Imaging, 23 (2014), 20110070

NEURORADIOLOGY

Imaging the temporal bone

I ZAMMIT-MAEMPEL, MRCP, FRCR
Department of Clinical Radiology, Freeman Hospital, Newcastle upon Tyne, UK
Summary
CT is the initial imaging of choice in the investigation of middle ear disease.
MRI is used in evaluating the inner ear in patients presenting with sensorineural

deafness, tinnitus and vertigo. It has an increasingly important role in the

detection of post-operative cholesteatoma recurrence.
Nuclear medicine and cone beam CT have limited roles.

doi: 10.1259/img.20110070
2014 The British Institute of
Radiology

Cite this article as: Zammit-Maempel I. Imaging the temporal bone. Imaging 2014;23:20110070.

Abstract. Interpretation of temporal bone imaging is

challenging for most general radiologists, as the temporal bone
is an anatomically highly complex region. This review aims to
provide an overview of the recent advances in imaging of the
temporal bone and to discuss problematic and currently topical
pathology.
Imaging of the temporal bone is guided by clinical and
audiological findings. Conductive hearing loss is mainly
evaluated by CT as most pathology is located within the
middle ear. Most causes of sensorineural deafness are
found in the inner ear or central auditory pathways and
on the whole evaluated by MRI. Recently, diffusionweighted MRI is gaining increasing importance in the
evaluation of the entire temporal bone.

CT technique
With the advent of multislice CT scanners, highresolution images of the temporal bone can be acquired
in the axial plane with exquisite coronal and sagittal
reconstructions, using thin collimation scanning obtained
as a volume acquisition. As some CT scanners do not
allow gantry tilt, correct positioning of the patient in the
chin-down position is important to reduce the eye dose.
Several techniques have been suggested to reduce radiation dose to the lens of the eye.1

MRI technique
High-resolution imaging of the inner ear with
heavily T2 weighted three-dimensional sequences such
as constructive interference in steady state or driven
equilibrium allows optimal imaging of the facial and
vestibulocochlear nerve complexes and the labyrinth.2
Address correspondence to: Dr Ivan Zammit-Maempel. E-mail: ivan.
zammit@nuth.nhs.uk

birpublications.org

Volumetric sequences have also been developed for

imaging at 3 T.3,4 Delayed gadolinium-enhanced T1
weighted images and diffusion-weighted sequences,
especially non-echo planar based, are being increasingly
used for assessing the entire temporal bone and, in particular, the middle ear for any residual cholesteatoma after
surgery.57

Basic anatomy
It is imperative that the radiologist is familiar with the
complex temporal bone anatomy on both CT and MRI. A
comprehensive review of this is beyond the scope of this
article, and readers are directed to other reviews.811 The
temporal bone comprises five parts, the squamous, petrous, tympanic, mastoid and styloid process. This review
will emphasize imaging and pathology of the petrous
temporal bone.

Computed tomography
The radiologist should be familiar with at least axial
and coronal anatomy.

Axial
The cochlear and vestibular aqueducts (VA), ossicles
and inner ear structures are well seen. The cochlear
aqueduct is a bony canal with a width of up to 6 mm
that connects the cochlear perilymph to the subarachnoid space and forms a potential route for meningeal spread of middle ear infection (Figure 1). The
VA lies posterior and parallel to the posterior semicircular canal and should not measure wider than
1.5 mm at its mid-point (Figure 2). It contains the endolymphatic sac and does not communicate with the
subarachnoid space. The ice cream appearance of the
malleoincudal joint is a useful landmark on axial
1 of 15

I Zammit-Maempel

Figure 1. Normal anatomy of the cochlear aqueduct on axial

CT (black arrow). Also, note the promontory (white arrow)
with the basal turn of the cochlea lying medially.

images. The facial nerve canal is seen well on both coronal and axial images.

Coronal
The scutum, Prussaks space, tegmen tympani, cochlea,
vestibule and semicircular canals are well visualized on
coronal images (Figure 3). The middle ear is divided into
three parts, the epitympanum, mesotympanum and
hypotympanum, on coronal images. The epitympanum
or attic lies above a line extending from the scutum to the
geniculate ganglion. The mesotympanum lies below the
epitympanum with its lower extent defined by a line
extending from the inferior aspect of the external auditory canal (EAC) to the bottom of the cochlear promontory. The hypotympanum occupies the rest of the middle
ear below the mesotympanum.

Figure 3. Normal coronal CT showing scutum (dashed white

arrow), malleus (white arrow), tegmen tympani (double
arrow), labyrinthine portion of the facial nerve (dashed black
arrow) and apical turn of the cochlea (long black arrow). The
space between the scutum and ossicles is Prussaks space.

MRI technique
The key structures to identify on high-resolution T2
volumetric sequences are the facial and vestibulocochlear
nerve complexes and membranous labyrinth (Figure 4).

External ear
EAC atresia, in the form of external canal stenosis and
pinna malformations, is often associated with middle ear
abnormalities such as fused malleus and incus.12
Necrotizing external otitis (NEO) (malignant otitis externa)
is a potentially fatal infection of the external ear canal,
skull base and adjacent soft tissues.
Patients usually present with extreme otalgia and
otorrhoea, often with an associated facial nerve palsy,
but can occasionally present as an acute neurological

Figure 4. Normal axial high-resolution volumetric driven

Figure 2. Normal anatomy of the malleus, incus, facial nerve
(white arrow) and vestibular aqueduct (black arrow) on axial
CT. The malleus body and the body and short process of the
incus simulate an ice cream cone (dashed black arrow).

2 of 15

equilibrium MRI through the internal auditory meatus

showing the facial and vestibulocochlear nerves (long white
double arrow), cochlea (short white arrow), vestibule, lateral
semicircular canal (double arrow) and posterior semicircular
canal (small arrow).

Imaging 2014, 23, 20110070

Imaging temporal bone

Figure 5. Technetium white

cell imaging in a patient with
necrotizing external otitis
demonstrating increased activity in the region of the
right skull base (arrows) but
poor anatomical localization.
Ant, anterior; L, left; R, right.

emergency with signs of skull base osteomyelitis and

intracranial extension.1315 Patients with diabetes, immunocompromised patients and the elderly are particularly affected. The prevalence of diabetes in a recent case
series of 37 patients with NEO was estimated at 51%,
with Pseudomonas aeruginosa the most common pathogen.16 Initial imaging of patients suspected of having
NEO is by contrast-enhanced CT or MRI, but these are
only of limited use in determining disease resolution if, as
is usually the case, some changes persist despite
adequate treatment with antibiotics.17,18 It is important
to note that follow-up cross-sectional imaging should not
be performed until at least 3 months after the commencement of treatment, as radiological changes lag behind clinical improvement.

