NEURORADIOLOGY REVIEW SERIES

NEURORADIOLOGY REVIEW SERIES

Imaging of Degenerative and Infectious Conditions

of the Spine
Lubdha M. Shah, MD*‡
Jeffrey S. Ross, MD§
Departments of *Radiology and Imaging
Sciences and ‡Neurosurgery, University
of Utah, Salt Lake City, Utah; §Depart-
ment of Radiology, Mayo Clinic Arizona,
Scottsdale, Arizona
Correspondence:
Lubdha M. Shah, MD,
Director of Spine Imaging,
Associate Professor of Radiology
and Neurosurgery,
University of Utah,
30 N 1900 E, No. 1A071,
Salt Lake City, UT 84132-2140.
E-mail: lubdha.shah@hsc.utah.edu
Received, December 16, 2015.
Accepted, May 11, 2016.
Published Online, June 28, 2016.
Copyright © 2016 by the
Congress of Neurological Surgeons.
Imaging is important in the evaluation of patients with degenerative disease and
infectious processes. There are numerous conditions that can manifest as low back pain
(LBP) or neck pain in a patient, and in many cases, the cause may be multifactorial.
Clinical history and physical examination are key components in the evaluation of such
patients; however, physical examination has variable sensitivity and specificity.
Although studies have demonstrated that uncomplicated acute LBP and/or radiculop-
athy are self-limited conditions that do not warrant any imaging, neuroimaging can
provide clear anatomic delineation of potential causes of the patient’s clinical pre-
sentation. Various professional organizations have recommendations for imaging of LBP,
which generally agree that an imaging study is not indicated for patients with
uncomplicated LBP or radiculopathy without a red flag (eg, neurological deficit such as
major weakness or numbness in lower extremities, bowel or bladder dysfunction, saddle
anesthesia, fever, history of cancer, intravenous drug use, immunosuppression, trauma,
or worsening symptoms). Different imaging modalities have a complementary role in the
diagnosis of pathologies affecting the spine. In this review, we discuss the standard
nomenclature for lumbar disk pathology and the utility of various clinical imaging
techniques in the evaluation of LBP/neck pain for potential neurosurgical management.
The imaging appearance of spinal infections and potential mimics also is reviewed.
Finally, we discuss advanced neuroradiological techniques that offer greater micro-
structural and functional information.
KEY WORDS: CT, Degenerative disease, Infectious disease, MRI, Spinal infection

Neurosurgery 79:315–335, 2016 DOI: 10.1227/NEU.0000000000001323 www.neurosurgery-online.com

I
maging plays an important role in the evaluation
of patients presenting with low back pain (LBP)
or neck pain. Because numerous conditions can
manifest as LBP/neck pain in a patient, clinical
history and physical examination can guide which
segment of the spine and which imaging modality
(computed tomography [CT] vs magnetic reso-
nance imaging [MRI]) will help elucidate the cause
ABBREVIATIONS: ADC, apparent diffusion coeffi-
cient; DTI, diffusion tensor imaging; DWI, diffusion-
weighted imaging; DOM, diskitis-osteomyelitis;
LBP, low back pain; MRM, magnetic resonance
myelography; SNA, spinal neuroarthropathy;
SPECT, single-positron emission computed tomog-
raphy; STIR, short tau inversion recovery
Supplemental digital content is available for this article.
Direct URL citations appear in the printed text and are
provided in the HTML and PDF versions of this article on
the journal’s Web site (www.neurosurgery-online.com).
of the patient’s LBP/neck pain. Multiple physical
examination tests have been used that collectively
significantly increase diagnostic precision.1
Although studies have demonstrated that uncom-
plicated acute LBP and radiculopathy are self-
limited conditions that do not warrant any
imaging,2-4 most professional organizations have
recommendations for imaging of LBP in patients
with LBP of . 6 weeks’ duration or with red flags
such as severe or progressive neurological deficit
(eg, bowel or bladder function, saddle parasthesia),
fever, trauma, sudden back pain with spinal
tenderness (especially with history of osteoporosis,
cancer, or steroid use), or history of serious
medical condition (eg, cancer). Imaging modalities
such as radiographs, CT, and MRI can provide
clear anatomic delineation of potential causes of
the patient’s clinical presentation. Here, we review
the fundamental role of imaging, focusing on the
complementary role of the different modalities, in

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 SHAH AND ROSS

the diagnosis of patients with degenerative and infectious processes
affecting the spine, with specific attention to the lumbar spine.
DEGENERATIVE SPINE
LBP is ubiquitous, affecting up to two-thirds of adults at some
period in their lives.3 Imaging, primarily with MRI and CT, is
used to evaluate the source of both LBP and neck pain. These
imaging modalities commonly identify disk degeneration, disk
herniations, and posterior element arthopathy; however, the
imaging findings of spine degeneration are present in a high
proportion of asymptomatic individuals and increase with age.5,6
Although many imaged-based degenerative changes are due to
the normal aging process, such imaging findings are often
interpreted as the cause of the patient’s back pain and initiate
a cascade of medical and surgical interventions, which may not be
helpful in relieving the symptoms.7
Nomenclature
Because imaging of the spine is used by all treating physicians,
a collaboration of multiple specialty societies yielded the nomen-
clature of lumbar disk pathology initially in 20018,9 and revised it
in 2014.10,11 Standard terms for normal and pathological
conditions of lumbar disks are described to accurately and
consistently communicate imaging findings for clinical and
therapeutic decision making. The focus of this nomenclature is
the lumbar spine; however, the principles and most definitions
can be extrapolated to the cervical and thoracic spine.
Full discussion of the nomenclature and classification is beyond
the scope of this article. Briefly, the diagnostic categories are normal,
congenital/developmental variation, degeneration, trauma, infection/
inflammation, neoplasia, and morphologic variant. Subcategories
of degeneration include annular fissures, which are separations
between the annular fibers or between the annular fibers and
their attachments to the vertebral body. These appear as linear
foci of hyperintensity on T2-weighted and short tau inversion
recovery (STIR) sequences (ie, high-signal-intensity zone). Disk
degeneration includes desiccation, mucinous degeneration of the
annulus, and fibrosis, which appears as low signal on T2-weighted
sequences with varying grades of obscuration of the nucleus
pulposus and annulus margins.12 With greater disk degeneration,
there is narrowing of the disk height. Intradiskal nitrogen gas is
a classic finding of degeneration (Figure 1).13
Diffuse bulging of disk beyond endplates can be seen with disk
degeneration, whereas herniation is defined as a localized or focal
disk material displacement beyond the limits of the disk space. The
disk material may be composed of $ 1 combinations of nucleus,
annular tissue, cartilage, and fragmented apophyseal bone.
Herniated disks may be further categorized into protrusion or
extrusion on the basis of the morphology of the displaced material.

FIGURE 1. Left, sagittal CT reconstruction demonstrates multilevel severe degenerative changes with loss of disk height, endplate
sclerosis, and vacuum phenomenon. Right, sagittal T2-weighted image shows corresponding intradiskal hypointensity and loss of
disk height. The levels of intradiskal vacuum phenomenon on the CT (yellow arrows) can become fluid-filled on MRI (red
arrows).

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 IMAGING OF SPINE DEGENERATIVE AND INFECTIOUS CONDITIONS

FIGURE 2. Sagittal (A) STIR and (B) T2-weighted images show a hyperintense disk sequestration along the posterior
margin of the L1 vertebral body (white arrows). C, sagittal postcontrast T1-weighted, fat-saturated image demonstrates
peripheral enhancement of the disk (red arrow), which is separate from the parent disk. D, sagittal CT reconstruction
reveals vacuum phenomenon in the sequestered disk (yellow arrow).

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 SHAH AND ROSS

FIGURE 3. Sagittal (A) T1-weighted, (B) T2-weighted, and (C) STIR images of the lumbar spine exhibit type 1 fibrovascular endplates changes at L5-S1 with hypointense
T1, heterogeneously hyperintense T2, and hyperintense STIR signal intensities.

A protrusion is used to describe disk material presenting outside
the disk space when its edges outside the disk space are less than the
distance between the edges of the base of the disk material
extending outside the disk space. An extrusion is present when any
one distance between the edges of the disk material beyond the
disk space is greater than the distance between the edges of the base
of the disk material beyond the disk space.10,11 A sequestered disk
is an extrusion that has lost contiguity with the parent disk (Figure
2). Disk herniation through a weakened subchondral vertebral
endplate is an intravertebral disk herniation (ie, Schmorl node).
With disk degeneration, the adjacent vertebral endplates and
subchondral bone will commonly show signal intensity changes on
MRI (ie, Modic changes). The 3 types are type I (low T1 and high
T2 signal; Figure 3), type II (high T1 and T2 signal; Figure 4),
and type III (low T1 and T2 signal; Figure 5).14 The histology of
type I shows disruption and fissuring of the endplate and
vascularized fibrous tissues within the adjacent marrow. If
contrast is administered, there will be enhancement of the
endplate that may involve the disk and is presumably related to
the vascularized fibrous tissue within the adjacent marrow.14
Type II endplate changes demonstrate endplate disruption with
yellow (lipid) marrow replacement in the adjacent vertebral body,
resulting in the high T1 signal. Type I changes may reflect the
inflammatory, active stage of degenerative disk disease, whereas

FIGURE 4. Sagittal (A) T1-weighted, (B) T2-weighted, and (C) STIR images of the lumbar spine exhibit type 2 fatty marrow endplate changes at the L4-L5 level with
hyperintense T1, hyperintense T2, and hypointense STIR signal intensities.

