A practical approach to spine imaging.

Review Article Address correspondence to Dr Joshua P. Klein, Department of Neurology, Room AB-124, Brigham and Women’s Hospital, 75 Francis Street, Boston, MA 02115, [email protected]. Relationship Disclosure: Dr Klein serves on the board of directors of The American Society of Neuroimaging; receives royalties from McGraw-Hill for Adams and Victor’s Principles of Neurology, 10th Edition; receives compensation for serving on the editorial boards of AccessMedicineYNeurology Collection and the Journal of Neuroimaging; and receives compensation for work as a consultant from Guidepoint Global. Unlabeled Use of Products/Investigational Use Disclosure: Dr Klein reports no disclosure. * 2015, American Academy of Neurology.

A Practical Approach to Spine Imaging Joshua P. Klein, MD, PhD ABSTRACT Purpose of Review: The spine is a complex mechanical structure that surrounds and protects the spinal cord and nerve roots. It is capable of multidirectional movement and is susceptible to a large variety of pathologies that can affect spinal cord and nerve root function. Detection of spinal pathology is aided by a familiarity with normal spinal anatomy and its appearance on CT and MRI studies. Imaging of the spine is performed frequently, and a systematic approach toward image interpretation can prevent overlooking or incompletely assessing a lesion. Recent Findings: CT and MRI of the spine provide detailed views of normal and abnormal structures and allow for differentiation of vascular, inflammatory, infectious, neoplastic, traumatic, and degenerative etiologies of spine disease. Summary: This article provides a strategy for interpreting CT and MRI studies of the spine and can be used as a primer for the other articles that follow in this issue of , in which specific etiologies of spine and spinal cord pathology are considered in detail. Continuum (Minneap Minn) 2015;21(1):36–51.

INTRODUCTION The spine is a complex mechanical structure that houses and protects the spinal cord and nerve roots. Unlike the immobile cranium, the spine is capable of multidirectional movement, including flexion, extension, rotation, and lateral bending. Just as in any machine with moving parts, a risk of malfunction exists; in the spine, malfunction is most often the result of progressive degeneration of joints and bones. Bipedal animals, including humans, endure additional stress on the spine, particularly the lumbar spine, caused by axial weight bearing against gravity. The mechanical demand of weight bearing is further exacerbated by the high prevalence of obesity in many populations. Imaging of the spine is performed frequently, and accurate interpretation of the images demands a systematic approach. This article provides a general strategy for interpreting CT and

36

MRI studies of the spine. An overview of this strategy is shown in Table 2-1. The goal is to enhance clinicians’ participation in spine image analysis and interpretation. IMAGING MODALITIES The spine is generally imaged using x-ray, CT, or MRI. Table 2-2 shows the imaging characteristics of various spinal structures on CT and MRI. It is best to localize potential spinal lesions clinically and image a focused area (eg, the cervical spine). When there is concern for diffuse or multiple spinal abnormalities, as may occur in metastatic disease, or when spinal cord or cauda equina compression is suspected following trauma, whole spine imaging (from occiput to coccyx) can be obtained. IV contrast should be administered when the differential diagnosis includes infection, neoplasm, inflammation, or demyelination.

www.ContinuumJournal.com

Copyright © American Academy of Neurology. Unauthorized reproduction of this article is prohibited.

February 2015

KEY POINTS

h It is best to localize

TABLE 2-1 Approach to Spine Imaging Structure

Task

Vertebral alignment

Count and label vertebrae, assess kyphosis, lordosis, scoliosis, and spondylolisthesis

Vertebral height and signal

Assess for compression fractures, masses, and pathologic marrow replacement

Disk height and signal

Assess for disk degeneration, bulging, herniation, and inflammation

Ligaments

Assess for nonlinearity, tears, hypertrophy, or inflammation

Paraspinal soft tissues

Assess for inflammation, masses, and muscle atrophy

Meninges

Assess for inflammation, nerve root clumping, and masses Assess for cord displacement

Cord position Cord caliber

Assess for focal or diffuse cord expansion or atrophy

Neural foramina

Assess for foraminal narrowing and nerve root compression, and for masses

Cord lesions

Assess whether cord abnormality is intrinsic or secondary to external compression, and whether regional cord involvement exists (ie, one tract, anterior/posterior/lateral/central)

potential spinal lesions clinically and image a focused area (eg, the cervical spine). When there is concern for diffuse or multiple spinal abnormalities, as may occur in metastatic disease, or when spinal cord or cauda equina compression is suspected following trauma, whole spine imaging (from occiput to coccyx) can be obtained.

h IV contrast should be administered when the differential diagnosis includes infection, neoplasm, inflammation, or demyelination.

TABLE 2-2 Imaging Modalities, Sequences, and Appearance of Various Structures Imaging Modalities and Sequences

Lipid

CSF/Edema

Bone

Spinal Cord/ White Nerve Matter

Gray Matter

CTa

-70 to -30

0 to 15

91000

20 to 45

35 to 45

T1-weighted

Hyperintense

Hypointense

Hypointense

Intermediate

Brighter

Darker

T2-weighted

Less hyperintense

Hyperintense Hypointense

Intermediate

Darker

Brighter

Short tau inversion recovery (STIR)

Hypointense

Hyperintense Hypointense

Intermediate

Darker

Brighter

T1-postcontrast

Normal enhancement of vascular structures, abnormal enhancement at sites of blood-brain barrier disruption and hypervascularity (tumor, infection, inflammation, demyelination)

Diffusion-weighted imaging (DWI)

Reduced diffusivity (DWI hyperintense, apparent diffusion coefficient hypointense) at foci of cytotoxic edema (acute infarction) or hypercellularity (abscesses and some tumors); enhanced diffusivity (DWI hyperintense, apparent diffusion coefficient hyperintense) at foci of vasogenic edema, sclerosis, gliosis

Susceptibility-weighted imaging (SWI)

Hypointense at foci of hemorrhage

20 to 30

CT = computed tomography. a Number values are in Hounsfield units.

Continuum (Minneap Minn) 2015;21(1):36–51



37

Practical Approach to Spine Imaging KEY POINTS

h The short tau inversion recovery sequence is a T2-weighted sequence in which the relatively hyperintense signal generated by lipid is suppressed and is often used with spine imaging to help differentiate lipid and edema.

h Although most often the spine is composed of 7 cervical vertebrae, 12 thoracic vertebrae, and 5 lumbar vertebrae, some variability exists, requiring a reliable system for numbering the vertebrae on radiographic studies.

38

X-ray and CT are the preferred modalities to assess for acute spinal trauma because they are fast, relatively inexpensive, widely available, and safe. X-ray images can be obtained in multiple positions, for example, in flexion, extension, or with rotation of the neck.1 This is helpful to assess for dynamic instability of the spine, which can result from spinal ligament injury, among other pathologies. Although CT is best for assessing bone injury and deformation, narrowing of the spinal canal and neural foramina leading to compression of the spinal cord and nerve roots can be easily detected as well. Contrast myelography, where contrast material is injected intrathecally and allowed to diffuse throughout the CSF surrounding the spinal cord, is still occasionally used to highlight the contour of the spinal subarachnoid space in relation to surrounding bones and soft tissue. In this way, it can demonstrate a block in free flow of CSF corresponding to narrowing of the spinal canal and potential compression of the spinal cord. CT myelography can also be used to identify the location of a CSF leak, in which case an extradural collection of contrast may be seen adjacent to a discontinuity in the dura. The CT myelography technique is also a useful substitute for patients who cannot undergo MRI of the spine. MRI provides a more nuanced evaluation of the spine, allowing excellent differentiation between bones, muscle, fat, ligaments, dura, CSF, spinal cord, nerve roots, and blood vessels.2 MRI is safe as well, so long as the patient has been screened for ferromagnetic material. On T1-weighted images, lipid has a shorter recovery time than water, meaning that tissues containing more lipid and less water appear brighter than tissues containing less lipid and more water; CSF and edema, therefore, appear hypointense, and gray matter is hypointense compared with white matter (Figure 2-1).

