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MRI Web Clinic — July 2012


Discitis
Alice B. Viroslav M.D.

Clinical history: A 91 year-old woman complains of low back pain. A routine


lumbar spine MR with (1a) T1-weighted sagittal and (1b,1c) T2-weighted
sagittal and axial images was performed. What are the findings? What is your
diagnosis?
1a
(http://radsource.us/wp-content/uploads/2012/07/1a.jpg)
1b
(http://radsource.us/wp-content/uploads/2012/07/1b.jpg)

1c
(http://radsource.us/wp-content/uploads/2012/07/1c.jpg)
Figure 1:
(1a) T1-weighted sagittal and (1b,1c) T2-weighted sagittal and axial images.
Findings

2a
(http://radsource.us/wp-content/uploads/2012/07/2a1.jpg)
Figure 2:
The T1-weighted sagittal image shows irregularity of the endplates at the L2-3 level
(arrowheads)with marked hypointensity in the adjacent endplates (asterisks).
3a
(http://radsource.us/wp-content/uploads/2012/07/3a.jpg)
Figure 3:
The T2-weighted sagittal image confirms endplate irregularity(arrowhead). The disc is markedly
hyperintense.

4a
(http://radsource.us/wp-content/uploads/2012/07/4a.jpg)
Figure 4:
The T2-weighted axial image reveals abnormal hyperintensity in the atrophic left iliopsoas
muscle(asterisk) and a small left paraspinous fluid collection (arrow), suspicious for abscess.
Diagnosis

Spontaneous pyogenic discitis.

Introduction

Discitis, infection of the disc and vertebral endplates, has significant morbidity
and mortality. Although early diagnosis and treatment leads to a better
outcome, a delay in diagnosis is common due to nonspecific and inconsistent
clinical signs and symptoms. A variety of imaging modalities may be used to
evaluate suspected discitis with varying degrees of effectiveness.

Epidemiology

Discitis exhibits a bimodal age distribution, with peaks in early childhood and
after age 50. A male predominance is seen. Risk factors for discitis include
diabetes, old age, immunosuppression, IV drug use, alcoholism, and renal
failure. Although rare, there is an increased risk of discitis following invasive
spinal procedures, estimated at 0.5% for anterior cervical discectomy and
0.25% for lumbar discectomy, with an overall rate of 0.1 to 4% of all invasive
spinal procedures. Postoperative discitis accounts for approximately 20-30% of
cases of discitis.1,2

Pathophysiology

Most cases of discitis are secondary to infection elsewhere in the body, with
the most common source being the genitourinary tract; other less common
sources include endocarditis, pneumonia, or the oral cavity.1,3 Contrary to its
name, due to the vascular anatomy of adults, discitis is a primary infection of
the vertebral endplate with secondary extension into the disc. The
metaphyseal arteries of the endplate are the target for septic emboli, which
cause bone infarction and secondary infection. The vascular supply of the disc
ends in the annulus fibrosis; the disc is largely supplied with nutrients via direct
diffusion from the vertebral endplate. Infection thus spreads contiguously to
the disc, spinal canal, and paraspinous soft tissues.1,2 Another postulated
source of blood-borne pathogens is the epidural venous plexus; retrograde
flow from the pelvis may allow the spread of infection from pelvic disease, and
the pelvis is in fact the most common source of infection in discitis. However,
this route of spread is not universally accepted, as pressures required to
generate retrograde flow in animal models are not physiologic.2

In children, the pathophysiology of discitis differs due to differences in arterial


anatomy; nutrient vessels penetrate into the nucleus pulposus, allowing direct
infection of the disc.1 Childhood discitis is also less likely to be associated with
a systemic infection.2

The most common organism in both adults and children is Staphylococcus


aureus. Less commonly seen are Pseudomonas aeruginosa in IV drug abusers,
and mycobacterial infection in immunocompromised patients.2 Blood cultures
are only positive in 50% of patients, and biopsy is often necessary to isolate the
causative organism.1