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 IMAGING OF SPINE DEGENERATIVE AND INFECTIOUS CONDITIONS

FIGURE 5. Sagittal (A) T1-weighted, (B) T2-weighted, (C) STIR, and (D) CT images of the lumbar spine exhibit type III
sclerotic marrow endplates changes at L5-S1 with hypointense T1, hypointense T2, and hypointense STIR signal intensities. On
CT, endplate sclerosis, subchondral cystic change, and endplate osteophytosis are seen. The intradiskal fluid on the MRI corresponds
to vacuum phenomenon on CT.

type II is related to a more quiescent stage. Others have proposed
that type I changes correspond to endplate edema, which could
correspond to microfractures of cancellous bone and endplate
fissures, along with increased vascular and nerve density.15 Lastly,
the type III appearance is due to the relative absence of marrow in
areas of advanced sclerosis seen on radiographs.16 Although these
diskogenic endplate changes have been observed in patients with
LBP and have therefore been suspected as a potential cause of
axial and radicular chronic LBP,17,18 such endplate changes have
also been observed on MRIs in the general population19,20 and
asymptomatic subjects.21-23 Such imaging findings are seen more
frequently among men, particularly increasing with age and signs
of disk degeneration.24,25 A recent study assessed the endplate
perfusion and found that increased enhancement in the endplate
of degenerating disks might be an indication of ongoing
damage.26 Endplate degeneration may result in intradiskal gas.16
Spinal stenosis is categorized as congenital or acquired. The
majority of congenital stenosis is seen in adults in combination
with acquired degenerative stenosis. This is seen as facet
arthropathy and bulging annulus plus congenitally short pedicles.
Severe multilevel congenital spinal stenosis may also be seen in
achondroplasia and other bony dysplasias. Acquired spinal stenosis
is usually degenerative, but it can also be due to degenerative
changes superimposed on spondylolisthetic or spondylolytic

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 SHAH AND ROSS

FIGURE 6. Left, sagittal T2-weighted image demonstrates severe spinal canal narrowing at L2-L3 and L3-L4 in a post-
laminectomy patient. Right, axial T2-weighted image at the L2-L3 level, just superior to the laminectomy, shows severe spinal
canal narrowing caused by a combination of symmetric disk bulge, facet hypertrophy, and ligamentum flavum thickening.

stenosis, iatrogenic stenosis (such as postlaminectomy stenosis; MRI, has low predictive value for posterior element pain.37
Figure 6), posttraumatic stenosis, or metabolic stenosis (such as There is moderate to good agreement between MRI and CT with
Paget disease).27 Patients with lumbar spinal stenosis may have regard to osteoarthritis of the lumbar facet joints.38 Hybrid
neurogenic intermittent claudication caused by venous conges-
tion and arterial hypertension around nerve roots (Figure 7).
Similarly, cervical spinal stenosis may result in myelopathy owing
to mechanical factors (eg, disk protrusion, osteophytes, and
ossified posterior longitudinal ligament) causing static and
dynamic compression and to secondary cord ischemia from
venous congestion (Figure 8).28-32
Acquired stenosis of the degenerative type most often involves
the L4-L5 level and is due to changes in the 3-joint complex, which
consists of the diskovertebral complex of the disk space, adjacent
endplates, and facet joints. Synovitis of the diarthrodial facet joints
may be the initiating factor,33 and as it progresses, the joint
cartilage thins and the facet capsule loosens. This loosening allows
greater spinal motion and accelerates degeneration of the
intervertebral disk. Facet joint effusion has been shown to be
correlated with instability in degenerative spondylolisthesis
(Figure 9).34 Osteophytes on the superior articular facet narrow
the subarticular zone, whereas osteophytes on the inferior
articular facet narrow the central canal.
The degree of facet degeneration is underestimated by current FIGURE 7. Left, sagittal T2-weighted and (right) postcontrast T1-weighted
imaging modalities.35 There is likely a continuum of facet images of the lumbar spine illustrate severe spinal stenosis at L3-L4. The cauda
equina nerve roots have a clumped appearance resulting from the impingement.
degeneration, from a normal to an obliterated joint. The severity
The venous congestion results in breakdown of the blood-nerve barrier, which
of disk and facet degeneration also is associated with interspinous manifests as patchy nerve root enhancement (white arrow).
degeneration.36 Standard imaging, including plain films, CT, and

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 IMAGING OF SPINE DEGENERATIVE AND INFECTIOUS CONDITIONS

FIGURE 8. Left, sagittal T2-weighted image demonstrates anterior disk osteophyte complexes and posterior ligamentum flavum
causing severe spinal canal narrowing at C4-C5 and C5-C6. There is abnormal cord T2 hyperintensity at the C4-C6 levels, which
reflects myelomalacia and gliosis. Right, axial T2-weighted image at the C4-C5 level shows severe spinal canal narrowing and
impingement of the cord caused by the anterior disk osteophyte complex and posterior ligamentum flavum.

single-positron emission CT (SPECT)/CT imaging can be a useful
adjunct in the management of suspected facet arthropathy. Facet
hypertrophy alone is not predictive of bone scan positivity, whereas
synovial abnormalities correlate with SPECT findings.39 In one
study, hybrid SPECT/CT imaging identified potential pain
generators in 92% of cervical spine scans and 86% of lumbar
spine scans and localized positive facet joint targets in 65% of the
referral population for steroid/anesthetic injection (Figure 10).40
Degeneration of the facet joint capsule may cause protrusion of
the synovial membrane through defects of the joint capsule. This
herniation causes the formation of a para-articular cavity filled with
synovial fluid: a synovial or juxta-articular cyst.41 The incidence of
lumbar facet synovial cysts detected by imaging ranges from 0.8%
to 2.0% (Figure 11).42 Most synovial cysts arise at the L4-L5
level, which is the most mobile level of the vertebral column, and
are frequently associated with spondylolisthesis. These features
suggest that instability is a pivotal factor in their pathogenesis.43
On MRI, synovial cysts are typically T2 hyperintense and T1
hypointense, but the signal intensity can vary, depending on
protein content, previous hemorrhage, and calcification.42
Synovial cysts projecting into the spinal canal can cause radicular
pain (87%), neurogenic claudication (44%), sensory loss (43%),
and motor weakness (27%).44
MRI signal abnormalities can also be seen within the pedicles in
association with spondylolysis and degenerative facet changes
(Figure 12).45-48 Similar to the classification of diskogenic endplate
changes,14 Borg et al49 showed that pedicle marrow signal intensity
changes corresponding to type I (T1 hypointense and T2
hyperintense) are strongly associated with LBP. This pedicle signal
abnormality may reflect stress reaction in the underlying bone,48 in
some cases caused by the segmental spinal motion. A similar
mechanism has been hypothesized in the vertebral endplates when
there is accelerated disk degeneration and associated biomechanical
stress.50 Studies report the conversion of type I endplate/pedicle
changes to type II or normal-appearing marrow, particularly with
instrumentation and fusion.15,51,52
Imaging
Radiographs are widely available, are relatively inexpensive, and
provide information on osseous anatomy. Dynamic views in the
upright, flexion, extension, and lateral bending positions give
functional information on alignment with axial loading and
segmental listhesis. The main disadvantage of radiographs is the
limited soft tissue resolution, particularly of the intervertebral
disks, ligaments, nerves, and paraspinal tissues. Multidetector CT
can be reconstructed in the axial, sagittal, and coronal planes such
that one can evaluate the integrity of the osseous structures with
exquisite detail. Processing in different algorithms (ie, soft tissue)
enables assessment of disk herniations into the spinal canal and
neural foramina. CT, however, is limited in its delineation of
marrow infiltrative processes and intrathecal pathology.
Myelography and CT myelography are informative imaging
modalities when MRI is not possible in patients because of safety
reasons (eg, pacemaker), severe image-quality degradation resulting

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 SHAH AND ROSS

FIGURE 9. A, axial T2-weighted image at the L3-L4 level shows facet hypertrophy and bilateral effusions. B, sagittal T2-
weighted image demonstrates grade 1 degenerative anterolisthesis of L3 on L4, where there is also a focal cranially extending disk
extrusion. C, lateral extension and (D) lateral flexion radiographs reveal abnormal motion at L3-L4.

from metallic implants, or claustrophobia or in cases in which myelography/CT myelography provides valuable diagnostic infor-
kyphoscoliosis makes image acquisition and interpretation mation beyond MRI. After intrathecal injection of myelographically
extremely difficult. The ability to obtain dynamic imaging with safe contrast, fluoroscopic images are obtained with the patient in

