Accepted Manuscript

Skull base osteomyelitis secondary to malignant otitis externa

mimicking advanced nasopharyngeal cancer: MR imaging
features at initial presentation

J.P.N. Goh, A. Karandikar, S.C. Loke, T.Y. Tan

PII: S0196-0709(16)30623-8
DOI: doi: 10.1016/j.amjoto.2017.04.007
Reference: YAJOT 1848
To appear in:
Received date: 26 January 2017

Please cite this article as: J.P.N. Goh, A. Karandikar, S.C. Loke, T.Y. Tan , Skull base
osteomyelitis secondary to malignant otitis externa mimicking advanced nasopharyngeal
cancer: MR imaging features at initial presentation. The address for the corresponding
author was captured as affiliation for all authors. Please check if appropriate. Yajot(2017),
doi: 10.1016/j.amjoto.2017.04.007

This is a PDF file of an unedited manuscript that has been accepted for publication. As
a service to our customers we are providing this early version of the manuscript. The
manuscript will undergo copyediting, typesetting, and review of the resulting proof before
it is published in its final form. Please note that during the production process errors may
be discovered which could affect the content, and all legal disclaimers that apply to the
journal pertain.
 ACCEPTED MANUSCRIPT

Grant support: Nil

Conflict of Interest: None
Financial Disclosure: Nil
This study was approved by the Institutional Review Board.
Presentation: Material previously presented at the 25th Congress and Refresher Course of the
European Society of Head and Neck Radiology 2012.

T
Skull base osteomyelitis secondary to malignant otitis externa mimicking advanced

IP
nasopharyngeal cancer: MR imaging features at initial presentation

CR
J.P.N Goha,* Julian_Goh@ttsh.com.sg, A. Karandikara, S.C. Lokea, T.Y. Tanb

US
a
Department of Diagnostic Radiology, Tan Tock Seng Hospital, Singapore 308433, Singapore
b
Department of Radiology, Changi General Hospital, Singapore 529889, Singapore
AN
*
Corresponding author at: Department of Diagnostic Radiology, Basement 1, Podium Block, Tan
Tock Seng Hospital, 11 Jalan Tan Tock Seng, S(308433), Republic of Singapore.
M

Abstract
ED

Purpose
PT

Skull base osteomyelitis (SBOM) is an inflammatory process which often arises from malignant
otitis externa (MOE); the diffuse skull base and adjacent soft tissue involvement may be
CE

mistaken at initial imaging for advanced nasopharyngeal carcinoma (NPC), especially if there is
no prior knowledge of MOE, direct spread from the sphenoid sinus or in atypical presentations of
AC

MOE. This study aims to evaluate imaging features on MR that may differentiate SBOM from
NPC.

Materials and Methods

The MR examinations of 26 patients diagnosed with SBOM between January 1996 and January
2013 were retrospectively reviewed. Comparison was also made with the MR images of 22
consecutive patients with newly diagnosed advanced T3 and T4 NPC between July 2011 and
August 2012. Imaging features in both conditions were compared, including the presence of a

[1]
 ACCEPTED MANUSCRIPT

nasopharyngeal bulge, nasopharyngeal mucosal irregularity, lateral extension, architectural

distortion (or lack thereof), increased T2 signal and enhancement patterns.

Results

The most prevalent findings in SBOM were lateral extension, increased T2 signal in adjacent
soft tissues, lack of architectural distortion and enhancement greater than or equal to mucosa.
The combination of these 4 findings was found to best differentiate SBOM from advanced NPC,

T
and found to be statistically significant (p < 0.001).

