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

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

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

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