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FIGURE 10. Fused SPECT/CT images in the (A) coronal and parasagittal (B) right and (C) left planes display the significant increased radionuclide uptake in the right C1-
C2 facet joint (white arrows) and moderate uptake in the left C2-C3 facet joint (yellow arrow). This modality can help localize pain generators, which is helpful in the
setting of severe spondylosis.
different positions to obtain functional information about align-
ment and motion of the diskovertebral and facet joints and the effect
on the spinal canal. The CT myelogram gives superb spatial and
contrast resolution, even with metallic implants, and without the
susceptibility artifact from osseous structures seen on MRI. The
superior osseous delineation on CT myelography enables detection
of the osseous components to the spinal canal, subarticular recess,
and neural foraminal narrowing. Myelography/CT myelography is
an important study to confirm degenerative root impingement in
the subarticular recess as the cause of radiculopathy, which can be
underestimated by MRI (Figure 13).53 In potential surgical cases, it
should be noted that MRI has been shown to overestimate spinal
and neural foraminal stenosis compared with myelography/CT
myelography.54,55
Nuclear medicine bone scans have high sensitivity for increased
bone turnover but low diagnostic specificity.56,57 The addition of
SPECT to a bone scan improves the spatial resolution, and the
digital fusion of a CT scan of the area of interest with a bone scan
with SPECT imaging provides the anatomic resolution for
accurate localization of a pain generator,58 particularly of
posterior element origin.
The principal modality for spinal pathology evaluation is MRI,
which allows highly detailed visualization of spine anatomy in
a noninvasive process without ionizing radiation. The routine
sequences in a degenerative spine protocol are T1-weighted,
T2-weighted, STIR, and gradient echo sequences. Images may be
obtained in the sagittal, axial, and coronal planes and with
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IMAGING OF SPINE DEGENERATIVE AND INFECTIOUS CONDITIONS
3-dimensional isotropic imaging. T1-weighted images provide
excellent depiction of the vertebral bodies, marrow, and interver-
tebral disks. The T2-weighted sequences show the nerve roots and
spinal cord surrounded by hyperintense cerebrospinal fluid,
whereas the STIR images increase the conspicuity of tissues with
high water content.
Diffusion-weighted imaging (DWI), which provides informa-
tion about the diffusion movement of water molecules, has been
investigated in degenerative disk disease. An estimate of this
movement is given by the apparent diffusion coefficients (ADCs)
by measuring the decrease in signal resulting from moving protons.
In the lumbar spine, ADC values are reportedly negatively
correlated with the degree of intervertebral disk degeneration.59
There is also a significant negative association between age and
ADC values at all levels. Not only do degenerated disks have
lower ADC values than normal disks, but the more caudal disks
show lower ADC values.60 DWI has also been applied to spinal
neural structures. When DWI of the dorsal root ganglion of the
affected nerve root in lumbar disk herniation was evaluated,
a study found that patients with decreased ADC tended to show
poor improvement in leg symptoms.61
Diffusion tensor imaging (DTI) quantifies the multidirectional
movement of water molecules, and in the highly anisotropic
architecture of the spinal cord, it can be used to assess structural
changes. DTI can detect cord changes in cervical spondylotic
myelopathy even with normal signal intensities on T1- and
T2-weighted images.62,63 DTI index alterations are dependent
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 SHAH AND ROSS
FIGURE 11. Left, parasagittal T2-weighted image demonstrates a large synovial cyst extending anteromedially from the left
facet joint (curved yellow arrow). Right, axial T2-weighted image shows severe thecal sac narrowing caused by the synovial cyst,
which has a characteristic hypointense rim (white arrow).
on the degree of cord damage, with decreased fractional
anisotropy at the affected level (Figure 14). Kerkovsky et al64
showed lower fractional anisotropy and higher ADC values in
symptomatic compared with asymptomatic patients with radio-
logical cord compression. However, studies have not shown
consistent correlations between DTI metrics and clinical scores in
patients with cervical spondylotic myelopathy.65-67
Magnetic resonance myelography (MRM) is a high-resolution
technique in which heavily fluid-weighted sequences provide sharp
contrast between the dark signal of the spinal cord and nerves and the
bright signal of the cerebrospinal fluid (Figure 15). A large study of
. 1000 patients found that MRM complements conventional MRI,
adding information that is relevant to the final MR diagnosis.68 In
combination with sequential axial images of the spine, MRM may
decrease the need for conventional myelography by showing the
cause of compression and degree of compressive effect in degener-
ative spine disease.69 However, others have shown that in routine
practice, MRM was of limited value and assisted in establishing
a diagnosis in a minority of cases (6%).70 In patients with multilevel
pathology and, to a lesser extent, in patients with scoliosis, MRM did
help to establish the level most likely to account for pathology.70
Standard imaging of the spine is static and in the supine position,
which does not provide important functional information on the role
of axial loading and motion on spinal biomechanics. Kinetic MRI
can demonstrate segmental diskovertebral instability by imaging in
multiple positions. This technique can be performed on typical
lower-strength open magnets with a horizontal configuration or on
MRI scanners with an upright configuration. With the upright
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configuration, the patient can be scanned in an upright, axially
loaded position and with weight-bearing neutral, flexion, and
extension positioning. Studies have shown the utility of flexion
and extension positioning during MRI of the cervical71 and
lumbar spine.72,73 Real-time flexion-extension dynamic cervical
MRI with a variety of steady state techniques (balanced steady-
state free precession, true fast imaging with steady-state pre-
cession, fast-field echo, fast imaging employing steady-state
acquisition) may be a functional adjunct to the standard static
MRI examination of the cervical spine. (Video, Supplemental
Digital Content, http://links.lww.com/NEU/A880, shows sag-
ittal real-time balanced steady-state free precession cine images of
the cervical spine demonstrate multilevel spondylotic disease.
With extension, there is impingement of the cord at the C5-C6
level resulting from anterior disk osteophyte complex and posterior
thickened ligamentum flavum. There is hyperdynamic motion of
the cord just distal to the cord impingement, likely resulting from
accelerated cerebrospinal fluid flow effects. With flexion, the cord
impingement decreases. Total cine clip time is 0:35 with repeated
flexion and extension motions showing the findings below: 0:05,
extension; 0:08, flexion. This is repeated through the course of the
cine clip.) Balanced steady-state free precession has a high signal-to-
noise ratio and, in the steady state, has T2/T1 contrast. It can be
acquired rapidly with conventional MRI coils and scanners. The
spatial and contrast resolution achieved with real-time balanced
steady-state free precession is helpful to assess exacerbation of spinal
stenosis from anterior and posterior degenerative factors and
movement of the cord and cerebellar tonsils.74
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FIGURE 12. Parasagittal STIR images display edema in the L4 and L5 pedicles (left, white arrow) and the L4-L5 facet joint
(right, yellow arrow) caused by a stress reaction.
This status of the disk proteoglycans has been evaluated by
a number of imaging techniques, most of which remain in the
research arena such as T2 relaxation times, T1rho, and magnetic
resonance spectroscopy. The Pfirrmann MRI classification of
lumbar disk degeneration is a widely accepted semiquantitative
method of evaluation of disk degeneration.12 Pfirrmann et al12
proposed a 5-tier grading system for disk degeneration on T2-
weighted MRI. A grade I disk is homogeneous with hyperintense
signal intensity and normal disk height, whereas a grade II disk is
inhomogeneous but maintains its hyperintensity and height.
There may be a horizontal linear gray band, and the nucleus and
annulus are distinct. Grade III and IV disks are inhomogeneous,
with greater hypointensity and nucleus-annulus obscuration as
the grade increases. With increasing grade, there is also further
disk height loss. The grade V disks are inhomogeneous with
hypointense dark signal intensity, collapsed disk, and complete
loss of distinction between the nucleus and annulus. However,
the Pfirrmann classification does not provide a reliable quanti-
fication in the early stages of degeneration, which are character-
ized by a loss of water or proteoglycan in an intact disk. The T2
relaxation time is an intrinsic property of tissue that reflects the
molecular composition of water, proteins, collagen, and other
solutes in the disk. There is a positive correlation of intervertebral
disk T2 relaxation times with hydration and, to a lesser extent,
with proteoglycan content and a negative correlation with
collagen.75,76 Good correlation between T2 mapping values
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IMAGING OF SPINE DEGENERATIVE AND INFECTIOUS CONDITIONS
and water or proteoglycan content in lumbar intervertebral disk
has been validated,76,77 as well as characterization of different
tissue compartments within the intervertebral disk based on T2
values (ie, the annulus fibrosus and nucleus pulposus).78 Painful
herniated disks have shown a lower T2 relaxation compared with
those without pain.79 Quantitative T2 mapping has also been
studied in the cervical disks in asymptomatic young adults for
detecting and characterizing early degeneration.80
T1rho MRI is a potential noninvasive tool for quantitatively
measuring disk degeneration that is particularly sensitive to loss of
proteoglycan.81,82 Conventional MRI techniques cannot detect
loss of proteoglycan in the nucleus pulposus that occurs during
early degeneration. Matrix changes such as loss of proteoglycan
are reflected in the T1rho time constant, which may be more
sensitive to early degenerative changes than even T2 mapping.83
In exploratory studies, T1rho has been significantly lower in
painful disks on diskography compared with control disks.84
Magnetic resonance spectroscopy may also be used to detect
metabolites and biochemicals associated with degenerative disk
disease. Specimens of those disks determined to be the cause of
diskogenic disease demonstrate significantly lower proteoglycan,
glycosaminoglycan/collagen, and glycosaminoglycan/lactate ratios
and a higher lactate/collagen ratio.85 In vivo single voxel magnetic
resonance spectroscopy has also been used to differentiate
diskography-confirmed painful disks from asymptomatic (vol-
unteer and diskography-negative) controls on the basis of changes
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 SHAH AND ROSS