IP
Conclusion

CR
We suggest that the combination of lateral extension, increased T2 signal, lack of architectural

US
distortion and enhancement greater than or equal to mucosa is helpful in differentiating SBOM
from advanced NPC.
AN
Keywords: MR, Head and Neck, nasopharyngeal carcinoma, malignant otitis externa, skull base
M

osteomyelitis
ED

1. INTRODUCTION
PT

Skull base osteomyelitis (SBOM) involves the temporal bone and is a known late complication
of malignant otitis externa (MOE). Central skull base osteomyelitis may also result from direct
CE

spread from sphenoid sinus infection or less commonly, hematogenous spread. Symptoms
include otalgia, otorrhoea and headache and, late in the disease course, cranial nerve palsies.
AC

With involvement of the deep soft tissues just below the skull base, intracranial extension and
cranial nerve palsies, SBOM may be mistaken for advanced malignancy. In East Asia, SBOM
can be mistaken for nasopharyngeal carcinoma (NPC), a common malignancy in East Asia
which predominantly affects the ethnic Chinese population. Undifferentiated carcinoma is the
most common subtype of NPC in this region, secondary to Epstein-Barr virus (EBV) infection,
affecting males more commonly (M:F incidence 2.7:1) [1]. The disease is often advanced at
diagnosis, as symptoms have a late onset.

[2]
 ACCEPTED MANUSCRIPT

Due to the overlap of features, differentiation between these 2 entities can be difficult, especially
for less experienced readers who may be unfamiliar with skull base anatomy and pathology. A
lack of relevant clinical information and the presence of atypical features (e.g. painless central
skull base involvement or a lack of constitutional symptoms) adds to the diagnostic difficulty.
This can lead to delayed diagnosis and treatment, with serious consequences.

As MR imaging is used in the setting of both NPC and SBOM, we attempted to identify imaging

T
features that may help differentiate SBOM from advanced NPC at initial presentation.

IP
CR
2. MATERIALS AND METHODS

US
A retrospective review was made of patients with a diagnosis of SBOM secondary to MOE
imaged with MR. The diagnosis of SBOM was made based on bacteriologic culture results,
AN
clinical presentation and elevated inflammatory markers. Institutional board approval to perform
this review was obtained. A waiver of consent was granted as this was a retrospective review.
M

These patients were imaged between January 1996 and January 2013. The images were reviewed
in consensus by 2 head and neck radiologists. The images were assessed for the following
ED

features:

a) presence or absence of a nasopharyngeal bulge,

PT

b) involvement of lateral structures such as the parotid gland or temporomandibular joint

CE

c) presence or absence of abscess formation.

AC

d) presence or absence of architectural distortion, specifically disruption of fascial planes and

distortion of normal muscle fibres in the masticator space and prevertebral musculature, in the
presence of abnormal signal and enhancement.

e) presence, extent and distribution of nodal disease. Only the retropharyngeal and level I and II
nodes were evaluated as patients imaged for suspected SBOM were routinely imaged only to the
level of the upper neck in our patients. Nodal enlargement was deemed to be present if the
shortest trans-axial diameter was greater than 0.8 cm and 1.1 cm for the retropharyngeal and
level I and II nodes respectively.

[3]
 ACCEPTED MANUSCRIPT

f) enhancement of the adjacent deep soft tissues relative to mucosa on MR images. Enhancement
was considered significant if this was equal to or greater than that of nasopharyngeal or nasal
mucosa

h) perineural extension and intracranial extension. Perineural extension was deemed present if
there was thickened enhancing tissue (with or without nodularity) extending along the cranial
nerves.

T
Comparison was then made with the MR images of 22 consecutive patients with newly

IP
diagnosed advanced T3 and T4 NPC between July 2011 and August 2012, with an aim to

CR
identify the above findings.

The medical records were reviewed, looking for the presence of underlying medical conditions

US
such as diabetes mellitus; elevated inflammatory markers (specifically ESR and CRP);
microbiology; and histology (where available).
AN
Statistical evaluation of the results was performed using the Fisher’s exact test.
M
ED

3. IMAGING TECHNIQUE

MR was performed using either a 1.5T (Signa; GE Healthcare, Milwaukee, Wisconsin) or 3T

PT

magnet (Trio; Siemens Medical Systems, Erlangen, Germany). Precontrast axial and coronal
T1W images were acquired, followed by post-contrast axial and coronal T1W fat-saturated
CE

images, unless there was impaired renal function. Axial and coronal STIR images were also
obtained.
AC

4. RESULTS

A total of 26 cases of SBOM were identified (M:F 15:11, age range 48 – 82 years). There were
17 Chinese and 9 non-Chinese patients (4 Malay, 4 Indian, 1 Thai). 24 patients were found to be
diabetic. 2 patients were immunocompetent. These findings are summarized in table 1.