The T1 sequence is useful for assessing fat-nerve and fat-fluid interfaces. On T2-weighted images, lipid has a shorter decay time than water, meaning that tissues containing more lipid and less water appear darker than tissues containing less lipid and more water. CSF and edema, therefore, appear hyperintense, and gray matter is hyperintense compared with white matter. The T2 sequence is useful for assessing spinal cord and nerve root interfaces with CSF, as well as for detecting inflammation and gliosis in the spinal cord. The short tau inversion recovery (STIR) sequence is often used with spine imaging to help differentiate lipid and edema. STIR is a T2-weighted sequence in which the relatively hyperintense signal generated by lipid is suppressed (Figure 2-1). Edema remains hyperintense on STIR. Several other MRI sequences, including diffusion-weighted and susceptibility-weighted imaging, are occasionally used in the spine to help characterize a lesion. The principles of each sequence are essentially the same as for brain imaging (Table 2-2). LANDMARKS AND ORIENTATION TO SPINAL LEVEL Imaging of the cervical spine by CT or MRI typically covers the inferior aspect of the posterior fossa to the upper thoracic vertebrae. Imaging of the thoracic spine covers the lower cervical vertebrae to the upper lumbar vertebrae, and imaging of the lumbosacral spine includes the lower thoracic vertebrae to the lower sacrum (Figure 2-1). Although most often the spine is composed of 7 cervical vertebrae, 12 thoracic vertebrae, and 5 lumbar vertebrae, some variability exists, requiring a reliable system for numbering the vertebrae on radiographic studies.3 For the cervical vertebrae, it is easiest to identify the odontoid process of C2 on a sagittal image and count inferiorly. On



February 2015

MRI of a normal cervical (AYC), thoracic (DYF), and lumbosacral (GYI) spine. The C2 and L5 vertebral bodies are labeled for orientation (A, arrow; G, arrow). The images in the left column (A, D, G) are T1-weighted, the images in the center column (B, E, H) are T2-weighted, and the images in the right column (C, F, I) are short tau inversion recovery (STIR). On T1-weighted images, CSF is hypointense and marrow within the vertebral bodies is hyperintense. On T2-weighted images, CSF is hyperintense and the nucleus pulposus is also hyperintense and easily distinguished from the surrounding hypointense annulus fibrosus. With STIR, the hyperintense signal from lipid is suppressed so the marrow as well as subcutaneous and abdominal fat is rendered hypointense, while all fluid remains as hyperintense as on T2-weighted images. Among many other structures, the basivertebral veins become more conspicuous on STIR (C, arrow).

FIGURE 2-1

Continuum (Minneap Minn) 2015;21(1):36–51



39


h The ventral root of a spinal nerve contains mostly motor information and appears as a thin fiber bundle. In contrast, the dorsal root expands into a ganglion containing the cell bodies of sensory neurons and is visible at the periphery of the spinal canal near the neural foramen.

h The normal spine appears curved when viewed in the sagittal plane, with cervical and lumbar lordoses and thoracic kyphosis.

h Scoliosis can occur as a secondary complication of a variety of diseases, including spinal dysraphism, neurofibromatosis, cerebral palsy, and other congenital movement disorders and neuromuscular diseases.

a sagittal view of the lumbar spine, one can count up from the first nonsacral vertebra or down from the first nonYrib-containing vertebra. Either method is acceptable, as long as the method of labeling is clear. Labeling the vertebrae of the thoracic spine is more challenging, particularly when the cervical or lumbar spine is not included. Here, one can count down from the first rib-containing vertebra (T1) or up from the most inferior ribcontaining vertebra (T12). Again, either method is acceptable, as long as the method of labeling is evident. An additional numbering problem arises from the fact that there are seven cervical vertebrae and eight cervical nerve roots.3 In the cervical spine, the nerve roots exit the spinal cord laterally and above their named vertebrae (ie, the C5 nerve root exits the neural foramina between the C4 and C5 vertebrae). The C8 nerve root exits the neural foramina between the C7 and T1 vertebrae. Below C8, nerve roots exit below their named vertebrae

MRI of the lumbar spine. A T1-weighted parasagittal view of a normal neural foramen containing a hypointense nerve root bundle surrounded by hyperintense fat (A, arrow). One vertebral level inferiorly, there is narrowing of the neural foramen, partial effacement of foraminal fat, and displacement of the nerve root bundle due to an intervertebral disk herniation. B, The normal appearance of dorsal root ganglia within neural foramina is shown on an axial T2-weighted image. Like the nerve roots on the sagittal image, the ganglia appear hypointense and are surrounded by hyperintense fat.

FIGURE 2-2

40

(ie, the T5 nerve root exits the neural foramina between the T5 and T6 vertebrae, and the L5 nerve root exits the neural foramina between the L5 and S1 vertebrae). In the lumbar spine, the nerve roots arising from the conus medullaris form the cauda equina and descend in the spinal canal before exiting a neural foramen. A nerve root destined to exit the lumbar or sacral spine at any given level begins to separate from the cauda equina one level above and move toward the lateral recess (the most lateral portion of the spinal canal medial to the pedicle and adjacent to the zygapophysial joint) of the spinal canal. At this point, is it called the traversing nerve root and is susceptible to compression by intervertebral disk herniations and facet hypertrophy. Thus, the L5 nerve root traverses between the L4 and L5 vertebrae and, as stated above, exits between the L5 and S1 vertebrae. The ventral root of a spinal nerve contains mostly motor information and appears as a thin fiber bundle. In contrast, the dorsal root expands into a ganglion containing the cell bodies of sensory neurons and is visible at the periphery of the spinal canal near the neural foramen (Figure 2-2). The dorsal root ganglion is surrounded by a venous plexus and, therefore, may demonstrate some enhancement when imaging is performed with contrast. Consequently, pathologic ganglionitis can be difficult to detect, although prominent enhancement with enlargement of a ganglia would be suspicious. Vertebral Alignment Assessment of vertebral alignment is best performed with sagittal and coronal images. The normal spine appears curved when viewed in the sagittal plane, with cervical and lumbar lordosis and thoracic kyphosis.4Y6 Average curvatures