Clinical Presentation and Laboratory Studies

The signs and symptoms of discitis are nonspecific, commonly leading to a


delay in diagnosis of 2 to 6 months on average after onset of symptoms. Over
90% of patients with bacterial discitis complain of back pain that is not relieved
by rest or common analgesics. Fever is not a consistent feature of discitis, seen
in only 60-70% of patients. Other non-specific symptoms such as weight loss
and anorexia may be present. Localized tenderness to palpation, muscle
spasm, and worsening of symptoms with movement are common. A
neurologic deficit is uncommon, but when present should raise suspicion for a
complicating epidural abscess. Epidural abscess is more common in
chronically ill patients who are unfortunately unlikely to exhibit constitutional
symptoms usually associated with abscess, such as fever and chills.1,2,3

The most common laboratory abnormalities in patients with discitis are an


elevated erythrocyte sedimentation rate (ESR) and elevated levels of C-reactive
protein (CRP), seen in over 90% of patients. Leukocytosis is not consistently
present, occurring in less than 50% of patients; therefore a normal white blood
cell count does not exclude discitis.1

In the postoperative patient, symptoms usually begin days to weeks after


surgery and are similar to spontaneous discitis. As the ESR and CRP are
normally elevated in the first few weeks post-operatively, laboratory studies are
not reliable indicators of discitis in these patients.3 Delayed onset of discitis up
not reliable indicators of discitis in these patients. Delayed onset of discitis up
to 7 years after surgery has been reported.4

5a
(http://radsource.us/wp-content/uploads/2012/07/5a.jpg)
Figure 5:
A 65 year-old male with history of L5 laminotomy several months prior, now with recurrent pain. A
T1-weighted sagittal image demonstrates marked hypointensity of the L4-5 disc(arrowhead) and
adjacent vertebral bodies(asterisks) with irregular, poorly defined endplates and a ventral epidural
soft tissue process (arrows).

6a
(http://radsource.us/wp-content/uploads/2012/07/6a.jpg)
Figure 6:
The corresponding T2-weighted sagittal image reveals a markedly hyperintense intervertebral disc
(arrowhead). Abnormal hyperintensity contiguous with the disc (arrow) extends into the ventral
epidural space.

7a
(http://radsource.us/wp-content/uploads/2012/07/7a.jpg)

7b
(http://radsource.us/wp-content/uploads/2012/07/7b.jpg)
Figure 7:
T1-weighted sagittal (7a) and axial (7b) images after IV gadolinium administration demonstrate
peripheral enhancement of the disc (arrowheads) and marked vertebral enhancement (asterisks). A
moderate amount of uniformly enhancing soft tissue is present in the ventral spinal canal at the
L4-5 level (arrows), suggesting epidural inflammatory changes. The recent left L5 laminotomy
defect is demonstrated (short arrow).
8a
(http://radsource.us/wp-content/uploads/2012/07/8a.jpg)
Figure 8:
A T2-weighted axial image demonstrates loss of normal paraspinous fat planes (arrowheads) and
abnormal signal in the left iliopsoas muscle (asterisk). Diagnosis: Post operative pyogenic discitis
with epidural phlegmon and paraspinous inflammation.

The clinical presentation of discitis in children differs from that of adults and is
characterized by fever, sudden onset of back pain, refusal to flex the lumbar
spine, irritability, and refusal to walk.1,2

Imaging of discitis

Discitis is most commonly seen in the lumbar spine, followed by the cervical
spine, and least commonly involves the thoracic spine (except for in atypical
cases, such as those caused by tuberculous involvement).2 Several imaging
modalities may be used in the assessment of discitis.