FIGURE 13. A, sagittal postcontrast T1-weighted, fat-saturated image and (B) axial T2-weighted image show soft tissue
protruding from the L4-L5 disk space into the right subarticular zone (yellow arrows). C, CT myelogram sagittal reconstruction
better delineates the osteophytic component (red arrow) impinging on the transiting L5 nerve. The edematous right L5 nerve can
be precisely followed along its course on the (D) axial CT myelogram (white arrow).

in the ratio between proteoglycan and combined lactate/lipid/
alanine peaks.86
SPINE INFECTION
Spinal infections may involve the intramedullary (eg, viral
myelitis, abscess), intradural extramedullary (eg, meningitis), and
extradural spaces. The latter includes epidural abscess, paraspinal
abscess, and diskitis-osteomyelitis (DOM). Spinal infection is the
most common form of hematogenous osteomyelitis in patients . 50
years of age and represents 3% to 5% of all cases of osteomyelitis.87
The increasing incidence has been attributed to an increase in
susceptible patients such as intravenous drug users, individuals
undergoing hemodialysis, and immunocompromised hosts. The
diagnosis of DOM may be difficult and requires the combination of
information obtained from many different modalities, including
serological, radiographic, and microbiological diagnostic tests.
Because the clinical diagnosis of spinal infection can be challenging
owing to vague symptoms of LBP or neck stiffness, radiological
evaluations have gained importance in the diagnosis, treatment
planning, and treatment monitoring of the spinal infections.
Spinal infections in each space have characteristic imaging
features that aid in the differential diagnosis. Typically, vertebral
bodies and disk spaces are involved in DOM, with the posterior

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 IMAGING OF SPINE DEGENERATIVE AND INFECTIOUS CONDITIONS

FIGURE 14. A, fractional anisotropy (left), red-green-blue (RGB; middle) map, and T2-weighted image (right) from a normal volunteer. Fractional anisotropy map shows
uniform values throughout the cord. RGB demonstrates the principal direction of diffusivity along the longitudinal direction as depicted with blue. T2-weighted image shows
a normal cervical cord without atrophy or lesions. B, fractional anisotropy (left), RGB map (middle), and T2-weighted images (right) from a patient with cervical spondylotic
myelopathy show severe degenerative disk disease and stenosis at C3-C4, C4-C5, and C5-C6. There is decrease in fractional anisotropy values at sites of stenosis. RGB map shows
admixing of colors at similar levels. Courtesy of fEun-Kee Jeong, PhD, Utah Center For Advanced Imaging Research, University of Utah.

elements less commonly affected. The infectious process may
extend into the epidural space, particularly in the anterior aspect
of the spinal canal. Although conventional radiographs are usually
the initial imaging study for vague complaints of LBP or neck pain,
the sensitivity and specificity of the plain radiographs are very low.
It takes 3 to 6 weeks after the onset of symptoms for osseous
destruction to be evident on plain radiographs (Figure 16). The
earliest sign on radiographs is the loss of definition and
irregularity of the vertebral endplates, usually anterosuperiorly.
The disk space initially increases, which is followed by loss of disk
height. Progressive endplate osteolysis causes obscuration of the
cortex.
CT has higher sensitivity than radiographs but lacks specificity
and plays a minor role in the diagnosis of early DOM compared
with MRI. CT is useful to assess the degree of osseous involvement
and destruction. Imaging features detected with CT include
osteopenia, soft tissue calcification, cortical bone erosion, perme-
ative bone destruction and fragmentation, and osseous sclerosis.
Involvement of the paraspinal soft tissues is suggested by
obliteration of fat planes.
MRI is the recommended initial diagnostic imaging of choice in
patients with suspected DOM because of its superior soft tissue
resolution.88-90 For diagnosing DOM, it has a sensitivity of 97%,
a specificity of 93%, and an accuracy of 94%.88,91 STIR sequences

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 SHAH AND ROSS

rim enhancement, and diffuse, homogeneous vertebral body

enhancement are distinctive MRI findings in pyogenic DOM.
The addition of fat saturation to gadolinium-enhanced
T1-weighted sequences can increase the conspicuity of the
paravertebral or epidural extension.
The most reliable MRI findings of spinal infection are the
hypointense T1 signal intensity of the vertebral body, abnormal
disk signal intensity on both T1-and T2-weighted images, and
contrast enhancement of the disk and vertebral body (Figure
17).91 Similarly, in a study of 44 patients with disk infection,
Ledermann et al88 found the MRI criteria with good to excellent
sensitivity were the presence of paraspinal or epidural inflam-
mation (97.7% sensitivity), disk enhancement (95.4% sensitiv-
ity), T2 hyperintensity in the disk space (93.2% sensitivity), and
erosion or destruction of at least 1 vertebral endplate (84.1%

FIGURE 15. Coronal half-Fourier acquisition single shot turbo spin echo
magnetic resonance myelograms of the (A) thoracic spine and (B) lumbar spine
illustrate the high-contrast resolution of this sequence. There is sharp contrast
between the dark signal of the spinal cord (white arrow) and nerves (red arrow)
and the bright signal of the cerebrospinal fluid. A nerve root sleeve diverticulum is
noted in the thoracic spine (yellow arrow).

have high positive and negative predictive values for detection of

vertebral bone marrow abnormalities (99.3% and 95.9%, respec-
tively).92 When STIR images are normal, contrast-enhanced
T1-weighted images do not provide additional information,
whereas further imaging is needed in cases of abnormal STIR
images.92 Gadolinium-based contrast agents increase the conspi-
cuity, specificity, and observer confidence in the diagnosis and
facilitate the treatment planning. The peridiskal bone destruction,

FIGURE 17. Sagittal (A) T1-weighted, (B) postcontrast T1-weighted, fat-

FIGURE 16. This patient had an L4-L5 microdiskectomy a12 weeks previously
and complains of increasing LBP. Left, posterior-anterior and (right) lateral
radiographs demonstrate loss of disk height with irregular endplate erosions and
obscuration of the cortical margins (white arrows).
saturated, (C) T2-weighted, and (D) STIR images of the lumbar spine exhibit
DOM at the L4-L5 level. There is T1 hypointensity, STIR hyperintensity, and
diffuse enhancement of the vertebral bodies. Peripherally enhancing (white
arrows), T2-hyperintense fluid (yellow arrow) is noted in the disk space. The
adjacent endplates exhibit irregular erosions (red arrow).

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FIGURE 18. Left, axial T2-weighted and (right) postcontrast axial T1-weighted, fat-saturated images shows T2-hyperin-
tense, peripherally enhancing abscesses in the left psoas muscle (white arrows). Amorphous T2 hyperintensity and enhancing soft
tissue, representing phlegmon, are observed in the anterior paraspinal region and ventral epidural space (yellow arrow).
sensitivity). Decreased height of the intervertebral space and disk
T1 hypointensity had a low sensitivity of 52.3% and 29.5%,
respectively. In their study of 37 patients, ring enhancement of
paraspinal and epidural lesions correlated with abscess and
homogeneous enhancement correlated with phlegmon at surgery
(Figure 18).91 Even without contrast, T2 hyperintensity of the
psoas musculature is highly correlated with DOM and can
significantly improve the diagnostic accuracy of DOM compared
with routine noncontrast variables alone.93 A repeat examination
may be warranted within 1 to 3 weeks if the initial imaging study
fails to show typical features of DOM.94
In patients in whom MRI cannot be performed, a combination
spine gallium/technetium-99 bone scan can be performed. Gallium
spine scan, in combination with a bone scan, has a specificity of
. 90%. Its sensitivity of 91% makes it a valuable test to exclude
DOM in patients with a questionable diagnosis.95,96 Intense
uptake on bone scintigraphy in 2 adjacent vertebrae with loss of the
disk space is highly suggestive of spinal osteomyelitis. Gallium not
only enhances the specificity of the diagnosis but also provides
information about surrounding soft tissue infection.
Image-guided diagnostic aspiration biopsy sampling is recommen-
ded as the first invasive diagnostic step in patients suspected of having
DOM when a microbiological diagnosis for a known associated
organism (eg, Staphylococcus aureus, Staphylococcus lugdunensis, and
Brucella species) has not been established by blood cultures or
serologic tests.94 The large proportion of negative results at
microbiological examination may be due to antibiotic treatment
initiated before the biopsy, an insufficient number of infectious agents
in the biopsied material, and sampling error with biopsy obtained
from a location without viable infectious agent. Histology combined
with microbiology increases the diagnostic yield of a biopsy.97
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IMAGING OF SPINE DEGENERATIVE AND INFECTIOUS CONDITIONS
Nonpyogenic causes of spinal infection can have distinguishing
imaging characteristics. In tuberculous spondylitis, the lower
thoracic and lumbar vertebrae are affected most frequently. The
anterior portion of the spine is affected primarily, with secondary
spread to the posterior elements. Multiple vertebral bodies are
invariably involved, and skip lesions may occur in up to 16.3% of
cases.98 Apposing endplate destruction with sparing of the
intervening disk, collapse of the vertebral body, epidural infection,
and intravertebral heterogeneous/ring enhancement can be seen.
Additional imaging features of tuberculous spondylitis are osseous
fragmentation, subligamentous spread, anterior wedging leading to
gibbus deformity, and intersegmental fusions (Figure 19). In
contradistinction to pyogenic paraspinal abscess, which shows ill-
defined signal abnormalities and enhancement, tuberculous para-
spinal abscesses have well-defined borders and are seen in up to
50% of cases.99 Focal brucellar spondylitis is seen as abnormal
signal intensities in the anterosuperior aspect of a vertebral body.
With diffuse brucellar spondylitis, abnormal signal intensity
extends throughout adjacent vertebrae and intervening disks.
Extension to the epidural space is common.
Fungal infection can affect the spinal column, particularly in
immunocompromised or immunosuppressed patients. In fungal
spondylitis, there may be only faint or absent T2 signal abnormalities.
In addition, contrast enhancement may be mild or absent, which is
thought to be due to the poor inflammatory reaction in immuno-
compromised patients. Some key imaging features in fungal
spondylitis are sparing of the disk space with preservation of the
equatorial intranuclear cleft, adjacent rib involvement, limited para-
spinal soft tissue extension, and relatively limited vertebral deformity.
The imaging differential diagnosis of DOM includes degenerative
endplate change, inflammatory arthropathy, spinal neuroarthropathy
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 SHAH AND ROSS