Figure 6. Coronal CT showing a small soft-tissue mass and

erosion of the inferior wall of the left external auditory canal
(arrow) in a patient with necrotizing external otitis presenting with left otalgia and otorrhoea.
birpublications.org

Nuclear medicine in the form of three-phase 99mTc

methylene diphosphonate scintigraphy (bone scan),
99m
Tc hexamethyl propylene white cell and gallium
scanning has been used for the diagnosis and follow-up
of NEO. Bone scanning is rapid and cheap and has a high
specificity for detecting osteomyelitis but does not detect
infection without bone involvement. It also remains
positive as long as osteoblastic activity persists, making
it of limited use to assess response to treatment.19 The

Figure 7. Axial CT on bone windows showing subtle erosion of

the left occipital condyle (arrow), underlying a soft-tissue mass,
in a patient presenting with otalgia and facial nerve palsy.

3 of 15

I Zammit-Maempel

Figure 10. Coronal CT showing a small rounded non-specific

soft-tissue mass in the right epitympanum (arrow), clinically
a cholesteatoma.

Figure 8. Unenhanced coronal T1 weighted MRI in a patient

presenting with left otalgia and facial nerve palsy, showing
a soft-tissue mass inferior to the left external auditory canal
around the carotid space (arrow) and abutting on to the
parotid gland.

radiolabelled technetium white cell scan (Figure 5) is

expensive and may be negative in low-grade infection.20
Gallium is absorbed by macrophages and reticular endothelial cells and concentrates in areas of active inflammation. Gallium scans quickly return to normal after
the infection has settled and are therefore useful to assess
response to treatment. Gallium scanning is however expensive, delivers a higher radiation dose than bone or
white cell scans and has poor anatomical detail.21
NEO usually begins insidiously at the osseous cartilaginous junction, as a focal area of ulceration and erosion
of the EAC. The disease usually extends inferiorly
allowing access to the soft tissues around the stylomastoid foramen and temporal fossa and from there can
spread anteriorly to involve the temporomandibular joint
and parotid gland. Medial extension to involve the jugular foramen can result in lower cranial nerve palsies and
patients may present with vocal cord palsy or swallowing
problems. Masses may be bilateral and central, mimicking a nasopharyngeal carcinoma. Extension through the

petro-occipital synchondrosis can result in secondary

meningitis, abscess formation and sinus thrombosis. Lee
et al22 evaluated the prognosis of NEO based on the
progression of disease in terms of extension patterns on
follow-up MRI. They found that retrocondylar fat infiltration was the earliest change in NEO and extension into
other areas such as the parapharyngeal space or nasopharyngeal musculature may be a poor prognostic factor.
A wide spectrum of radiological findings are seen in
NEO, including erosion of the EAC or tympanic plate
with or without an associated soft-tissue mass in the
EAC or periauricular region (Figure 6), erosion of the
clivus and occipital condyles (Figure 7), soft-tissue
masses around the mastoid process, stylomastoid foramen, carotid sheath (Figure 8), jugular foramen, parotid
gland and temporomandibular joint, meningeal enhancement and jugular vein/sigmoid sinus thrombosis.23 It should be pointed out that, as many of these
patients would have been treated with empirical short
courses of antibiotics, no abnormality may be seen in the
EAC and assessment of the soft tissues below the skull
base is imperative.

External auditory canal cholesteatoma

This is a mass of exfoliated keratin within stratified
squamous epithelium most commonly seen involving the
posterior and inferior EAC wall. Patients usually present
with otorrhoea and a chronic dull pain and less commonly with hearing loss. The classic imaging appearance
is of a focal soft-tissue mass with bony fragments and
adjacent bone erosion. The cholesteatoma may extend

Figure 9. (a, b) Axial CT on

bone (a) and soft-tissue (b)
settings showing destroyed
right temporal bone with
associated soft-tissue mass
(arrow) engulfing the right
external auditory canal and
middle ear and extending
on to the dura of the temporal lobe.

4 of 15

Imaging 2014, 23, 20110070

Imaging temporal bone

Middle ear
Cholesteatoma

Figure 11. Coronal CT showing a cholesteatoma with

erosion of the scutum and ossicles and labyrinthine fistula
(arrow).

into the mastoid or middle ear and may involve the facial
nerve canal or tegmen tympani.24

External auditory canal squamous cell carcinoma

Malignant tumours of the EAC are relatively rare, with
squamous cell carcinoma (SCC) being the most frequently encountered and primarily a disease of the elderly. Radiologists should be aware that SCC of the EAC
is occasionally seen in young patients and vigilance
maintained in interpreting scans with an osteitis picture.
SCC may begin in the EAC, arise from the pinna or, in
rare cases, originate in the middle ear. Secondary involvement of the EAC from regional tumour extension is
commoner than primary neoplasia. The classic imaging
appearances are of an aggressive mass with variable
degrees of underlying bone destruction (Figure 9) but, in
the early stages, may be mistaken for a benign process.
Presentation may be similar to otitis externa and early
symptoms include otorrhoea, otalgia and hearing loss.
Surgery is nearly always performed, and with localized
tumours, en bloc resection is often curative.25,26

A cholesteatoma is a collection of keratinizing squamous epithelium in the middle ear cleft associated with
bone erosion. Keratin squames normally migrate laterally
with cerumen from the tympanic membrane along the ear
canal. Acquired cholesteatomas develop in a retraction
pocket in the tympanic membrane and disturbance of the
normal clearance mechanism leads to keratin accumulation in an expanding mass. Congenital cholesteatomas
are rare, occurring in patients with an intact tympanic
membrane and likely to be caused by the persistence of
foetal epidermoid tissue. They have similar appearances
to the acquired type. Cholesteatomas classically present
with offensive otorrhoea associated with conductive
hearing loss but may also present with complications
such as vertigo, facial paralysis, mastoiditis or meningitis.
The acquired cholesteatomas usually arise in a retraction
pocket in the superior tympanic region, the classic pars
flaccida mass starting in Prussaks space and enlarging
into the posterior epitympanum and mastoid antrum.
Less commonly, it arises in a retraction pocket in the
posterosuperior tympanic membrane, the pars tensa
cholesteatoma producing a mass in the mesotympanum.
The initial diagnosis of cholesteatoma is generally made
by otoscopic examination when a pearly white mass is
seen behind a frequently retracted tympanic membrane.
CT may be performed to evaluate the extent or complications of disease. On CT, differentiating a small
cholesteatoma (Figure 10) from granulation tissue or inflammatory change is impossible. Imaging findings that
support a CT diagnosis of cholesteatoma include erosion
of the scutum, ossicles (Figure 11), tegmen tympani
or bone overlying the lateral semicircular canal.27,28
MRI, specifically diffusion-weighted imaging (DWI), is
not necessary in most of these patients. MRI is useful if
there is erosion of the tegmen tympani to determine if
intracranial extension is present or if there is an associated meningocele or encephalocele (Figure 12).
As there is no effective non-surgical management for
cholesteatoma, surgical eradication is necessary. The
earliest technique, a radical mastoidectomy, converted
the EAC and middle ear into a large cavity devoid of

