Imaging Techniques Relative to Rehabilitation

Imaging Techniques Relative to Rehabilitation (39)

 A brief presentation of imaging techniques of interest to the physiatrist must necessarily be selective. Because the diagnosis and initial treatment of fractures are primarily the responsibility of the orthopedic surgeon, with the rehabilitation professional typically involved only later in the course, a full discussion of fractures is not presented in this chapter. Only those fractures that bring patients under the long-term care of the physiatrist are included (e.g., vertebral fractures with the potential to damage the spinal cord). Similarly, tumors and infectious processes are de-emphasized. Rather, emphasis is placed on imaging degenerative musculoskeletal processes, spine and head trauma, stroke, and degenerative central nervous system (CNS) diseases commonly seen by the physiatrist. We will also cover imaging in sport medicine as this is a rapidly changing area in radiology and review the current applications of diagnostic ultrasound in the evaluation of musculoskeletal disorders.

In the past two decades, computed tomography (CT) and magnetic resonance imaging (MRI) have become the most sophisticated imaging modalities for evaluating the musculoskeletal system and the CNS. Therefore, this chapter focuses mainly on the recent applications of CT and MRI in the imaging of musculoskeletal and neural pathology of interest to the physiatrist. In the final section, we will introduce some relatively new imaging technologies of interest to the physiatrist, including advanced MRI methods and ultrasound imaging (USI).

The role of plain film examinations in the assessment of abnormalities of specific joint disorders is well established in the medical literature. A brief review of the most commonly performed radiographic examinations of the extremities will be done when addressing the specific subject. 


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Musculoskeletal Imaging

Musculoskeletal Imaging (21)

The advent of the multidetector CT (MDCT) scanner has increased the applicability of this imaging technique for the assessment of the musculoskeletal system. This technology allows for the acquisition of large data set in the axial plane that can be reconstructed in multiple planes of imaging with the use of multiplanar reconstruction (MPR) algorithm. 


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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. 


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Brain Imaging

Brain Imaging (10)

The following section will be dedicated to brain imaging relevant to rehabilitation. Emphasis is placed on the imaging of ischemic and hemorrhagic strokes, head trauma, and common degenerative diseases. The imaging of brain neoplasms and infections will not be covered in this section, as it is beyond the scope of this text. 

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The aging brain is characterized on CT or MRI as demonstrating volume increases in both cortical sulci and ventricles (Fig. 6-96). T2-weighted MR images also frequently display small areas of hyperintense signal along the anterolateral margins of the anterior horns of the lateral ventricles. These changes may or may not be associated with neurologic findings.

FIGURE 6-96. A case of cortical atrophy of aging as seen by CT. Enlargement of cortical sulci and sylvian fissures (arrows) with ex vacuo ventricular dilatation (arrowheads).

Patients with Alzheimer’s disease (AD) and other dementing disorders consistently show these age changes, but because many normal elderly do also, these changes cannot be used to diagnose AD. However, the absence of these findings typically excludes AD. Findings more specifically related to AD are those involving the temporal lobe. The earliest findings in AD involve atrophy of the temporal lobe with dilation of the temporal horn of the lateral ventricle, as well as dilation of the choroidal and hippocampal fissures caused by atrophy of the hippocampus, subiculum, and parahippocampal gyrus (89).


Source: Physical Medicine and Rehabilitation - Principles and Practice

White matter diseases can be divided into demyelinating diseases, in which the white matter is normally formed and then pathologically destroyed, and dysmyelinating diseases, in which there is usually a genetically determined enzymatic disorder that interferes with the normal production or maintenance of myelin (86). The enzymatic disturbances are relatively rare; therefore, their imaging characteristics will not be described.

The most common of the demyelinating disorders is multiple sclerosis (MS). The demyelinating plaques of MS are better visualized by MRI than by CT. In fact, MRI has become the primary complementary test to confirm a clinical diagnosis of MS. It also provides a quantitative means of evaluating the present state of a patient’s disease and a mode of following its progress (87). Although the T1-weighted MR images are usually normal, the FLAIR and T2-weighted images demonstrate MS plaques as high–signal-intensity areas. These are most frequently seen in the periventricular white matter, especially around the atrium and the tips of the anterior and posterior horns of the lateral ventricles (Fig. 6-94A,B). The high–signal-intensity plaques also can be seen in other white matter areas of the cerebral hemispheres, the brain stem, and even the upper spinal cord. When these lesions are seen in patients younger than 40 years of age, they tend to be relatively specific for MS (86). In patients more than 50 years of age, the MRI findings of MS are similar to findings in some aging brains, and correlation with the clinical findings helps establish the diagnosis. Recent MS plaques that involve damage to the blood-brain barrier frequently enhance with the use of IV gadolinium-DTPA (Fig. 6-95).

FIGURE 6-94. T2-weighted (A) and FLAIR (B) MRI demonstrates the periventricular demyelinating plaques of MS as hyper- intense areas (arrows ) adjacent to the anterior horns and atria of the lateral ventricles.

FIGURE 6-95. Active MS. T1 gadolinium enhanced MR image shows periventricular enhancing MS plaques (arrows).