FIGURE 19. Sagittal (A) postcontrast T1-weighted, fat-saturated, (B) STIR, and axial (C) T2-weighted and (D) postcontrast T1-weighted images of the thoracic spine
exhibit 3-level tuberculous spondylodiskitis. There are T2/STIR hyperintensity and diffuse enhancement in the vertebral bodies. Peripherally enhancing, T2/STIR–
hyperintense fluid is noted in the disk space with subligamentous spread. Affected vertebral bodies demonstrate anterior wedging and slight kyphotic deformity.

(SNA), and dialysis arthropathy. MRI can usually differentiate DOM
from more common degenerative, traumatic, or neoplastic diseases.
In metastases, the disk space is spared. However, stages of DOM may
be difficult to differentiate from type I endplate change.88,100 The
main imaging findings of disk degeneration are lack of diskal T2
hyperintensity (often decreased signal), lack of soft tissue involve-
ment, and mild linear subchondral endplate enhancement. The
presence of gas within the disk usually suggests degenerative
disease16,101; however, spinal infection may rarely be accompanied
by intradiskal or intraosseous gas.102 In addition to the expected
signal changes and enhancement on routine imaging sequences in
DOM, DWI may be helpful in showing diffusely increased signal in
the involved osseous structures and increased conspicuity of epidural
involvement. The differentiation between degenerative type 1

FIGURE 21. Left, sagittal diffusion tensor and (right) postcontrast

FIGURE 20. Left, sagittal STIR images and (right) DTIs demonstrate mul- T1-weighted, fat-saturated images demonstrate diffuse hyperintensity and het-
tilevel endplate hyperintensity. The DTI exhibits the “claw sign,” which is linear erogeneous enhancement in the L3 and L4 vertebral bodies, in keeping with
hyperintensity at the border between normal marrow and the edematous marrow osteomyelitis. There is also hyperintense diffusion signal in the ventral epidural
and granulation tissue about the endplates. phlegmon (arrow).

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FIGURE 22. Left, sagittal STIR and (right) postcontrast T1-weighted, fat-
saturated images demonstrate vertebral osteitis with high STIR signal intensity
with contrast enhancement at the anterosuperior and anteroinferior vertebral
body corners. These are examples of Romanus lesions in a patient with ankylosing
spondylitis.
diskogenic endplate changes and inflammatory disease can be
problematic with conventional unenhanced and contrast-enhanced
MRI sequences.103 However, the “claw sign” is a qualitative and
morphological finding on DWI that can be used to differentiate
degenerative type 1 endplate changes from infection (Figure 20).
With the claw sign, there are paired linear regions of diffusion
hyperintensity at the border between normal marrow and the
edematous marrow and granulation tissue about the endplates.
DOM, the other hand, shows diffusely increased diffusion signal
throughout the involved vertebral bodies (Figure 21).104 Absence of
diffusion hyperintensity in the intervertebral disk space in
degenerative disease is also a helpful discriminator from infectious
processes.103
The imaging features of inflammatory arthropathy can overlap
those of DOM. The hallmark of inflammatory arthropathy is
a generalized enthesopathy with secondary inflammatory changes
within the synovial joints. A spectrum of inflammatory and
destructive lesions is seen in ankylosing spondylitis that involves
predominantly the cartilaginous diskovertebral junction. Inflam-
mation (active enthesitis and fibro-osteitis) at the attachments of
the outer fibers of the annulus fibrosus and longitudinal ligaments
to the vertebral body causes small erosions at the anterosuperior
and anteroinferior vertebral body corners (ie, Romanus lesions).
The typical MR appearance of this early vertebral osteitis is low T1
and high T2 signal intensity with marked contrast enhancement
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IMAGING OF SPINE DEGENERATIVE AND INFECTIOUS CONDITIONS
FIGURE 23. Left, sagittal CT reconstruction and (right) T2-weighted images
illustrate midthoracic adjacent endplate destructive changes in a patient with
end-stage renal disease and on long-term hemodialysis. The diffuse osteosclerosis is
likely due to the hyperparathyroidism. There is mild intradiskal and vertebral
body marrow T2 hyperintensity, but no paraspinal mass is identified.
(Figure 22). Reactive sclerosis of healing erosions produces
a “shiny corner” configuration. Other destructive diskovertebral
lesions are the Andersson lesions, of which there are 2 types. Type
A is an early inflammatory reaction with focal destruction of the
intervertebral disk and herniation through the adjacent vertebral
endplate. In the relatively acute stage, marrow edema demon-
strates T2/STIR hyperintensity and enhancement. Type B is
a later noninflammatory pseudoarthrosis that occurs after fracture
at the point of motion in the extensively ossified axial skeleton.
Destruction of the entire diskovertebral junction with a normal or
widened disk space and reactive sclerosis in the adjacent vertebral
bodies may mimic infectious spondylodiskitis or neuropathic
spine.
Hemodialysis-related arthropathy may be seen in patients
receiving long-term dialysis, typically . 3 years. The changes of
the vertebral endplates can be identical to those of infectious
spondylitis on radiographs, including a decrease in disk height with
subchondral bone erosions at the anterior superior and inferior
margins. The destructive changes may be due to either infiltration
by b-amyloid or subchondral resorption from the secondary
hyperparathyroidism. MRI often does not show marrow edema,105
although some studies have reported vertebral body T2 hyper-
intensity and enhancement.106 Absence of paravertebral soft tissue
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 SHAH AND ROSS
FIGURE 24. A, sagittal T2-weighted, (B) sagittal postcontrast T1-weighted, fat-saturated, (C) coronal CT, and (D) axial CT images in a patient with SNA at the L2-L3
level. The intradiskal space is fluid-filled with destruction and heterogeneous enhancement of irregular endplates. The CT images show debris, sclerosis, disorganization, vacuum
disk phenomenon (indicating excessive motion), and osteophytes.
infiltration is a helpful differentiating feature (Figure 23). Bone and
gallium scans are typically negative.
SNA (ie, Charcot joint) is a progressive destructive arthropathy
occurring after the loss of neuroprotective sensation and pro-
prioceptive reflexes. The radiographic changes of SNA are difficult
to distinguish from the destructive changes of infection. One of
the most helpful imaging clues to the diagnosis of SNA is the
involvement of both anterior and posterior elements in the
thoracolumbar and lumbosacral junctions. The presence of debris,
disorganization, vacuum disk phenomenon (indicating excessive
motion), and facet involvement favors SNA (Figure 24).107
Although bone scan will have intense increased metabolic activity
in both conditions, Indium-111–labeled white blood cells may be
an informative imaging tool to differentiate infection from SNA.
In some cases, findings overlap with infection, or SNA can be
superinfected, and biopsy may be necessary for further workup.
Distinguishing infection from expected postoperative changes in
the spine also can be problematic. The diagnosis is strongly
suggested by a persistently elevated erythrocyte sedimentation rate
and C-reactive protein values. A postoperative rise in C-reactive
protein usually decreases by about 10 days, whereas erythrocyte
sedimentation rate takes about 3 to 6 weeks to reduce. MRI is the
imaging modality of choice in diagnosing postoperative infection,
with a reported sensitivity and specificity of . 92%.108,109 In
a study of 15 asymptomatic patients who had uncomplicated
lumbar diskectomy and 7 patients with postoperative diskitis,
Boden et al110 suggested that the triad of intervertebral disk space
enhancement, annular enhancement, and vertebral body enhance-
ment leads to the diagnosis of disk space infection when present
with the appropriate laboratory findings. However, asymptomatic
postoperative patients may have annular enhancement at the
curette site, disk enhancement, and vertebral endplate enhance-
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ment without evidence of disk space infection.111 In postoperative
studies with the challenge of discerning DOM from expected
surgical changes, psoas T2 hyperintensity was demonstrated to
have a statistically significant association with DOM compared
with the noninfected postoperative patients.93
CONCLUSION
Neuroradiological examinations play a valuable role in the
assessment of the spine disorders. The different imaging
modalities can provide specific diagnostic information. Cur-
rently, CT and MRI are the primary techniques to investigate
spine pathology, each having their advantages. Multidetector CT
displays exquisite osseous detail, with rapidity and multiplanar
reconstruction capability. MRI has a complementary role in
delineation of soft tissue abnormalities, which is helpful for
evaluating the extent of soft tissue involvement in spinal
infections. For degenerative spine evaluation, MRI is the
fundamental modality, providing soft tissue (eg, disk and
ligament) and osseous (eg, endplate diskogenic change) infor-
mation. With continued advances in imaging techniques such as
dynamic MRI and DTI, more functional and microstructural
information may be obtained.
Disclosure
The authors have no personal, financial, or institutional interest in any of the
drugs, materials, or devices described in this article.
REFERENCES
1. van der Wurff P, Buijs EJ, Groen GJ. A multitest regimen of pain provocation
tests as an aid to reduce unnecessary minimally invasive sacroiliac joint
procedures. Arch Phys Med Rehabil. 2006;87(1):10-14.
www.neurosurgery-online.com