[4]
 ACCEPTED MANUSCRIPT

23 patients with SBOM received intravenous gadolinium. 3 patients did not receive intravenous
contrast as they had impaired renal function. Of these 23 patients, 21 showed significant
enhancement. In contrast, only 1 NPC patient demonstrated significant tumor enhancement.

A nasopharyngeal bulge was seen in 14 patients with SBOM, and in all 22 patients with NPC.

Involvement of lateral structures was demonstrated in 24 of 26 patients with SBOM (Fig. 1a, 1b
and 2a). However, only 1 patient with NPC showed involvement of lateral structures; this was an

T
advanced case with extensive locoregional spread.

IP
Abscess formation was seen in 15 of 26 SBOM patients (Fig. 2b). 1 NPC patient developed

CR
tumor necrosis mimicking abscess; however, no necrosis was seen in the remaining NPC
patients.

US
Architectural distortion was seen in all 22 cases of NPC (Figs. 3a, 3b, 3c and 4a). In contrast,
AN
only 1 patient with SBOM showed evidence of architectural distortion.

Enlarged lymph nodes were found in all 22 patients with NPC, whereas only 3 of 26 patients
M

with SBOM showed enlarged nodes. The nodal stations involved in NPC were predominantly the
retropharyngeal nodes and level II (Fig. 5).
ED

Increased T2 signal, representing edema, was also seen in the adjacent deep soft tissues in 24
PT

patients with SBOM. Elevated T2 signal was only seen in 3 NPC patients.

The above results were all found to be statistically significant (p < 0.001). The results are
CE

summarised in table 2.
AC

The most prevalent findings in SBOM were involvement of lateral structures, increased T2
signal, lack of architectural distortion and enhancement greater than or equal to mucosa. The
combination of these 4 findings was found to best differentiate between SBOM and advanced
NPC, and found to be statistically significant (p < 0.001).

Amongst the SBOM patients, 13 patients had clinical evidence of cranial nerve palsy. However,
perineural involvement involving at least 1 cranial nerve was seen in 14 patients with SBOM. 3
patients showed involvement of at least 2 nerves. For the NPC patients, perineural involvement
was seen in 17 patients with NPC. On imaging, CN V (specifically V3) was the most commonly

[5]
 ACCEPTED MANUSCRIPT

affected (11 patients), followed by CN XII (4 patients) and VII (2 patients) (Figs. 6a and 6b).
Intracranial extension was seen in 15 of the SBOM patients, manifesting as dural thickening in
all 15 cases; extension into the cavernous sinus was seen in 4 patients, into the right internal
auditory canal in 1 patient and Meckel’s cave in 2 patients.

No gender predilection was seen with SBOM, with an almost equal distribution between genders
(15 M; 11 F). In contradistinction, males were more frequently affected with NPC, compared to

T
females (19 M; 3 F); this is similar to published data.

IP
Bacteriologic culture results (obtained from the ear) were available in 24 SBOM patients. The

CR
most common organism was Pseudomonas Aeruginosa (13 patients). Staphylococcus Aureus
was the next most common organism (5 patients). Other organisms successfully identified

US
included Klebsiella Pneumoniae, Streptococcus Anginosus, Enterobacter and skin flora. No
bacterial growth was identified in 2 patients. In these patients, the diagnosis was presumptive,
AN
based on the clinical features. Histology was available in 16 patients with SBOM – inflammatory
tissue was identified in all 16 patients. Elevated inflammatory markers (ESR & CRP) were seen
M

in all 26 patients with SBOM. Inflammatory markers are not routinely performed in patients with
NPC. 24 patients with SBOM responded to antibiotic treatment while 2 patients died despite
ED

antibiotic treatment.
PT
CE
AC

[6]
 ACCEPTED MANUSCRIPT

5. DISCUSSION

In 1959 Meltzer and Keleman [2] described a Pseudomonas chondritis with osteomyelitis
involving the external auditory canal and the temporal bone. Chandler [3] then described the
classical features in his case series in 1968, calling the condition MOE in view of the high
mortality rate. Patients are often elderly diabetics, and increasingly, immunocompromised
individuals. The condition starts as an external otitis, which spreads to the skull base via the

