microcysts. It is thought that the myelomalacic areas become larger intramedullary cysts because the scar tissue about the injured cord tethers the cord to the dura so that the episodic changes in CSF pressure that occur during daily activities tend to be concentrated on the injured cord segment as stretching forces. It is hypothesized that these stresses cause coalescence of the myelomalacic microcysts into a progressively enlarging gross cyst. CSF is theorized to enter the cysts along enlarged perivascular Virchow-Robin spaces that connect the subarachnoid space to the cyst.

On T1-weighted images, myelomalacia appears within the segment of the spinal cord near the area of injury as a region of lower signal intensity than the spinal cord but higher signal intensity than the CSF. It has indistinct margins with the surrounding spinal cord. In contrast, intramedullary cysts have signal intensity approximating that of CSF and sharply marginated borders with the surrounding spinal cord or an adjacent area of myelomalacia. The development of an intramedullary cyst in a spinal cord patient whose clinical picture had previously stabilized may cause the patient to develop progressive sensory and motor deficits. Although myelomalacia has no definitive treatment mode, a spinal cord cyst can be surgically decompressed with a shunt to achieve improvement or at least an arrest of the patient’s neurologic deterioration. Therefore, the MRI distinction between cysts and myelomalacia is important. MRI can also be used in postoperative follow-up to ensure that the cyst has been fully decompressed and that the catheter is continuing to function to prevent reaccumulation of fluid within the cyst.

FIGURE 6-69. Sagittal T2-weighted image at the cervicothoracic junction in a patient with fracture dislocation at the C5-6 segment. There is compression and swelling to the cord. A focal area of decreased signal within the cord secondary to methemoglobin deposition associated to the acute bleed (arrow ).


Source: Physical Medicine and Rehabilitation - Principles and Practice

Spondylolysis is a defect in the pars interarticularis, commonly involving the L5 and occasionally the L4 vertebrae. Most spondylolysis is thought to be produced by repetitive stress. The gravitational and muscular loads acting across the steep incline of the upper surface of the sacrum can be resolved into a shearing component, which tends to displace the L5 vertebral body forward on S1, and a compressive component at right angles to the superior surface of S1 (Fig. 6-63). In accordance with Newton’s third law, S1 will exert an equal and opposite force against the inferior aspect of the L5 vertebral body. The tendency of L5 to be displaced forward on S1 is primarily resisted by the impaction of the inferior articular processes of L5 on the superior articular processes of S1. Again, Newton’s third law dictates that there will be an equal and opposite force exerted against the inferior articular process of L5. The upward and forward force of the sacral body on the L5 body and the upward and backward force of the superior articular process of the sacrum on the inferior articular process of L5 cause shearing stresses to be concentrated on the pars interarticularis, and this can produce a stress fracture.

FIGURE 6-63. The gravitational load (G) is applied across the lumbosacral junction. The equal and opposite forces acting on the inferior aspect of the L5 body and the anterior aspect of the inferior articular

FIGURE 6-64. Spondylolysis and spondylolisthesis. An oblique radiograph demonstrates a spondylolytic defect in the pars interarticularis of L4 (arrow). Note the intact neck in the “Scotty dog” outline in the L3 vertebra.

Spondylolisthesis is an anterior subluxation of one vertebral body on another. It can occur at any vertebral level, but the mechanics of the lumbosacral junction cause a higher incidence at this level. The most common cause at this level is spondylolysis, where the impaction of the inferior articular process of L5 or L4 will no longer be able to resist forward displacement of the vertebral body. Whether or not a spondylolisthesis follows a spondylolysis is largely determined by the resistance of the other supporting structures of the lumbosacral junction, which include the intervertebral disc, the anterior longitudinal ligament, and the iliolumbar ligaments. When they fail, the lysis becomes a listhesis.

Other causes of spondylolisthesis include degenerative changes in the facet joints and disc that produce joint instability, fractures, dysplasia of the upper sacrum or the neural arch of L5, generalized pathology such as Paget’s disease, or iatrogenically induced laminectomy or facetectomy (62).