2. Ren XS, Selim AJ, Fincke G, et al. Assessment of functional status, low back
disability, and use of diagnostic imaging in patients with low back pain and
radiating leg pain. J Clin Epidemiol. 1999;52(11):1063-1071.
3. Jarvik JG, Deyo RA. Diagnostic evaluation of low back pain with emphasis on
imaging. Ann Internal Med. 2002;137(7):586-597.
4. Jarvik JG, Hollingworth W, Martin B, et al. Rapid magnetic resonance imaging
vs radiographs for patients with low back pain: a randomized controlled trial.
JAMA. 2003;289(21):2810-2818.
5. Brinjikji W, Luetmer PH, Comstock B, et al. Systematic literature review of
imaging features of spinal degeneration in asymptomatic populations. AJNR Am J
Neuroradiol. 2015;36(4):811-816.
6. Boden SD, Davis DO, Dina TS, Patronas NJ, Wiesel SW. Abnormal magnetic-
resonance scans of the lumbar spine in asymptomatic subjects: a prospective
investigation. J Bone Joint Surg Am. 1990;72(3):403-408.
7. Carragee E, Alamin T, Cheng I, Franklin T, van den Haak E, Hurwitz E. Are
first-time episodes of serious LBP associated with new MRI findings? Spine J.
2006;6(6):624-635.
8. Fardon DF. Nomenclature and classification of lumbar disc pathology. Spine
(Phila Pa 1976). 2001;26(5):461-462.
9. Fardon DF, Milette PC, Combined Task Forces of the North American Spine
Society, American Society of Spine Radiology, and American Society of
Neurology.Nomenclature and classification of lumbar disc pathology: recom-
mendations of the combined task forces of the North American Spine Society,
American Society of Spine Radiology, and American Society of Neuroradiology.
Spine. 2001;26(5):E93-E113.
10. Fardon DF, Williams AL, Dohring EJ, Murtagh FR, Gabriel Rothman SL,
Sze GK. Lumbar disc nomenclature: version 2.0: recommendations of the
combined task forces of the North American Spine Society, the American Society
of Spine Radiology and the American Society of Neuroradiology. Spine J. 2014;
14(11):2525-2545.
11. Fardon DF, Williams AL, Dohring EJ, Murtagh FR, Gabriel Rothman SL,
Sze GK. Lumbar disc nomenclature: version 2.0: recommendations of the
combined task forces of the North American Spine Society, the American Society
of Spine Radiology, and the American Society of Neuroradiology. Spine (Phila Pa
1976). 2014;39(24):E1448-E1465.
12. Pfirrmann CW, Metzdorf A, Zanetti M, Hodler J, Boos N. Magnetic resonance
classification of lumbar intervertebral disc degeneration. Spine (Phila Pa 1976).
2001;26(17):1873-1878.
13. Ford LT, Gilula LA, Murphy WA, Gado M. Analysis of gas in vacuum lumbar
disc. AJR Am J Roentgenol. 1977;128(6):1056-1057.
14. Modic MT, Steinberg PM, Ross JS, Masaryk TJ, Carter JR. Degenerative disk
disease: assessment of changes in vertebral body marrow with MR imaging.
Radiology. 1988;166(1 Pt 1):193-199.
15. Vital JM, Gille O, Pointillart V, et al. Course of Modic 1 six months after lumbar
posterior osteosynthesis. Spine (Phila Pa 1976). 2003;28(7):715-720; discussion 721.
16. Modic MT, Ross JS. Lumbar degenerative disk disease. Radiology. 2007;245(1):
43-61.
17. Rahme R, Moussa R. The Modic vertebral endplate and marrow changes:
pathologic significance and relation to low back pain and segmental instability of
the lumbar spine. AJNR Am J Neuroradiol. 2008;29(5):838-842.
18. Kuisma M, Karppinen J, Niinimaki J, et al. Modic changes in endplates of lumbar
vertebral bodies: prevalence and association with low back and sciatic pain among
middle-aged male workers. Spine (Phila Pa 1976). 2007;32(10):1116-1122.
19. Jensen TS, Bendix T, Sorensen JS, Manniche C, Korsholm L, Kjaer P.
Characteristics and natural course of vertebral endplate signal (Modic) changes in
the Danish general population. BMC Musculoskelet Disord. 2009;10:81.
20. Kjaer P, Leboeuf-Yde C, Korsholm L, Sorensen JS, Bendix T. Magnetic
resonance imaging and low back pain in adults: a diagnostic imaging study of 40-
year-old men and women. Spine (Phila Pa 1976). 2005;30(10):1173-1180.
21. Chung CB, Vande Berg BC, Tavernier T, et al. End plate marrow changes in the
asymptomatic lumbosacral spine: frequency, distribution and correlation with age
and degenerative changes. Skeletal Radiol. 2004;33(7):399-404.
22. Kanayama M, Togawa D, Takahashi C, Terai T, Hashimoto T. Cross-sectional
magnetic resonance imaging study of lumbar disc degeneration in 200 healthy
individuals. J Neurosurg Spine. 2009;11(4):501-507.
23. Weishaupt D, Zanetti M, Hodler J, et al. Painful lumbar disk derangement:
relevance of endplate abnormalities at MR imaging. Radiology. 2001;218(2):
420-427.
NEUROSURGERY
Downloaded from https://academic.oup.com/neurosurgery/article-abstract/79/3/315/2835698
by UB Frankfurt/Main user
Copyright © Congress of Neurological Surgeons. Unauthorized reproduction of this article is prohibited
on 24 February 2018
IMAGING OF SPINE DEGENERATIVE AND INFECTIOUS CONDITIONS
24. Albert HB, Briggs AM, Kent P, Byrhagen A, Hansen C, Kjaergaard K. The
prevalence of MRI-defined spinal pathoanatomies and their association with
Modic changes in individuals seeking care for low back pain. Eur Spine J. 2011;20
(8):1355-1362.
25. Arana E, Kovacs FM, Royuela A, et al. Modic changes and associated features in
Southern European chronic low back pain patients. Spine J. 2011;11(5):402-411.
26. Arpinar VE, Rand SD, Klein AP, Maiman DJ, Muftuler LT. Changes in
perfusion and diffusion in the endplate regions of degenerating intervertebral
discs: a DCE-MRI study. Eur Spine J. 2015;24(11):2458-2467.
27. Arnoldi CC, Brodsky AE, Cauchoix J, et al. Lumbar spinal stenosis and nerve
root entrapment syndromes: definition and classification. Clin Orthop Relat Res.
1976(115):4-5.
28. Tavee JO, Levin KH. Myelopathy due to degenerative and structural spine
diseases. Continuum (Minneap Minn). 2015;21(1 Spinal Cord Disorders):52-66.
29. Zhang C, Das SK, Yang DJ, Yang HF. Application of magnetic resonance imaging
in cervical spondylotic myelopathy. World J Radiol. 2014;6(10):826-832.
30. Tracy JA, Bartleson JD. Cervical spondylotic myelopathy. Neurologist. 2010;16
(3):176-187.
31. Baptiste DC, Fehlings MG. Pathophysiology of cervical myelopathy. Spine J.
2006;6(suppl 6):190S-197S.
32. Baron EM, Young WF. Cervical spondylotic myelopathy: a brief review of its
pathophysiology, clinical course, and diagnosis. Neurosurgery. 2007;60(1 suppl 1):
S35-S41.
33. Yong-Hing K, Kirkaldy-Willis WH. The pathophysiology of degenerative disease
of the lumbar spine. Orthop Clin North Am. 1983;14(3):491-504.
34. Lattig F, Fekete TF, Grob D, Kleinstuck FS, Jeszenszky D, Mannion AF.
Lumbar facet joint effusion in MRI: a sign of instability in degenerative
spondylolisthesis? Eur Spine J. 2012;21(2):276-281.
35. Lee JC, Cha JG, Yoo JH, Kim HK, Kim HJ, Shin BJ. Radiographic grading of
facet degeneration, is it reliable? A comparison of MR or CT grading with
histologic grading in lumbar fusion candidates. Spine J. 2012;12(6):507-514.
36. Keorochana G, Taghavi CE, Tzeng ST, et al. Magnetic resonance imaging
grading of interspinous ligament degeneration of the lumbar spine and its relation
to aging, spinal degeneration, and segmental motion. J Neurosurg Spine. 2010;13
(4):494-499.
37. Gorbach C, Schmid MR, Elfering A, Hodler J, Boos N. Therapeutic efficacy of
facet joint blocks. AJR Am J Roentgenol. 2006;186(5):1228-1233.
38. Weishaupt D, Zanetti M, Boos N, Hodler J. MR imaging and CT in
osteoarthritis of the lumbar facet joints. Skeletal Radiol. 1999;28(4):215-219.
39. Kim KY, Wang MY. Magnetic resonance image-based morphological predictors of
single photon emission computed tomography-positive facet arthropathy in patients
with axial back pain. Neurosurgery. 2006;59(1):147-156; discussion 147-156.
40. Matar HE, Navalkissoor S, Berovic M, et al. Is hybrid imaging (SPECT/CT)
a useful adjunct in the management of suspected facet joints arthropathy? Int
Orthop. 2013;37(5):865-870.
41. Hemminghytt S, Daniels DL, Williams AL, Haughton VM. Intraspinal synovial
cysts: natural history and diagnosis by CT. Radiology. 1982;145(2):375-376.
42. Apostolaki E, Davies AM, Evans N, Cassar-Pullicino VN. MR imaging of lumbar
facet joint synovial cysts. Eur Radiol. 2000;10(4):615-623.
43. Shah RV, Lutz GE. Lumbar intraspinal synovial cysts: conservative management
and review of the world’s literature. Spine J. 2003;3(6):479-488.
44. Pytel P, Wollmann RL, Fessler RG, Krausz TN, Montag AG. Degenerative spine
disease: pathologic findings in 985 surgical specimens. Am J Clin Pathol. 2006;
125(2):193-202.
45. Ulmer JL, Elster AD, Mathews VP, Allen AM. Lumbar spondylolysis: reactive
marrow changes seen in adjacent pedicles on MR images. AJR Am J Roentgenol.
1995;164(2):429-433.
46. Ulmer JL, Mathews VP, Elster AD, Mark LP, Daniels DL, Mueller W. MR
imaging of lumbar spondylolysis: the importance of ancillary observations. AJR
Am J Roentgenol. 1997;169(1):233-239.
47. Morrison JL, Kaplan PA, Dussault RG, Anderson MW. Pedicle marrow signal
intensity changes in the lumbar spine: a manifestation of facet degenerative joint
disease. Skeletal Radiol. 2000;29(12):703-707.
48. Sairyo K, Katoh S, Takata Y, et al. MRI signal changes of the pedicle as an
indicator for early diagnosis of spondylolysis in children and adolescents: a clinical
and biomechanical study. Spine (Phila Pa 1976). 2006;31(2):206-211.
49. Borg B, Modic MT, Obuchowski N, Cheah G. Pedicle marrow signal
hyperintensity on short tau inversion recovery- and T2-weighted images:
VOLUME 79 | NUMBER 3 | SEPTEMBER 2016 | 333
 SHAH AND ROSS
