Otolaryngol Clin N Am

41 (2008) 179–193

Imaging of Tinnitus
Melissa Kang, MD*, Edward Escott, MD
University of Pittsburgh Medical Center, 200 Lothrop Street, Pittsburgh, PA 15213, USA

Tinnitus is the experience of auditory sensation in the absence of external

stimuli. In the western countries, it is estimated that 12% of the population
is affected by tinnitus to varying degrees. Most patients present in the sev-
enth to eighth decade of life [1].
Many classification schemes for tinnitus are available. Many investiga-
tors characterize tinnitus according to subjective or objective, and pulsatile
or nonpulsatile. Others evaluate pitch or loudness of the noise. Pulsatile tin-
nitus coincides with the patient’s heartbeat. Nonpulsatile tinnitus does not
and can be either intermittent or continuous. Tinnitus can be subjective (ex-
perienced by the patient only) or objective (perceptible to another). Full
neurotologic clinical examination typically precedes imaging workup. Clin-
ically, pulsatile tinnitus can further be divided into arterial or venous origin.
Differentiation between the two can be made by applying pressure over the
ipsilateral internal jugular vein (IJV). This maneuver usually has no effect on
the intensity of the arterial type, whereas the venous type should subside
with this technique [2].
From a radiologic workup perspective, tinnitus is classified into pulsatile,
which can be objective, and nonpulsatile, which is typically subjective.
There is considerable discrepancy within the literature regarding the per-
centage of positive findings in patients with pulsatile tinnitus. Weissman
and Hirsch [3] found that most patients with subjective tinnitus and normal
otoscopic examination have no imaging abnormalities to explain the tinni-
tus. Sonmez and colleagues [4] described radiographic abnormalities in
61.9% of patients with subjective tinnitus; however, it remains unclear
whether these positive abnormalities were the cause of the subjective tinni-
tus or incidentally found.
In objective pulsatile tinnitus, Weissman and Hirsch [3] found that most
patients have no imaging abnormalities while Sonmez and colleagues [4]
postulated that radiographic abnormalities can be detected in up to 100%

* Corresponding author. 144 Hidden Hollow Terrace, Palm Beach Gardens, FL 33418.
E-mail address: melissakang@yahoo.com (M. Kang).

0030-6665/08/$ - see front matter Ó 2008 Elsevier Inc. All rights reserved.
doi:10.1016/j.otc.2007.10.008 oto.theclinics.com
180 KANG & ESCOTT

of patients and De Ridder and colleagues [5] have found 15% of patients
with pulsatile tinnitus have no imaging abnormality. The variability of the
results is likely because of the uncertainty as to whether the radiographic
findings are indeed the etiology of the patient’s tinnitus or just incidental
findings. For example, Sonmez and colleagues [4] considered jugular bulb
variants as positive findings in patients with tinnitus. However, jugular
bulb venous variants are common findings and can be seen in asymptomatic
patients. It is unclear what percentage of these imaging abnormalities were
indeed the cause of tinnitus in these patients and a very large study would be
necessary to have enough statistical power to truly determine the relation-
ship between relatively common normal variants and clinical symptoms.
The goal of imaging is to identify treatable causes of tinnitus.
Many radiologic findings associated with tinnitus have been seen in
asymptomatic patients. Koesling and colleagues [6] presented a review of
223 thin-section CT temporal bone scans where only 5% of these patients
were referred for tinnitus. They detected the following vascular variations:
mastoid emissary vein (82%), lateral sigmoid sinus (28%), high-riding jug-
ular bulb (6%), and anterior sigmoid sinus (55%). Less than 1% showed
persistent stapedial artery, aberrant internal carotid artery, jugular bulb
diverticulum, and dehiscent sigmoid sinus. All of these findings have been
seen in asymptomatic patients as well as in patients with tinnitus [7]. There-
fore, it is critical to correlate the radiographic findings with the full neuro-
tological exam and the overall clinical picture [1].