On oblique plain films, spondylolysis is visualized as a break in the neck of the “Scotty-dog” outline, which is produced by the ipsilateral transverse process forming a nose; the ipsilateral pedicle, an eye; the pars interarticularis, a neck; the ipsilateral inferior articular process, a forelimb; the lamina, a body; the contralateral inferior articular process, a hind limb; and the spinous process, a tail (Fig. 6-64). When spondylolysis is suspected clinically or on plain film studies, a volumetric CT with sagittal reconstruction, MR, or plain film examination with nuclear medicine scintigraphy can be useful for diagnosis (Fig. 6-65A,B) (70).

Spondylolisthesis is graded by the amount of subluxation, with grade I being a forward displacement of less than 25%; grade II, a forward displacement of 25% to 50%; grade III, a displacement of 50% to 75%; and grade IV, a displacement of greater than 75%. Grading the spondylolisthesis is usually accomplished by lateral plain films or sagittal reconstructed images in CT (Fig. 6-65C,D).

FIGURE 6-65. Spondylolysis and spondylolisthesis. A: Right parasagittal reconstruction of an MDCT demonstrates a spondylolytic defect in the pars interarticularis of L5 (PD arrow ). B: Parasagittal reconstructed image form a volumetric CT demonstrating the pars defect in a patient with stage II spondylolisthesis (PD arrow ). C: Midplane sagittal reconstruction demonstrates the grade II spondylolisthesis. D: Volume rendering, oblique posterior view demonstrating the pars defect (PD) and a normal pars (NP) above.

On CT, the defect of spondylolysis is differentiated from the facet joint interval by its location at the axial level of the pedicles rather than at the level of the neural foramen, as well as by the defect’s irregular margins and adjacent sclerosis. By MRI, the defect in the pars is visualized as a low–signalintensity zone within the high–signal-intensity marrow of the pars.


Source: Physical Medicine and Rehabilitation - Principles and Practice

Like cervical stenosis, lumbar spinal stenosis is frequently precipitated by disc degeneration with subsequent marginal osteophytosis of the vertebral body ends, hypertrophic degeneration of the facet joints, and bulging of the ligamenta flava. Lumbar stenosis may be lateral, central, or combined. The lower lumbar vertebrae normally have shorter pedicles that cause the superior articular processes to intrude into the spinal canal to cut off narrow lateral recesses (Fig. 6-61A–E). The lateral nerve roots of the next spinal nerve to exit as they descend recesses are bordered by the pedicles laterally, the vertebral within their dural sleeve. Osteophytes that develop on the body anteriorly, and, most important, the superior articular anteromedial margin of the superior articular processes of the processes posteriorly. The lateral recesses are occupied by the next lower vertebra are most likely to encroach on the lateral recess to produce lateral stenosis. Because the inferior articular processes of the next higher vertebra are situated posteromedial to the superior articular processes, osteophytes developing on their anterior margin are more likely to produce central steno- sis. In central stenosis, any or all of the rootlets of the cauda equina can be encroached on. Vertebral body margin osteophytes and buckling of the ligamentum flavum can contribute to lumbar spinal stenosis.

FIGURE 6-61. MDCT of the lumbar spine in a patient with degenerative spondylosis and spinal canal steno- sis. At the L4-5 level, there are hypertrophic degenerative changes of the facet joints and ligamentum flavum (long white arrow), which produce lateral stenosis, and hypertrophic changes of the articular process, which cause central stenosis (short white arrow). A: Bone windows. B: Soft-tissue windows that demonstrate to a better advantage the hypertrophied ligamentum flavum (short arrow ). C: Soft-tissue windows and D: bone windows. There is congenital canal stenosis as well. Compression to the superior end plate of L1 is appreciated. E: Volume rendering reconstruction looking at the central canal demonstrates the significant narrowing to the central canal.

