European Journal of Radiology 139 (2021) 109722

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European Journal of Radiology

journal homepage: www.elsevier.com/locate/ejrad

Review

Detecting causes of pulsatile tinnitus on CT arteriography-venography: A

pictorial review
Raekha Kumar a, b, Scott Rice a, Ravi Kumar Lingam a, *
a
Northwick Park, London North West University Healthcare NHS Trust, Watford Road, Harrow, HA13UJ, United Kingdom
b
Watford General Hospital, West Hertfordshire Hospitals NHS Trust, Vicarage Road, Watford, Hertfordshire, WD180HB, United Kingdom

A R T I C L E I N F O A B S T R A C T

Keywords: Pulsatile tinnitus (PT) can be a mild or debilitating symptom. Following clinical examination and otoscopy, when
Head and neck the underlying aetiology is not apparent, radiological imaging can be used to evaluate further. CT arteriography-
Pulsatile tinnitus venography (CT A–V) of the head and neck has recently been introduced as a single ‘one catch’ modality for
CT arteriography-venography
identifying the many causes of PT including those which are treatable and potentially serious whilst also
Vascular aetiologies
providing reassurance through negative studies or studies with benign findings.
Tumours
Bony dysplasia CT A–V is performed as a single phase study allowing both arterial and venous assessment, hence limiting
radiation exposure. Additional multiplanar reformats and bone reconstructions are desirable. Understanding the
limitations of CT A–V is also required, with an awareness of the scenarios where other imaging modalities should
be considered.
The causes of PT can be divided into systemic and non-systemic categories. Non-systemic aetiologies in the
head and neck should be carefully reviewed on CT A–V and include a variety of vascular causes (arteriovenous
malformations/fistulas, venous or arterial aetiologies) and non-vascular causes (tumours and bony dysplasias).
Venous causes (dominant, aberrant, stenosed or thrombosed venous vessels) are more common than arterial
aetiologies (aberrant or stenosed internal carotid artery, aneurysms or a persistent stapedial artery). Glomus
tumours that are not visible on otoscopy and osseous pathologies such as bony dehiscence and otospongiosis
should also be excluded.
Careful assessment of all the potential vascular and non-vascular causes should be reviewed in a systematic
approach, with correlation made with the clinical history. A structured reporting template for the reporting
radiologist is provided in this review to ensure all the potential causes of PT are considered on a CT A–V study.
This will help in providing a comprehensive radiological evaluation, hence justifying the radiation dose and for
patient assessment and prognostication.

1. Introduction
Pulsatile tinnitus (PT) is defined as a repetitive, auditory perception
that imitates the patient’s cardiac rhythm. This differs from non-
pulsatile tinnitus which lacks a rhythmic quality, with less than 10 %
of tinnitus patients developing pulsatile features [1]. This can manifest
as unilateral or bilateral ringing, buzzing or whistling, causing distress
to the affected patient and adversely affecting their daily performance.
When audible to both the patient and clinician, this is subclassified as
‘objective PT’ or when solely audible to the patient as ‘subjective PT’
[2].
The mechanism of PT is widely presumed to be secondary to either
abnormal blood flow due to acceleration/turbulent flow (likely objec­
tive PT) or normal flow with an increased perception of ordinary flow
sounds due to sound conduction disturbances (likely subjective PT) [3].
Hence the aetiology of PT can be divided into vascular or non-vascular
categories (Table 1). Vascular character can be subdivided into arterial
or venous, clinically audible as an arterial bruit or a venous hum

Abbreviations: PT, pulsatile tinnitus; CT, computed tomography; CT A–V, CT arteriography-venography; MRI, magnetic resonance imaging; MRA, magnetic
resonance arteriography; MRV, magnetic resonance venography; DSA, digital subtraction angiography; MPR, multiplanar reformats; IIH, idiopathic intracranial
hypertension; MEV, mastoid emissary vein; ICA, internal carotid artery; IJV, internal jugular vein; AVM, arteriovenous malformation; dAVF, dural arteriovenous
fistula; PSA, persistent stapedial artery; CPA, cerebellar-pontine angle; AICA, anterior inferior cerebellar artery; IAM, internal auditory meatus.
* Corresponding author.
E-mail addresses: raekha.kumar@nhs.net (R. Kumar), s.rice@nhs.net (S. Rice), ravi.lingam@nhs.net (R.K. Lingam).

https://doi.org/10.1016/j.ejrad.2021.109722
Received 1 March 2021; Received in revised form 7 April 2021; Accepted 12 April 2021
Available online 14 April 2021
0720-048X/Crown Copyright © 2021 Published by Elsevier B.V. All rights reserved.
R. Kumar et al. European Journal of Radiology 139 (2021) 109722