Plain films

Findings on plain radiographs usually require 10-14 days to develop and lag
behind clinical symptoms. As a result, a negative plain film does not exclude
early discitis. Eventual changes include loss of definition of the end plates and
decrease in disc space height, followed by lucency of the vertebral body, loss
of trabeculations, and finally frank bone destruction. Progressive kyphosis or
scoliosis can develop in cases of chronic infection. Sclerosis is seen after
2,3
healing with a high incidence of fusion of the disc space.2,3

Nuclear medicine studies

Gallium scans and technetium-99M scans are highly sensitive for the detection
of discitis, with positive scans seen in 90% of patients that have been
symptomatic for longer than 2 days. The increased uptake in the affected
endplates and decrease in disc space height produces a characteristic
“sandwich” appearance. However, because of the poor anatomic resolution of
nuclear medicine studies and the advent of more sensitive and specific
imaging modalities, these studies are usually utilized in cases of fever of
unknown origin or, in the case of gallium scan, as part of treatment follow-up.
Technetium-99m scans remain positive long after healing has occurred, and
are thus not useful in assessing treatment efficacy.3

Computed tomography

CT scanning allows earlier detection of endplate involvement and bone


destruction than plain films, and may allow identification of paraspinous
inflammatory changes and psoas abscess formation, especially on contrast-
enhanced scans. Post-contrast studies and sagittal and coronal reconstructed
images are helpful in defining extent of disease. CT is not ideal for detection of
bone marrow changes or epidural involvement.3

Magnetic resonance imaging

MR is the imaging modality of choice in suspected discitis due to its


multiplanar imaging capabilities, lack of ionizing radiation, excellent anatomic
resolution, and ability to assess bone marrow changes.1 It allows detection of
early discitis with a reported sensitivity of 96% and a specificity of 94%. In
animal studies, changes of discitis were seen as early as five days post
infection.9 MR also allows accurate assessment of complications of discitis,
including direct assessment of effect on neural structures. Multiplanar pre- and
post-gadolinium T1- and T2-weighted images should be performed, including
a STIR sequence which helps distinguish between normal and edematous
marrow.6
9a
(http://radsource.us/wp-content/uploads/2012/07/9a.jpg)
Figure 9:
A 48 year-old male with lumbar pain, tenderness, and positive straight leg raise sign. A T1-
weighted sagittal image reveals hypointensity of the L4 and L5 vertebral bodies (asterisks) with loss
of disc space height at L4-5 and poor definition of the endplates (arrowheads). A contiguous soft
tissue inflammatory mass is present at the anterior disc margin (arrows).
10a
(http://radsource.us/wp-content/uploads/2012/07/10a.jpg)
Figure 10:

The T2-weighted sagittal image shows hyperintensity of the disc and vertebral bodies (asterisks)
and confirms endplate destruction (arrowheads). The anterior soft tissue process demonstrates
increased T2 signal (arrows).

11a
(http://radsource.us/wp-content/uploads/2012/07/11a.jpg)
Figure 11:
The T2-weighted axial image demonstrates a large, irregular fluid collection along the left pelvic
sidewall (arrowheads) extending into the left sacroiliac joint (arrow), with abnormal hyperintensity
of the left iliac bone and left sacral ala (asterisks). Diagnosis: L4-5 discitis with secondary infection
of the left sacroiliac joint and associated pelvic sidewall abscess.

In acute discitis, hypointensity of the disc and destruction of the endplate are
often seen on T1-weighted imaging, due to inflammation and necrosis
replacing the normal fatty marrow. However, these findings are not consistent.
A phenomenon known as “pseudosparing” of the endplate has been described
in up to 71% of patients, caused by loss of the normal chemical shift
phenomenon seen with fatty marrow that typically causes the superior
endplate to appear thin and the inferior endplate to appear thick. When the
normal marrow is lost in discitis, the decrease in the chemical shift artifact in
the inferior endplate allows visualization of the actual endplate thickness,
masking endplate thinning and erosion.5

The “nuclear cleft sign” is another traditionally described MRI finding in discitis.
However, Ledermann et al. found that loss of the nuclear cleft was not
consistently seen in affected discs and was not a reliable indicator of the
presence or absence of discitis; in fact, in many patients, the nuclear cleft
could not be identified in unaffected discs.6 Loss of disc space height is
another common finding in discitis that is nonspecific and found in many other
conditions.