CT demonstrates MS plaques with less reliability than does MRI. On CT, these plaques appear as areas of hypodensity. Recent plaques in the acute phase of an exacerbation of the disease will have damage to the blood-brain barrier, and IV contrast will then enhance the periphery of the lesion. In the chronic plaque, no contrast enhancement occurs on CT or MRI. Other demyelinating diseases, although numerous, are of relatively low incidence and therefore are not described.


Source: Physical Medicine and Rehabilitation - Principles and Practice

Brain injuries may be accompanied by a number of late or long-term complications. These secondary brain injuries include cerebral herniations, which may occur under the falx cerebri or through the tentorium. Herniations can cause compression of adjacent brain substance or vessels, with the production of secondary signs and symptoms (Fig. 6-93). Penetrating injuries or fractures can injure nearby large or small vessels, producing thrombosis, embolism, traumatic aneurysm formation, or internal carotid–cavernous sinus fistula. Basal skull fractures involving the dura and arachnoid can cause CSF leaks that show up as CSF rhinorrhea or otorrhea. Local or diffuse brain swelling can compress the cerebral aqueduct or fourth ventricle, producing obstructive hydrocephalus. Subarachnoid hemorrhage may obstruct CSF resorption and cause a late-developing communicating hydrocephalus. Focal cerebral atrophy can occur at sites of infarction, hemorrhage, or trauma. Generalized atrophy can follow diffuse injuries and can be demonstrated by an increased size of sulci, fissures, cisterns, and ventricles.

FIGURE 6-93. Nonenhanced CT scan shows a left MCA infarct with mass effect causing contralateral midline shift (arrow ) corresponding to subfalcine herniation.


Source: Physical Medicine and Rehabilitation - Principles and Practice

Diffuse brain injuries include diffuse axonal injury, diffuse cerebral swelling, and edema. Diffuse axonal injury is produced by high shearing stresses that occur at different parts of the brain, including at the gray matter-white matter interface. These shearing stresses cause axonal stretching commonly involving the corpus callosum, anterior commissure, and upper brain stem. Blood vessels may or may not be disrupted. When vessels are uninterrupted, the scattered small areas of edema are best demonstrated by T1-weighted MR images as slightly hypointense or isointense regions that become hyperintense on T2-weighted images. When vessel disruption produces hemorrhages, they appear early on CT as multiple sites of hyperdensity (Fig. 6-91).

FIGURE 6-91. Diffuse axonal injury. Nonenhanced CT scan shows hemorrhagic foci at the genu of the corpus callosum (arrows).

Diffuse cerebral swelling occurs with many types of head injury. It is thought to be produced by a rapidly increased volume of circulating blood. By MRI and CT, the general brain enlargement is visualized by an obliteration or encroachment of the normal CSF spaces: the cortical sulci, the perimesencephalic and basal cisterns, and the ventricles (85). By CT, the enlarged brain may show slightly increased density.

In generalized cerebral edema, the enlarged brain also encroaches on the CSF spaces, but by CT the edema produces a generalized hypodensity that usually takes longer to develop than diffuse cerebral swelling (Fig. 6-92). The edema may obscure gray matter-white matter boundaries.

Both diffuse brain swelling and generalized cerebral edema are emergencies, because if not treated promptly they may lead to brain herniation sometimes with fatal outcomes.


FIGURE 6-92. Diffuse brain edema. Nonenhanced CT scan shows diffuse hypodensity with sulci effacement and loss of gray/white matter differentiation. Mass effect is causing almost complete obliteration of the ventricular system. Compare low parenchymal attenuation with normal cerebellar density.


Source: Physical Medicine and Rehabilitation - Principles and Practice

Focal parenchymal injuries such as contusions and intraparenchymal hemorrhage usually develop as a result of contact of the brain with the osseous walls of the cranial cavity. The coup-type injuries occur at the point of contact, and the contrecoup injuries occur on the opposite side of the brain. Contusions often occur in areas where the walls of the cranial cavity are irregular, such as the anterior and middle cranial fossae. Therefore, frontal and temporal lobe contusions are common as the brain glides along these irregular surfaces (85) (Fig. 6-90A,B).

FIGURE 6-90. A: Nonenhanced CT scan shows a small left frontal hyperdense hemorrhagic foci (arrow ). Acute extra-axial bleed is also noted (arrowhead ). B: Left temporal post-traumatic hemorrhagic contusions (arrow ). Overlying acute extra-axial bleed is noted (arrowhead).

Cerebral contusions are heterogeneous lesions containing edema, hemorrhage, and necrosis, with any element predominating. When blood makes a major contribution, the contusion appears on CT as a poorly delimited irregular area of hyperdensity. A contusion with mostly edema or necrosis may not be detectable immediately, but after a few days it appears as a hypodense region. Where there is a general admixture of elements, contusions may have a heterogeneous density. Old contusions appear as hypodense areas. By MRI, the edematous and necrotic areas have low signal intensity on T1-weighted images and high signal intensity on T2-weighted images, and thus MRI is more sensitive than CT in identifying these non- hemorrhagic contusions. The areas of hemorrhage in a contusion older than a few days will be hyperintense on both T1- and T2-weighted images.