Hypertrophic degenerative changes involving the facet joints can also encroach on the posterior aspect of the neural foramen and produce foraminal stenosis with compression of the nerve roots exiting that foramen. Therefore, hypertrophic degenerative changes involving a single superior articular process can involve the roots of two closely adjacent nerves, with the possibility of producing both foraminal and lateral spinal stenosis. With disc degeneration and loss of disc height, the neural foramen can be further compromised by the upward and forward displacement of the superior articular process into the upper part of the neural foramen, where the nerve roots are situated. In addition, because of the obliquity of the facet joint, the accompanying downward displacement of the inferior articular process of the next higher vertebra can produce retrolisthesis (i.e., backward displacement) of its vertebral body into the upper portion of the neural foramen.

By standard myelography, the protruding disc anteriorly and the bulging ligamenta flava posteriorly can produce an hourglass appearance of the thecal sac (Fig. 6-62). By CT, all osteophytes are clearly visualized, and measurements of the AP dimension of lateral recesses that are less than 3 mm are strongly suggestive of lateral stenosis (69). The hypertrophic changes producing central and foraminal stenosis are also well visualized. Sagittal reformations are especially helpful in evaluating foraminal stenosis.

FIGURE 6-62. Lumbar spinal stenosis caused by both protruding process of L5 cause shearing stresses to be concentrated on the pars discs and bulging ligamentum flavum. Lateral myelogram showing the interarticularis of L5 (curved arrows). This produces the stress fracture hourglass appearance of the thecal sac. of spondylolysis.

Facet anatomy is well seen by MRI, with subchondral bone appearing as a signal void. On T1-weighted images, articular cartilage is visualized as a moderate–signal-intensity interval between the subchondral bone of the two articular processes. This becomes more signal intense on T2-weighted images. Facet joint degeneration appears as an irregularity or reduction in the thickness of the articular cartilage. Osteophytes are usually displayed as signal voids encroaching into the foramen, lateral recess, or spinal canal. Occasionally, osteophytes show high– signal-intensity interior, indicating the presence of marrow.


Source: Physical Medicine and Rehabilitation - Principles and Practice

The correlation of lumbar disc herniation with a patient’s complaints of low back pain or sciatica is not always clearly established. It has been estimated that as many as 20% of patients with radiologic findings of disc herniation are asymptomatic (67). Furthermore, when disc herniation occurs in symptomatic patients, other findings are often present that also could explain the clinical findings.

Lumbar disc herniations occur most frequently posterolaterally because the annulus is thinnest in the posterior quadrants but reinforced in the midline by the posterior longitudinal ligament. Also, flexion is the most prevalent lumbar spine motion, which places greatest stress on the posterior part of the disc. When the disc herniates to the posterolateral direction, it frequently does not impinge on the spinal nerve roots emerging from the neural foramen to which the disc is related, because the nerve roots occupy the upper portion of the foramen, whereas the disc is situated in the anterior wall of the lower part of the foramen. Therefore, when the L5-S1 disc herniates posterolaterally, it frequently spares the L5 nerve roots, exiting through the upper portion of the L5-S1 neural foramen. Instead, it more commonly involves the S1 nerve roots that descend across the posterolateral aspect of the L5-S1 disc before their exit from the S1 sacral foramina. Less common lumbar disc herniations are placed centrally or far laterally. Central herniations can involve any or all of the rootlets of the cauda equina. The infrequent far lateral herniations occur outside of the neural foramina. When present, they usually impinge on the ventral ramus that has just emerged from that foramen.

FIGURE 6-57. Axial T2-weighted images in the same patient as in Figure 6-54. Note deformity to the cord that has assumed a bean shape in the transaxial plane. There is compression and increased signal intensity to the cord compatible with myelopathy (arrow ).