prevalence and relationship to clinical symptoms. AJNR Am J Neuroradiol. 2011;
32(9):1624-1631.
50. Masaryk TJ, Boumphrey F, Modic MT, Tamborrello C, Ross JS, Brown MD.
Effects of chemonucleolysis demonstrated by MR imaging. J Comput Assist
Tomogr. 1986;10(6):917-923.
51. Lang P, Chafetz N, Genant HK, Morris JM. Lumbar spinal fusion: assessment of
functional stability with magnetic resonance imaging. Spine (Phila Pa 1976).
1990;15(6):581-588.
52. Buttermann GR, Heithoff KB, Ogilvie JW, Transfeldt EE, Cohen M. Vertebral
body MRI related to lumbar fusion results. Eur Spine J. 1997;6(2):115-120.
53. Bartynski WS, Lin L. Lumbar root compression in the lateral recess: MR
imaging, conventional myelography, and CT myelography comparison with
surgical confirmation. AJNR Am Journal Neuroradiol. 2003;24(3):348-360.
54. Grams AE, Gempt J, Förschler A. Comparison of spinal anatomy between
3-Tesla MRI and CT-myelography under healthy and pathological conditions.
Surg Radiol Anat. 2010;32(6):581-585.
55. Naganawa T, Miyamoto K, Ogura H, Suzuki N, Shimizu K. Comparison of magnetic
resonance imaging and computed tomogram-myelography for evaluation of cross
sections of cervical spinal morphology. Spine (Phila Pa 1976). 2011;36(1):50-56.
56. Pneumaticos SG, Chatziioannou SN, Hipp JA, Moore WH, Esses SI. Low back
pain: prediction of short-term outcome of facet joint injection with bone
scintigraphy. Radiology. 2006;238(2):693-698.
57. Dolan AL, Ryan PJ, Arden NK, et al. The value of SPECT scans in identifying
back pain likely to benefit from facet joint injection. Br J Rheumatol. 1996;35
(12):1269-1273.
58. Willick SE, Kendall RW, Roberts ST, Morton K. An emerging imaging technology
to assist in the localization of axial spine pain. PM R. 2009;1(1):89-92.
59. Zhang W, Ma X, Wang Y, et al. Assessment of apparent diffusion coefficient in
lumbar intervertebral disc degeneration. Eur Spine J. 2014;23(9):1830-1836.
60. Kealey SM, Aho T, Delong D, Barboriak DP, Provenzale JM, Eastwood JD.
Assessment of apparent diffusion coefficient in normal and degenerated
intervertebral lumbar disks: initial experience. Radiology. 2005;235(2):569-574.
61. Takashima H, Takebayashi T, Yoshimoto M, Terashima Y, Ida K, Yamashita T.
Efficacy of diffusion-weighted magnetic resonance imaging in diagnosing spinal
root disorders in lumbar disc herniation. Spine (Phila Pa 1976). 2013;38(16):
E998-E1002.
62. Demir A, Ries M, Moonen CT, et al. Diffusion-weighted MR imaging with
apparent diffusion coefficient and apparent diffusion tensor maps in cervical
spondylotic myelopathy. Radiology. 2003;229(1):37-43.
63. Kara B, Celik A, Karadereler S, et al. The role of DTI in early detection of cervical
spondylotic myelopathy: a preliminary study with 3-T MRI. Neuroradiology.
2011;53(8):609-616.
64. Kerkovsky M, Bednarik J, Dusek L, et al. Magnetic resonance diffusion tensor
imaging in patients with cervical spondylotic spinal cord compression:
correlations between clinical and electrophysiological findings. Spine (Phila Pa
1976). 2012;37(1):48-56.
65. Budzik JF, Balbi V, Le Thuc V, Duhamel A, Assaker R, Cotten A. Diffusion
tensor imaging and fibre tracking in cervical spondylotic myelopathy. Eur Radiol.
2011;21(2):426-433.
66. Jones JG, Cen SY, Lebel RM, Hsieh PC, Law M. Diffusion tensor imaging
correlates with the clinical assessment of disease severity in cervical spondylotic
myelopathy and predicts outcome following surgery. AJNR Am J Neuroradiol.
2013;34(2):471-478.
67. Arima H, Sakamoto S, Naito K, et al. Prediction of the efficacy of surgical intervention
in patients with cervical myelopathy by using diffusion tensor 3T-magnetic resonance
imaging parameters. J Craniovertebr Junction Spine. 2015;6(3):120-124.
68. Ferrer P, Marti-Bonmati L, Molla E, Arana E. MR-myelography as an adjunct to
the MR examination of the degenerative spine. MAGMA. 2004;16(5):203-210.
69. Stone JA. MR myelography of the spine and MR peripheral nerve imaging. Magn
Reson Imaging Clin N Am. 2003;11(4):543-558.
70. O’Connell MJ, Ryan M, Powell T, Eustace S. The value of routine MR
myelography at MRI of the lumbar spine. Acta Radiol. 2003;44(6):665-672.
71. Chen CJ, Hsu HL, Niu CC, et al. Cervical degenerative disease at flexion-
extension MR imaging: prediction criteria. Radiology. 2003;227(1):136-142.
72. Wei FHS, Zou J, Tow B, et al. The effect of lumbar flexion and extension on the
central canal with dynamic MRI; Paper #79 presented at: 22nd Annual Meeting
of the North American Spine Society 2007, Austin, Texas. doi: 10.1016/j.spinee.
2007.07.096.
334 | VOLUME 79 | NUMBER 3 | SEPTEMBER 2016
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by UB Frankfurt/Main user
Copyright © Congress of Neurological Surgeons. Unauthorized reproduction of this article is prohibited
on 24 February 2018
73. Wildermuth S, Zanetti M, Duewell S, et al. Lumbar spine: quantitative and
qualitative assessment of positional (upright flexion and extension) MR imaging
and myelography. Radiology. 1998;207(2):391-398.
74. Shah LM, Lazzaro N, Rassner UA, Wiggins RH, Quigley EP. Dynamic cervical spine
MRI: a new view of spinal stenosis. Paper presented at: American Society of Spine
Radiology (ASSR) Annual Symposium; February 18-21, 2010; Las Vegas, NV.
75. Weidenbaum M, Foster RJ, Best BA, et al. Correlating magnetic resonance
imaging with the biochemical content of the normal human intervertebral disc.
J Orthop Res. 1992;10(4):552-561.
76. Marinelli NL, Haughton VM, Munoz A, Anderson PA. T2 relaxation times of
intervertebral disc tissue correlated with water content and proteoglycan content.
Spine (Phila Pa 1976). 2009;34(5):520-524.
77. Niu G, Yang J, Wang R, Dang S, Wu EX, Guo Y. MR imaging assessment of
lumbar intervertebral disk degeneration and age-related changes: apparent diffusion
coefficient versus T2 quantitation. AJNR Am J Neuroradiol. 2011;32(9):1617-1623.
78. Stelzeneder D, Welsch GH, Kovacs BK, et al. Quantitative T2 evaluation at 3.0T
compared to morphological grading of the lumbar intervertebral disc: a stan-
dardized evaluation approach in patients with low back pain. Eur J Radiol. 2012;
81(2):324-330.
79. Boos N, Dreier D, Hilfiker E, et al. Tissue characterization of symptomatic and
asymptomatic disc herniations by quantitative magnetic resonance imaging.
J Orthop Res. 1997;15(1):141-149.
80. Chen C, Huang M, Han Z, et al. Quantitative T2 magnetic resonance imaging
compared to morphological grading of the early cervical intervertebral disc
degeneration: an evaluation approach in asymptomatic young adults. PLoS One.
2014;9(2):e87856.
81. Johannessen W, Auerbach JD, Wheaton AJ, et al. Assessment of human disc
degeneration and proteoglycan content using T1rho-weighted magnetic reso-
nance imaging. Spine (Phila Pa 1976). 2006;31(11):1253-1257.
82. Auerbach JD, Johannessen W, Borthakur A, et al. In vivo quantification of
human lumbar disc degeneration using T(1rho)-weighted magnetic resonance
imaging. Eur Spine J. 2006;15(suppl 3):S338-S344.
83. Boos N, Wallin A, Schmucker T, Aebi M, Boesch C. Quantitative MR imaging
of lumbar intervertebral disc and vertebral bodies: methodology, reproducibility,
and preliminary results. Magn Reson Imaging. 1994;12(4):577-587.
84. Borthakur A, Maurer PM, Fenty M, et al. T1rho magnetic resonance imaging
and discography pressure as novel biomarkers for disc degeneration and low back
pain. Spine (Phila Pa 1976). 2011;36(25):2190-2196.
85. Keshari KR, Lotz JC, Link TM, Hu S, Majumdar S, Kurhanewicz J. Lactic acid
and proteoglycans as metabolic markers for discogenic back pain. Spine (Phila Pa
1976). 2008;33(3):312-317.
86. Hu SS, Peacock J, Clad J, Lotz J, Bradford DS, Berven SH. Modified magnetic
resonance spectroscopy diagnosis of painful and non-painful lumbar interverte-
bral discs. Paper presented at: the Annual Meeting of the Orthopaedic Research
Society; October 2010.
87. Jensen AG, Espersen F, Skinhøj P, Rosdahl VT, Frimodt-Møller N. Increasing
frequency of vertebral osteomyelitis following Staphylococcus aureus bacteraemia
in Denmark 1980-1990. J Infect. 1997;34(2):113-118.
88. Ledermann HP, Schweitzer ME, Morrison WB, Carrino JA. MR imaging
findings in spinal infections: rules or myths? Radiology. 2003;228(2):506-514.
89. Tali ET, Oner AY, Koc AM. Pyogenic spinal infections. Neuroimaging Clin N
Am. 2015;25(2):193-208.
90. Tali ET. Spinal infections. Eur J Radiol. 2004;50(2):120-133.
91. Dagirmanjian A, Schils J, McHenry M, Modic MT. MR imaging of vertebral
osteomyelitis revisited. AJR Am J Roentgenol. 1996;167(6):1539-1543.
92. Mahnken AH, Wildberger JE, Adam G, et al. Is there a need for contrast-
enhanced T1-weighted MRI of the spine after inconspicuous short tau inversion
recovery imaging? Eur Radiol. 2005;15(7):1387-1392.
93. Ledbetter LN, Salzman KL, Shah LM. Psoas Sign in Lumbar Vertebral Infections:
“Look at Me Lesion!” Chicago, IL: Radiological Society of North America; 2014.
94. Berbari EF, Kanj SS, Kowalski TJ, et al. 2015 Infectious Diseases Society of
America (IDSA) clinical practice guidelines for the diagnosis and treatment of
native vertebral osteomyelitis in adults. Clin Infect Dis. 2015;61(6):e26-e46.
95. Palestro CJ, Torres MA. Radionuclide imaging in orthopedic infections. Semin
Nucl Med. 1997;27(4):334-345.
96. Love C, Patel M, Lonner BS, Tomas MB, Palestro CJ. Diagnosing spinal
osteomyelitis: a comparison of bone and Ga-67 scintigraphy and magnetic
resonance imaging. Clin Nucl Med. 2000;25(12):963-977.
www.neurosurgery-online.com