The most reliable MRI findings in discitis are hyperintensity of the disc on T2-
weighted imaging (sensitivity 93%); the presence of paraspinous or epidural
inflammation/abscess, (sensitivity 98%); and contrast enhancement of the disc
and adjacent bone marrow (sensitivity 95%). Vacuum disc phenomenon is
rarely seen in discitis and is a negative predictor, usually indicating a
degenerative etiology.6

MRI is also superior to all other imaging modalities in the assessment of


epidural disease, either phlegmon or abscess. Post-gadolinium images are
excellent in assessing the extent of epidural involvement as well as the degree
of mass effect upon adjacent structures. Uniformly enhancing soft tissue is
consistent with phlegmon, while peripheral enhancement is highly suggestive
of abscess. Epidural disease typically involves between two and four vertebrae
and is ventral in location. MRI is also excellent in evaluating soft tissue
involvement of discitis, such as paraspinous inflammation and psoas
abscess.3,6
12a
(http://radsource.us/wp-content/uploads/2012/07/12a.jpg)
Figure 12:
A 28 year-old male three months status post L5-S1 microdiscectomy, now with progressive back
pain. The T2-weighted sagittal image reveals focal edema and irregularity of the endplates at L5-S1
(arrowheads) with areas of hyperintensity in the disc and a small contiguous fluid collection in the
ventral epidural space (arrow). These findings have developed in the interim since a previous MRI
two months prior.
13a
(http://radsource.us/wp-content/uploads/2012/07/13a.jpg)
Figure 13:
The corresponding post-contrast fat-suppressed T1-weighted sagittal view demonstrates
enhancement of the vertebral endplates (asterisks) and peripheral enhancement of the disc
(arrowheads) and the epidural fluid collection (arrow).

14a
(http://radsource.us/wp-content/uploads/2012/07/14a.jpg)
14b
(http://radsource.us/wp-content/uploads/2012/07/14b.jpg)
Figure 14:
(14a) T2-weighted and (14b) post-gadolinium T1-weighted axial images show a peripherally
enhancing fluid collection in the ventral epidural space at L5-S1 (arrows) displacing the let S1 nerve
root. Diagnosis: Post operative discitis with epidural abscess.

Diffusion-weighted MRI has been advocated as a method of distinguishing


discitis from degenerative endplate changes. Restricted diffusion has been
shown to be present in the endplates of patients with infection, but not in
those with degenerative disease. Diffusion sequences are not routinely
performed in the spine, but can be useful in cases where there is a specific
question regarding degeneration versus infection.7

Tuberculous discitis

Tuberculous discitis is often seen in immunocompromised patients or IV drug


abusers and can have a more indolent clinical course than the more
commonly seen pyogenic discitis, with a subsequent longer delay in diagnosis
of up to 6-8 months.1 Tuberculous discitis is more common in the thoracic
spine due to spread from mediastinal lymph nodes. On imaging studies, the
typical MRI signal intensity changes in the bone marrow may be absent, and
bony destruction can be pronounced with relative sparing of the disc space.
TB can also solely involve the posterior elements or only a portion of the
vertebral body. Skip lesions, extensive paraspinous inflammation, and abscess
formation are common.1,6

Differential diagnosis
Several other conditions can mimic the appearance of discitis on various
imaging modalities.

Degenerative disc disease in the early, inflammatory stage can mimic discitis.
Modic Type 1 changes in the endplates due to disruption of the endplate and
vascularized fibrous tissue in the adjacent marrow cause hyperintensity in the
endplate on T2-weighted images and enhancement after the administration of
gadolinium. However, lack of disc hyperintensity on T2-weighted images and
the absence of paraspinous inflammation indicate a degenerative etiology.3,10
In addition, while endplate irregularities are common in degenerative disease,
actual loss of endplate definition or endplate destruction are not
characteristics of Modic Type 1 changes.