Figure 12. (a, b) Coronal CT

(a) showing a rounded mass
in the left epitympanum with
a defect in the tegmen tympani (arrow). Coronal unenhanced T1 weighted MRI (b)
showed this to be a left
encephalocele (arrow).
birpublications.org

5 of 15

I Zammit-Maempel

Figure 13. (a, b) Axial CT (a) showing a large destructive lesion in the left middle ear with ossicular fragments and tegmen tympani
dehiscence. This mass is shown to be of high signal on T2 weighted axial MRI (b). Contrast-enhanced coronal T1 weighted MRI
(c) shows differentiation between enhancing granulation tissue (single arrow) and non-enhancing cholesteatoma (double arrow).

ossicles or tympanic membrane, but poor epithelialization generally caused a chronic discharging cavity. The
later modified radical mastoidectomy or canal wall down
(CWD) procedure was still associated with a discharge
and required regular attendance for suction clearance,
but recurrence of cholesteatoma was uncommon and residual disease easy to identify. CWD procedures are
performed usually when the cholesteatoma has eroded
through a large portion of the EAC, if there is evidence of
a labyrinthine fistula or if there is limited surgical access
via sclerotic mastoids. Subsequent surgical development
of the canal wall up procedure by preserving the posterior canal wall results in a closed mastoidectomy cavity
with better hearing results and avoids cavity problems.
However, residual cholesteatoma occurs in 1336% of
cases and recurrent disease in 513% of cases.29 This
failure to eradicate the disease in relatively inaccessible
sites makes a re-exploration or second look procedure
mandatory after 12 months.
The primary role of imaging in the management of
post-operative cholesteatoma is to detect any residual or
recurrent disease. If rounded non-dependent soft tissue is
present on CT, then the findings are suggestive of recurrent disease. However, if there is amorphous soft tissue or complete opacification of the middle ear, then the
findings are considered non-specific, and recurrent cholesteatoma cannot be differentiated from granulation tissue,
fibrosis or inflammatory tissue.30 The cardinal CT sign
of cholesteatoma, bony and ossicular erosion, is not
applicable in the post-operative ear because of the
surgical alteration of the bony and ossicular landmarks.7 CT does however have a high negative predictive value in the well-aerated middle ear cleft with
no abnormal soft tissue.31
Post-contrast T1 weighted MRI has been advocated as
an effective technique for distinguishing granulation tissue from residual cholesteatoma. Although both cholesteatoma and granulation tissue are of low T1 and high T2
signal, cholesteatoma is avascular and does not enhance
following contrast administration, whereas granulation
tissue is poorly vascularized but does enhance on
6 of 15

delayed images (Figure 13), allowing detection of a large

cholesteatoma.32,33 However, obtaining such images after
delays of 3045 min is inconvenient for patients and
decreases patient throughput. Over the past few years,
a lot of data have been published advocating DWI for
evaluation of residual or recurrent cholesteatoma following
mastoidectomy.6,7,3447 Cholesteatomas are hyperintense
on diffusion-weighted images (Figure 14) compared with
cerebrospinal fluid and brain parenchyma, like epidermoid
cysts, which are histologically identical.
Initially, echo planar imaging (EPI) was performed but
susceptibility artefacts in the temporal bone made detection of cholesteatomas that are ,5 mm difficult. The
overall sensitivity and specificity for detecting residual
or recurrent cholesteatoma is 13100% and 73100%,
respectively.3945 Non-echo planar techniques using a
single-shot turbo spin echo (STE) sequence such as the
half-Fournier acquired STE (HASTE) sequence can detect
cholesteatomas as small as 2 mm, as the sequence does

Figure 14. Single-shot non-echo planar coronal diffusionweighted imaging showing a right cholesteatoma as a bright
focus.

Imaging 2014, 23, 20110070

Imaging temporal bone

Figure 15. (ac) Axial CT (a) showing opacification of the right middle ear (arrow) in a patient presenting with hearing loss and
bluish discoloration to the drum. Both the coronal unenhanced T1 weighted (b) and axial T2 weighted MRI (c) showed this mass to
be of high signal (arrows), consistent with a middle ear cholesterol granuloma. Note the incidental opacified maxillary antra.

not exhibit the image distortion and susceptibility artefacts present in EPI-based techniques. The periodically
rotated overlapping parallel lines with enhanced reconstruction (PROPELLER) and HASTE sequences have
also been used successfully on 3-T machines, but the
PROPELLER sequence can only be performed in the axial
plane.46,47 Although most early studies have reported
a sensitivity and specificity of 90100% in detecting recurrent or residual cholesteatoma, some more recent
studies have raised doubts about the reliability of these
DWI sequences for definitely excluding very small
cholesteatomas.4850 A recent systematic review of DWI
in the assessment of post-operative cholesteatoma suggested sensitivity, specificity, positive and negative predictive values of 91%, 96%, 97% and 85%, respectively,
for non-EPI techniques.51

Other middle ear masses

Recurrent haemorrhage in the middle ear can result
in specialized granulation tissue called cholesterol
granuloma (CG). Patients usually present with slowly
progressive conductive hearing loss or pulsatile tinnitus
and otoscopy reveals a non-pulsating bluish discoloration of a retracted tympanic membrane. On CT,
small lesions appear as soft-tissue density opacification
of the middle ear without ossicular erosion (Figure 15a),
but larger lesions are expansile with ossicular loss. MRI
reveals characteristic high T1 (Figure 15b) and high T2
signals (Figure 15c), due to the paramagnetic effect of
methaemoglobin. Glomus tympanicum is a benign
paraganglioma that arises in the glomus bodies along
Arnolds and Jacobsens nerves on the cochlear promontory. Patients usually present with pulsatile tinnitus
or conductive hearing loss, and, at otoscopy, a vascular
mass is noted in the anteroinferior quadrant of the
tympanic membrane. Unenhanced high-resolution CT
is the imaging modality of choice for small tumours and
shows a rounded mass around the promontory with no
bone erosion. If the floor of the middle ear is not intact,
then there is likely to be jugular vein involvement, the
so-called glomus jugulotympanicum (Figure 16), an
birpublications.org

important radiological differentiation for any surgeon

contemplating surgery, and, in such cases, MRI is imperative. Aberrant carotid artery is a congenital anomaly, where the cervical internal carotid artery regresses
during embryogenesis resulting in an anastomosis between the inferior tympanic and caroticotympanic
arteries.52 This results in the aberrant artery entering the
posterior middle ear cavity, crossing the middle ear
closely applied to the promontory and then joining the
horizontal portion of the internal carotid artery through
a dehiscence in the carotid plate.53,54 The CT appearance
of aberrant carotid artery (Figure 17a) is diagnostic and
MR angiogram (Figure 17b) complementary, but conventional MR does not reliably pick up this anomaly. A
persistant stapedial artery, suspected by the presence of
an absent foramen spinosum and an enlarged anterior
tympanic segment of the facial nerve, is often found in
association.