Table 1 2.1.3. Ultrasound

Table categorizing the different aetiologies of pulsatile tinnitus which must be The role of US is limited to the dynamic assessment of the vascular
excluded on a CT arterio-venography study for pulsatile tinnitus. (ICA: internal structures (e.g. carotid artery stenosis, proximal jugular vein thrombosis
carotid artery). and superficial vascular malformations). It is commonly used an adjunct
Vascular to CT/MRI examinations.
Venous Dominant vein/sinus
Aberrant/emissary veins 2.1.4. Digital subtraction angiography
Venous stenosis/thrombosis Digital subtraction angiography (DSA) is a dynamic test for assessing
Idiopathic intracranial hypertension vascular pathology which provides excellent characterization of the
Venous-osseous High riding jugular bulb/dehiscence
Sigmoid plate dehiscence/diverticulum
angioarchitecture. It is especially useful for complex treatment planning
Arterial ICA stenosis [6] however it is invasive and its role in initial assessment has been
ICA dissection superseded by CT/MR angiography.
Aberrant ICA
Persistent stapedial artery
2.2. Abnormal otoscopy
Aneurysm
Vascular loops
Mixed Arteriovenous malformation A glomus tumour is a recognised cause of PT and readily identified
Dural arteriovenous fistula on otoscopy, where it manifests typically as a reddish mass within the
Non-Vascular inferior half of the middle ear cavity. If a glomus tumour is suspected
then CT imaging of the temporal bones or contrast enhanced MRI is
Tumours Glomus tympanicum
Glomus jugulare indicated in the first instance.
Meningiomas
Hypervascular metastases 3. CT arteriography-venography
Bone dysplasias Otospongiosis
Intraosseous haemangioma
Paget’s Disease
CT A–V is a quick imaging technique for identifying the majority of
causes of PT in patients with a normal otoscopic examination [4,8,9]. It
provides an assessment of both the vascular flow dynamics and the
respectively, and also includes systemic triggers which increase blood osseous structures of the head and neck. It not only detects the
flow such as hyperthyroidism, pregnancy, severe anaemia or hyperten­ correctable, potentially serious causes of PT but also provides reassur­
sion. Non-vascular causes include glomus tumours due to their intrinsic ance when a benign cause or no obvious cause has been detected.
hypervascularity and otospongiosis due to bony dysplasia at the bony Additionally, many ‘soft’ aetiologies detected on CT A–V represent
labyrinth. anatomical variants or benign pathology which are best left untreated
[4].
2. Imaging options and strategy for pulsatile tinnitus CT A–V is performed at our institution most frequently utilising a
Siemens Definition AS + scanner. A single bolus of 70mls of iodinated
The initial choice of imaging is guided by clinical and otoscopic contrast (Omnipaque 350) is administered at a rate of 3–5 ml s/seconds
evaluation. This should include the side, character (objective/subjec­ with an overall 40–50 second delay before image acquisition. Images are
tive, intermittent/constant, soft/intrusive, arterial/venous), identifica­ acquired from the skull vertex to the carotid bifurcation (in line with the
tion of potentially reversible systemic causes (e.g. anaemia or C4 vertebra) at a 1 mm slice thickness (128 × 0.6 mm acquisition) with
thyrotoxicosis, where the resulting hyperdynamic circulatory state is an a 0.7 mm increment (scan parameters: kV 120, mA 120, pitch 1.2).
aetiological factor) and assessment of the tympanic membrane for an Reconstruction filters are utilised for acquiring soft tissue and bone re­
underlying glomus tumour. Assessment may be limited where symptoms constructions. The window width (W) and window length (L) utilised at
are not present at consultation (intermittent PT). our institution vary for general soft tissue assessment (W 400; L40), bone
window assessment (W2000; L500) and angiogram assessment (W700;
2.1. Normal otoscopy W80).
This CT A–V protocol ensures we limit radiation exposure with one
Traditionally, multidetector CT and MRI have been the modalities of single sequence whilst retaining appropriate arterial and venous
choice for investigating PT in patients with a normal otoscopy. Ultra­ enhancement of the head and neck vasculature. This permits optimal
sound or digital subtraction angiogram (DSA) has a role in limited but assessment of the position, calibre and normal developmental variants
specific scenarios. arising from the arteries or veins in the head and neck and their rela­
tionship to the cranial bones. Additional reconstructed high resolution
2.1.1. CT bone images are also obtained to provide excellent assessment of the fine
CT imaging can be provided with CT arteriography-venography (CT bony detail at the temporal bones. Multiplanar (coronal and sagittal)
A–V), a non-invasive imaging tool reviewing the vessels, bones and tu­ reformats are vital for accurate assessment particularly in assessing the
mours in the head and neck and hence provides a valuable ‘one catch’ course of the vasculature, skull base assessment and assessing for bony
imaging modality in detecting the multitude of causes of PT [4]. The role dehiscence [6] (Fig. 1).
of CT A–V is further described below. Other options include 4D CT
arteriography (4D CTA), a new test with flow dynamic evaluation but a 4. Causes of pulsatile tinnitus
higher radiation dose [5,6].
All CT A–V studies should be carefully assessed for the many po­
2.1.2. MRI tential causes of PT. The recognized causes of pulsatile tinnitus are
MRI, MR angiography (MRA) and MR venography (MRV) are subdivided into vascular and non-vascular aetiologies).
commonly used to detect intracranial and vascular causes of PT with
high diagnostic accuracy [7]. There is no ionizing radiation exposure. 4.1. Vascular aetiologies
However, MRI is suboptimal in assessing bony structures and
vessel-bone relationships and require multiple sequences resulting in a Venous causes are more commonly detected as a cause of PT [4].
long examination. They are benign and are typically left untreated, hence their causality