Intraparenchymal hemorrhage differs from contusions by having better demarcated areas of more homogeneous hemorrhage. The CT and MRI characteristics of acute and evolving intraparenchymal hemorrhage are the same as for hemorrhagic stroke.


Source: Physical Medicine and Rehabilitation - Principles and Practice

Subdural hematoma is most commonly caused by acceleration- deceleration shearing stresses that rupture the bridging veins that extend from the movable brain to the fixed dural venous sinuses. The blood accumulates in a pre-existing but essentially volumeless subdural space. Normally, the pressure of the CSF holds the arachnoid in contact with the dura, thereby creating a real interval that is without significant volume. Because the subdural space is a real space surrounding all external surfaces of the brain, subdural hemorrhage tends to spread extensively over many aspects of the brain surface.

On CT examination, the typical acute subdural hematoma appears as a diffuse crescent-shaped radiodensity that may extend onto many surfaces of the brain, including the cerebral convexity, skull base, interhemispheric fissure, upper or lower surface of the tentorium, and area around the brain stem (Fig. 6-89). One way to differentiate subdural from epidural hematomas is that subdural hematomas cross sutures lines yet do not cross midline, whereas epidural hematomas do not cross suture lines yet can cross midline. There are two ways of classifying subdural hematomas based on their changing radiographic appearance over time (83). One scheme divides them into acute (i.e., more radiodense than adjacent gray matter), subacute (i.e., isodense to gray matter), and chronic (i.e., hypodense to gray matter). Another scheme simply lumps the subacute and chronic into the chronic category. The subdural hematoma typically effaces the adjacent gyri, produces inward displacement of the gray-white matter junction, and may compress the ventricle or cause brain herniation under the falx or through the tentorium.

FIGURE 6-89. Bilateral panhemispheric chronic subdural hematomas with superimposed acute bleed and hematocrit levels (arrows).

As the subdural hematoma ages, the hemoglobin protein producing its radiodensity is broken down and removed, and a vascular granulation tissue develops along its inner surface. Over a few weeks, the subdural hematoma usually becomes isodense or hypodense to gray matter (84). Because of volume loss, the chronic subdural hematoma may lose its concave inner border and become more focal, even occasionally assuming a biconvex outline. Isodense subdural hematomas are more difficult to discriminate. Their presence can be implied indirectly by their mass effects on the underlying brain. An injection of contrast material will enhance both the vascular membrane and the displaced cortical vessels, allowing discrimination of the hematoma from the adjacent cortex.

Patients who present first with a chronic subdural hematoma may have no recollection of any antecedent trauma because the traumatic episode may have been so slight that it was forgotten. Chronic hematomas commonly involve the elderly, where loss of cerebral volume puts the bridging veins under increased stress and makes them more susceptible to rupture by minor trauma.

MRI has valuable unique imaging properties that make it very sensitive to the detection of some extracerebral hemorrhages. First, the high signal intensity that subacute hematomas display on T1- and T2-weighted images makes MRI more sensitive than CT for detecting hematomas that are isodense by CT (73). Even chronic subdural hematomas remain hyperintense to CSF and gray matter for several months, which is long after they have become isodense or hypodense on CT. Also, the ability of MRI to discern the displaced signal voids of cortical or dural vessels facilitates the identification of small extracerebral hemorrhages. In addition, when the hematoma collects around the obliquely placed tentorium, axial CT images may average it into adjacent tissues. In these cases, the multiplanar imaging properties of MRI can be very valuable. Also, small hematomas next to the calvarium can be better seen by MRI because they are contrasted against the osseous signal void.


Source: Physical Medicine and Rehabilitation - Principles and Practice

Epidural hematoma is caused by tears of the middle meningeal artery or vein, or of a dural venous sinus. The blood accumulates in the interval between the inner table of the calvarium and the dura by gradually stripping the dura from its bony attachment. CT visualizes the epidural hematoma as a well-localized biconvex radiodense mass (83) (Fig. 6-88). It is commonly, though not invariably, associated with a skull fracture. It causes mass effect upon the adjacent brain parenchyma with effacement of the underlying sulci, compression of the brain and ventricles, and possible contralateral midline shift. It is important to note that midline shift is a secondary injury caused by subfalcine herniation, which is herniation of the cingulate gyrus under the falx cerebi, and can eventually lead to ipsilateral anterior cerebral artery infarction. When there is a question about whether the mass might be intraparenchymal, contrast injection enhances the dura, establishing the epidural position of the clot. As the clot lyses over the next few weeks, it shrinks and changes to isodense and then hypodense relative to the brain. The inner aspect of the clot vascularizes, and this may produce a thicker rim of enhancement on late contrast studies. The overlying dura may calcify. Epidural hematoma may be associated with subdural, subarachnoid, or intraparenchymal hemorrhages.

FIGURE 6-88. Epidural hematoma. Nonenhanced CT scan of the head shows a left parietal biconvex extra-axial hyperdensity (arrow).


Source: Physical Medicine and Rehabilitation - Principles and Practice

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
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