Figure 16. Coronal unenhanced CT showing a small rounded

mass in the left middle ear but also bone erosion of the skull
base (arrow) consistent with a glomus jugulotympanicum.

7 of 15

I Zammit-Maempel

Figure 17. (a, b) Axial CT

(a) showing an aberrant left
internal carotid artery as a
middle ear mass close to
the promontory (arrow), confirmed by time of flight MR
angiogram (b).

Inner ear
Vestibular schwannoma
The investigation of patients with sensorineural deafness, tinnitus and vertigo is an increasingly heavy workload on MR machines, with the aim of predominantly
excluding a vestibular schwannoma (VS) or acoustic
neuroma, as it is often known. VS is a slow-growing
benign tumour arising from the nerve sheath of the vestibular divisions of the vestibulocochlear nerve. It is the
most common mass of the internal auditory meatus
(IAM) or cerebellopontine angle and is usually unilateral,
but 5% of patients have bilateral tumours as part of
neurofibromatosis Type 2.55 High-resolution volumetric
T2 weighted sequences are now accepted as a rapid and
cheap diagnostic tool in diagnosing VS (Figure 18) and
gadolinium scans are reserved for the few cases of doubt
or positive scans. It is important to emphasize the importance of careful evaluation of all the inner ear structures, as small schwannomas can also be found within
the vestibule (Figure 19) and inner ear malformations
may be seen in all age groups.

The Mondini deformity, the best known deformity of the

inner ear is due to arrested inner ear development during
the 8th and 9th week of gestation. The middle and apical
turns of the cochlea are fused (Figure 21), resulting in
a low-frequency hearing deficit, but the basal turn is
present, resulting in some preservation of high-frequency
hearing. In 20% of patients, there are associated malformations of the vestibule, semicircular canals or endolymphatic duct and sac.56 Cochlear implantation is the
treatment of choice but, because of an associated defect of
the modiolus, can be associated with a gusher, the immediate emptying of the endolymph the moment the
electrode is inserted. Careful radiological evaluation of the
modiolus is therefore important.

Dehiscence of superior semicircular canal

Superior semicircular canal dehiscence (SSCD) occurs
when there is a defect of the bone overlying the canal58
and may be due to erosion of the bone, trauma or congenital absence. Normally, the oval and round windows
are the only two openings in the fluid-filled system of the
inner ear. The presence of a dehiscence results in a third

Dilated vestibular aqueduct

The VA is the bony canal that runs along the posterior
surface of the petrous temporal bone to communicate
with the vestibule superiorly and contains the endolymphatic sac. As previously mentioned, it should not be
wider than 1.5 mm at its mid-point and, as a rule of
thumb, not wider than the adjacent posterior semicircular
canal. The large VA is the most common abnormality in
children with sensorineural deafness and is often overlooked on both CT and MRI.56 Classically, patients have
a moderate hearing deficit in early childhood, but this
gradually deteriorates in a fluctuating stepwise manner
over the years; in many cases, after minor head injury or
barometric pressure changes.57 Accordingly, patients
with an enlarged VA are advised to avoid contact sports
and scuba diving. The abnormality is best visualized by
axial CT (Figure 20) or MRI (Figure 21). A dilated VA can
be associated with other congenital inner ear anomalies,
especially the Mondini deformity and Pendred syndrome.
8 of 15

Figure 18. Axial driven equilibrium MRI showing bilateral

intracanalicular masses (arrows) consistent with vestibular
schwannomas in a patient with neurofibromatosis Type 2.

Imaging 2014, 23, 20110070

Imaging temporal bone

Figure 19. (a, b) Axial driven

equilibrium MRI (a) showing
a low-signal focus (arrow)
within the high-signal fluid
in the right vestibule and
axial T1 weighted post gadolinium MRI (b) showing enhancement within this focus
(arrow), consistent with a labyrinthine schwannoma.

window, and fluid movement within the semicircular

canal can occur in response to sound vibration of the stapes. This causes slight movement of the perilymph, which
is transmitted to the endolymph, and the brain perceives
this as body movement, and the patient has dizziness or vertigo.59,60 This dizziness or vertigo in response to
loud noises is called the Tullio phenomenon. SSCD can
also cause a conductive hearing loss.61
High-resolution axial CT with coronal and sagittal
reconstructions is the imaging modality of choice in
demonstrating the small defect in the bony wall of the
semicircular canal (Figure 22a) but may be suspected on
MRI (Figure 22b). SSCD has been observed in up to 10%
of patients imaged for different reasons.62 To make
a confident diagnosis, the imaging findings must be accompanied by the appropriate vestibular function tests
and typical symptoms.

Labyrinthine ossificans
This refers to ossification of the membranous labyrinth
as a healing response to an infectious, inflammatory,

traumatic or surgical insult to the inner ear. Children

developing hearing loss following meningitis should be
scanned as a matter of urgency, as labyrinthine ossificans
(LO) can develop rapidly and affect both inner ears
making cochlear implantation difficult. The CT appearance of LO varies from a slight increase in density within
the membranous labyrinth to complete sclerosis. MRI
findings vary from low-density foci within the highsignal fluid on T2 weighted sequences to complete obliteration of this fluid (Figure 23).

Cochlear implantation
A cochlear implant (CI) is an electronic device used to
rehabilitate patients with sensorineural hearing loss. It
takes the place of the damaged organ of Corti and directly stimulates the spiral ganglion cells that innervate
fibres of the auditory nerve. An individual deafened after
the critical period of language acquisition will have
had his or her central auditory pathways stimulated

Figure 21. Axial T2 weighted MRI showing a Mondini

Figure 20. Axial CT showing bilateral dilated vestibular
aqueducts (arrows).

birpublications.org

deformity with markedly dilated endolymphatic sacs within

widened vestibular aqueducts (double arrow) and loss of the
normal cochlear turns (single arrow).

9 of 15

I Zammit-Maempel

Figure 22. (a, b) Coronal CT

(a) and coronal driven equilibrium MRI (b) showing dehiscence of the left superior
semicircular canal (arrow).

normally, and, in such individuals, cochlear implantation

has a good chance of success many years after the hearing
loss. A child born with congenital deafness or who is
deafened before language has been acquired, however,
has only a short window during which stimulation with
a CI can be expected to result in the acquisition of speech
and language.
The National Institute for Health and Clinical Excellence issued guidelines in 2009 on the use of CIs for severe
to profound deafness.63 Unilateral cochlear implantation
was recommended for people with severe to profound
deafness who did not receive adequate benefit from
acoustic hearing aids. Simultaneous bilateral cochlear
implantation was recommended for children and for
adults who were blind or who had other disabilities that
increased their reliance on auditory stimuli as a primary
sensory mechanism for spatial awareness.
Pre-CI imaging evaluation with CT and MRI aims to
identify patients with contraindications for cochlear implantation, as well as to guide the choice of device and
surgical approach. Absolute contraindications include the
absence or obliteration of the cochlea or embryonic cochlear cavity, absent cochlear nerve and severe damage to