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R. Kumar et al.
Fig. 1. Normal CT arterio-venography (CT A-V) examination.
A 40 year old male patient presented with bilateral pulsatile tinnitus (PT) with a normal otoscopy examination. Axial soft tissue CT A–V images (A) and with bone
windows (B,C) show both arterial and venous enhancement at the level of the extracranial ICA (A), sigmoid sinus (B) and circle of Willis (C). Multiplanar soft tissue
reformats with bone windows in the coronal (D) and sagittal (E) planes from the vertex to the carotid bifurcation are also obtained, and are essential for radio­
logical assessment.
with symptoms has not been robustly demonstrated [4]. However, CT
A–V has been shown to demonstrate a significant association between
the side of the patient’s symptoms and the source of PT such as venous
dominance, suggesting a causal relationship and hence its utility in PT
assessment [4]. On encountering such various venous anatomical vari­
ants, their contributing relationship in a patient with PT needs to be
considered individually, correlating with the side of symptoms, clinical
examination and the presence of other potential causes. Mixed and
arterial causes are less common, the former includes arteriovenous
malformations and the latter internal carotid artery stenoses (ICA)
which are more frequent in the elderly population and hence should be
correlated with the clinical history and other imaging findings.
4.1.1. Venous causes
4.1.1.1. Dominant jugular vein/sigmoid sinus. A dominant jugular or a
sigmoid venous sinus is a common, incidental finding on CT A–V
(Fig. 2). The vessels are defined as co-dominant if there is ≤3 mm be­
tween the diameters at the mid-transverse sinuses bilaterally [9]. If there
is a difference of >3 mm, the side with the larger diameter is regarded as
the side with the dominant cerebral venous system [9]. With a history of
PT, a significant association has been shown on CT A–V between a
dominant jugular vein or sigmoid sinus and the ipsilateral side of the
patient’s symptoms, with increased turbulent flow through the larger
venous system postulated as a contributory factor [4]. It has been shown
that without another underlying cause, right sided venous PT is more
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European Journal of Radiology 139 (2021) 109722
common due to background dominance of the right jugular vein in
70–80 % of the population [10]. Venous dominance may also be a sol­
itary finding on CT A–V or can be associated with other causes [4,11].
4.1.1.2. Aberrant venous channels and prominent emissary veins. An
aberrant venous channel is a prominent vein which traverses through
the head and neck and may be a developed collateral related to a hy­
poplastic sigmoid sinus or jugular vein (contralateral to the side of a
dominant venous system). CT A–V with MPR can characterize the size,
path, and relationships of the aberrant vessel. Increased flow in the
aberrant vein can manifest as PT, particularly if it is in close proximity to
the middle ear cleft (Fig. 3). It is also important to note that aberrant
venous channels may be incidental hence the side of the abnormality
must be correlated with the patient’s symptoms.
Emissary veins related to PT most commonly occur in the mastoid. A
mastoid emissary vein (MEV) is a venous tract which develops at the
embryonic stage and by traversing the mastoid connects the sigmoid
sinus with the posterior auricular or occipital vein, allowing exit of
diploic venous blood [12]. They can be unilateral or bilateral (Fig. 4).
This may be a solitary finding on CT A–V or be associated with a hy­
poplastic sigmoid sinus or jugular vein. Such emissary veins are valve­
less allowing bidirectional flow which can lead to turbulence, increased
velocity or increased intracranial pressure leading to increased flow, all
potentially audible through the mastoid as PT. [13]. The size of the vein
may also be important as suggested by a recent report reviewing a case
of PT related to a single large MEV [13]. Other radiologically evident
R. Kumar et al.
Fig. 2. Dominant sigmoid sinus and internal jugular vein A 30 year old female patient presented with right sided PT. CT A-V axial (A,C) and coronal (B, D) images
demonstrate a dominant right sigmoid sinus (A, long arrow) draining into a dominant right internal jugular vein (IJV) (C, short arrow). The contralateral non-
dominant left sigmoid sinus (B, long dashed arrow) and left IJV (D, short dashed arrow) are smaller in calibre.
emissary veins which are of clinical importance include posterior
condylar veins (courses between the superior bulb of the internal jugular
vein and deep cervical vein) and occipital emissary veins (drains from
the confluence of the sinuses into the internal vertebral plexus) [12]
which theoretically could transit flow related sounds to the mastoid.
4.1.1.3. Venous stenosis. Venous sinus stenosis describes a sudden
change in venous calibre. This can be intrinsic narrowing due to acute
venous sinus thrombosis or due to post thrombotic related fibrosis.
Venous stenosis can also be secondary to extrinsic compression and
subsequently lead to PT. CT A–V with MPR evaluation can identify
extrinsic compression of the suprahyoid internal jugular vein (IJV)
typically caused by the C1 transverse process, styloid process or poste­
rior belly of digastric (Fig. 5) [4]. Elevated intracranial CSF pressure can
also lead to external compression of the sigmoid and transverse sinuses.
It has been postulated that this results in turbulent venous flow due to
stenosis or periodic narrowing caused by arterial narrowing secondary
to pulsating arteries, the affects of which are transmitted to the venous
sinuses across the CSF space [14]. This can then create a vicious feed­
back loop leading to a further increase in intracranial pressure and
consequently increasing venous narrowing which may present as PT [3,
15]. However, narrowing of the venous sinuses, related to contralateral
dominance, is a common incidental finding. Hence true pathological
venous stenosis should be considered when there are signs of raised
intracranial pressure/idiopathic intracranial hypertension (IIH), taking
into account the laterality of PT and excluding other causes.
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European Journal of Radiology 139 (2021) 109722
4.1.2. Venous-osseous causes
4.1.2.1. High riding jugular bulb and dehiscent jugular bulb. A high riding
jugular bulb is a normal variant and a recognised cause of PT, more
commonly noted on the right side of the neck [11,16–18]. Anatomically,
this is defined by the position of the superior aspect of the jugular bulb
being posterosuperior to the floor of the internal auditory canal (IAC).
The jugular bulb consequently lies at the level of the basal turn of the
cochlea (Fig. 6). The jugular foramen and sigmoid plate are intact with
no extension into the middle ear cavity. The presence of a high riding
jugular bulb is also important to report for surgical planning during a
mastoidectomy. However, given jugular bulb variations are normal
variants and hence can be noted incidentally in asymptomatic patients,
care must be taken to ensure there are no other causes of PT on the study.
A dehiscent jugular bulb, whilst also considered a normal variant,
has been associated with PT in the literature [16,18,19]. On CT A–V,
there is superolateral extension of the jugular bulb through a dehiscent
petrous septum of the sigmoid plate and into the middle ear cavity
where it can contact the ossicles, restricting their mobility, or invade the
bony labyrinth leading to conductive hearing loss. This should be
reviewed on high resolution bone windows on CT A–V (Fig. 7). This may
be seen otoscopically as a retrotympanic blue mass. A jugular bulb
diverticulum arises as a focal outpouching of the bulb, most commonly
superior and posterior to the IAC, and protrudes into the temporal bone
(anterior, posterior and medial positions are also possible) [16,20].
Turbulent flow within the diverticulum can result in PT. They are rare
and unlike a high riding jugular bulb, diverticulae are more common on
the left despite a right sided venous dominance in 75 % of cases [20,21].
R. Kumar et al. European Journal of Radiology 139 (2021) 109722