97. Michel SC, Pfirrmann CW, Boos N, Hodler J. CT-guided core biopsy of
subchondral bone and intervertebral space in suspected spondylodiskitis. AJR Am
J Roentgenol. 2006;186(4):977-980.
98. Polley P, Dunn R. Noncontiguous spinal tuberculosis: incidence and manage-
ment. Eur Spine J. 2009;18(8):1096-1101.
99. Tekkok IH, Berker M, Ozcan OE, Ozgen T, Akalin E. Brucellosis of the spine.
Neurosurgery. 1993;33(5):838-844.
100. Longo M, Granata F, Ricciardi K, Gaeta M, Blandino A. Contrast-enhanced MR
imaging with fat suppression in adult-onset septic spondylodiscitis. Eur Radiol.
2003;13(3):626-637.
101. Li FC, Zhang N, Chen WS, Chen QX. Endplate degeneration may be the
origination of the vacuum phenomenon in intervertebral discs. Med Hypotheses.
2010;75(2):169-171.
102. Bielecki DK, Sartoris D, Resnick D, Van Lom K, Fierer J, Haghighi P.
Intraosseous and intradiscal gas in association with spinal infection: report of
three cases. AJR Am J Roentgenol. 1986;147(1):83-86.
103. Eguchi Y, Ohtori S, Yamashita M, et al. Diffusion magnetic resonance imaging to
differentiate degenerative from infectious endplate abnormalities in the lumbar
spine. Spine (Phila Pa 1976). 2011;36(3):E198-E202.
104. Patel KB, Poplawski MM, Pawha PS, Naidich TP, Tanenbaum LN. Diffusion-
weighted MRI “claw sign” improves differentiation of infectious from degenerative
Modic type 1 signal changes of the spine. AJNR Am Journal Neuroradiol. 2014;35(8):
1647-1652.
NEUROSURGERY
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IMAGING OF SPINE DEGENERATIVE AND INFECTIOUS CONDITIONS
105. Sheldon PJ, Forrester DM. Imaging of amyloid arthropathy. Semin Musculoskelet
Radiol. 2003;7(3):195-203.
106. Leone A, Sundaram M, Cerase A, Magnavita N, Tazza L, Marano P. Destructive
spondyloarthropathy of the cervical spine in long-term hemodialyzed patients: a five-
year clinical radiological prospective study. Skeletal Radiol. 2001;30(8):431-441.
107. Jones EA, Manaster BJ, May DA, Disler DG. Neuropathic osteoarthropathy:
diagnostic dilemmas and differential diagnosis. Radiographics. 2000;20 Spec No:
S279-S293.
108. Frank AM, Trappe AE. The role of magnetic resonance imaging (MRI) in the
diagnosis of spondylodiscitis. Neurosurg Rev. 1990;13(4):279-283.
109. Rohde V, Meyer B, Schaller C, Hassler WE. Spondylodiscitis after lumbar
discectomy: incidence and a proposal for prophylaxis. Spine (Phila Pa 1976).
1998;23(5):615-620.
110. Boden SD, Davis DO, Dina TS, Sunner JL, Wiesel SW. Postoperative diskitis:
distinguishing early MR imaging findings from normal postoperative disk space
changes. Radiology. 1992;184(3):765-771.
111. Ross JS, Zepp R, Modic MT. The postoperative lumbar spine: enhanced MR
evaluation of the intervertebral disk. AJNR Am J Neuroradiol. 1996;17(2):323-331.
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