February 2015

are: cervical lordosis 20 degrees, thoracic kyphosis 35 degrees, and lumbar lordosis 29 degrees.7 Abnormal lateral deviation of the spine, or scoliosis, is easily detected if some vertebrae appear out of the plane of a midsagittal image.8 On coronal images, lateral deviation of the spine (levoscoliosis is bowing to the left; dextroscoliosis is bowing to the right) can be precisely measured. Other elements of the vertebrae, such as the transverse and spinous processes, should be aligned as well. Alignment abnormalities can be generally classified as regional versus diffuse. Scoliosis is defined as a lateral deviation of the spine of greater than 10 degrees. Scoliosis can occur as a secondary complication of a variety of diseases, including spinal dysraphism (malformation of the spine), neurofibromatosis, cerebral palsy, and other congenital movement disorders and neuromuscular diseases.9 Scoliosis in association with congenital fusion of one or more cervical vertebrae constitutes the rare Klippel-Feil syndrome. Adjacent vertebrae articulate at intervertebral disks and zygapophysial (facet) joints and are further supported by several longitudinal ligaments. The anterior and posterior surfaces of adjacent vertebral bodies should be parallel. Malposition of one vertebral body over another is termed spondylolisthesis. By convention, the position of the upper vertebrae is described in relation to the inferior: anterolisthesis is anterior displacement; retrolisthesis is posterior displacement. These misalignments can cause narrowing of the neural foramen as well as of the spinal canal. Spondylolistheses are graded radiographically based on the degree of slippage: grade 1 is less than 25%, grade 2 is 26% to 50%, grade 3 is 51% to 75%, and grade 4 is 76% to 100%. Grade 5, referring to complete dislocation of two adjacent vertebrae, is termed spondyloptosis.10 Continuum (Minneap Minn) 2015;21(1):36–51

While the most common cause of spondylolisthesis in adults is degenerative osteoarthritis, in the pediatric population, the more frequent etiology is spondylolysis. Spondylolysis refers to a defect in the pars interarticularis that lies in the interfacet space between the vertebral lamina and pedicle.10 The defect allows for slippage of one vertebra over another, most often in the lower lumbar spine. Pars interarticularis defects are seen in 3% to 6% of the population and are known to run in families.11 Spondylolysis often follows repetitive trauma to the spine and has been linked to a variety of high-impact sports. The pars interarticularis defect is best seen on lateral radiographs or CT and appears as a discontinuity in the bone with or without accompanying spondylolisthesis. Pars interarticularis defects, as well as other vertebral fractures, deformities, and misalignments, should be sought whenever spondylolisthesis is present. In addition to osteoarthritic pain, the obvious clinical relevance of these defects is potential narrowing of the spaces through which neural structures pass. Narrowing of the spinal canal can be subjectively graded, with ‘‘mild’’ corresponding to effacement of CSF, ‘‘moderate’’ corresponding to contact and displacement of the spinal cord or the cauda equina nerve roots, and ‘‘severe’’ corresponding to compression of these neural structures. Likewise, narrowing of the neural foramina due to spondylolisthesis with or without disk herniation can be subjectively graded, with ‘‘mild’’ corresponding to effacement of intraforaminal fat, ‘‘moderate’’ corresponding to contact and displacement of an exiting nerve root, and ‘‘severe’’ corresponding to compression of a nerve root. Although exceptions exist, the severity of clinical deficits most often corresponds to the degree of spinal cord and nerve root compression.

KEY POINTS

h By convention, the position of the upper vertebrae is described in relation to the inferior: anterolisthesis is anterior displacement; retrolisthesis is posterior displacement.

h While the most common cause of spondylolisthesis in adults is degenerative osteoarthritis, in the pediatric population, the more frequent etiology is spondylolysis. Spondylolysis refers to a defect in the pars interarticularis that lies in the interfacet space between the vertebral lamina and pedicle.

h Narrowing of the spinal canal can be subjectively graded, with ‘‘mild’’ corresponding to effacement of CSF, ‘‘moderate’’ corresponding to contact and displacement of the spinal cord or the cauda equina nerve roots, and ‘‘severe’’ corresponding to compression of these neural structures.

h Narrowing of the neural foramina due to spondylolisthesis with or without disk herniation can be subjectively graded, with ‘‘mild’’ corresponding to effacement of intraforaminal fat, ‘‘moderate’’ corresponding to contact and displacement of an exiting nerve root, and ‘‘severe’’ corresponding to compression of a nerve root.



41


h The MRI appearance of progressive osteoarthritic degeneration of the vertebral endplates has been classified into three types by Modic.

h Vertebral collapse is most often the result of trauma but can be seen in pathologic processes that weaken bone architecture, including osteoporosis, osteogenesis imperfecta, osteomyelitis, and lytic lesions from primary or metastatic tumors.

42

Degenerative osteoarthritis produces a pattern of imaging abnormalities that are important to recognize and distinguish from other pathophysiologic processes. Osteoporosis of the spine is recognized on x-ray and CT as thinning of cortical bone and increased radiolucency. Osteoporosis becomes evident on these imaging modalities when loss of bone density is greater than approximately 30%. If focal lytic lesions of bone are seen, processes such as metastases and disseminated multiple myeloma should be considered. On MRI, osteoporosis is more difficult to detect since bone appears hypointense on most sequences. The MRI appearance of progressive osteoarthritic degeneration of the vertebral endplates (the edge of the vertebral bone facing the intervertebral disk) has been classified into three types by Modic.12 Type I change appears T1 hypointense and T2 hyperintense and correlates with formation of granulation tissue subjacent to the endplates. Type II change appears T1 and T2 hyperintense and correlates with fat replacement of bone marrow. Suppression of the T2 hyperintensity on STIR sequence further confirms the presence of fat. Type III change appears T1 and T2 hypointense and correlates with chronic degeneration of the endplates. In a given patient, different Modic types may be seen at different vertebral levels, depending upon the degree and chronicity of degeneration. Beyond osteoarthritic degeneration, fatty replacement of bone marrow can also be seen following radiation therapy and in other settings. In addition to degenerative bone loss, a common finding is bony overgrowth at sites of disk and endplate degeneration. The resulting osteophytes or diskosteophyte complexes are easily recognized on CT and MRI and often impinge upon neural structures. For more information, refer to the article ‘‘Myelopathy

Due to Degenerative and Structural Spine Diseases’’ by Jinny O. Tavee, MD, and Kerry H. Levin, MD, FAAN, in this . issue of Vertebral Height Vertebral height increases fairly consistently from the cervical spine down to the lower lumbar spine. Adjacent vertebral bodies should be nearly the same height. Average vertebral heights are cervical 1.4 cm, upper thoracic 1.8 cm, lower thoracic 2.3 cm, upper lumbar 2.6 cm, and lower lumbar 2.8 cm.6,7 Loss of vertebral height should raise concern for collapse of a vertebra. Vertebral collapse is most often the result of trauma but can be seen in pathologic processes that weaken bone architecture, including osteoporosis, osteogenesis imperfecta, osteomyelitis, and lytic lesions from primary or metastatic tumors. The main risks of vertebral collapse are compression of neural structures and an unstable vertebral column. Fractures are graded by loss of vertebral height: grade 0 is no loss of height; grade 1 is 20% to 25%; grade 2 is 26% to 40%; and grade 3 is greater than 40%.10 Vertebral fractures are further distinguished by the shape of the deformity.13 Wedged vertebrae are most compressed anteriorly, whereas crushed vertebrae are most compressed posteriorly. Biconcave deformities are seen as well. These deformities can produce abrupt angularities of the spine when viewed in the sagittal plane. Severe compression fractures resulting from high axial loads can cause bursting of a vertebra, with shards of bone penetrating into adjacent tissues including the spinal cord. A Chance fracture is a complex fracture consisting of a wedge-shaped anterior vertebral compression fracture with a transverse fracture through the posterior elements of the vertebra, resulting from hyperflexion of the spine.