Fig. 3. Aberrant venous channels.

(A,B) A 37 year old female patient presented with left sided PT. CT A–V axial (A) and sagittal (B) images at the level of the middle ear cleft demonstrate an aberrant
venous channel (solid arrows) that arises from the non-dominant left sigmoid sinus (dashed arrows) and passes along the floor of the left middle cranial fossa, just
adjacent to the left tegmen mastoid.
(C,D) A 67 year old female patient with a history of right sided unilateral PT. CT A–V axial (C) and coronal (D) images at the level of the middle ear cleft demonstrate
an anomalous venous channel at the medial aspect of the right petrous apex (solid arrows) draining inferiorly into the right jugular bulb (dashed arrow).

Fig. 4. Emissary veins.

A 53 year old female patient with a history of bilateral PT. CT A–V coronal (A) and axial (B) images on a CT A–V study demonstrate bilateral mastoid emissary veins
(solid arrows), larger on the left, which are closely related to the mastoid air cells and connecting with the co-dominant sigmoid sinuses bilaterally (dashed arrows).

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R. Kumar et al. European Journal of Radiology 139 (2021) 109722

Fig. 5. Suprahyoid extracranial internal jugular vein compression.

(A,B) 49 year old female patient with left sided PT. CT A–V axial (A) and sagittal (B) images demonstrate compression of the non-dominant left IJV between the
posterior digastric belly and the internal carotid artery (solid arrow) and by the styloid process in the styloid tunnel (dashed arrow).
(C,D) A 60 year old male patient with right sided PT. CT A–V axial (C) and sagittal (D) images demonstrate a dominant right IJV with compression by the styloid
process at the styloid tunnel (dotted arrows).
(E,F) A 68 year old male patient with right sided PT. CT A–V coronal (E) and axial (F) images demonstrate a 13 mm short segment of narrowing of the dominant right
proximal IJV (arrowheads) due to compression from the adjacent right C1 transverse process.

4.1.2.2. Sigmoid plate dehiscence and associated diverticulum. Sigmoid
plate dehiscence and diverticulum formation have been associated with
PT in up to 20 % of cases [22,23]. These abnormalities are one of the few
surgically correctable causes of PT with successful resolution of symp­
toms reported post treatment in several studies [23–25]. An intact sig­
moid plate is likely to insulate vibrations from the adjacent flow through
the sigmoid sinus, however with dehiscence, flow sounds may be
transmitted into the mastoid and cochlea leading to PT (Fig. 8) [26].
Extensive pneumatisation of the mastoid segment of the temporal bone
is thought to amplify this phenomenon [27]. A sigmoid plate divertic­
ulum is believed to arise from forceful flow in the adjacent sigmoid sinus
with the lumen consequently protruding into the mastoid cortex/air

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Fig. 6. High riding jugular bulb.

A 59 year old female patient with a history of right sided PT. CT A–V axial (A) and sagittal (B) images demonstrate a high riding right jugular bulb (solid arrow). This
is confirmed with the jugular bulb noted superior to the floor of the internal auditory canal and level with the basal turn of the cochlea (dashed arrow). The right
jugular foramen and sigmoid plate are intact. Note the normal appearances at the level of the left internal auditory meatus and the left jugular bulb is not visible at
this level (arrowhead).

Fig. 7. Dehiscent jugular bulb.

A 50 year old middle aged man presenting with right sided PT. CT A–V axial (A) and coronal (B) images demonstrate a very thin /dehiscent intervening bony wall
between the right dominant jugular bulb and the right middle ear cavity (solid arrows). Normal appearances are noted on the left (dashed arrow). CT A–V axial (C)
image also demonstrates a high riding right jugular bulb (arrowhead).