Imaging workup algorithm

When an imaging abnormality is found in pulsatile tinnitus, it is usually
from a vascular mass (neoplasm), vascular malformation, or bony/develop-
mental abnormality of the middle ear cavity and otic capsule where MRI is
less sensitive [1,8,9].
Imaging of objective pulsatile tinnitus begins with contrast-enhanced
temporal bone CT [1].
If the examination is normal and clinical suspicion is high, then consider
conventional angiography to evaluate for dural arteriovenous fistula or mal-
formation. If both studies are normal or if there is low suspicion for dural
vascular abnormality, then consider enhanced CT of the neck through the
superior mediastinum to look for venous compression or CT angiography
of the neck to evaluate for atherosclerotic disease.
Imaging of subjective pulsatile tinnitus begins with contrast-enhanced
temporal bone CT [1].
If this study is normal, then consider contrast-enhanced CT of the neck
through the superior mediastinum to look for venous compression or ath-
erosclerotic disease.
Imaging of nonpulsatile tinnitus begins with MRI of the internal auditory
canal with intravenous contrast [8].
 IMAGING OF TINNITUS 181

Refer to Box 1 for Imaging Protocols from University of Pittsburgh Med-

ical Center.

Pulsatile tinnitus
Neoplasm
Glomus tumors, or paragangliomas, are benign vascular neoplasms that
arise from paraganglia that follow the cranial nerves. The most common
paragangliomas that present with pulsatile tinnitus are the glomus tympani-
cum, glomus jugulare, and glomus jugulotympanicum, which is a glomus
jugulare that has grown into the middle ear.
Glomus tympanicum are the most common tumors of the middle ear cav-
ity and arise along the medial middle ear cavity along the course of Jacob-
son’s nerve, a branch of the glossopharyngeal nerve (CN 9). Typically they
occur along the cochlear promontory but can occur throughout the meso-
tympanum along the course of Jacobson’s nerve. Glomus tumors may
also arise from Arnold’s nerve, a branch of the Vagus nerve (CN10), which
enters the facial canal to course along the facial nerve. They appear as red
retrotympanic pulsatile masses on otoscopic exam (Fig. 1) [10].
Glomus jugulare tumors arise from the paraganglia of the adventitia at
the jugular bulb. They grow superiorly into the middle ear cavity and
then can be visible on otoscopic exam. CT scan can show early characteristic
moth-eaten or permeative erosive changes of the jugular foramen. Glomus
jugulare tumors can avidly enhance and be indistinguishable from normal

Box 1. Imaging protocols from the University of Pittsburgh

Medical Center
Contrast-enhanced temporal bone CT [1]:
 64 detector row CT scanner
 125 cc nonionic contrast with 60-second delay for both arterial
and venous opacification
 Kvp 120, mA 280, slice thickness 0.625 mm
 Coronal reconstructions
MRI of the IAC (1.5T):
 Brain: 5-mm axial fluid attenuated inversion recovery (FLAIR),
T1-weighted sagittal images, and contrast-enhanced fat-
suppressed T1-weighted axial images.
 IAC: 2- to 3-mm T1-weighted axial and coronal images (pre and
post contrast enhancement), and high-resolution thin-section
three-dimensional (3D) T2-weighted axial images, using either
Fast Spin Echo or fast imaging employing steady state
acquisition techniques (FIESTA).
182 KANG & ESCOTT

Fig. 1. Glomus tympanicum. (A) Thin-section axial unenhanced CT through the level of the
temporal bones. At the level of the right basal turn of the cochlea in the middle ear cavity, there
is a soft tissue density mass with extension anteriorly (solid arrow). No osseous erosion is seen.
(B) Coronal reformatted image through temporal bones. A soft tissue density mass is present
along the cochlear promontory (solid arrow). No osseous erosion is seen.