February 2015

Several other traumatic vertebral fractures may be encountered.14 The Jefferson fracture refers to a fracture of the anterior and posterior arches of the C1 vertebra, usually resulting from neck hyperextension or a severe axial load on the occiput. The hangman’s fracture (traumatic spondylolisthesis of C2) refers to bilateral pedicle or pars interarticularis fractures of the C2 vertebra, caused by similar mechanisms. The clay shoveler’s fracture is an avulsion fracture of the spinous process of the C6 or C7 vertebra caused by abrupt hyperflexion of paraspinal muscles. Several fractures of the odontoid process (dens) of C2 have also been identified: (1) type I fractures are oblique and involve the tip or body of the dens; (2) type II fractures are more transverse and involve the base of the dens; and (3) type III fractures involve the base of the dens with extension into the body of C1. On CT, traumatic fractures appear as linear interfaces between the fracture line and the surrounding bone.13 With small fractures, cortical bone margins are preserved and bone expansion is not seen. With larger or comminuted (broken into several pieces) fractures, bone margins may be less distinct. On MRI, cortical bone appears hypointense on standard sequences, and small fractures may be impossible to visualize. However, fractures cause edema of surrounding tissue, which can be detected on MRI. The STIR sequence reduces the normal hyperintensity from bone marrow so that any residual hyperintensity in the bone is due to fluid (either edema or blood). The presence of a fracture is, therefore, inferred by a focus of edema within or adjacent to bone. CT and MRI reveal imaging features that favor the presence of a malignant etiology of a fracture such as underlying infection or tumor.13 These inContinuum (Minneap Minn) 2015;21(1):36–51

clude indistinct cortical bone margins, heterogenous bone marrow signal that could represent marrow replacement by tumor, bone expansion due to tumor growth, pedicle involvement representing spread of infection or tumor beyond the vertebral body, the presence of an adjacent soft tissue mass that could represent infection or tumor, and multilevel lesions that could represent a diffuse underlying process such as metastatic disease. Osseous metastases rarely cross intervertebral disk spaces, whereas infectious osteomyelitis often erodes the vertebra and extends into the disk space. Systemic autoimmune inflammatory conditions, including rheumatoid arthritis and the seronegative spondyloarthropathies, affect the vertebral bones as well. The most commonly encountered abnormalities associated with rheumatoid arthritis are of the cervical spine and include a retrodental (C2) pannus, anterior subluxation of C1 on C2, vertical subluxation of C1 on C2 (basilar invagination), and bony erosions, all of which can reduce normal range of motion and, in severe cases, lead to spinal instability and spinal cord compression.15 Atlantoaxial instability is also seen in ankylosing spondylitis, along with several other characteristic abnormalities discussed later in this article.15,16 Two intravertebral abnormalities are common enough to warrant their inclusion in this section. The first is a hemangioma, typically seen within the trabecular bone of the vertebral body and consisting of a mix of vascular and adipose tissue.17 These lesions are fairly well circumscribed and appear hyperintense on both T1-weighted and T2-weighted sequences (Figure 2-3). The lesion remains hyperintense on the STIR sequence, in distinction to focal fat deposits whose hyperintense signal is suppressed. Because of the

KEY POINT

h The most commonly encountered abnormalities associated with rheumatoid arthritis are of the cervical spine and include a retrodental (C2) pannus, anterior subluxation of C1 on C2, vertical subluxation of C1 on C2 (basilar invagination), and bony erosions, all of which can reduce normal range of motion and, in severe cases, lead to spinal instability and spinal cord compression.



43

Practical Approach to Spine Imaging

hypointense, T2 hyperintense, and nonenhancing). These lesions are usually the result of axial loading and are more prevalent in the lower thoracic and lumbar spine. Acute prolapses induce variable degrees of edema and inflammation in the adjacent vertebral body.20 In these cases, infectious diskitis and osteomyelitis, which cause abnormal enhancement and destruction of the disk and endplate, must be considered.21Y23 Last, when there has been prior surgical instrumentation of the spine, it is important to evaluate all implanted hardware for malposition, disconnection, or bone erosion.3,24 An air or fluid collection surrounding an implanted device should be interpreted as a potential abscess until proven otherwise.

Some common spinal abnormalities. A, B, An intravertebral hemangioma is shown on sagittal T1-weighted (A) and T2-weighted (B) images (arrows). The lesion appears relatively hyperintense compared with surrounding marrow on both sequences since the lesion is partially composed of fat. C, D, Typical Schmorl nodes are shown in sagittal T1-weighted (C) and T2-weighted (D) images of the upper lumbar spine (arrows). The focal discontinuities in the vertebral endplates contain herniated disk material that has the same intensity as the parent disk. E, F, A perineural (Tarlov) cyst is seen at the location of nerve roots exiting the spinal canal at L5 (arrows). Note that, like CSF, the cyst contents are T1 hypointense (E) and T2 hyperintense (F). Hypointense nerve fibers can be seen within the cyst on the T2-weighted image.

FIGURE 2-3

KEY POINT

h An air or fluid collection surrounding an implanted device should be interpreted as a potential abscess until proven otherwise.

44

vascular nature of a hemangioma, contrast enhancement is evident. Hemangiomas rarely bleed and rarely weaken surrounding bone. The second common lesion is the Schmorl node, which describes a focal prolapse of disk and cartilage through a defect in the vertebral body endplate and into the trabecular compartment of the vertebra (Figure 2-3).18,19 These nodes are identified by the contour deformity of the vertebral endplate as well as by their signal characteristics, typically that of disk material (T1

Disk Height Intervertebral disks absorb direct, oblique, and torsional forces applied to the vertebral column, so they are highly susceptible to use-related and age-related degeneration. Neck and back pain, much of which is undoubtedly due to disk degeneration, is one of the most common medical concerns. Therefore, recognizing the imaging appearance of normal and injured intervertebral disks is of great importance. The normal disk contains a gelatin matrix called the nucleus pulposus, a remnant of the fetal notochord, which appears T2 hyperintense and is bounded by the vertebral endplates on its superior and inferior surfaces, and the annulus fibrosus and longitudinal spinal ligaments laterally.3 The disk material should not extend beyond the lateral margins of the vertebral bones. Average normal disk height is upper cervical 6 mm, lower cervical 4.5 mm, upper thoracic 4.5 mm, lower thoracic 5.9 mm, upper lumbar 11 mm, and lower lumbar 12 mm.6,7 As might be expected, one of the clearest signs of disk degeneration is