cells due to bony remodelling, thus leading to a diverticulum (Fig. 8)
[26]. PT is widely thought to result from the consequent turbulent flow
in the pouch (46). It is more common on the side of the dominant venous
sinus but with a similar prevalence on both sides in co-dominant systems
[26,28,29].
On CT A–V, bone window assessment of the sigmoid plate using the
acquired high resolution bone reformats should be performed, with
dehiscence/diverticulum more likely noted on the dominant side of
venous outflow and within the lateral wall of the sigmoid plate [28]. On
review of the literature, there remains no apparent size classification for
sigmoid plate dehiscence. Consequently, various studies have used
different criteria to identify dehiscence such as a minimum width of
5 mm on 2 consecutive slices [4,30]. Eisemann reported the following
criteria as useful in identifying dehiscence/diverticulae: irregularity of
the bony sigmoid sinus wall, focal thinning of the calvarial cortex
overlying the adjacent sinus wall, absence of the normal thin layer of
cortical bone overlying the sinus or the ‘air on sinus’ sign (mastoid air
cells directly contact the sinus wall) [23]. The affected side and
maximum diameter of the dehisced segment should be reported because
sigmoid plate dehiscence can also be an incidental finding, hence the
size and side affected should be correlated clinically. [31]. A divertic­
ulum can be more readily identified on CT A–V bone windows as an
outpouching from the sigmoid sinus into the mastoid with venous phase
enhancement. The AP and transverse circumference on axial images of a
sigmoid plate diverticulum can be measured and reported, aiding sur­
gical management.
4.1.2.3. Idiopathic intracranial hypertension. There has been a known
association in the literature between IIH and PT [15,32]. The aetiology
is complex; external compression (e.g. styloidogenic, posterior belly of
digastric or C1 transverse process) with IJV stenosis, dural sinus stenosis

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Fig. 8. Sigmoid plate dehiscence and diverticulum.

(A,B) 62 year old female patient with a history of left sided PT. CT A–V axial (A) and coronal (B) images demonstrate a 6 mm area of bony dehiscence (long arrow) at
the left lateral sigmoid plate between the sigmoid sinus and mastoid cells. Note the intact right sigmoid plate (short arrow).
(C,D) 40 year old male patient presents with right sided PT. CT A–V axial (C) and coronal (D) images demonstrate a right sigmoid plate bony dehiscence with a
diverticulum posterior to the mastoid air cells, abutting the outer table of the skull vault (dashed arrow).
(E) A 33 year old male patient presents with right sided PT. CT A–V axial (E) image demonstrates a diverticulum of the right sigmoid sinus penetrating into the right
mastoid through a dehiscent sigmoid plate (arrowhead).

or venous sinus thrombosis have all been linked with IIH [4,6,33].
Conversely, raised intracranial pressure can also lead to venous
compression [3]. Several of the ancillary findings of IIH such as an
empty sella and increased fluid around the optic nerves are
sub-optimally assessed on CT A–V, and can be better demonstrated on
MRI brain imaging. However an elevated opening pressure on lumbar
puncture confirms the diagnosis [34].
4.1.3. Arterial causes
stenosed segment (Fig. 9).
A carotid arterial dissection is a more unusual cause of pulsatile
tinnitus. Patients often present with acute neck pain and can develop
sympathetic symptoms indicative of Horner’s syndrome and cerebral
compromise. PT may be an accompanying symptom with other stroke-
like symptoms or may rarely occur in isolation [38]. CT A–V can
assess for a dissected ICA lumen due to an intramural haematoma with
the crescent shaped ‘pseudolumen sign’ on the ipsilateral side of
symptoms.

4.1.3.1. Arterial stenosis and dissection. In the elderly population, arte­
rial stenoses due to atherosclerotic disease in the head and neck
vasculature are reported as the most common cause of PT [35]. One
study has demonstrated this can account for up to 16 % of PT cases [36].
This can lead to ipsilateral PT or even contralateral PT due to compen­
satory increased flow through contralateral open/collateral channels
which is perceived as a pulsing auditory phenomenon [37]. Arterial
stenoses are more common in the ICA hence imaging to the level of the
carotid bulb is preferred in our institution. In younger patients, fibro­
muscular dysplasia (patients present due to widespread
non-atheromatous segmental stenoses) may also trigger symptoms of
PT. Careful clinical assessment for signs of neurovascular compromise in
the form of stroke like symptoms and radiological assessment of the
arterial vasculature on CT A–V using a systematic approach with MPR is
required to accurately identify and assess the location and length of a
4.1.3.2. Aneurysm. An intracranial aneurysm has also been reported in
the literature as a cause of PT and can be depicted on CT A–V, although
this is remarkably rare. Abnormally increased flow within the aneurysm
can be perceived by the auditory apparatus as PT. An example includes
an anterior communicating artery aneurysm published by Austin et al.
[39], with other locations including an ICA, basilar or vertebral artery
aneurysm.
4.1.3.3. Persistent stapedial artery. This is a rare congenital, arterial
developmental anomaly related to the persistence of the embryological
stapedial artery. This frequently arises from the vertical or horizontal
petrous ICA or an aberrant ICA. Consequently, the proximal middle
meningeal artery fails to develop leading to an absent foramen spinosum
[6]. This is often bilateral. Patients can be asymptomatic or present with
PT due to turbulent flow in the stapedial artery [11]. CT A–V cannot