jugular vein making the inferior extent difficult to define. Moreover, it can
invade the lumen of the jugular vein. There can be variable signals within
the jugular vein that may reflect slow flow, turbulent flow, or tumor involve-
ment, which can be difficult to distinguish on MRI [10,11]. MRI may show
a salt-and-pepper appearance to the lesion illustrating the multiple flow
voids of the tumor; however, this is not always present. The classic described
‘‘salt-and-pepper’’ appearance is seen on long TR/TE images. The ‘‘pepper’’
component represents flow void while the ‘‘salt’’ component represents
hyperintense foci due to slow flow or hemorrhage. This is usually seen in
glomus tumors greater than 1 cm (Figs. 2 and 3) [11].
Hemangiomas within the internal auditory canal are rare. They are typ-
ically hyperintense on T1- and T2-weighted MR images but there have
been reports of either isointensity or hypointensity on T1-weighted images.
They typically show strong enhancement patterns. When large, they can
demonstrate stippled calcifications, although it is not the rule. When stip-
pled calcifications are present, they may help differentiate hemangioma
from schwannoma [12]. Depending on location and the nerve of origin,
these lesions can cause severe and progressive sensorineural hearing loss,
tinnitus, facial nerve palsy, or vertigo [12]. Hemangiomas can occur any-
where along the facial nerve. When they occur at the geniculate ganglion,
patients typically present with facial nerve dysfunction (96%) and rarely
 IMAGING OF TINNITUS 183

Fig. 2. Right glomus jugulotympanicum. (A, B) Sequential enhanced axial 3D spoiled gradient
recalled images show an enhancing mass arising from the right jugular foramen (solid arrow)
with extent into the middle ear cavity (arrowhead).

hearing loss (5%) [13]. Hemangiomas found in the internal auditory canal
have a higher rate of hearing loss with variable degrees of hearing loss [13].
When they do occur in the internal auditory canal, they typically involve
the facial nerve.

Fig. 3. Left glomus jugulotympanicum. (A) Axial enhanced CT image through temporal bones
shows an enhancing mass extending from the left jugular foramen (solid arrow) into the left
middle ear cavity (arrowhead) causing a permeative osseous pattern (asterisk). (B) Coronal
reformatted image through temporal bones shows the enhancing mass extending from the
jugular foramen (solid arrow) into the middle ear cavity (arrowhead) with permeative pattern
of osseous bony erosion (asterisk).
184 KANG & ESCOTT

Vascular malformation
A dural arteriovenous fistula or arteriovenous malformation is the most
frequent cause of objective pulsatile tinnitus in patients with a normal oto-
scopic exam [12,14–29]. Any dural sinus may be involved, but the two most
frequent sinuses involved are the cavernous sinus and the transverse sinus.
The dural arteriovenous fistula to most commonly cause pulsatile tinnitus
is in the transverse sinus region. CT or MRI are often normal but may dem-
onstrate too many or enlarged vascular structures including cortical veins,
and the sigmoid or transverse sinuses. Conventional angiography remains
the gold standard for this diagnosis (Fig. 4) [1].

Vascular anomalies
An aberrant internal carotid artery is not the true internal carotid artery
but rather a hypertrophied inferior tympanic artery that arises from the
ascending pharyngeal branch of the external carotid artery. The inferior
tympanic artery enlarges to anastomose with the caroticotympanic artery
in the middle ear and resumes the course of the petrous internal carotid
artery. Along the way, the inferior tympanic canaliculus enlarges and resem-
bles the carotid canal. It may or may not be dehiscent in the middle ear. This
occurs in response to a carotid artery that never develops. CT scan will show
the dehiscence and abnormal course of the vessel into the middle ear. Mag-
netic resonance angiography (MRA) and conventional angiography will
show the abnormal lateral course of the aberrant carotid artery. Often, it
may be best appreciated on CT since one can see the bony landmarks [1,3].
The persistent stapedial artery can occur with an aberrant internal
carotid artery or with a normal carotid artery. It is persistence of a fetal cir-
culation that courses between the crura of the stapes (obturator foramen)
then courses along the tympanic segment of the facial nerve and exits to sup-
ply the middle meningeal artery territory. It generally regresses with birth
[3]. When there is a persistent stapedial artery, the middle meningeal artery
does not develop and thus there is no foramen spinosum. These abnormal-
ities can be seen on thin-section CT scan. The persistent stapedial artery is
likely too small to be seen on MRA [30,31].
Redundant anterior inferior cerebellar artery has been implicated by
some authors as an etiology of tinnitus. Vascular contact with the cisternal
segment of the vestibulocochlear nerve has been associated with nonpulsa-
tile tinnitus while vascular contact with cranial nerve (CN) 8 in the internal
auditory canal has been associated with pulsatile tinnitus [5,32]. De Ridder
and colleagues [5] postulate that the etiology of pulsatile tinnitus may be
caused by direct transmission of pulsation to the cochlea via the internal au-
ditory canal. They further state that the pulsations are heard via a so-called
bone conduction mechanism, rather than via cochlear nerve compression. It
is well known that intrameatal vascular loops can be present without gen-
erating pulsatile tinnitus. Potentially, the sharpness of the vascular loop
 IMAGING OF TINNITUS 185