February 2015

loss of disk height. Coincident with loss of disk height is progressive loss of T2 hyperintensity in the nucleus pulposus. Loss of T2 hyperintensity corresponds to reduction of disk turgor, or so-called disk desiccation. As this degeneration proceeds, there can be diffuse (circumferential) bulging of the disk or more focal protrusion of disk material beyond its normal margins. Focal disk protrusions may disrupt the integrity of the annulus fibrosus. The normal annulus fibrosus is T2 hypointense; an anular tear appears as a radially or longitudinally oriented focus of T2 hyperintensity in the annulus fibrosus adjacent to the protruding disk. Focal disk herniations are classified as protrusions when the diameter of the herniated material is less than the diameter of the base of herniation. They are classified as extrusions when the diameter of the herniated material is greater than the diameter of the base of herniation (ie, there is a ‘‘waist’’). When herniated material separates from the disk of origin, herniations are classified as sequestrations. Fragments of sequestered disks can migrate craniocaudally in the spinal canal. Disk bulges and herniations, if posteriorly oriented, can impinge upon the spinal canal and its contents. Posterolateral bulges and herniations may impinge upon the lateral recess as well as the neural foramina. Lateral bulges and herniations may compress exiting nerve roots. Ligaments The vertebral column is supported by three longitudinal ligaments and additional intervertebral ligaments that provide structural support to the spine and aid in its flexibility. The anterior longitudinal ligament runs anterior to the vertebral bodies, and the posterior longitudinal ligament runs posterior to the vertebral bodies and adjacent to the anterior thecal sac. These ligaments, along with the annulus fibrosus, help contain the Continuum (Minneap Minn) 2015;21(1):36–51

intervertebral disks. Similarly, the facet joint between the superior and inferior articular processes is bounded by a ligamentous structure called the zygapophysial capsule. The supraspinous ligament runs posteriorly, connecting the spinous processes. Interspinous ligaments provide further support between adjacent spinous processes. A variety of pathologies can affect the spinal ligaments; two of the most dramatic pathologies are diffuse idiopathic skeletal hyperostosis (DISH), where linear ‘‘flowing’’ ossification of the anterior longitudinal ligament limits range of motion of the spine,25 and ankylosing spondylitis, where calcification of the anterior longitudinal ligament, along with zygapophysial and sacroiliac arthritis, atlantoaxial subluxation, and diffuse peripheral enthesitis (inflammation at the point of insertion of tendon or ligament into bone), produces pain and limits movement.16 The ligamentum flavum (ligaments that extend between the laminae of adjacent vertebrae), although comparatively small in size, assumes clinical relevance owing to its location immediately posterior to the thecal space in the spinal canal. With osteoarthritic degeneration, the ligamentum flavum can hypertrophy and bunch, potentially compressing neural structures. Unique ligaments of the upper cervical spine should also be mentioned. The transverse ligament of C1 is a dense band of tissue that prevents distraction of the odontoid process of C2 (the dens) from its articulation with the posterior aspect of the anterior arch of C1. The alar ligament, connecting the odontoid process with the occipital condyles, provides additional support. Laxity of these ligaments can produce atlantoaxial instability.

KEY POINTS

h The normal annulus fibrosus is T2 hypointense; an anular tear appears as a radially or longitudinally oriented focus of T2 hyperintensity in the annulus fibrosus adjacent to the protruding disk.

h A variety of pathologies can affect the spinal ligaments; two of the most dramatic pathologies are diffuse idiopathic skeletal hyperostosis, where linear ‘‘flowing’’ ossification of the anterior longitudinal ligament limits range of motion of the spine, and ankylosing spondylitis, where calcification of the anterior longitudinal ligament, along with zygapophysial and sacroiliac arthritis, atlantoaxial subluxation, and diffuse peripheral enthesitis, produces pain and limitation of movement.

Paraspinal Soft Tissues Imaging of the spine invariably includes the paraspinal musculature, www.ContinuumJournal.com


45

Practical Approach to Spine Imaging KEY POINT

h A separate re-review of all images will help avoid overlooking nonspinal lesions. If an abnormality is incompletely visualized or assessed, or if ambiguity exists about the nature of the lesion, further imaging is generally recommended.

which should appear symmetric. Denervation or other injury to paraspinal muscles can cause muscle edema, inflammation, or atrophy. Similarly, unexpected abnormalities in other organs are often revealed, as summarized in Table 2-3.26 A separate re-review of all images will help avoid overlooking these nonspinal lesions. If an abnormality is incompletely visualized or assessed, or if ambiguity exists about the nature of the lesion, further imaging is generally recommended. Spinal Canal The cross-sectional area of the spinal canal is greatest in the cervical and lower lumbar spine. These regional enlargements of the canal are due mostly to increases in spinal canal width rather than depth. Canal width (transverse) ranges from approximately 25 mm to 30 mm in the cervical and lumbar spine and 18 mm to 22 mm in the thoracic spine. Canal depth (anterior to posterior) is fairly consistently 15 mm to 20 mm throughout the spine.7 Congenital or acquired canal stenoses can be assessed by comparison with these normal values. Focal canal stenoses most often result

from osteoarthritic degeneration, and spondylolisthesis is frequently seen. Besides the thecal sac, the spinal canal contains several other structures, and precise assessment of the compartment of origin of a lesion determines its most likely etiology, as shown in Table 2-4. As described earlier, the anterior and posterior margins of the spinal canal are bounded by the posterior longitudinal ligament and the ligamentum flavum, respectively. Between these ligaments and the dura is a narrow epidural space that contains fat. With CT, epidural fat is difficult to distinguish from adjacent ligament and dura since all of these structures are relatively hypodense. These structures can more easily be distinguished on MRI since epidural fat is T1 hyperintense compared with ligament and dura. Spinal lipomas appear as focal epidural lesions that indent the thecal sac. Lipomas are easily recognized by their homogeneity, lack of enhancement with contrast, and T2 signal suppression on STIR sequence. Epidural lipomatosis refers to longitudinally extensive hypertrophy of adipose tissue that can compress neural

TABLE 2-3 Unexpected Findings in Paraspinal Structures

46

Region

Finding

Throughout spine

Paraspinal muscle atrophy or hypertrophy, paraspinal fluid collections, soft tissue masses

Cervical spine

Thyroid nodule, goiter, vocal cord or cartilage asymmetry, lymphadenopathy, vascular atheromatosis and stenosis, lung apex pathology, pneumonia, pulmonary embolism, pleural effusion or mass

Thoracic spine

Aortic aneurysm or dissection, vascular atheromatosis and stenosis, pulmonary embolism, pleural effusion or mass, pneumonia or lung mass

Lumbosacral spine

Peritoneal or retroperitoneal mass, cyst or calcification, conceptus, dilated or obstructed bowel or bladder, free abdominal air or fluid, vascular atheromatosis and stenosis



February 2015

KEY POINT

h The thecal sac protrudes

TABLE 2-4 Differential Diagnosis by Compartment Compartment

Differential Diagnosis

Epidural

Lipoma, lipomatosis, abscess, hematoma, herniated disk, ligament hypertrophy, osteophytes, synovial and other cysts, metastases

Intradural extramedullary

Meningioma, ependymoma, CSF flow voids, dilated surface veins of a dural arteriovenous fistula, schwannoma, neurofibroma, sarcoidosis, meningitis, arachnoiditis, syringomyelia, metastases

Intramedullary

Glioma or astrocytoma, ependymoma, hemangioblastoma, cavernous hemangioma, arteriovenous malformation, demyelinating and autoimmune myelopathies, neurodegenerative disease including wallerian degeneration, spinal cord trauma, metabolic myelopathies, metastases

into the lateral recess of each vertebral segment. The transition from intradural to extradural space occurs in the neural foramen, just distal to the dorsal root ganglia.