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R. Kumar et al.
Fig. 9. Internal carotid artery stenosis.
A 71 year old male patient presenting with right sided PT. CT A–V sagittal (A) and axial (B) images demonstrate moderate narrowing of the proximal internal carotid
artery (ICA) immediately distal to the carotid bifurcation (solid arrows). There are two associated partially calcified atheromatous plaques (dashed arrow). The sagittal
reformats are useful in assessing the length of stenosed segment.
identify the persistent stapedial artery itself however its utility is in
assessing for indirect signs of its existence. This includes absence of the
foramen spinosum (however this can be a normal finding in 3% of cases
[40] (Fig. 10), subtle enlargement of the anterior tympanic segment of
the facial nerve canal or an associated aberrant ICA [11]. DSA can be
used for confirmation if required [16].
4.1.3.4. Aberrant internal carotid artery. An aberrant ICA is another
congenital variant which can lead to PT. This vascular anomaly arises
due to absent formation of the extracranial ICA, leading to the devel­
opment of an arterial collateral. This runs horizontally through the
middle ear cavity, entering through an enlarged inferior tympanic
canaliculus, coursing anteriorly across the cochlear promontory, then
entering the carotid canal due to dehiscence of the carotid plate
(Fig. 11). The transfer of pulsating sounds by bone conduction to the
inner ear may be the cause of PT. 30 % have a coexisting persistent
stapedial artery [40].
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European Journal of Radiology 139 (2021) 109722
4.1.3.5. Vascular loops. Vascular loops within the cerebellar-pontine
angle (CPA) are common incidental findings [41,42] but are also
another recognised cause of PT [43]. They frequently arise from the
anterior inferior cerebellar artery (AICA) and can contact or compress
the vestibulocochlear nerve [44]. Reports have suggested that distortion
of the vestibulocochlear nerve at the intrameatal segment towards the
fundus rather than the cisternal segment at the nerve root entry zone
may result in PT [45] with improvement post surgical treatment [46].
Vascular loops can be confidently identified on CT A–V by assessing the
CPA and internal auditory meatus (IAM) in both the axial and coronal
planes. However, given these are frequent incidental findings, further
characterisation with heavily T2 weighted high resolution MRI IAM
imaging should be reserved for those cases with vascular loops
traversing at or near the IAM fundus when no other cause of PT has been
identified.
Fig. 10. Persistent stapedial artery.
A 44 year old female patient presenting with left sided PT.
Axial CT A–V image (A) demonstrates an absent left foramen
spinosum indicating the failure of development of the middle
meningeal artery and presence of a persistent stapedial artery
(PSA). The normal relationship of the foramen spinosum pos­
terior to the foramen ovale is shown on the right (solid arrow).
This should be reviewed on all CT A–V examinations. A PSA
cannot be directly visualised on cross-sectional imaging. Other
supportive imaging findings include enlargement of the ante­
rior tympanic segment of the of the facial nerve canal or an
associated aberrant ICA (not present on this study).
R. Kumar et al. European Journal of Radiology 139 (2021) 109722

Fig. 11. Aberrant internal carotid artery.

A 57 year old female patient presenting with left sided PT. An
unenhanced CT temporal bone study was performed instead of
CT A–V, with axial (A) and coronal (B) bone weighted images
shown at the level of the middle ear cleft. They demonstrate an
anomalous lateral course of the left internal carotid artery
(ICA) (solid arrows) at the left middle ear cavity via an enlarged
inferior tympanic canaliculus. This then passes anteriorly
across the cochlear promontory to join the horizontal petrous
ICA through a dehiscent carotid plate. Note the normal
configuration of the right petrous ICA (arrowhead). CT A–V
would have depicted the internal carotid artery more
conspicuously by virtue of its intense enhancement.

4.1.4. Mixed aetiology then resolves, subsequently leading to an artery to sinus anastomosis
[47]. They can be known as a ‘dural AVF’ (dAVF) if there is a connection
4.1.4.1. Arteriovenous malformation and dural arteriovenous fistula. An between dural arteries and dural veins/venous sinuses. A dAVF is a well
arteriovenous malformation (AVM) is an abnormal collection of ectatic, recognised cause of PT, with PT being the initial symptom in over 10 %
dilated arteries and veins (nidus) which act as a shunt between the of patients with a dAVF [51–53]. One study suggested that the most
arterial and venous systems. They are congenital and often present in 40 common typical sites are the transverse sigmoid sinus (70 %), hypo­
or 50 year olds due to a high flow state which can lead to PT [47]. In the glossal canal (10 %) and middle cranial fossa (6.7 %) [52]. However the
head and neck, these AVMs are commonly found intracranially and can detection of a dAVF is challenging on CT A–V and can be missed if the
be confidently assessed with CT A–V given there is dual enhancement in degree of vascular enhancement is suboptimal, hence other indicators
the arterial and venous phases (Fig. 12). There are also reported cases of include the presence of dilated vessels, cerebral oedema or haemorrhage
PT secondary to parotid and external ear AVMs [48–50]. [6,9]. In particular, CT A–V may not detect a small AVM/dAVF due to
An arteriovenous fistula (AVF) is an acquired anomaly usually due to the lack of flow dynamics and magnetic resonance
thrombosis of a dural venous sinus secondary to a prior insult which arteriogram-venogram (MRAV) may not provide further

Fig. 12. Intracranial arteriovenous malformation.

A 76 year old female patient presented with left sided PT. CT A–V axial (A), coronal (B) and sagittal (C) post contrast images demonstrate asymmetric intracranial,
tortuous, dilated vessels at the peripheral aspect of the left parietal and temporal cortical lobes (solid arrows) in keeping with an arteriovenous malformation.