15a
(http://radsource.us/wp-content/uploads/2012/07/15a.jpg)
Figure 15:
A 62 year-old male with back pain radiating to both legs. A T1-weighted sagittal image shows loss
of disc space height at T12-L1 (arrow) with marked hypointensity of the endplates. Mild endplate
irregularity is present and a Schmorl's node is seen within the superior endplate of L1 (arrowhead).
16a
(http://radsource.us/wp-content/uploads/2012/07/16a.jpg)
16b
(http://radsource.us/wp-content/uploads/2012/07/16b.jpg)
Figure 16:
Corresponding (16a) T2-weighted and (16b) STIR sagittal images redemonstrate the Schmorl's
node at the superior endplate of L1 (arrowheads), hypointensity of the disc (arrows) and edema in
the adjacent endplates (asterisks).

17a
(http://radsource.us/wp-content/uploads/2012/07/17a.jpg)
Figure 17:
The T1 weighted axial image shows well-defined paraspinous fat planes at the level of T12-L1
(asterisks). Diagnosis: Modic Type 1 degenerative endplate changes. The lack of hyperintensity of
the disc on T2 weighted images, the clearly defined endplates, and the lack of paraspinous
inflammation make infection highly unlikely.

Dialysis-related spondyloarthropathy is most likely related to amyloid


deposition in the disc and ligamentum flavum. On plain films and CT,
destruction of the end plates and severe disc space narrowing can mimic
infectious discitis. However, on MRI, the T2 hyperintensity of the disc
characteristic of discitis is not present. In addition, dialysis-related disease
often involves the posterior elements, a rare finding in discitis. Unlike discitis,
the most commonly involved area is the lower cervical spine.8 Neurogenic
spondyloarthropathy caused by paralysis can cause changes similar to dialysis-
related spondyloarthropathy on plain film and CT, but also fails to show disc
hyperintensity on T2-weighted images.3,12

18a
(http://radsource.us/wp-content/uploads/2012/07/18a.jpg)
18b
(http://radsource.us/wp-content/uploads/2012/07/18b.jpg)
Figure 18:
A 56 year-old female with chronic back pain radiating into right hip; the patient is on dialysis for
renal failure. T1- (18a) and T2- (18b) weighted sagittal images show endplate destruction at the L4-
5 and L5-S1 levels (arrowheads). Of note, the discs remain relatively isointense to the unaffected
discs on T2 weighted images. Marrow signal intensity is markedly decreased in all vertebral bodies,
consistent with the history of renal failure.

19a
(http://radsource.us/wp-content/uploads/2012/07/19a.jpg)
Figure 19:
T1-weighted off-midline sagittal images show erosion and inflammation of the right facet joint at
L4-5 (arrow) with surrounding soft tissue inflammatory changes (asterisk). Involvement of the
facets by discitis is uncommon.

20a
(http://radsource.us/wp-content/uploads/2012/07/20a.jpg)
Figure 20:
The T2-weighted axial image at the L4-5 level shows involvement of the facet joints and absence
of paraspinous inflammation. Diagnosis: Dialysis-related spondyloarthropathy.