CSF = cerebrospinal fluid.

structures and is most often encountered as a complication of long-term steroid use.27 The epidural space can also harbor hematomas and abscesses, which may produce acute compressive myelopathy. Epidural hematoma can be differentiated from lipid on CT and MRI. Unlike hematomas, epidural abscesses demonstrate marked peripheral enhancement. Subdural hematomas and abscesses are not restricted by epidural ligaments and fat and may have a more longitudinal extension compared to epidural hematomas and abscesses within the spinal canal. Refer to Case 6-4 in the article ‘‘Myelopathy Associated With Microorganisms’’ by Jennifer L. Lyons, MD, in this issue . of The thecal sac protrudes into the lateral recess of each vertebral segment. The transition from intradural to extradural space occurs in the neural foramen, just distal to the dorsal root ganglia. At this location and particularly in the lumbosacral spine, CSF-filled sacs lined by nerve fibers known as perineural, or Tarlov, cysts, are encountered incidentally in less than 5% of patients (Figure 2-3).28 These cysts Continuum (Minneap Minn) 2015;21(1):36–51

are most often asymptomatic but may slowly grow over time, leading to remodeling of surrounding vertebral bones and, in rare cases, radicular symptoms. Multiple Tarlov cysts are sometimes found in inherited connective tissue syndromes such as Marfan and Ehlers-Danlos. Solid (noncystic) masses in the lateral recesses and neural foramina include meningiomas, schwannomas, and neurofibromas, among others. Subarachnoid processes can spread throughout the CSF and, therefore, have the potential to affect the leptomeninges of the spinal cord and nerve roots, including the cranial nerves. A polyradiculopathy or sensory neuronopathy can result. Involvement of the CSF space can be primary (autoimmune, paraneoplastic), secondary by direct extension from adjacent soft tissue (infection, sarcoma), or by hematologic spread (metastases, septic emboli). A serious complication of intradural spine surgery is arachnoiditis, a chronic inflammation of the meninges causing fibrous adhesions throughout the spinal canal that can disrupt the position and function of neural structures, in www.ContinuumJournal.com


47


h Displacement of the spinal cord should raise concern for a mass, which may be epidural, intradural, or subdural.

h Focal expansion of the spinal cord, particularly with associated edema and abnormal enhancement, should raise concern for acute inflammation. Atrophy or shrinkage of the cord may reflect prior inflammation, trauma, or degeneration.

particular, the nerve roots of the cauda equina.24 Inflammation of the subarachnoid space may result in abnormal clumping of nerve roots, which is best seen on T2-weighted MRI. Postcontrast images may also reveal abnormal enhancement of nerve roots, sensory ganglia, or leptomeninges. As stated earlier, a venous plexus surrounds the dorsal root ganglia, and subtle enhancement without edema or inflammation may not be a pathologic finding. Cord Position Because of normal cervical and lumbar lordoses and thoracic kyphosis, the spinal cord may lie somewhat anteriorly in the thoracic spinal canal, but in all regions the spinal cord should be completely surrounded by CSF. Displacement of the spinal cord should raise concern for a mass, which may be epidural, intradural, or subdural. Rarely, a segment of spinal cord herniates through a defect in the dura.29,30 This can occur spontaneously or as a result of trauma, and the most common site of herniation is the upper thoracic spine. On sagittal views, an abrupt notch and deflection of the spinal cord is noted, without evidence of a disk herniation or other mass. The herniation most often extends for one or two vertebral levels, below which the spinal cord resumes a normal appearance. On axial views, the thecal sac appears empty at the level of herniation. Clinically, myelopathic symptoms are variable, and the defect can be corrected surgically if needed. Cord Caliber Besides slight enlargements due to anterior horn expansions in the cervical and lumbar spinal cord, the normal cord gradually tapers in cross-sectional area from the cervical spine to the conus medullaris. Like the cross-sectional dimensions of the spinal canal, the spinal

48

cord is wider and more oblong in the cervical spine and less ovoid in the thoracic spine. Normal spinal cord segment cross-sectional areas are roughly 53 mm2 to 58 mm2 cervical, 28 mm2 to 35 mm2 thoracic, and 31 mm2 to 40 mm2 lumbar.31 The conus medullaris most often terminates between the L1 and L2 vertebral levels. Focal expansion of the spinal cord, particularly with associated edema and abnormal enhancement, should raise concern for acute inflammation. Atrophy or shrinkage of the cord may reflect prior inflammation, trauma, or degeneration. Blood Supply The spinal column and its neural structures are perfused by a complex and highly collateralized arterial supply arising from the vertebral arteries near the cervicomedullary junction and from segmental branches of the aorta via radicular arteries inferiorly.32 A dominant radiculomedullary artery of Adamkiewicz is most often encountered in the lower thoracic spine. Each radicular artery branches into tiny arterioles that directly supply the vertebral bones and a larger spinal artery that transits the neural foramen alongside the nerve roots and pierces the dura. The spinal artery then branches into radiculomedullary and radiculopial arterioles that anastomose with the anterior and posterior spinal arteries to perfuse the spinal cord. The spinal cord has one midline anterior spinal artery that receives segmental perfusion from multiple radicular arteries and supplies the anterior two-thirds of the spinal cord. Occlusion of the anterior spinal artery can produce ischemia to the anterior spinal cord. The anterior horns are most affected clinically, and if the descending corticospinal tracts are spared, a suspended paraparesis can be seen. Occlusion of the two posterior



February 2015

spinal arteries can produce ischemia to the posterior one-third of the spinal cord. Infarction of the posterior spinal cord is quite rare. A venous plexus within each vertebral body coalesces into a basivertebral vein in the middle of each vertebral body, best seen on sagittal images (Figure 2-1). This vein merges into an epidural venous plexus. The venous drainage of the spinal cord is into medullary venules that merge on the surface of the spinal cord. Larger surface veins form a radicular vein that transits the neural foramen and joins with venous blood from the epidural venous plexus to form the intervertebral vein, which ultimately drains into the inferior vena cava. Obstruction of venous outflow from the spinal cord, whether due to venous thrombosis or venous hypertension, produces central spinal cord edema with hemorrhage and ischemia in the most severe cases. Subacute myelopathy due to a spinal dural arteriovenous malformation or fistula, the Foix-Alajouanine syndrome, is diagnosed on imaging studies by the combined findings of spinal cord edema and dilated surface veins appearing as enlarged tortuous vascular flow voids.33 Magnetic resonance angiography (MRA) or catheter angiography can delineate the vertebral segmental location of the fistula, which can then be repaired either by endovascular or open spinal surgery. Refer to the article ‘‘Vacular Myelopathies’’ by Alejandro A. Rabinstein, MD, . FAAN, in this issue of The intervertebral disks are avascular structures in the adult,34 although they are directly perfused during fetal development.35 Insufficient nutrient supply to the cells of the nucleus pulposus is a strong determinant of disk incompetence and degeneration. In the adult, diskitis is presumed to arise secondarily from infection of adjacent Continuum (Minneap Minn) 2015;21(1):36–51