Fig. 4. Right dural arteriovenous fistula. (A, B) Sequential enhanced axial 3D SPGR images
show too numerous multiple small vessels in the region of the right transverse sinus (solid
arrow). (C) Lateral view of the right vertebral artery selective injection angiogram shows an ar-
teriovenous fistula with feeding vessels from the posterior circulations (dashed arrows). (D) AP
view of a right common carotid artery injection shows feeding vessels extending from the inter-
nal and external circulation (arrowhead) with an early venous drainage and opacification of the
internal jugular vein (dotted arrow).

as well as the size of the internal auditory canal may be contributory to the
development of tinnitus. Furthermore, these authors postulate that the rea-
son we do not hear our carotid arteries as they course through the petrous
bone is the presence of a perivenous plexus that surrounds the carotid and is
most prominent between the carotid artery and the cochlea. The venous
186 KANG & ESCOTT

plexus acts as a sound barrier and dampens the acoustic effect of the carotid
[5].
Improvement in tinnitus has been described with microvascular decom-
pression of the CN 8. However, many patients are scanned for other reasons
that have vessels in close proximity to the CN 8 without symptoms of tinni-
tus. MRI optimally illustrates this finding (Fig. 5).
Venous variants may be associated with pulsatile tinnitus [33]. A stenosed
transverse sinus can be seen in patients with tinnitus [33]. Additionally,
asymmetric transverse and sigmoid sinuses, and sigmoid sinus diverticulum
have all been associated with tinnitus [7]. An aberrant sigmoid sinus that
courses anteriomedially from its normal course may run near the endolym-
phatic sac and the posterior semicircular canal and transmit pulses to the
inner ear. CT scan illustrates these abnormalities well in relation to key
structures. Magnetic resonance venography (MRV) phase contrast will
show the anatomy and patency of the venous structures well; however,
the relationship to key inner ear structures is not well delineated.
There are a number of different definitions for ‘‘high-riding jugular
bulb.’’ A jugular bulb is considered high riding when it extends over the
tympanic annulus and the round window or the basal turn of the cochlea.
Atilla and colleagues [34] showed an incidence of 20.3% of high-riding jug-
ular jugular bulb. Dietz and colleagues [33] and Remley and colleagues
define high-riding jugular bulb when the tip of the jugular bulb extends to
the level of the external auditory canal. When the jugular bulb reached
the level of the internal auditory canal, it can be considered to be very

Fig. 5. Looping anterior inferior cerebellar artery. FIESTA image shows a looping anterior
inferior cerebellar artery (solid arrow) into the right IAC contacting the seventh and eighth
cranial nerve complex (arrowhead).
 IMAGING OF TINNITUS 187