Figure 23. Axial driven equilibrium MRI showing loss of the

normal high T2 signal from the right cochlea (arrow) and
lateral semicircular canal (double arrow) consistent with
labyrinthine ossificans.
10 of 15

the auditory pathways and/or auditory cortex. CT gives

excellent bone detail of the temporal bone with bony
malformations of the otic capsule and deformities to the
modiolus easily demonstrated. The diameter of the IAM
can be measured and ossification and fracture lines easily
identified. In addition, pneumatization of the mastoid
and facial nerve position provide valuable information to
the surgeon. However, CT does not show neural structures and, in particular, the cochlear nerve, inner ear fluid
or cochlear fibrosis.
MRI elegantly demonstrates the nerves in the IAM and
is very sensitive to cochlear sclerosis/fibrosis but does not
show the bony structures, in particular the facial canal.
Although some studies64,65 have shown that an absent
cochlear nerve is associated with a narrowed IAM,
Casselman et al66 reported one patient with a normal CT
and absent cochlear nerve on MRI. As cochlear implantation in a patient with an absent cochlear nerve would
be a catastrophe, MRI should be performed in all children
prior to implantation. As CT adds valuable bony information, some authors suggest performing MRI and CT in
the paediatric population.67 However, Mackeith at al68
showed that omitting CT and using MRI alone missed no
critical abnormalities and that the overall frequency of
abnormalities and their detection rate did not depend on

Figure 24. Modified Stenvers view showing a normally

positioned cochlear implant.

Imaging 2014, 23, 20110070

Imaging temporal bone

Figure 25. (a, b) Axial T2 weighted MRI (a) showing high signal in the left petrous apex (arrow) and axial CT (b) showing
opacified but non-eroded cells (arrow), consistent with simple retained secretions.

age. However, in adults, assuming a VS has been previously excluded, CT should suffice. Post-implantation
evaluation can be performed by a plain radiograph in the
form of a modified Stenvers view (Figure 24) and highresolution CT reserved for patients with implant failure,
as malpositioned or extruded electrodes are well demonstrated.69 Over the past few years, cone beam CT is
being increasingly used following cochlear implantation,
as it results in reduced artefact, high-resolution bony
detail and a considerable lower radiation dose than
conventional CT.70 These machines are, however, predominantly found in dental departments.
As CIs are electronically activated devices, MRI may be
contraindicated in patients with CIs because of the possibility of injuring the patient and altering the function of
the device. Based on studies conducted to determine the
safety of patients with CIs to safely undergo MRI,71,72
highly specific guidelines are now available for the different CIs available on the market, as well as the strength
of magnets. Some implants require the use of 0.2- or 0.3-T
systems, and some require the removal of the magnet
associated with the CI and its replacement following the
scan. Crane et al73 showed that there was no ill effect
while scanning patients with three different types of CI
where the device was tightly bound, but Deneuve et al74
reported a case of CI magnet displacement during MRI.
In practice, most MRI units in the UK elect not to image
patients with CIs.

space simulating a mass lesion on MRI, appearing as

a bright signal on T1 sequences. A fat-suppressed sequence or high-resolution CT will clarify matters, should
there be any doubt. Petrous apex effusions can also develop from previous otitis media and subsequent obstruction of the tracts leading from the petrous apex to
the middle ear. This results in variable signal on T1
depending on the protein content of secretions and usually a high T2 signal (Figure 25a), but CT will show no
erosion of the cell septae (Figure 25b). These findings are
often noted on routine MRI and require no further investigation or treatment.
Another lesion to ignore is the petrous apex cephalocele,76 which is a congenital or acquired herniation of
the posterolateral dural wall of Meckels cave into the
anterolateral aspect of the petrous bone (Figure 26),
resulting in a sharply delineated scalloping of the petrous
apex.

The petrous apex

The petrous apex is the portion of the petrous temporal
bone anteromedial to the inner ear and lateral to the
petro-occipital suture. It is divided by the IAM into
a larger anterior compartment that consists of either bone
marrow or air cells (30% of individuals) and a smaller
posterior compartment.75

Petrous apex pseudolesions to ignore

In about 5% of patients, there is asymmetric aeration of
the petrous apex with the non-pneumatized marrow
birpublications.org

Figure 26. Axial driven equilibrium MRI showing a right

petrous apex cephalocele (arrow) communicating with Meckels
cave.

11 of 15

I Zammit-Maempel

Figure 27. (a, b) Axial CT

(a) showing an expansile
mass in the right petrous
apex (arrow) and MR angiogram (b) confirming this to
be a petrous carotid aneurysm (black arrow).

Petrous apex cholesterol granuloma

Petrous apex metastasis

CG, also known as cholesterol cyst, is an expansile mass

of the petrous apex arising from air cell obstruction and
recurrent haemorrhage.77 It usually presents in young to
middle-aged adults with sensorineural deafness but may
also present with tinnitus, hemifacial spasm, facial numbness, trigeminal neuralgia and abducens palsy. It is the
most common primary lesion of the petrous apex, accounting for about 60% of all lesions in this region. CT
reveals a smooth expansile mass with trabecular breakdown and cortical thinning, whereas MRI shows a classical
high signal on both T1 and T2 weighted sequences.

This is the most common site for metastases to the

temporal bone and is due to haematogenous spread from
breast, bronchus or renal primaries. The imaging appearances are of a destructive lesion on CT (Figure 28) and an
irregular enhancing mass on contrast-enhanced MRI.
Other destructive lesions to consider in the differential
diagnosis are myeloma in the elderly and sarcoma,
lymphoma or Langerhans cell histiocytosis in younger
patients.

Petrous apex cholesteatoma

These lesions, also known as epidermoid cysts, present
with sensorineural deafness and are due to epithelial rests
of embryonal origin and present as expansile nonenhancing masses of low T1 and high T2 signal and
demonstrate restricted diffusion on DWI with a clear
hyperintensity on b1000 images.

Conclusion
MRI and CT have become essential and complementary tools in the investigation of patients with symptoms
related to the middle and inner ear. Nuclear medicine
studies and cone beam CT play a limited role in the
evaluation of temporal bone disease. The interpretation of
this temporal bone imaging can be difficult and may put
many radiologists off. Appreciation of the temporal bone
anatomy, normal anatomical variants and the wide range

Apical petrositis
This is due to an infectious nidus in the petrous apex
cells with trabecular degeneration and meningeal involvement. The classical triad of Gradenigo syndrome
includes ear pain, sixth nerve palsy and deep facial pain
referable to the trigeminal nerve. CT demonstrates a petrous effusion often with variable bone erosion, whereas
contrast-enhanced MRI shows enhancement of bone,
adjacent dura and Meckels cave. Possible complications
include meningitis, focal cerebral abscess and venous sinus thrombosis.78

Petrous internal carotid artery aneurysm

This is congenital or acquired and may present with
hearing loss or as an incidental expansile petrous apex
mass (Figure 27a). MRI reveals a rounded or fusiform
mass with complex signal due to intraluminal clot of
various ages and flow voids, with the aneurysm confirmed by CT or MR angiography (Figure 27b).
12 of 15

Figure 28. Unenhanced axial CT showing destruction of the

right petrous apex (arrow) in a patient with known metastatic
bronchogenic carcinoma.
Imaging 2014, 23, 20110070

Imaging temporal bone

of pathological entities is crucial in correct interpretation.