10
R. Kumar et al.
characterisation [6,8]. If there is ongoing high clinical suspicion
(objective PT, headache, dizziness, conjunctival/orbital congestion or
neurological symptoms) further imaging is warranted [54]. In such
cases, a DSA is a more sensitive test providing further characterisation
with the added benefit of treatment planning, and hence remains the
gold standard [6,8,55–57]. However, a caveat is that it is an invasive
procedure. 4D CT imaging is emerging as a promising new non-invasive
assessment tool which is comparable to DSA in providing data on flow
patterns and visualizing retrograde venous flow in cortical veins in
diagnosing dAVF [5,58].
4.2. Non-vascular causes
Non-vascular causes of PT are a rarer finding on CT A–V imaging.
They include glomus tumours, bone dysplasias such as otospongiosis
and Paget’s disease, and miscellaneous causes such as intraosseous
haemangiomas or mengingiomas.
4.2.1. Tumours
4.2.1.1. Paragangliomas / Glomus tumours. Pulsatile tinnitus is a well
recognised symptom of glomus tumours, specifically the tympanic
(glomus tympanicum) and jugular (glomus jugulare) types. The former
refers to a paraganglioma within the middle ear cavity while the latter
pertains to a paraganglioma within the jugular bulb; involvement at
both sites is described as a glomus jugulotympanicum.
Glomus tympanicum tumours are usually visible on otoscopic ex­
amination, but should be excluded on all CT A–V studies with the
presence or absence of such a tumour noted in the report. They usually
arise from glomus bodies anywhere along the Jacobsen nerve (tympanic
branch of the glossopharyngeal nerve), and typically present as a small
focal round mass with a flat base, usually sited at the cochlear prom­
ontory (Fig. 13) [6]. High resolution bone-weighted reconstructions are
11
European Journal of Radiology 139 (2021) 109722
essential to detect these small tumours on CT A–V. They can then extend
into the mesotympanum and towards the tympanic membrane whilst
larger lesions may erode the medial wall of the middle ear cavity and the
ossicular chain [11]. The floor of the middle ear cavity and jugular fo­
ramen are intact.
Jugular paragangliomas arise from glomus bodies in the jugular fo­
ramen, from the tympanic branch of the glossopharyngeal nerve or the
auricular branch of the vagus nerve [59]. They are frequently visible on
otoscopy in 75 % of patients [60]. These tumours are often larger than
tympanic paragangliomas and show diffuse enhancement. As the mass
expands, there is erosion of the adjacent petrous bone and a risk of
compression of the adjacent glossopharyngeal, vagus or accessory
nerves. There may also be compression of the internal jugular vein as it
exits the foramen. Many tumours extend superolaterally with perme­
ative destruction through the jugular plate into the hypo/­
mesotympanum (glomus jugulotympanicum) [61]. This can lead to
ossicular chain destruction. The tumour can also spread laterally to
involve the facial nerve canal and inferiorly into the infratemporal fossa
(Fig. 14) [62]. Differentials which must be considered on CT A–V for
mass lesions in the jugular foramen include nerve sheath tumours, me­
ningiomas, metastases, primary bone tumours e.g. myeloma, jugular
vein thrombosis or a dehiscent/high riding jugular bulb [63].
4.2.1.2. Meningiomas. Meningiomas, a slow growing benign tumour
arising from the meninges, can lead to adjacent bony hyperostosis and
sclerosis. If they are in contact with the temporal bone, there is a
theoretical risk of associated PT. On CT A–V, meningiomas should avidly
enhance and show a pathognomonic dural tail.
4.2.1.3. Hypervascular metastases. Any hypervascular metastases which
deposit in the temporal bone may lead to increased vascularity that may
be referred to the middle ear cleft, and hence audible as PT. Common
primary malignancies with hypervascular metastases include renal cell,
Fig. 13. Glomus tympanicum.
A 47 year old female patient presenting with left sided PT. The
patient was unable to tolerate otoscopy. Bone weighted CT A–V
axial (A) and coronal (B) images at the level of the middle ear
cleft demonstrate a 1 cm enhancing mass, closely applied to
the cochlear promontory (solid arrow). This is characteristic of
a glomus tympanicum tumour. The mass encases the stapes,
distal end of the long process of incus and partially involves the
handle of malleus. The tympanic floor is intact. Normal ap­
pearances of the right middle ear cavity are noted.
R. Kumar et al. European Journal of Radiology 139 (2021) 109722

Fig. 14. Glomus jugulare.

A 43 year old female patient presenting with right sided PT and normal otoscopy. CT A–V coronal (A), axial (B) and sagittal (C) images demonstrate a diffusely
enhancing, expansile soft tissue mass at the jugular foramen (dashed arrow) with associated erosive changes at the adjacent bone including the jugular spine, petrous
ICA and mastoid segment of the facial nerve. The tumour extends inferiorly into the infratemporal fossa (solid arrows). There is no extension into the middle ear cavity
and hence this was not detected on otoscopy.

thyroid, melanoma, neuroendocrine tumours, choriocarcinomas and lung cancers [65].

sarcomas [64]. However, the most common cancers to metastasise
specifically to the temporal bone are hematological malignancies and

Fig. 15. Otospongiosis.

A 41 year old female patient presenting with right sided PT and
bilateral conductive hearing loss. Bone weighted CT A–V axial
image at the level of the middle ear cleft demonstrates bilateral
foci of bony lucency at the anterior margin of the oval window
(fissula ante fenestram) in keeping with fenestral otospongiosis
(solid arrows). Bone reconstructions on CT A–V studies should
be performed to assess for this cause of PT.