Metastatic involvement of the spine can cause destructive changes similar to


those seen in discitis. However, the disc space is rarely involved by neoplasm,
and paraspinous fat planes are usually preserved. Vertebral lesions are usually
hypointense to CSF on T2-weighted images, as opposed to infectious
involvement, which is generally hyperintense.11 Involvement of contiguous
vertebral bodies is more typical of infection.3
21a
(http://radsource.us/wp-content/uploads/2012/07/21a.jpg)

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21b
(http://radsource.us/wp-content/uploads/2012/07/21b.jpg)
21c
(http://radsource.us/wp-content/uploads/2012/07/21c.jpg)
Figure 21:
A 67 year-old male with lower back pain radiating into the right leg. (21a) T1- and (21b) T2-
weighted sagittal images and a (21c) fat saturated T2-weighted sagittal image reveal
heterogeneous, abnormal signal in the T11 vertebral body (asterisk) with loss of vertebral body
height and posterior epidural extension (arrowheads). The vertebral body is predominantly
hypointense to CSF on T2 weighed images. The endplates are intact, and the adjacent discs are
spared. Diagnosis: Metastatic disease involving the T11 vertebrae with pathologic fracture.

SAPHO syndrome (synovitis, acne, pustulosis, hyperostosis, and osteitis) can


cause abnormal marrow signal intensity, paraspinous soft tissue swelling, end
plate irregularity and disc space narrowing, disc hyperintensity on T2-weighted
images, and disc enhancement, and can be difficult to differentiate from
pyogenic discitis. The multiplicity of foci and lack of abscess formation in
SAPHO syndrome can be helpful in distinguishing between the two
entities.3,13,14

Treatment and follow-up

Non-operative treatment is effective in the majority of patients (up to 90%) and


consists of 4-8 weeks of parenteral antibiotics and immobilization.
Percutaneous CT-guided drainage of paraspinous abscesses larger than 2 cm
may also be performed. Surgery is indicated in cases of spinal cord
compression, instability, correction of mechanical deformity, abscess, or
severe persistent pain. In cases where instability is present, the placement of
fixation devices has not been shown to impede healing.1,2,3

Although MRI is frequently used to follow patients during treatment, it has not
been shown to be an effective modality for assessing response to treatment.
Although paraspinous inflammation and epidural enhancement improves in
most patients, other findings such as disc space enhancement, marrow
edema, and vertebral body enhancement can persist and actually worsen
despite a favorable clinical response. In addition, post-gadolinium
enhancement can persist for longer than 4 months; this may be due to
development of hypervascular fibrous scar tissue during the healing phase. For
these reasons, the use of MRI in routine follow-up of patients with discitis is
not recommended.1,16

Monitoring of clinical symptoms and laboratory studies is the most effective


method of assessing treatment. Reduction in back pain and decreased
constitutional symptoms are expected. A decrease in serum ESR and CRP
indicates a successful response, with CRP being the more sensitive of the two;
ESR levels should fall by one third to one half, but frequently never return to
pre-disease levels. Serial plain films may also be performed to determine
whether bony deformity or collapse has developed. These parameters are
usually followed during treatment and for one year after its completion.1,2

Morbidity and mortality

The overall mortality rate of discitis is between 2 and 11%. The presence of an
epidural abscess increases mortality to 10% or greater. Up to 16% of patients
with spontaneous discitis experience a recurrence, usually within 6 months of
cessation of antibiotic treatment. Recurrence in cases of discitis complicating
spine surgery is less common, ranging from 0 to 4%; this may be in part due to
increased vigilance in the postoperative period leading to earlier diagnosis of
infection.1,2,17

The morbidity of discitis is significant. Approximately one third of patients have


residual disability. 15% of patients have permanent neurologic deficits. Only
45% of patients with postoperative discitis are able to return to normal daily
activities.1,2,17

Early diagnosis and treatment of discitis and completion of antibiotic regimen


is correlated with a better prognosis; a delay in diagnosis leads to poorer
outcomes.1,2,17
Conclusion

Discitis commonly presents with nonspecific signs and symptoms and has
significant morbidity and mortality, but prognosis is improved by early
diagnosis. MRI is the imaging study of choice in evaluating possible discitis due
to its high sensitivity and ability to define associated complications, such as
epidural and paraspinous abscess, and should be performed if discitis is
suspected even if plain films and CT are non-diagnostic. MRI can also
distinguish between discitis and other conditions with similar presentations,
allowing the clinician to make informed treatment decisions. However,
because MRI findings do not correlate well with treatment response, follow up
with serial plain films and monitoring of laboratory studies is recommended.