structures such as bone, ligament, or paraspinal soft tissues. Primary disk infections can occur with trauma or as a complication of surgery.23,24,36 SPINAL CORD LESIONS Familiarity with spinal cord anatomy aids in the diagnosis of cord lesions, particularly those lesions that affect specific tracts or structures.37 When a spinal cord lesion is encountered, one should consider whether a particular longitudinal tract is affected, or alternatively, whether the pathophysiology involves gray matter only, white matter only, or both. As stated earlier, anterior spinal artery infarctions affect the anterior two-thirds of the spinal cord, and posterior spinal artery infarctions affect the posterior one-third of the spinal cord. ALS produces atrophy and gliosis in the anterior horn cells and corticospinal tracts. Poliomyelitis produces atrophy of the anterior horn cells. Cobalamin (vitamin B12) and copper deficiency preferentially affect the posterior columns of the spinal cord. Some forms of spinocerebellar ataxia have shown degeneration of the posterior and lateral ascending white matter tracts. Multiple sclerosis (MS) lesions in the spinal cord are small and ovoid and preferentially affect white matter structures such as the posterior columns and corticospinal tracts.38 Neuromyelitis optica, venous outflow obstruction, venous hypertension, and autoimmune myelitides most often produce longitudinally extensive (extending greater than three vertebral segments) central cord lesions. Cavernous hemangiomas can occur anywhere in the spinal cord and have characteristic internal heterogeneity and an outer rim of T1 and T2 hypointense hemosiderin.33 Spinal cord tumors have variable imaging features but most often produce cord expansion and do not reliably respect gray and white matter boundaries.39 The same is true of

KEY POINTS

h Subacute myelopathy due to a spinal dural arteriovenous malformation or fistula is diagnosed on imaging studies by the combined findings of spinal cord edema and dilated surface veins appearing as enlarged tortuous vascular flow voids.

h The intervertebral disks are avascular structures in the adult, although they are directly perfused during fetal development. Insufficient nutrient supply to the cells of the nucleus pulposus is a strong determinant of disk incompetence and degeneration.

h When a spinal cord lesion is encountered, one should consider whether a particular longitudinal tract is affected, or alternatively, whether the pathophysiology involves gray matter only, white matter only, or both.

h Multiple sclerosis lesions in the spinal cord are small and ovoid and preferentially affect white matter structures such as the posterior columns and corticospinal tracts.

h Neuromyelitis optica, venous outflow obstruction, venous hypertension, and autoimmune myelitides most often produce longitudinally extensive (extending greater than three vertebral segments) central cord lesions.



49


h The tethered cord syndrome results from an abnormally taut filum terminale or from other lesions (such as lipoma of the filum terminale) that exert tension on the inferior aspect of the spinal cord.

h Although a larger syrinx can cause cord expansion, the internal contents of a syrinx have the imaging characteristics of CSF and, therefore, can be distinguished from other mass-producing lesions such as tumors and acute demyelination.

h Spinal dysraphisms encompass a variety of defects of spinal cord formation that are easily recognized. In spina bifida, incomplete closure of the neural tube may allow the spinal cord or nerve roots to exit the spinal canal to form a myelomeningocele.

infectious myelitides.40 Metastatic lesions can occur anywhere in the spinal cord as well as in the meninges and paraspinal soft tissues. Syringomyelia, referring either to formation of a fluid-filled cyst in the spinal cord parenchyma or to cystic expansion of the central canal of the spinal cord, can damage both spinothalamic fibers as they decussate in the anterior commissure and other cord structures as well. Cervical syringomyelia often coexists with Chiari malformations. Although a larger syrinx can cause cord expansion, the internal contents of a syrinx have the imaging characteristics of CSF and, therefore, can be distinguished from other massproducing lesions such as tumors and acute demyelination. Spinal dysraphisms encompass a variety of defects of spinal cord formation that are easily recognized. In spina bifida, incomplete closure of the neural tube may allow the spinal cord or nerve roots to exit the spinal canal to form a myelomeningocele. Lumbar myelomeningoceles are also seen in Chiari II malformations. Diastematomyelia refers to an abnormal congenital longitudinal splitting of the spinal cord due to a bony or cartilaginous septum in the spinal canal. As described earlier, dural tears may allow a segment of the spinal cord to herniate outside the dura. The tethered cord syndrome results from an abnormally taut filum terminale or from other lesions (such as lipoma of the filum terminale) that exert tension on the inferior aspect of the spinal cord. CONCLUSION In this review, a practical approach toward interpretation of spine imaging is presented. The goal is to allow the clinician to take a more active role in understanding the significance of abnormal imaging findings. Recognition of normal anatomy is paramount so that pathologies involving nervous system structures, meninges,

50

bones, ligaments, muscles, and vessels can be readily identified. REFERENCES 1. Mink JH, Gordon RE, Deutsch AL. The cervical spine: radiologist’s perspective. Phys Med Rehabil Clin N Am 2003;14(3):493Y548. doi:10.1016/S1047-9651(03)00035-4. 2. Bitar R, Leung G, Perng R, et al. MR pulse sequences: what every radiologist wants to know but is afraid to ask. Radiographics 2006;26(2):513Y537. doi:10.1148/rq.262055063. 3. Kasdan RB, Howard JL. Neuroimaging of spinal diseases: a pictorial review. Semin Neurol 2008;28(4):570Y589. doi:10.1055/ s-0028-1083693. 4. Smith JS, Shaffrey CI, Fu KM, et al. Clinical and radiographic evaluation of the adult spinal deformity patient. Neurosurg Clin N Am 2013;24(2):143Y156. doi:10.1016/ j.nec.2012.12.009. 5. Johnson RD, Valore A, Villaminar A, et al. Sagittal balance and pelvic parametersVa paradigm shift in spinal surgery. J Clin Neurosci 2013;20(2):191Y196. doi:10.1016/ j.jocn.2012.05.023. 6. Frobin W, Brinckmann P, Biggemann M, et al. Precision measurement of disc height, vertebral height and sagittal plane displacement from lateral radiographic views of the lumbar spine. Clin Biomech (Bristol, Avon) 1997;12(suppl 1): S1YS63. doi:10.1016/S0268-003(96)00067-8. 7. Busscher I, Ploegmakers JJW, Verkerke GJ, Veldhuizen AG. Comparative anatomical dimensions of the complete human and porcine spine. Eur Spine J 2010;19(7): 1104Y1114. doi:10.1007/s00586-010-1326-9. 8. Berven SH, Lowe T. The Scoliosis Research Society classification for adult spinal deformity. Neurosurg Clin N Am 2007;18(2):207Y213. 9. Cassar-Pullicino VN, Eisenstein SM. Imaging in scoliosis: what, why and how? Clin Radiol 2002;57(7):543Y562. doi:10.1016/j.nec.2007.03.002. 10. Murthy NS. Imaging of stress fractures of the spine. Radiol Clin North Am 2012;50(4):799Y821. doi:10.1016/j.rcl.2012.04.009. 11. Standaert CJ, Herring SA. Spondylolysis: a critical review. Br J Sports Med 2000;34(6): 415Y422. doi:10.1136/bjsm.34.6.415. 12. Modic MT, Ross JS. Lumbar degenerative disk disease. Radiology 2007;245(1):43Y61. doi:10.1148/radiol.2451051706. 13. Link TM, Guglielmi G, van Kuijk C, Adams JE. Radiologic assessment of osteoporotic vertebral fractures: diagnostic and prognostic implications. Eur Radiol 2005;15(8):1521Y1532. doi:10.1007.s00330-005-2773-2.