This review has attempted to clarify some of these points
with special emphasis on recent imaging advances and
topics which may cause confusion.

19.

20.

References
1. Niu Y, Wang Z, Liu Y, Liu Z, Yao V. Radiation dose to the
lens using different temporal bone CT scanning protocols.
AJNR Am J Neuroradiol 2010; 31: 2269. doi: 10.3174/ajnr.
A1807
2. Rabinov JD, Barker FG, McKenna MJ, Curtin HD. Virtual
cisternoscopy: 3D MRI models of the cerebellopontine angle
for lesions related to the cranial nerves. Skull Base 2004; 14:
939. doi: 10.1055/s-2004-828701
3. Byun JS, Kim HJ, Yim YJ, Kim ST, Jeon P, Kim KH, et al. MR
imaging of the internal auditory canal and inner ear at 3T:
comparison between 3D driven equilibrium and 3D balanced fast field echo sequences. Korean J Radiol 2008; 9:
21218. doi: 10.3348/kjr.2008.9.3.212
4. Naganawa S, Koshikawa T, Fukatsu H, Ishigaki T, Aoki I,
Ninomiya A. Fast recovery 3D fast spin-echo MR imaging
of the inner ear at 3T. AMJR Am J Neuroradiol 2002; 23:
299302.
5. Dubrulle F, Souillard R, Chechin D, Vaneecloo FM, Desaulty
A, Vincent C. Diffusion-weighted MR imaging sequence in
the detection of postoperative recurrent cholesteatoma. Radiology 2006; 238: 60410. doi: 10.1148/radiol.2381041649
6. De Foer B, Vercruysse JP, Spaepen M, Somers T, Pouillon M,
Offeciers E, et al. Diffusion-weighted magnetic resonance
imaging of the temporal bone. Neuroradiology 2010; 52:
785807. doi: 10.1007/s00234-010-0742-1
7. Khemani S, Singh A, Lingam RK, Kalan A. Imaging of
postoperative middle ear cholesteatoma. Clin Radiol 2011;
66: 7607. doi: 10.1016/j.crad.2010.12.019
8. Gunlock MG, Gentry LR. Anatomy of the temporal bone.
Neuroimaging Clin N Am 1998; 8: 195209.
9. Swartz JD, Loevner LA. Imaging of the temporal bone. New
York, NY: Thieme; 2009.
10. Curtin HD, Gupta R, Bergeron RT. Embryology, anatomy
and imaging of the temporal bone. In: Som PM, Curtin HD,
eds. Head and neck imaging. 5th edn. St Louis, MO: Elsevier
Mosby; 2011. pp. 105396.
11. Ahuja AT, Yuen HY, Wong KT, Yue V, Van Hasselt AC.
Computed tomography imaging of the temporal bone
normal anatomy. Clin Radiol 2003; 58: 6816.
12. Yuen HY, Ahuja AT, Wong KT, Yue V, van Hasselt AC.
Computed tomography of common congenital lesions of the
temporal bone. Clin Radiol 2003; 58: 68793.
13. Clark MP, Pretorius PM, Byren I, Milford CA. Central or
atypical skull base osteomyelitis: diagnosis and treatment.
Skull Base 2009; 19: 24754. doi: 10.1055/s-0028-1115325
14. Chang PC, Fischbein NJ, Holliday RA. Central skull base
osteomyelitis in patients without otitis externa: imaging
findings. AJNR Am J Neuroradiol 2003; 24: 131016.
15. Cavel O, Fliss DM, Segev Y, Zik D, Khafif A, Landsberg R.
The role of the otorhinolaryngologist in the management of
central skull base osteomyelitis. Am J Rhinol 2007; 21: 2815.
16. Ali T, Meade K, Anari S, ElBadawey MR, Zammit-Maempel
I. Malignant otitis externa: case series. J Laryngol Otol 2010;
124: 84651. doi: 10.1017/S0022215110000691
17. Sudhoff H, Rajagopal S, Mani N, Moumoulidis I, Axon PR,
Moffat D. Usefulness of CT scans in malignant external
otitis: effective tool for the diagnosis, but of limited value in
predicting outcome. Eur Arch Otorhinolaryngol 2008; 265:
536. doi: 10.1007/s00405-007-0416-8
18. Grandis JR, Curtin HD, Yu VL. Necrotizing (malignant)
external otitis: prospective comparison of CT and MR

birpublications.org

21.

22.

23.

24.

25.

26.

27.

28.
29.

30.

31.

32.

33.

34.

35.

36.

imaging in diagnosis and follow-up. Radiology 1995; 196:

499504. doi: 10.1148/radiology.196.2.7617867
Carfrae MJ, Kesser BW. Malignant otitis externa. Otolaryngol
Clin North Am 2008; 41: 53749. doi: 10.1016/j.otc.2008.01.
004
Okpala NC, Siraj QH, Nilssen E, Pringle M. Radiological and
radionuclide investigation of malignant otitis externa. J Laryngol Otol 2005; 119: 715. doi: 10.1258/0022215053222978
Stokkel MP, Boot IC, van Eck-Smit BL. SPECT gallium
scintigraphy in malignant external otitis: initial staging and
follow-up. Case reports. Laryngoscope 1996; 106: 33840.
Lee JE, Song JJ, Oh SH, Chang SO, Kim CH, Lee JH. Prognostic value of extension patterns on follow-up magnetic
resonance imaging in patients with necrotizing otitis
externa. Arch Otolaryngol Head Neck Surg 2011; 137: 68893.
doi: 10.1001/archoto.2011.98
Mehrotra P, Elbadawey MR, Zammit-Maempel I. Spectrum
of radiological appearances of necrotising external otitis:
a pictorial review. J Laryngol Otol 2011; 125: 110915. doi:
10.1017/S0022215111001691
Heilbrun ME, Salzman KL, Glastonbury CM, Harnsberger
HR, Kennedy RJ, Shelton C. External auditory canal cholesteatoma: clinical and imaging spectrum. AJNR Am J Neuroradiol 2003; 24: 7516.
Moffatt DA, Wagstaff SA. Squamous cell carcinoma of the
temporal bone. Curr Opin Otolaryngol Head Neck Surg 2003;
11: 10711.
Ong CK, Pua U, Chong VF. Imaging of carcinoma of the
external auditory canal: a pictorial essay. Cancer Imaging
2008; 8: 1918. doi: 10.1102/1470-7330.2008.0031
Yates PD, Flood LM, Banerjee A, Clifford K. CT scanning of
middle ear cholesteatoma: what does the surgeon want to
know? Br J Radiol 2002; 75: 84752.
Morley S, Beale TJ. Imaging of deafness and tinnitus. Imaging 2007; 19: 5570.
Mills RP. Management of chronic otitis media. In: ScottBrown WG, Hibbert J, Kerr AG, eds. Scott-Browns otolaryngology. 6th edn. Oxford, UK: Butterworth-Heinemann; 1997.
Tierney PA, Pracy P, Blaney SP, Bowdler DA. An assessment of the value of the preoperative computed tomography scans prior to otoendoscopic second look in intact
canal wall mastoid surgery. Clin Otolaryngol Allied Sci 1999;
24: 2746.
Lemmerling MM, De Foer B, VandeVyver V, Vercruysse JP,
Verstraete KL. Imaging of the opacified middle ear. Eur J
Radiol 2008; 66: 36371. doi: 10.1016/j.ejrad.2008.01.020
Ayache D, Williams MT, Lejeune D, Corre A. Usefulness of
delayed postcontrast magnetic resonance imaging in the
detection of residual cholesteatoma after canal wall-up
tympanoplasty. Laryngoscope 2005; 115: 60710. doi:
10.1097/01.mlg.0000161360.66191.29
Williams MT, Ayache D, Alberti C, Heran F, Lafitte F,
Elmaleh-Berges M, et al. Detection of postoperative residual
cholesteatoma with delayed contrast-enhanced MR imaging: initial findings. Eur Radiol 2003; 13: 16974. doi:
10.1007/s00330-002-1423-1
Schwartz KM, Lane JI, Bolster BD Jr, Neff BA. The utility of
diffusion-weighted imaging for cholesteatoma evaluation.
AJNR Am J Neuroradiol 2011; 32: 4306. doi: 10.3174/ajnr.
A2129
De Foer B, Vercruysse JP, Bernaerts A, Maes J, Deckers F,
Michiels J, et al. The value of single-shot turbo spin-echo
diffusion-weighted MR imaging in the detection of middle
ear cholesteatoma. Neuroradiology 2007; 49: 8418. doi:
10.1007/s00234-007-0268-3
Huins CT, Singh A, Lingam RK, Kalan A. Detecting cholesteatoma with non-echo planar (HASTE) diffusion-weighted
magnetic resonance imaging. Otolaryngol Head Neck Surg
2010; 143: 1416. doi: 10.1016/j.otohns.2010.02.021

13 of 15

I Zammit-Maempel
37. De Foer B, Vercruysse JP, Bernaerts A, Meersschaert J, Kenis
C, Pouillon M, et al. Middle ear cholesteatoma: non-echo
planar diffusion-weighted MR imaging versus delayed
gadolinium-enhanced T1-weighted MR imagingvalue in
detection. Radiology 2010; 255: 86672. doi: 10.1148/
radiol.10091140
38. Vercruysse JP, De Foer B, Somers T, Casselman J, Offeciers
E. Long-term follow up after bony mastoid and epitympanic
obliteration: radiological findings. J Laryngol Otol 2010; 124:
3743. doi: 10.1017/S002221510999106X
39. Vercruysse JP, De Foer B, Pouillon M, Somers T, Casselman
J, Offeciers E. The value of diffusion-weighted MR imaging
in the diagnosis of primary acquired and residual cholesteatoma: a surgical verified study of 100 patients. Eur Radiol
2006; 16: 14617. doi: 10.1007/s00330-006-0160-2
40. Aikele P, Kittner T, Offergeld C, Kaftan H, Huttenbrink KB,
Laniado M. Diffusion-weighted MR imaging of cholesteatoma in pediatric and adult patients who have undergone middle ear surgery. AJR Am J Roentgenol 2003; 181:
2615. doi: 10.2214/ajr.181.1.1810261
41. Venail F, Bonafe A, Poirrier V, Mondain M, Uziel A. Comparison of echo-planar diffusion-weighted imaging and
delayed postcontrast T1-weighted MR imaging for the detection of residual cholesteatoma. AJNR Am J Neuroradiol
2008; 29: 13638. doi: 10.3174/ajnr.A1100
42. Stasolla A, Magliulo G, Parrotto D, Luppi G, Marini M.
Detection of postoperative relapsing/residual cholesteatomas
with diffusion-weighted echo-planar magnetic resonance
imaging. Otol Neurotol 2004; 25: 87984.
43. Jindal M, Doshi J, Srivastav M, Wilcock D, Irving R, De R.
Diffusion-weighted magnetic resonance imaging in the
management of cholesteatoma. Eur Arch Otorhinolaryngol
2010; 267: 1815. doi: 10.1007/s00405-009-1023-7
44. Jeunen G, Desloovere C, Hermans R, Vandecaveye V. The
value of magnetic resonance imaging in the diagnosis of
residual or recurrent acquired cholesteatoma after canal
wall-up tympanoplasty. Otol Neurotol 2008; 29: 1618. doi:
10.1097/MAO.0b013e31815dbae8
45. Cimsit NC, Cimsit C, Baysal B, Ruhi IC, Ozbilgen S, Aksoy
EA. Diffusion-weighted MR imaging in postoperative follow up: reliability for detection of recurrent cholesteatoma.
Eur J Radiol 2010; 74: 1213. doi: 10.1016/j.ejrad.2009.01.
025
46. Lehmann P, Saliou G, Brochart C, Page C, Deschepper B,
Vallee JN, et al. 3T MR imaging of postoperative recurrent
middle ear cholesteatomas: value of periodically rotated
overlapping parallel lines with enhanced reconstruction
diffusion-weighted MR imaging. AJNR Am J Neuroradiol
2009; 30: 4237.
47. Pizzini FB, Barbieri F, Beltramello A, Alessandrini F, Fiorino
F. HASTE diffusion-weighted 3-Tesla magnetic resonance
imaging in the diagnosis of primary and relapsing cholesteatoma. Otol Neurotol 2010; 31: 596602. doi: 10.1097/
MAO.0b013e3181dbb7c2
48. Clark MP, Westerberg BD, Fenton DM. The ongoing dilemma of residual cholesteatoma detection: are current
magnetic resonance imaging techniques good enough? J
Laryngol Otol 2010; 124: 13004.
49. Kasbekar AV, Scoffings DJ, Kenway B, Cross J, Donnelly N,
Lloyd SWK, et al. Non echo planar, diffusion-weighted
magnetic resonance imaging (periodically rotated overlapping parallel lines with enhanced reconstruction sequence) compared with echo planar imaging for the
detection of middle-ear cholesteatoma. J Laryngol Otol 2011;
125: 37680.
50. Plouin-Gaudon I, Bossard D, Fuchsmann C, Ayari-Khalfallah
S, Froehlich P. Diffusion-weighted MR imaging for evaluation of pediatric recurrent cholesteatomas. Int J Pediatr Otorhinolaryngol 2010; 74: 226. doi: 10.1016/j.ijporl.2009.09.035