T
fissures of Santorini and the tympanomastoid suture, with subsequent spread along fascial planes

IP
[4]. Symptoms include deep-seated otalgia, otorrhoea, fever and headache. Cranial nerve palsies

CR
occur late in the disease. SBOM is a late complication of MOE, although central and atypical
presentations of SBOM may occur (e.g. in immunocompromised patients), leading to diagnostic
difficulty. Pseudomonas is the most common causative organism; this Gram negative organism

US
colonizes the external auditory canal after significant water exposure or minor trauma e.g.
irrigation with tap water. Other documented causative organisms include Staphylococcus,
AN
Proteus mirabilis [5] and Malassezia sympodialis [6].
M

NPC is a malignancy commonly seen in East Asia, predominantly affecting the Chinese
population. Of the three subtypes undifferentiated carcinoma is the most common; this subtype is
ED

associated with EBV infection, which is ubiquitous in the East Asia region [7]. A neck lump
from cervical adenopathy is the most common presenting symptom; the tumor itself is often not
PT

apparent clinically. Patients often present with advanced disease, with skull base invasion,
perineural spread and intracranial extension.
CE

The imaging features of SBOM, even in the setting of MOE, can be difficult to differentiate from
advanced NPC (e.g. on a brain MR), as both conditions produce bony destruction and soft tissue
AC

changes, with middle ear and mastoid opacification. Even with dedicated skull base imaging,
differentiation between SBOM and advanced NPC can be difficult. This situation is further
complicated when SBOM occurs as a result of superimposed infection upon osteoradionecrosis
after treatment for NPC. SBOM may also be difficult to identify if it presents in an atypical
fashion (e.g. multiple cranial nerve palsies without pain or otorrhoea), in the central skull base,
or when the imager is unaware of a clinical history of infection. Differentiating between the two

[7]
 ACCEPTED MANUSCRIPT

conditions, however, is of great clinical importance, as a misdiagnosis of NPC in a patient with

SBOM will lead to delayed treatment of the infection, with potentially devastating consequences.

The nasopharyngeal bulge seen in many cases with SBOM (noted in 14 of our cases) can be
mistaken for a nasopharyngeal mass during imaging, especially if the fossa of Rosenmuller is
involved (Fig 4c). However, with SBOM, clinical examination reveals smooth mucosa with no
evidence of irregularity, unlike NPC, where mucosal irregularity is clinically evident. However,

T
mucosal irregularity can be difficult to differentiate on radiologic images, and when a

IP
nasopharyngeal bulge is identified at imaging, SBOM can be misdiagnosed as NPC, especially

CR
with an atypical clinical presentation. Nevertheless, we feel that several radiologic features may
help differentiate between these 2 clinical entities.

US
Given the extensive involvement of soft tissue structures below the skull base in SBOM,
architectural distortion might be expected. However, architectural distortion could only be seen
AN
in 1 patient with SBOM; the remaining cases demonstrated architectural preservation (Fig. 4b
and 4c). In contrast, all 22 patients with NPC showed architectural distortion (Fig. 4a). We
M

postulate this lack of architectural distortion in SBOM may be due to infection extending along
(rather than violating) fascial planes. This is opposed to NPC, where invasion and distortion of
ED

soft tissue structures occurs once fascial planes have been breached.

Abscess formation (Fig. 2b) should also alert the radiologist to the likelihood of infection rather
PT

than NPC, because tumor necrosis (which can conceivably mimic an abscess) is uncommon in
CE

the latter condition.