Noncontrast CT has been described as being accurate in diagnosing disc herniations. On CT examination, the herniated disc appears as a focal protrusion of the disc that displaces the epidural fat (Fig. 6-58). The herniated disc material is typically slightly hyperdense relative to the non–contrast-enhanced dural sac and its adjacent nerve roots. The dural sac or adjacent nerve roots may be seen to be indented, displaced, or compressed. In more lateral herniations, the soft-tissue material of the disc can encroach on the neural foramen or the extraforaminal soft tissues, where it also displaces fat, and here it may encroach on the dorsal root ganglion, spinal nerve, or its ventral ramus. Herniated lumbar discs may calcify or contain gas. Extruded disc fragments can become separated from the disc and are thus able to migrate superiorly, inferiorly, or laterally. A herniated disc should be distinguished from a bulging annulus. A bulging annulus is produced by dehydration and volume loss within the nucleus pulposus. In contrast to the focal protrusion of a herniated disc, the bulging annulus typically has a symmetrical smooth contour, bulging beyond all margins of the vertebral body.

FIGURE 6-58. Sagittal reconstructed image of a MDCT acquisition of the lumbar spine demonstrates a large disc protrusion.

FIGURE 6-59. A: Left parasagittal T2WI of the lumbar spine with an extruded disk at the L5-S1 segment. B: Axial T2WI demonstrates elevation of the thecal sac (TS) by the extrusion (E). There is mass effect and posterior displacement of the first sacral root (S1).

On T1-weighted sagittal and axial MR images, the herniated lumbar disc appears as a moderate–signal-intensity intrusion into the high–signal-intensity epidural fat or on the moderate– to low–signal-intensity thecal sac or the lumbar nerve roots within their dural sleeves (Fig. 6-59A,B). Similarly, disc herniation into the neural foramen is visualized by a moderate– signal-intensity mass displacing the foraminal fat and encroaching on the dorsal root ganglion or nerve roots.

On T2-weighted sagittal MR images, the low signal intensity of a degenerated disc contrasts sharply with the high signal intensity of the nucleus pulposus of adjacent well- hydrated discs (Fig. 6-60). Any intrusion of the low–signalintensity disc herniation on the thecal sac is well seen because of the high–signal-intensity myelographic effect of the CSF on T2-weighted images.

FIGURE 6-60. Small central extrusion (E) at the L5-S1 segment. Note decreased signal to the intervertebral disk when compared to the remaining intervertebral segments, a sign of degeneration.

Discography remains a controversial diagnostic imaging modality. It appears that its major diagnostic value lies in the reproduction of the patient’s specific pain on contrast injection of a given disc, with controls demonstrating that injection of adjacent discs produces either no pain or foreign pain (68). Discography, especially when combined with CT, may provide information about degeneration and the extent of fissures and rupture.


Source: Physical Medicine and Rehabilitation - Principles and Practice

Cervical spinal stenosis can be congenital or acquired. In the less common congenital stenosis, a small spinal canal is produced by short pedicles and thick laminae (62). It commonly remains asymptomatic until degenerative changes are superimposed on the congenital stenosis later in life.

Acquired stenosis can be produced by a host of hyper- trophic degenerative changes often collectively referred to as cervical spondylosis. These include osteophytic lipping of the posterior margins of the vertebral body ends bordering the disc, hypertrophic degenerative changes involving Luschka’s joints or the facet joints, buckling or hypertrophy of the ligamenta flava, and OPLL. All these structures border the spinal canal; therefore, hypertrophic degenerative changes can produce spinal canal stenosis. Because Luschka’s joints, the facet joints, and the ligamenta flava also border the neural foramen, their involvement by degenerative processes can produce foraminal stenosis.

Although hypertrophic degenerative changes of any of the structures bordering the spinal canal or neural foramen can occur in isolation, they are commonly precipitated by intervertebral disc degeneration. As the disc degenerates and loses its normal load-dispersing ability, loads tend to become concentrated on the vertebral body margin toward which the spine is bent. This excessive loading can produce marginal osteophytes around the entire circumference of the vertebral body end plates. Those osteophytes developing on the posterior margin can encroach on the spinal canal to produce spinal stenosis (Fig. 6-54A,B). Luschka (i.e., uncovertebral) joints are situated between the uncinate processes that protrude from the lateral or posterolateral margins of the upper surface of the vertebral bodies and a reciprocal convexity on the lateral aspect of the inferior surface of the next higher vertebral body. Recent evidence indicates that they are not true joints (63). Rather, they are degenerative clefts within the lateral part of the intervertebral disc that begin in the second decade of life. The increased loading of Luschka joints produced by these degenerative changes produces bony spurs that can extend posteriorly into the lateral part of the spinal canal or posterolaterally into the neural foramen (Fig. 6-55A–C).