14 of 15

51. Jindal M, Riskalla A, Jiang D, Connor S, OConnor AF. A

systematic review of diffusion-weighted magnetic resonance
imaging in the assessment of postoperative cholesteatoma.
Otol Neurotol 2011; 32: 12439.
52. Lo WW, Solti-Bohman LG, McElveen JT Jr. Aberrant carotid
artery: radiologic diagnosis with emphasis on highresolution computed tomography. Radiographics 1985; 5:
98593. doi: 10.1148/radiographics.5.6.3880011
53. Rojas R, Palacios E, DAntonio M, Correa G. Aberrant internal carotid artery as a cause of pulsatile tinnitus and an
intratympanic mass. Ear Nose Throat J 2003; 82: 1734.
54. Sauvaget E, Paris J, Kici S, Kania R, Guichard JP, Chapot R,
et al. Aberrant internal carotid artery in the temporal bone:
imaging findings and management. Arch Otolaryngol Head
Neck Surg 2006; 132: 8691. doi: 10.1001/archotol.132.1.86
55. Gillespie JE. Imaging in neurofibromatosis type 2: screening
using magnetic resonance imaging. Ear Nose Throat J 1999;
78: 1023, 106, 1089.
56. Krombach GA, Honnef D, Westhofen M, Di Martino E,
Gunther RW. Imaging of congenital anomalies and acquired
lesions of the inner ear. Eur Radiol 2008; 18: 31930. doi:
10.1007/s00330-007-0759-y
57. Koesling S, Rasinski C, Amaya B. Imaging and clinical
findings in large endolymphatic duct and sac syndrome. Eur
J Radiol 2006; 57: 5462. doi: 10.1016/j.ejrad.2005.09.005
58. Minor LB. Superior canal dehiscence syndrome. Am J Otol
2000; 21: 919.
59. Offiah CE, Ramsden RT, Gillespie JE. Imaging appearances
of unusual conditions of the middle and inner ear. Br J Radiol
2008; 81: 50414. doi: 10.1259/bjr/17051473
60. Belden CJ, Weg N, Minor LB, Zinreich SJ. CT evaluation of
bone dehiscence of the superior semicircular canal as a cause
of sound- and/or pressure-induced vertigo. Radiology 2003;
226: 33743. doi: 10.1148/radiol.2262010897
61. St Martin MB, Hirsch BE. Imaging of hearing loss. Otolaryngol Clin North Am 2008; 41: 15778. doi: 10.1016/j.
otc.2007.10.007
62. Krombach GA, Schmitz-Rode T, Haage P, DiMartino E,
Prescher A, Kinzel S, et al. Semicircular canal dehiscence:
comparison of T2-weighted turbo spin-echo MRI and CT.
Neuroradiology 2004; 46: 32631. doi: 10.1007/s00234-0030948-6
63. National Institute for Health and Clinical Excellence. Cochlear implants for children and adults with severe to profound
deafness. NICE Technology Appraisal Guidance 166. London,
UK: NICE; 2009.
64. Sennaroglu L, Saatci I, Aralasmak A, Gursel B, Turan E.
Magnetic resonance imaging versus computed tomography
in pre-operative evaluation of cochlear implant candidates
with congenital hearing loss. J Laryngol Otol 2002; 116:
80410. doi: 10.1258/00222150260293619
65. Shelton C, Luxford WM, Tonokawa LL, Lo WW, House WF.
The narrow internal auditory canal in children: a contraindication to cochlear implants. Otolaryngol Head Neck Surg
1989; 100: 22731.
66. Casselman JW, Offeciers FE, Govaerts PJ, Kuhweide R,
Geldof H, Somers T, et al. Aplasia and hypoplasia of the
vestibulocochlear nerve: diagnosis with MR imaging. Radiology 1997; 202: 77381. doi: 10.1148/radiology.202.3.9051033
67. Trimble K, Blaser S, James AL, Papsin BC. Computed tomography and/or magnetic resonance imaging before pediatric cochlear implantation? Developing an investigative
strategy. Otol Neurotol 2007; 28: 31724.
68. Mackeith S, Joy R, Robinson P, Hajioff D. Pre-operative
imaging for cochlear implantation: magnetic resonance imaging, computed tomography, or both? Cochlear Implants Int
2012; 13: 1336. doi: 10.1179/1754762811Y.0000000002
69. Jain R, Mukherji SK. Cochlear implant failure: imaging evaluation of the electrode course. Clin Radiol 2003; 58: 28893.

Imaging 2014, 23, 20110070

Imaging temporal bone

70. Hodez C, Griffaton-Taillandier C, Bensimon I. Cone-beam
imaging: applications in ENT. Eur Ann Otorhinolaryngol
Head Neck Dis 2011; 128: 6578. doi: 10.1016/j.anorl.2010.10.
008
71. Teissl C, Kremser C, Hochmair ES, Hochmair-Desoyer IJ.
Cochlear implants: in vitro investigation of electromagnetic
interference at MR imagingcompatibility and safety
aspects. Radiology 1998; 208: 7008. doi: 10.1148/radiology.
208.3.9722849
72. Majdani O, Leinung M, Rau T, Akbarian A, Zimmerling M,
Lenarz M, et al. Demagnetization of cochlear implants and
temperature changes in 3.0T MRI environment. Otolaryngol
Head Neck Surg 2008; 139: 8339. doi: 10.1016/j.otohns.2008.
07.026
73. Crane BT, Gottschalk B, Kraut M, Aygun N, Niparko JK.
Magnetic resonance imaging at 1.5T after cochlear implantation. Otol Neurotol 2010; 31: 121520. doi: 10.1097/MAO.
0b013e3181ec1d61

birpublications.org

74. Deneuve S, Loundon N, Leboulanger N, Rouillon I,

Garabedian EN. Cochlear implant magnet displacement
during magnetic resonance imaging. Otol Neurotol 2008; 29:
78990. doi: 10.1097/MAO.0b013e3181825695
75. Connor SEJ, Leung R, Natas S. Imaging of the petrous apex:
a pictorial review. Br J Radiol 2008; 81: 42735. doi: 10.1259/
bjr/54160649
76. Moore KR, Fischbein NJ, Harnsberger HR, Shelton C,
Glastonbury CM, White DK, et al. Petrous apex cephaloceles. AJNR Am J Neuroradiol 2001; 22: 186771.
77. Greenberg JJ, Oot RF, Wismer GL, Davis KR, Goodman ML,
Weber AE, et al. Cholesterol granuloma of the petrous apex:
MR and CT evaluation. AJNR Am J Neuroradiol 1988; 9:
120514.
78. Boardman JF, Rothfus WE, Dulai HS. Lesions and pseudolesions of the cavernous sinus and petrous apex. Otolaryngol
Clin North Am 2008; 41: 195213. doi: 10.1016/j.otc.2007.10.
006

15 of 15