Involvement of lateral structures (parotid gland, temporomandibular joint) was a prominent

AC

finding in our patients with SBOM (seen in 24 out of 26 patients) (Figs. 1a, 1b, 1c and 4b). This
finding is not unexpected, given that these patients developed SBOM as a consequence of MOE.
In comparison, NPC originates in the nasopharynx, which is centrally located, and subsequently
involves the contiguous soft tissue structures and central skull base. Lateral extension is rarely
seen except in late cases of NPC, secondary to contiguous spread or perineural extension along
the auriculotemporal nerve [8]. Indeed, lateral extension (secondary to contiguous spread) was
seen in only 1 NPC patient with very advanced disease in our study; no evidence of

[8]
 ACCEPTED MANUSCRIPT

auriculotemporal nerve extension could be identified in this patient. We feel this involvement of
lateral structures is also an important feature that helps differentiate infection from NPC.

Soft tissue enhancement equal to or greater than mucosa was seen in patients with SBOM (21
patients) (Fig. 4b and 4c). This was felt to be due to inflammatory tissue. Interestingly, we found
the degree of tumor enhancement in NPC patients was less conspicuous (Fig. 3b), with only 1
NPC patient showing enhancement equal to or greater than mucosa. To our knowledge, this has

T
not been reported in previous papers.

IP
It has been reported that T2-weighted sequences in patients with SBOM evidence isointense or

CR
slightly hyperintense signal, in contrast to the high T2-weighted signal in most inflammatory
disorders. It is postulated that the underlying fibrosis and necrotizing process, together with the

US
presence of microangiopathic changes and compromised vascular supply, are contributory
factors [9]. However, we found the T2 signal in our patients to be at least of moderate signal
AN
intensity. Also, we noted the T2-weighted soft tissue signal in the patients with SBOM was
higher than that of NPC. This may be due to more densely packed cells in NPC (thus limiting the
M

T2-weighted signal), whereas the edema and inflammatory infiltrate in patients with SBOM
would lead to increased T2-weighted signal, especially in the adjacent soft tissues e.g. in the
ED

tensor and levator veli palatini muscles and masticator spaces. This finding may be useful in
differentiating tumor from inflammatory disease, although this would require further study.
PT

Patients with SBOM may present with cranial nerve palsies. We identified perineural extension
CE

on imaging in 14 patients (Figs. 6a and 6b), although only 13 presented with clinical features of
cranial nerve palsy. However, as we only included patients in whom there was extension of the
disease process into the respective cranial nerve canal, we acknowledge that we may have
AC

underestimated the actual extent of involvement. Nevertheless, cranial nerve palsies would be
clinically evident and unlikely to be missed. Similarly, dural enhancement would not
satisfactorily distinguish SBOM from NPC.

Metastatic nodal disease is a common finding in patients with NPC. This generally behaves in an
orderly fashion beginning with the retropharyngeal nodes, with subsequent extension to levels II,
III and IV, and in advanced cases, the supraclavicular nodes. Level V nodes are also often
involved. The retropharyngeal nodes may be bypassed in up to 1/3 of cases [10, 11, 12]. In

[9]
 ACCEPTED MANUSCRIPT

SBOM, although reactive nodal enlargement may occur, the typical features associated with
metastatic nodal disease in NPC should be absent. As expected, all patients with NPC showed
evidence of nodal metastases (involving the retropharyngeal nodes in 18, level II in all 22
patients and level III in 7 patients; table 2). An enlarged retropharyngeal node was seen in 1
patient with SBOM; this later returned to normal on subsequent imaging studies. Only the
retropharyngeal, level II and level III nodes are included in this discussion as this is the area
normally imaged in patients with suspected SBOM.

T
IP
Inflammatory myofibroblastic tumor, previously termed inflammatory pseudotumor, is an

CR
uncommon non-neoplastic inflammatory lesion of the skull base with a variable clinical
presentation, including multiple cranial nerve palsies, facial pain and numbness, depending on
the location of the lesion. This lesion itself is composed of myofibroblastic cells amidst a