12
R. Kumar et al.
4.2.2. Bone dysplasias
4.2.2.1. Otospongiosis. Otospongiosis (or otosclerosis) is an idiopathic
process with infiltration and foci of lucency within the petrous bone
which typically leads to conductive hearing loss. It can be associated
with the development of PT, with one study demonstrating that up to 11
% of patients can have underlying otopsongiosis [11,36,66]. This is
commonly fenestral (85 %) with hypoattenuated bone at the anterior
margin of the oval window (fissula ante fenestram) (Fig. 15) or less
commonly retrofenestral/cochlear (15 %) often at the basal turn of the
cochlea [16]. In chronic cases, the bone appears sclerotic. Assessment on
CT A–V relies on high resolution, axial, bone-weighted reconstructions
of the temporal bones.
4.2.2.2. Intraosseous haemangioma. An intraosseous haemangioma is a
well-defined, intradiploic, expansile mass with trabecular thickening
(polka dot pattern) which abuts the outer table of the calvarium. They
account for 10 % of benign neoplasms of the skull [67]. In the context of
pulsatile tinnitus, assessment should be focused at the temporal bone
and skull base, including the occipital condyles. CT A–V should identify
the lesion on bone windows (Fig. 16) however an MRI study often
confirms the diagnosis due to T1 and T2 hyperintensities (related to fat
and vascular contents respectively), confirming the diagnosis [68].
4.2.2.3. Paget’s disease. Paget’s disease at the skull base, particularly
the temporal bone, can be linked to PT due to diffuse bony expansion,
sclerosis and possibly associated intraosseous AV shunts [[16,69]. CT
A–V imaging, with appropriate differentials based on the clinical history
and other imaging findings, can be used to help determine whether this a
contributory factor in the patient’s PT.
5. Clinical value and limitations of CT A–V
In contrast to the other imaging modalities that are currently avail­
able, CT A–V is a quick ‘one-catch’ scan that can reliably identify the
majority of causes of PT. It is not the modality of choice in non-pulsatile
Fig. 16. Skull base intraosseous haemangioma.
A 40 year old male patient presented with right sided PT. An unenhanced CT temporal bone study with coronal (A) and axial (B) images demonstrate an expansile
lesion with a few calcific foci in the right occipital condyle, extending into the adjacent right mastoid air cells (solid arrow). MRI T2 STIR axial (C) image demonstrates
signal hyperintensities with signal voids within the lesion (dashed arrow). Findings would be consistent with an intraosseous haemangioma. Such bony dysplasias
should be excluded on all CT A–V studies.
13
European Journal of Radiology 139 (2021) 109722
tinnitus where MRI of the internal auditory meatus is preferred, typi­
cally to detect acoustic neuromas. Given that the majority of the rec­
ognised causes and associations of PT are benign and do not require
treatment, when detected on CT A–V it can provide reassurance to both
clinicians and patients that one or more likely ‘soft’ causes have been
identified and no action with only conservative management is required.
The true value of the scan is to reliably detect the harmful (aneurysm or
AVM) or treatable (otospongiosis or sigmoid plate dehiscence) causes of
PT. A diagnostic algorithm summarizing the role of CT A–V is provided
(Fig. 17).
Clinical and otoscopic assessment is crucial as this determines the
choice of subsequent imaging required. It is also necessary to clinically
assess for systemic causes for a more comprehensive evaluation of PT. It
is vital that the clinician provides essential information such as the side
of PT, whether it is arterial or venous in character and subjective or
objective in nature, to allow accurate radiological interpretation, espe­
cially in light of the many normal anatomical variants the radiologist
may encounter during imaging evaluation.
CT A–V is not without risks or limitations. There is radiation expo­
sure (average total DLP 240mGycm) and hence imaging needs to be
justified and preferably reserved for debilitating or progressive symp­
toms. CT A–V also requires intravenous contrast administration and
hence should be used with caution where there is significant renal
impairment and contraindicated with contrast allergy. In these situa­
tions, alternate non-contrast imaging such as a CT temporal bone study
and a MRI with a MRV study and MRA head and neck could be
considered. As noted earlier, CT A–V can also be suboptimal in the
evaluation of IIH and dAVF, where in the latter DSA is the gold standard
with 4D CT imaging emerging as a promising new non-invasive assess­
ment tool [5,58].
Given the myriad of aetiologies for PT that can be detected on CT
A–V, it is important that the reading radiologist is familiar with the
various causes and their imaging features. Indeed, a methodical and
thorough review is necessary to avoid under-reporting the potential
causes of PT. We have therefore devised a reporting checklist (Fig. 18)
for the radiologist which can help in providing a systematic and
comprehensive report for the CT A–V scan. Where necessary, discussion
R. Kumar et al. European Journal of Radiology 139 (2021) 109722

Fig. 17. Diagnostic algorithm for the use of CT A-V in pulsatile tinnitus.

Fig. 18. Reporting checklist provided for the assessment of pulsatile tinnitus on CT A-V.

14
R. Kumar et al.
at a multidisciplinary team meeting can provide insight into the clinical
significance and relevance of any incidental ‘soft’ radiologic findings
and normal variants, which may not be implicated in the patient’s PT.
6. Conclusion
There are many recognized causes of pulsatile tinnitus and they can
be broadly classified as vascular and non-vascular causes. CT A–V pro­
vides a quick, single ‘one catch’ imaging technique which can reliably
detect almost all causes of PT including those that are harmful and
treatable. A reporting checklist, supported by the relevant clinical in­
formation, allows a comprehensive and methodical approach in
reporting this examination.
Declaration of Competing Interest
There are no conflicts of interest to declare.
Acknowledgements
I would like to thank Mr. Sachin Samji, CT superintendent radiog­
rapher, for his advice and expertise pertaining to the pulsatile tinnitus
protocol utilised in our institution.
There has been no external funding.
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