high riding and is also a less frequent finding (7.3%), according to Atilla and
colleagues [34]. The frequency of high-riding jugular bulb ranges from 4%
to 20%. Approximately 4.5% of patients with high-riding jugular bulbs
have pulsatile tinnitus. Tinnitus can be reduced with jugular replacement
in 30% of patients with pulsatile tinnitus and a high-riding jugular bulb [4].
The jugular bulb is considered dehiscent when the jugular plate is dehis-
cent. If it is dehiscent, then it may be visible on otoscopic exam as a bluish
mass. MRI may show variable signal intensity within the bulb and can be
a signal void, which is the same as the adjacent cortical bone thereby making
MRI relatively unreliable for this diagnosis.
Jugular bulb diverticulum is defined as extension of a diverticulum supe-
riorly and medially from the jugular fossa extending toward the area
between the posterior wall of the internal auditory canal and the vestibular
aqueduct. Patients with jugular diverticulum may be dizzy and vertiginous.
High jugular bulb, dehiscence, and diverticulum formation were noted to be
seen more frequently on the right side, being up to 2 to 3 times more fre-
quent (Fig. 6) [34].
It remains unclear how or why these vascular anomalies cause sudden
onset of pulsatile tinnitus [3]. These findings may be seen incidentally in
patients who do not have complaints of tinnitus but have undergone imag-
ing for other reasons. When these anomalies are found, other etiologies
should be pursued. A very large sample size would be necessary to truly val-
idate any statistically significance.
Vascular abnormalities such as atherosclerotic disease, fibromuscular
dysplasia, or petrous aneurysm can be associated with tinnitus. Atheroscle-
rotic plaque is usually located distant from the skull base and is typically in
the extracranial carotid artery [35]. Sismanis and colleagues [35] found that
atherosclerosis of the extracranial carotid artery was the second most com-
mon cause of pulsatile tinnitus. However, these patients did not undergo
endarterectomy as they were neurologically stable. Thus, no postoperative

Fig. 6. Dehiscent jugular bulb with a diverticulum. (A) Contrast-enhanced CT temporal bones
show a dehiscent and high-riding jugular bulb (solid arrow) with a diverticulum into the right
middle ear cavity (asterisk). (B) Coronal reformat image through temporal bones shows the
dehiscent jugular bulb (solid arrow) with small diverticulum (asterisk).
188 KANG & ESCOTT

follow-up data were presented. Some authors have shown case reports illus-
trating patients who had successful treatment and relief of pulsatile tinnitus
with carotid artery stenting for stenosis; however, no series in the literature
statistically validates this finding (Fig. 7) [36].
Internal carotid artery dissection can present with tinnitus; although it
usually presents with cerebral ischemia, Horner’s syndrome, or intracranial
hemorrhage. Dissection is a diagnosis that may be missed on contrast-
enhanced CT. MRI with axial T1 images (preferably with fat-saturation)
are used to show the methemoglobin in the wall of the vessel. MRA, com-
puted tomography angiography, and conventional angiography will show
a narrowed vessel (Fig. 8).
Occasionally, an obstructed vein within the neck may be the cause of pul-
satile tinnitus. When detailed imaging fails to reveal the cause of pulsatile
tinnitus, imaging of the neck may be undertaken to evaluate for cervical
causes [14]. Subclavian stenosis, occlusion proximal to the origin of the ver-
tebral artery, typically causes subclavian steal syndrome; however, it has
also been reported to be a cause of pulsatile tinnitus because of anastomosis
between the left vertebral artery and occipital artery [14]. Because some of
these anomalies may be located in the neck, cervical imaging studies are
included in the workup for pulsatile tinnitus [3,10].

Osseous Etiologies
Otosclerosis is an osseous dysplasia that causes both sensorineural and
conductive hearing loss and occasionally tinnitus. Abnormal vascular haver-
sian bone replaces the normal enchondral bone of the otic capsule.

Fig. 7. Atherosclerotic disease. Marked narrowing of the left internal carotid artery with non-
calcified plaque at its origin (dashed arrow).
 IMAGING OF TINNITUS 189

Fig. 8. Right Internal carotid artery dissection. (A) Axial T1 MRI shows a crescentic-shaped T1
shortening with central flow void in the right internal carotid artery (solid arrow). (B) Contrast-
enhanced CT shows contrast filling the true lumen of the right ICA corresponding to the dimin-
utive flow void on MRI (arrowhead). (C) A Reformatted image from a CTA shows tapering
opacified true lumen.