US
background of plasma cells and lymphocytes, together with fibrosis. In the head and neck, the
orbit is the most common site of involvement; the skull base is rarely involved. The radiologic
AN
appearance can mimic malignancy, and the diagnosis should be considered as a differential for
a destructive skull base lesion. Histology is required for final diagnosis. On imaging,
M

inflammatory myofibroblastic tumor shows hypointense T1W signal with variable enhancement.
Typically the T2W signal is hypointense, due to the fibrotic component [13, 14]. The patients
ED

with histologic correlation in our series showed evidence of inflammatory tissue and did not
demonstrate the presence of myofibroblastic cells and fibrosis. Although we did not have
PT

histologic correlation for all patients, we felt that inflammatory myofibroblastic tumor was
unlikely given the typical clinical presentation of otalgia and aural discharge, the positive
CE

bacteriologic result in 24 patients and the patients’ response to antibiotics. In contrast,

inflammatory myofibroblastic tumor responds to corticosteroid treatment and not antibiotic
AC

therapy. While 2 of our patients died, patients with inflammatory myofibroblastic tumor do not
typically perish from this disease, whereas patients with MOE and SBOM can die from their
disease. Finally the T2W signal was elevated in our patients, unlike the reduced T2W signal
typically seen in inflammatory myofibroblastic tumor.

Clinical information is very helpful in making a diagnosis of SBOM. The presence of otorrhoea,
unremitting otalgia (particularly at night) and elevated inflammatory markers (ESR, CRP) should

[10]
 ACCEPTED MANUSCRIPT

all raise the suspicion of an infective process rather than a malignancy. However, this
information may not be available to the radiologist at the time of imaging.

Diabetes mellitus was seen in 22 of 26 patients with SBOM, while Pseudomonas was the most
common causative organism. These findings concur with previous studies. Other organisms were
also identified in our study, such as Staphylococcus aureus and Klebsiella pneumoniae.

T
We acknowledge several limitations in our study. Firstly, our sample size is small. However,

IP
despite the increasing incidence, SBOM is still a relatively uncommon condition, and as such
clinical numbers will be small. Secondly, culture results were also unavailable for 2 patients, as

CR
no bacterial growth was available. Nevertheless, the diagnosis of SBOM was made based on the
clinical presentation, patient profiles, serological results and radiologic findings. Thirdly, we did

US
not perform DWI in our patients. A large number of our patients were imaged prior to the advent
of DWI; DWI was also not a part of our routine imaging protocol, although we recognize DWI
AN
may have utility. Ozgen et al [15] found ADC values in SBOM were higher than in NPC and
lymphoma cases. However, severe susceptibility artefacts at the skull base limit its utility
M

although new software reduces the degree of susceptibility. While tumor necrosis may
conceivably mimic abscesses, necrosis was not a prominent feature in our series, and we felt that
ED

this should not pose a diagnostic difficulty for radiologists.

In conclusion, the increasing prevalence of diabetes and the increased number of

PT

immunocompromised patients (e.g. HIV, post-transplant patients) and the similarities at imaging
CE

between SBOM and NPC make early differentiation between these two conditions important to
prevent a delay in diagnosis and allow early institution of appropriate treatment. The presence of
lateral extension, elevated T2W signal (likely due to inflammatory fluid), enhancement greater
AC

than or equal to mucosa and the lack of architectural distortion and lymphadenopathy, together
with relevant clinical and biochemical features (immunocompromised status, otorrhoea,
unremitting otalgia, elevated inflammatory markers) should alert the radiologist to an underlying
inflammatory process rather than malignancy.

ACKNOWLEDGEMENTS

[11]
 ACCEPTED MANUSCRIPT

Nil

CONFLICT OF INTEREST

The authors declared no conflicts of interest.

FUNDING

This research did not receive any specific grant from funding agencies in the public, commercial,

T
or not-for-profit sectors.

IP
CR
US
AN
M
ED
PT
CE
AC

[12]
 ACCEPTED MANUSCRIPT

REFERENCES
[1] Singapore Cancer Registry Annual Registry Report. Trends in Cancer Incidence in Singapore
2010 - 2014. National Registry of Diseases Office.
https://www.nrdo.gov.sg/publications/cancer
[2] Meltzer PE, Keleman, G. Pyocyaneous osteomyelitis of the temporal bone, mandible and
zygoma. Laryngoscope 1959; 69:1300 – 1316
[3] Chandler JR. Malignant external otitis. Laryngoscope 1968; 78:1257-1294

T
[4] Ganghadar SS, Kwartler JA. Skull base osteomyelitis secondary to malignant otitis externa.