FIGURE 6-54. (A) Midplane sagittal and (B) right parasagittal T2-weighted images in a patient with congenital stenosis and superimposed degenerative spondylosis with central canal narrowing and cord compression. There is increased AP dimension to the C4, C5, and C6 vertebral bodies. Annular bulge and hypertrophy to the supporting ligamentous structures is responsible for compression to the cord. There is linear increased signal to the cord on the T2-weighted image (arrow ) compatible with early myelopathy.

FIGURE 6-55. Hypertrophic Luschka joints with associated bilateral foraminal stenosis. A: Axial image at the C5-6 segment shows the hypertrophic changes to the uncovertebral joints (arrow ) and associated foraminal stenosis. B: Coronal and C: sagittal oblique MPR images demonstrates to a better advantage the associated foraminal stenosis, the deformity at the uncovertebral joint and the subchondral bone sclerosis.

Disc degeneration is accompanied by dehydration and loss of disc height, with decreased space between vertebral bodies resulting in increased facet joint loads. The resultant facet joint degeneration involves cartilage erosion with joint space narrowing, subchondral bone sclerosis, and osteophyte formation. The osteophytes may encroach on the spinal canal or the neural foramen.

Loss of disc height results in decrease of the laminae inter- space, which causes the ligamentum flavum to buckle and bulge into the spinal canal, contributing to the spinal stenosis. Because the ligamentum flavum continues laterally into the facet joint capsule, buckling of this part of the ligamentum flavum can cause foraminal stenosis.

OPLL occurs more commonly at cervical than at other vertebral levels. It is best visualized via CT, where it appears as an ossification extending over several vertebral levels, separated from the posterior margin of the vertebral bodies by a thin radiolucent interval (Fig. 6-56A,B).

FIGURE 6-56. Ossification of the posterior longitudinal ligament OPLL. A: Axial CT at the level of C3 demonstrates the calcification to the fibers of the posterior longitudinal ligament. There is narrowing to the central canal by the mass effect exerted by the enlarged calcified ligament. B: Sagittal multi-planar reformatted image. The short arrows at the flowing calcifications within the anterior longitudinal ligament. The calcification extends from C2 up to C7. The OPLL (long arrow) extends from C2 up to the proximal border of C5.

When any of these potential causes of cervical stenosis sufficiently narrow the spinal canal, cord compression can produce myelopathic signs and symptoms. Spinal stenosis most frequently narrows the AP dimension of the spinal canal. Although the cross-sectional area of the spinal canal is smallest at the C4 and C7 levels, the smallest AP diameter is usually at the C3 through C5 levels (62). It has been stated that all spinal stenosis that reduces the AP dimension to less than 10 mm could produce quadriplegia (64).

Although the uppermost cervical cord segments are nearly round, at most cervical levels the cord has an elliptical outline with its major axis transversely oriented. With encroachment of the cord by spinal stenosis, it is usually first flattened anteriorly by an encroaching osteophyte. With progression, the anterior median fissure becomes indented and widened until the cord assumes a kidney bean shape (Fig. 6-57) (48). The lateral funiculi may become tapered anterolaterally because of tension on the denticulate ligaments. The cord may become notched dorsally because of posterior white column atrophy. It has been estimated that a 30% reduction in cord cross-sectional area may be required to produce signs of ascending and descending tract degeneration (65).


Source: Physical Medicine and Rehabilitation - Principles and Practice

Disc herniation is typically preceded by degenerative changes in the mucopolysaccharides of the nucleus pulposus, which produce fibrillation of the collagen (60). This eventually causes dehydration and loss of disc volume. As a result, the nucleus pulposus no longer serves as a normal load-dispersing mechanism, and excessive stress is borne by the annulus fibrosus. This produces annular fissuring and tears that can culminate in herniation of the nucleus pulposus. The loss of the load-diffusing function of the normal disc also causes facet joint degeneration and marginal osteophytosis of the vertebral body ends by virtue of the increased loads these joints must bear.