Arteriovenous shunting may contribute to tinnitus. Hyperemic mucosa over

the otosclerotic bone can be seen at otoscopy (Schwartse sign). There are
two forms of otosclerosis: the fenestral form, which is more common, and
the retrofenestral (cochlear) form. Vestibular symptoms are more often as-
sociated with retrofenestral otosclerosis [37]. The findings of otosclerosis are
best seen on thin-section temporal bone CT scans as hypoattenuation in the
region of the fissula ante fenestrum (fenestral otosclerosis) or around the co-
chlea (retrofenestral otosclerosis), which is seen as lucency around the co-
chlea (Fig. 9).
190 KANG & ESCOTT

Fig. 9. Retrofenestral otosclerosis (aka cochlear otosclerosis). (A) Unenhanced CT temporal

bones show bilateral lucencies surrounding both cochlea (solid arrows). (B) Enhanced T1
MRI with fat saturation shows enhancement in the pericochlear region (solid arrows) corre-
sponding to the areas of hypoattenuation on the CT.

MRI does not reliably illustrate this finding. Occasionally, hyperintense

signal may be seen on T2-weighted images; however the relevant anatomy
of the inner ear structures may not be well enough defined to confidently
make this diagnosis. T1-weighted images with gadolinium may show
enhancement in the pericochlear region [37].
Patients with Paget disease may have tinnitus related to the intraosseous
arteriovenous shunting associated with pagetic bone.
Benign intracranial hypertension has been associated with tinnitus, and
has been said to be a fairly common cause in the appropriate demographic
[38]. MRI may show sequelae of long-standing intracranial hypertension
such as flattening of the optic disc or an enlarged fluid-filled sella.

Nonpulsatile tinnitus
Nonpulsatile tinnitus is almost always subjective. Most patients do not
show an abnormality on radiologic workup. However, imaging is performed
to exclude potentially treatable causes of nonpulsatile tinnitus. The most
common cause apparent on imaging is a cerebellopontine angle mass or
internal auditory canal mass, typically a vestibular schwannoma (Fig. 10).
Brainstem lesions such as microvascular disease, stroke, and demyelinat-
ing disease also have been associated with continuous tinnitus. Chiari mal-
formations have been associated with a myriad of symptoms including
tinnitus, which may be possibly related to the stretching of the CN 8 [1].
Moreover, vascular compression along the cisternal segment of the vestibu-
locochlear nerve may cause nonpulsatile tinnitus [5]. The goal of imaging is
to exclude the possibility of a treatable lesion such as a vestibular schwan-
noma (Fig. 11).
 IMAGING OF TINNITUS 191

Fig. 10. Right vestibular schwannoma. (A) Enhanced axial T1 MRI image with fat saturation
shows an enhancing mass in the right internal auditory canal (solid arrow). (B) Enhanced cor-
onal T1 MRI image with fat saturation shows an enhancing mass in the right internal auditory
canal (solid arrow).

Other etiologies of nonpulsatile tinnitus include medication side effects

from aspirin, nonsteroidal anti-inflammatory agents, aminoglycoside antibi-
otics, furosemide, and noise-induced hearing loss. Additionally, posttrau-
matic tinnitus has been described. Meniere disease is associated with
hearing loss, tinnitus, and vertigo and often has no imaging abnormalities.

Fig. 11. Brainstem microangiopathic disease. Axial fluid attenuated inversion recovery image
through the brainstem shows central and bilateral abnormal signal within the pons.
192 KANG & ESCOTT

A potential cause of tinnitus is muscular tinnitus, which is tinnitus and/or

palatal myoclonus associated with rhythmic contractions of the muscles
around the skull base. There is no correlative imaging abnormality. Senso-
rineural hearing loss is often accompanied by tinnitus, particularly in the
elderly population [1,3]. Valvular heart disease has been implicated as
a potential cause of tinnitus as well.
There is considerable overlap in the radiographic findings detected in
association with tinnitus in both asymptomatic patients and symptomatic
patients. It is most important for imaging to detect treatable causes, such
as vestibular schwannoma. It remains unclear whether the radiographic
abnormalities detected in all of these patients are responsible for their symp-
toms, particularly, ‘‘normal’’ venous variants which are detected not uncom-
monly in the asymptomatic population. The association with the fairly
commonly seen vascular loops are also controversial. Therefore, correlation
with the patient’s symptoms, neuro-otological exam, and clinical history is
necessary in the overall care of the patient.

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