IP
Curr Opin Otolaryngol Head Neck Surg 2003; 11:316-323

CR
[5] Huang KL, Lu CS. Skull base osteomyelitis presenting as Villaret’s syndrome. Acta Neurol
Taiwan 2006; 15:255-8

US
[6] Chai FC, Auret K, Christiansen K, Yuen PW, Gardam D. Malignant otitis externa caused by
Malassezia sympodialis. Head Neck 2000; 22:87-9
AN
[7] Goh J, Lim K. Imaging of nasopharyngeal carcinoma. Ann Acad Med Singapore. 2009 Sep;
38(9):809-16.
M

[8] Schmalfuss IM, Tart RP, Mukherji S, Mancuso AA. Perineural tumor spread along the
auriculotemporal nerve. AJNR Am J Neuroradiol. 2002 Feb; 23(2):303-11
ED

[9] Adams A, Offiah C. Central skull base osteomyelitis as a complication of necrotizing otitis
externa: Imaging findings, complications and challenge of diagnosis. Clin Radiol. 2012 Oct;
PT

67(10):e7-e16. doi: 10.1016/j.crad.2012.02.004. Epub 2012 Apr 7

[10] King AD et al. Neck node metastases from nasopharyngeal carcinoma: MR imaging of
CE

patterns of disease. Head Neck. 2000 May; 22(3): 275 - 81

[11] Ng SH, Chang JT, Chan SC, et al. Nodal metastases of nasopharyngeal carcinoma:
AC

patterns of disease on MRI and FDG PET. Eur J Nucl Med Mol Imaging. 2004; 31:1073 -
1080
[12] Chong VF, Fan YF, Khoo JB. Retropharyngeal lymphadenopathy in nasopharyngeal
carcinoma. Eur J Radiol. 1995 Dec 15; 21(2): 100 - 5
[13] Narla LD, Newman B, Spottswood SS, Narla S, Kolli R. Inflammatory pseudotumor.
Radiographics 2003 May-Jun;23(3):719-29
[14] Park SB, Lee JH, Weon YC. Imaging findings of head and neck inflammatory
pseudotumor. AJR Am J Roentgenol. 2009 Oct;193(4):1180-6

[13]
 ACCEPTED MANUSCRIPT

[15] B Ozgen, KK Oguz, A Cila. Diffusion MR Imaging Features of Skull Base Osteomyelitis
Compared with Skull Base Malignancy. AJNR Am J Neuroradiol. 2011 Jan; 32(1):179-84

T
IP
CR
US
AN
M
ED
PT
CE
AC

[14]
 ACCEPTED MANUSCRIPT

Table 1. Patient demographics in patients with SBOM

N = 26
Male 15

Female 11

Ethnicity Chinese 17; non-Chinese 9

T
IP
Diabetic 24

CR
Raised inflammatory markers
26
(CRP, ESR)

US
AN
M
ED
PT
CE
AC

[15]
 ACCEPTED MANUSCRIPT

Table 2. MRI findings

Feature SBOM (N=26) NPC (N=22)

Nasopharyngeal bulge 14 22

Lateral extension 24 1

Significant soft tissue enhancement 21# 1

T
IP
Abscess formation/necrosis 15 1

CR
Architectural distortion 1 22

Nodes 3* 20+

US
Elevated T2 signal AN 24 3

SBOM: Skull base osteomyelitis; NPC: Nasopharyngeal carcinoma

p value < 0.001 for all findings above
M

#
3 non-contrast exams; 2 cases did not show significant enhancement
ED

*Retropharyngeal node
+
Nodes involved: retropharyngeal – 18; level II – 20; level III – 7
PT
CE
AC

[16]
 ACCEPTED MANUSCRIPT

Fig. 1. a – c. 75-year old lady with diabetes and SBOM presenting with multiple cranial nerve
palsies. Axial T1-weighted pre-contrast (a), T1-weighted post-contrast (b) and STIR (c) images
show extensive clival marrow signal change and cortical erosion, with reduced T1W signal (* in
a) and enhancement (seen in b). Lateral extension to temporomandibular joints (arrows in b).
Fluid tracking between tissue planes but relatively little distortion of masticator space and longus
capitis muscles (arrow in c). Biopsies were repeatedly negative for malignancy. S aureus
cultured.