Cervical disc herniation occurs with less frequency than lumbar disc herniation. About 90% of cervical disc herniations occur, in order of decreasing frequency, at C5-6, C6-7, and C4-5 (61,62). On CT examination, a herniated cervical disc appears as a dense soft-tissue mass protruding from the disc space centrally or paracentrally into the spinal canal or posterolaterally into the neural foramen (Fig. 6-51).

FIGURE 6-51. CT evaluation of a herniated C5-6 nucleus pulposus. An axial CT myelogram shows a radiodense protrusion of the C5-6 disc (arrow ) that distorts the left anterior aspect of both the thecal sac and the spinal cord.

On T1-weighted MR images, the herniated cervical disc appears as a posterior extension of the moderate signal intensity of the disc into the low–signal-intensity region of the thecal sac (Fig. 6-52A,B). Because the spinal cord appears as a relatively high–signal-intensity structure outlined by the low–signal-intensity CSF, the relationship of the herniated disc to the spinal cord can be visualized directly by MRI. On T2-weighted MR images, the degenerated disc appears as a narrowed disc interval. The disc herniation appears as a moderate– to low– signal-intensity impingement on the now high–signal-intensity CSF. The posterior margin of the herniated disc may have a to determine its probability of causing a patient’s myelopathic very-low-signal-intensity margin interfacing with the CSF. This findings (Fig. 6-53A,B). It is sometimes difficult to differentiate may be a posterior longitudinal ligament elevated by the herni-lateral herniations of the disc into the neural foramen from osteoated disc, or it may be fragments of the posterior part of the phytic encroachments by MRI because they may both demon- annulus fibrosus (61). T2-weighted images also permit evalua-strate low signal intensity. In these circumstances, CT provides tion of the relationship of the herniated disc to the spinal cord good differentiation between bone and soft-tissue density.

FIGURE 6-52. A: T2*-weighted axial MRI of the cervical spine shows a left posterolateral herniated C6-7 nucleus pulposus (between arrow) indenting the thecal sac (arrowhead ) and extending into the ostium of the ipsilateral nerve root foramina. B: A T2-weighted left parasagittal MRI shows the disc fragment (arrow ) impinging upon the intermediate–signal-intensity thecal sac (arrowheads) and low–signal-intensity posterior longitudinal ligament.

FIGURE 6-53. A: Axial T2-weighted image at the C4-5 level demonstrates a bilobed protrusion contained in the midline by the posterior longitudinal ligament. Note complete obliteration of the normal CSF signal anterior to the cord, posterior displacement, and compression of the cord. B: The herniated disc elevates the posterior longitudinal ligament, compresses the cervical cord, which demonstrates increased signal intensity as a sign of myelopathy.


Source: Physical Medicine and Rehabilitation - Principles and Practice

The intervertebral disc space is a cartilaginous joint with a central nucleus pulposus surrounded by an annulus fibrosus. Degenerative change in the nucleus pulposus is termed inter-vertebral osteochondrosis (Fig. 6-49A,B). Early signs of disc disease may include loss of fluid signal within the nucleus pulposus (dehydration), which results in decreased signal within the central portion of the disc on T2-weighted images, and blurring of the transition between the nucleus pulposus and the annulus fibrosus. This is followed later by narrowing of the intervertebral disc, which sometimes results in vertebral body end-plate degenerative changes. These end-plate changes are referred to as Modic changes (58). Modic type I changes are characterized by signal of edema, that is decreased signal on T1-weighted images and increased signal on T2-weighted images. Type II changes (Fig. 6-50A,B) follow the signal characteristic of fat, with intermediate to increased signal on T1-weighted images and increased signal on T2-weighted images. This is the most common type of reactive end-plate changes appreciated on degenerative osteochondrosis. Type III changes represent osseous sclerosis, characterized by decreased signal on both the T1- and the T2-weighted images.