References
1
Cottle L, Riordan T. Infectious Spondylodiscitis. J Infect, Jun 2008; 56(6):401-
12.
2
Jallo GI, Keenan MA. Diskitis. Medline, Feb 2011.
3Varma R, Lander P, Assaf A. Imaging of Pyogenic Infectious Spondylodiskitis.
Radiol Clin of N Amer, March 2001; 39(2):203-213.
4 Viola RW, King HA, Adler SM, et al. Delayed Infection After Elective Spinal
Instrumentation and Fusion: A Retrospective Analysis of Eight Cases. Spine,
1997; 22:2444-2450 (tel:2444-2450).
5Wolansky LJ, Heary RF, Patterson T, Friedenberg JS, Tholany J, et al.
Pseudosparing of the Endplate: A Potential Pitfall in Using MR Imaging to
Diagnose Infectious Spondylitis. AJR, 1999; 172:777-780.
6 Ledermann HP, Schweitzer ME, Morrison WB, Carrino JA. MR Imaging
Findings in Spinal Infections: Rules or Myths? Radiology, 2003; 228:506-514.
7 Eguchi Y, Ohtori S, Yamashita M, Yamaguchi K, Suzuki M, Orita S, et al.
Diffusion Magnetic Resonance Imaging to Differentiate Degenerative from
Infectious Endplate Abnormalities in the Lumbar Spine. Spine, Feb 2011;
36(3):E198-202.
8Kiss E, Keutch G, Zanetti M, Jung T, Schwartz A, Schocke M, Jaschke W,
Czermak BV. Dialysis-Related Amyloid Revisited. AJR, 2005; 185:1460-1467.

9
9Taylor DJ, Brown GC, Moore RJ, Walters R, Chapple DC, Goss DL, Fraser RJ.
Early Detection of Lumbar Discitis by MRI. Proc Intl Soc Mag Reson Med, 2001;
9:249.
10Modic MT, Ross JS. Lumbar Degenerative Disc Disease. Radiology, October
2007; 245(1):43-57.
11Hovi I, Lamminen A, Salomen O, et al. MR Imaging of the Lower Spine. Acta
Radiol, 1994;35:532-540.
12Park YH, Taylor JA, Szollar SM, et al. Imaging Findings in Spinal
Neuroarthropathy. Spine, 1994; 19:1499-1504.
13Nachtigal A, Cardinal E, Bureau NJ, et al. Vertebral Involvement in SAPHO
Syndrome: MRI Findings. Skeletal Radiol, 1999; 28:163-168.
14Toussirot E, Dupond JL, Wendling D. Spondylodiscitis in SAPHO Syndrome:
A Series of Eight Cases. Ann Rheum Dis, 1997; 56:52-58.
15Karadimas EJ, Bunger C, Lindblad BE, Hansen ES, Hoy K, et al.
Spondylodiscitis: A Retrospective Study of 163 Patients. Acta Orthop, Oct
2008; 79(5):650-659.
16
Kowalski, TJ, Layton, KF, Berbari, EF, Steckelberg, JM, Huddleston PM, et al.
Follow-up MRI Imaging in Patients with Pyogenic Spine Infections: Lack of
Correlation with Clinical Features. Am J Neuroradiol, Apr 2007; 28:693-699.
17Jimenez-Mejias ME, de Dios Colmenero J, Sanchez-Lora FJ, Palomino-
Nicas J, et al. Postoperative Spondylodiskitis: Etiology, Clinical Findings,
Prognosis, and Comparison with Non-Operative Pyogenic Spondylodiskitis.
Clin Inf Dis, 1999; 29:339-345.

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Hospital.pdf)

(/protonpacs-pacs/)

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