T
IP
Fig. 2. a, b. SBOM in two different 69-year old males. Axial T1-weighted post-contrast image

CR
(a) in the first patient shows lateral extension to left mandibular condyle. Note condylar
involvement by inflammatory process (arrow) and preservation of masticator space architecture.

US
Axial T1-weighted post-contrast image (b) shows abscess formation in prevertebral soft tissue
(starred) in the second patient.
AN
Fig. 3. a – c. 53-year old male with NPC. Axial T1-weighted pre-contrast (a), T1-weighted post-
M

contrast (b) and STIR (c) images show a mass in a NPC patient filling the right fossa of
Rosenmuller (arrows in a-c), with clivus infiltration (* in a). Note lack of fluid tracking within
ED

soft tissues (arrowhead in c), and lack of enhancement of adjacent soft tissues and lateral
extension into the right masticator space (b, c). Tumor also shows T2 signal and enhancement
PT

less than nasal turbinates.

CE

Fig. 4. a – c. Axial T1-weighted pre-contrast image (a) in a 66-year old male with NPC showing
architectural distortion involving left longus capitis and masticator space (* in a). Axial T1-
AC

weighted post-contrast (b) and STIR (c) images in an 84-year old male with SBOM show
architectural preservation (arrows in b and c) and a left nasopharyngeal bulge (star in b and c);
this bulge can be mistaken for NPC by inexperienced readers.

Fig. 5. 57-year old male with NPC. Axial T1-weighted post-contrast image shows bilateral
necrotic level II nodes.

[17]
 ACCEPTED MANUSCRIPT

Fig. 6. a, b. 48-year old female with SBOM. Axial T1-weighted post-contrast (a) and coronal T1-
weighted post-contrast image (b) images show perineural extension along left main trigeminal
and hypoglossal nerves (arrows in a) and left V3 nerve (block arrow in b). This can be mistaken
for perineural spread in a patient with NPC.

T
IP
CR
US
AN
M
ED
PT
CE
AC

[18]
 ACCEPTED MANUSCRIPT

T
IP
CR
US
AN
M
ED
PT
CE
AC

[19]
 ACCEPTED MANUSCRIPT

T
IP
CR
US
AN
M
ED
PT
CE
AC

[20]
 ACCEPTED MANUSCRIPT

T
IP
CR
US
AN
M
ED
PT
CE
AC

[21]
 ACCEPTED MANUSCRIPT

T
IP
CR
US
AN
M
ED
PT
CE
AC

[22]
 ACCEPTED MANUSCRIPT

T
IP
CR
US
AN
M
ED
PT
CE
AC

[23]
 ACCEPTED MANUSCRIPT

T
IP
CR
US
AN
M
ED
PT
CE
AC

[24]
 ACCEPTED MANUSCRIPT

T
IP
CR
US
AN
M
ED
PT
CE
AC

[25]
 ACCEPTED MANUSCRIPT

T
IP
CR
US
AN
M
ED
PT
CE
AC

[26]
 ACCEPTED MANUSCRIPT

T
IP
CR
US
AN
M
ED
PT
CE
AC

[27]
 ACCEPTED MANUSCRIPT

T
IP
CR
US
AN
M
ED
PT
CE
AC

[28]
 ACCEPTED MANUSCRIPT

T
IP
CR
US
AN
M
ED
PT
CE
AC

[29]
 ACCEPTED MANUSCRIPT

T
IP
CR
US
AN
M
ED
PT
CE
AC

[30]
 ACCEPTED MANUSCRIPT

T
IP
CR
US
AN
M
ED
PT
CE
AC

[31]
 ACCEPTED MANUSCRIPT

T
IP
CR
US
AN
M
ED
PT
CE
AC

[32]