FIGURE 6-49. A: Sagittal T2WI of the lumbar spine demonstrating different stages of intervertebral osteochondrosis. Normal disk (ND) demonstrates increased signal to the nucleus pulposus and normal height. With early degeneration (ED), the nucleus pulposus loses signal in part related to the decreased water content of the intervertebral disc but preserves the intervertebral height. With advanced degeneration (AD), there is near complete loss to the normal signal of the intervertebral disk and early traction osteophyte formation (TO). Note herniated disk (DH) at the L5-S1 segment. B: Advanced degenerative osteochondrosis on a different patient. There is loss of the intervertebral disk height, Schmorl’s node formation (SN) representing end-plate herniation and moderate traction osteophyte formation (arrow).

FIGURE 6-50. Sagittal T1- (A) and T2- (B) weighted images with degenerative osteochondrosis of the cervical spine. There is decreased T2 signal to most intervertebral discs, decreased disc height throughout, annular bulge, and traction osteophytosis. Note increased signal to the inferior end plate of C5 both on the T1- and T2-weighted images (arrows) characteristic of Modic type II changes.

When the disc becomes degenerated, it may undergo tearing of the annulus fibrosus collagen bundles, which is often a precursor to herniation of the nucleus pulposus, particularly at the posterolateral aspect of the disc. Protrusion is herniation of the nucleus pulposus that is contained by the annulus. In the axial plane, it usually demonstrates a base broader than the height against the parent disc (59). Extrusion is defined as a herniation of the nucleus pulposus beyond the fibers of the

The loss of the load-diffusing function of the normal disc also causes facet joint osteoarthrosis and marginal osteophytosis of the vertebral body ends (spondylosis deformans) by virtue of the increased loads these joints must bear.


Source: Physical Medicine and Rehabilitation - Principles and Practice

CT and MRI provide complementary information about degenerative diseases of the spine. MRI is often the modality of choice in assessing degenerative changes within the spine due to its superior soft-tissue contrast. CT has superior spatial resolution and provides better conspicuity of osseous and calcified structures. The advent of MDCT technology allows for superb reconstruction in the sagittal and the coronal planes that allows for better depiction of pathologic processes and hardware evaluation in the post–operative spine (57). MRI permits noninvasive visualization of the spinal cord and subarachnoid space within the spinal canal and the nerve roots within the neural foramina. Discrimination of these structures by CT requires injection of intrathecal contrast agents. MRI has a superior ability to evaluate intramedullary abnormalities. It also offers direct multiplanar imaging capabilities.

Axial CT images of the normal cervical and lumbar spine (Figs. 6-44 and 6-45) provide good visualization of all osseous elements, including the facet joints. In the cervical spine, the uncovertebral joints (i.e., Luschka) are well depicted with coronal reformatted and sagittal oblique images. Sagittal oblique images through the lumbar spine provide excellent anatomical reconstruction of the pars interarticularis for the assessment of spondylolysis. Soft-tissue windows typically permit visualization of the moderate radiodensity of the soft- tissue structures, such as the intervertebral disc, ligamentum flavum, and thecal sac. Sagittal images provide assessment of anatomical alignment, intersegmental instability and allows for adequate evaluation of foraminal stenosis. The epidural fat contains the internal vertebral venous plexus, which can be enhanced by a circulating bolus of contrast material to improve visualization of soft-tissue encroachments into the spinal canal, such as herniated discs. Introduction of contrast material into the subarachnoid space (i.e., CT myelography) delimits the contained spinal cord and the nerve roots (Fig. 6-46).

FIGURE 6-44. MDCT of the normal cervical spine. A: Bone window CT of the cervical spine in the axial plane at the level of C5-6 displays normal facet joints (short arrow) and Luschka joints (long arrow). B: Coronal multiplanar reformatted images (MPR) through the level of the uncovertebral joints (arrow). C: Midplane sagittal reconstructed images of the cervical spine shows mild reverse of the normal lordosis that could be secondary to spasm or associated to positioning. Note adequate alignment and no intersegmental subluxations. D: Sagittal oblique MPR demonstrates the nerve root foramina, uncovertebral joints, and facet joints.