February 2015

14. Marx JA, Hockberber RS, Walls RM. Rosen’s emergency medicine: concepts and clinical practice. 6th ed. St. Louis, MO: Mosby, Inc, 2006. 15. Jurik AG. Imaging the spine in arthritisVa pictorial review. Insights Imaging 2011;2(2): 177Y191. doi:10.1007/s13244-010-0061-4. 16. Amrami KK. Imaging of the seronegative spondyloarthropathies. Radiol Clin North Am 2012;50(4):841Y854. doi:10.1007/s11926-000-0065-z. 17. Vande Berg BC, Lecouvet FE, Galant C, et al. Normal variants and frequent marrow alterations that simulate bone marrow lesions at MR imaging. Radiol Clin North Am 2005;43(4):761Y770. doi:10.1016/j.rcl.2005.01.007. 18. Kyere KA, Than KD, Wang AC, et al. Schmorl’s nodes. Eur Spine J 2012;21(11):2115Y2121. doi: 10.1007/s00586-012-2325. 19. Hamanishi C, Kawabata T, Yosii T, Tanaka S. Schmorl’s nodes on magnetic resonance imaging. Their incidence and clinical relevance. Spine (Phila Pa 1976) 1994;19(4):450Y453. 20. Wu HT, Morrison WB, Schweitzer ME. Edematous Schmorl’s nodes on thoracolumbar MR imaging: characteristic patterns and changes over time. Skeletal Radiol 2006;35(4):212Y219. doi:10.1007/ s00256-005-0068-y. 21. Go JL, Rothman S, Prosper A, et al. Spine infections. Neuroimag Clin N Am 2012;22(4):755Y772. doi:10.1016/ j.nic.2012.06.2002. 22. Do-Dai DD, Brooks MK, Goldkamp A, et al. Magnetic resonance imaging of intramedullary spinal cord lesions: a pictorial review. Curr Probl Diagn Radiol 2010;39(4):160Y185. doi: 10.1067/ j.cpradiol.2009.05.004. 23. Lury K, Smith JK, Castillo M. Imaging of spinal infections. Semin Roentgenol 2006;41(4): 363Y379. doi:10.1053/j.ro.2006.07.008. 24. Salgado R, Van Goethem JW, van den Hauwe L, Parizel PM. Imaging of the postoperative spine. Semin Roentgenol 2006;41(4):312Y326. doi:10.1053/ j.ro.2006.07.004. 25. Taljanovic MS, Hunter TB, Wisneski RJ, et al. Imaging characteristics of diffuse idiopathic skeletal hyperostosis with an emphasis on acute spinal fractures: review. AJR Am J Roentgenol 2009;193(3 suppl):S10YS19. doi:10.2214/AJR.07.7102. 26. Quattrocchi CC, Giona A, Di Martino AC, et al. Extra-spinal incidental findings at lumbar spine MRI in the general population: a large cohort study. Insights Imaging 2014;4(3): 301Y308. doi:10.1007/s13244-013-0234-z. Continuum (Minneap Minn) 2015;21(1):36–51

27. Al-Khawaja D, Seex K, Eslick GD. Spinal epidural lipomatosisVa brief review. J Clin Neurosci. 2008;15(12):1323Y1326. doi:10.1016/j.jocn.2008.03.001. 28. Lucantoni C, Than KD, Wang AC, et al. Tarlov cysts: a controversial lesion of the sacral spine. Neurosurg Focus 2011;31(6):E14. doi:10.3171/2001.9.FOCUS11221. 29. Parmar H, Park P, Brahma B, Gandhi D. Imaging of idiopathic spinal cord herniation. Radiographics 2008;28(2):511Y518. doi:10.1148/rq.282075030. 30. Le TC, Grunch BH, Karikari IO, et al. Dorsal thoracic spinal cord herniation: report of an unusual case and review of the literature. Spine J 2012;12(10):e9Ye12. doi:10.1016/ j.spinee.2012.09.039. 31. Kameyama T, Hashizume Y, Sobue G. Morphologic features of the normal human cadaveric spinal cord. Spine (Phila Pa 1976) 1996;21(11):1285Y1290. 32. Santillan A, Nacarino V, Greenberg E, et al. Vascular anatomy of the spinal cord. J Neurointervent Surg 2012;4(1):67Y74. doi:10.1136/neurintsurg-2011-010018. 33. Boo S, Hartel J, Hogg JP. Vascular abnormalities of the spine: an imaging review. Curr Probl Diagn Radiol 2010;39(3): 110Y117. doi:10.1067/j.cpradiol.2009.07.003. 34. Grunhagen T, Wilde G, Soukane DM, et al. Nutrient supply and intervertebral disc metabolism. J Bone Joint Surg Am 2006;88(suppl 2):30Y35. doi:10.2106/ JBJS.E.01290. 35. Nerlich AG, Schaaf R, Walchli B, Boos N. Temporo-spatial distribution of blood vessels in human lumbar intervertebral discs. Eur Spine J 2007;16(4):547Y555. doi:10.1007/ s00586-006-0213-x. 36. DeSanto J, Ross JS. Spine infection/inflammation. Radiol Clin North Am 2011;49(1):105Y127. doi:10.1016/j.rcl.2010.07.018. 37. Cosnard G. Tips and traps in spinal cord pathology. Diagn Interv Imaging 2012;93(12):975Y984. doi:10.1016/ j.diii.2012.08.003. 38. Goh C, Phal PM, Desmond PM. Neuroimaging in acute transverse myelitis. Neuroimaging Clin N Am 2011;21(4):951Y973. doi:10.1016/ j.nic.2011.07.010. 39. Smith JK, Lury K, Castillo M. Imaging of spinal and spinal cord tumors. Semin Roentgenol 2006;41(4):274Y293. doi:10.1053/j.ro.2006.07.002. 40. Cho TA, Vaitkevicius H. Infectious myelopathies. Continuum (Minneap Minn) 2012;18(6 Infectious Disease):1351Y1373. doi:10.1212/01.CON.0000423851.63017.2a. www.ContinuumJournal.com


51

A practical approach to imaging the axilla.

A practical approach to transverse-section gamma-ray imaging.

A practical approach to patenting.

A Practical Approach to Hypocalcaemia in Children.

A practical approach to relapsed multiple myeloma.

A practical approach to fetal growth restriction.

A practical approach to the genetic neuropathies.

Frostbite: a practical approach to hospital management.

Dysphagia. A practical approach to diagnosis.

A practical approach to investigation of syncope.

A practical approach to cutaneous sarcoidosis.

A practical approach to acid-base disorders.

A practical approach to fasting hypoglycemia.

Hyponatremia: A practical approach.

A practical approach to the imaging interpretation of sphenoid sinus pathology.

Pruritus: a practical approach.

A Practical Approach to Quantitative Processing and Analysis of Small Biological Structures by Fluorescent Imaging.

Periodontics: a practical approach.

A Practical Approach to Excessive Daytime Sleepiness: A Focused Review.

Chronic diarrhea. A practical approach.

A practical approach to a low protein diet in Brazil.

Practical approach to hypertension. 2. Treatment.

Practical approach to hypertension. 1. Diagnostic evaluation.

Practical approach to pediatric hearing problems.