FIGURE 6-45. Normal lumbar spine CT. A: Axial soft-tissue window CT of L5 demonstrating thecal sac (T), L5 nerve root (NR) within the lateral recess, epidural fat (E), and ligamentum flavum (LF). B: Bone windows axial through the same level demonstrate the sclerotic margins of the facet joint and the right sacroiliac joint. C: Midplane sagittal reconstruction (MPR image). Normal homogeneous trabecular pattern. Note intervertebral space distance and anatomical alignment of the anterior and posterior surface to the vertebral bodies. D: The density of the nucleus pulposus (NP) and annulus fibrosus (AF) can be appreciated. Note decreased attenuation to the CSF in the thecal sac. E: Oblique reconstruction through the posterior elements demonstrating the normal facet joints and pars interarticularis.


FIGURE 6-46. Metrizamide CT myelogram at L1 level delimiting the spinal cord (SC), nerve roots (NR) arising from the cord, and the contrast-enhanced CSF.

The introduction of MDCT technology allows for the acquisitions of multiple thin cut images in the axial plane that can be reconstructed in the sagittal and the coronal planes. The high spatial resolution of the acquired data allows for near-perfect isometric reconstruction in different planes. In addition, computer-generated volume rendering images provide superb 3D images of the spine (Fig. 6-47A–C).

Sagittal T1-weighted MR images of the cervical, thoracic, or lumbar spine provide excellent noninvasive survey to evaluate patients with suspected regional spinal pathology. Midsagittal T1-weighted images display the high–signal-intensity marrow of the vertebrae bordered by low–signal-intensity cortical bone. Structures displaying very low signal intensity include the peripheral part of the annulus fibrosus of the intervertebral disc, all ligaments, the dura, and the cerebrospinal fluid (CSF), and these are usually indistinguishable from each other (Fig. 6-48A–C). The nucleus pulposus, and probably the inner portion of the annulus fibrosus, shows moderate signal intensity. The spinal cord and the nerve roots display moderate signal intensity, which is well contrasted against the low–signal-intensity CSF. Collections of epidural fat, which are largest at lumbar levels, produce high signal intensity on T1-and T2-weighted images. On T2-weighted MR images, CSF and the normal well-hydrated nucleus pulposus assume high signal intensity.

FIGURE 6-47. Volume rendering images of the normal lumbar spine. A: Coronal (frontal) projection. Arrow points to a hypoplastic right transverse process, a normal anatomical variant. B: Sagittal (lateral) view, note relationship of pars interarticularis (PI) to the facet joint (FJ) and root foramina (RF). C: Midplane sagittal view through the central canal. Facet joint (FJ), pars interarticularis (PI), and pedicle (P).

FIGURE 6-48. MRI of the normal spine and spinal cord. A: A T2-weighted axial MRI at the L5-S1 disk level shows the thecal sac (T) as an area of high signal intensity, the nerve roots (S1, S2) within the posterior thecal sac are of low signal intensity. Note the ligamentum flavum (LF), and fluid within the facet joints (FJ) with high–signal-intensity fluid. B: T1-weighted midsagittal MRI of the lumbosacral spine displays the nucleus pulposus (NP) of the intervertebral discs, spinal cord (SC), conus medullaris (CM), and nerve roots of the cauda equina (CE) as areas of moderate signal intensity. Cerebrospinal fluid (CSF) is of low signal intensity, and epidural fat (E) is hyperintense. C: T2-weighted midsagittal MRI of the lumbosacral spine demonstrates the increased intensity of the nucleus pulposus (NP) and CSF. peripheral annulus. In the axial plane, it can demonstrate a narrower base in relationship to the height of the herniation. A sequestered or free fragment is an extruded disc without contiguity to the parent disc. The majority of disc herniation are central or paracentral (subarticular) in location.


Source: Physical Medicine and Rehabilitation - Principles and Practice

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