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 ‘objective PT’ or when solely audible to the patient as ‘subjective PT’
[2].
Pulsatile tinnitus (PT) is defined as a repetitive, auditory perception The mechanism of PT is widely presumed to be secondary to either
that imitates the patient’s cardiac rhythm. This differs from non- abnormal blood flow due to acceleration/turbulent flow (likely objec­
pulsatile tinnitus which lacks a rhythmic quality, with less than 10 % tive PT) or normal flow with an increased perception of ordinary flow
of tinnitus patients developing pulsatile features [1]. This can manifest sounds due to sound conduction disturbances (likely subjective PT) [3].
as unilateral or bilateral ringing, buzzing or whistling, causing distress Hence the aetiology of PT can be divided into vascular or non-vascular
to the affected patient and adversely affecting their daily performance. categories (Table 1). Vascular character can be subdivided into arterial
When audible to both the patient and clinician, this is subclassified as 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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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 common due to background dominance of the right jugular vein in
A–V has been shown to demonstrate a significant association between 70–80 % of the population [10]. Venous dominance may also be a sol­
the side of the patient’s symptoms and the source of PT such as venous itary finding on CT A–V or can be associated with other causes [4,11].
dominance, suggesting a causal relationship and hence its utility in PT
assessment [4]. On encountering such various venous anatomical vari­ 4.1.1.2. Aberrant venous channels and prominent emissary veins. An
ants, their contributing relationship in a patient with PT needs to be aberrant venous channel is a prominent vein which traverses through
considered individually, correlating with the side of symptoms, clinical the head and neck and may be a developed collateral related to a hy­
examination and the presence of other potential causes. Mixed and poplastic sigmoid sinus or jugular vein (contralateral to the side of a
arterial causes are less common, the former includes arteriovenous dominant venous system). CT A–V with MPR can characterize the size,
malformations and the latter internal carotid artery stenoses (ICA) path, and relationships of the aberrant vessel. Increased flow in the
which are more frequent in the elderly population and hence should be aberrant vein can manifest as PT, particularly if it is in close proximity to
correlated with the clinical history and other imaging findings. 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
4.1.1. Venous causes must be correlated with the patient’s symptoms.
Emissary veins related to PT most commonly occur in the mastoid. A
4.1.1.1. Dominant jugular vein/sigmoid sinus. A dominant jugular or a mastoid emissary vein (MEV) is a venous tract which develops at the
sigmoid venous sinus is a common, incidental finding on CT A–V embryonic stage and by traversing the mastoid connects the sigmoid
(Fig. 2). The vessels are defined as co-dominant if there is ≤3 mm be­ sinus with the posterior auricular or occipital vein, allowing exit of
tween the diameters at the mid-transverse sinuses bilaterally [9]. If there diploic venous blood [12]. They can be unilateral or bilateral (Fig. 4).
is a difference of >3 mm, the side with the larger diameter is regarded as This may be a solitary finding on CT A–V or be associated with a hy­
the side with the dominant cerebral venous system [9]. With a history of poplastic sigmoid sinus or jugular vein. Such emissary veins are valve­
PT, a significant association has been shown on CT A–V between a less allowing bidirectional flow which can lead to turbulence, increased
dominant jugular vein or sigmoid sinus and the ipsilateral side of the velocity or increased intracranial pressure leading to increased flow, all
patient’s symptoms, with increased turbulent flow through the larger potentially audible through the mastoid as PT. [13]. The size of the vein
venous system postulated as a contributory factor [4]. It has been shown may also be important as suggested by a recent report reviewing a case
that without another underlying cause, right sided venous PT is more of PT related to a single large MEV [13]. Other radiologically evident

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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 4.1.2. Venous-osseous causes
condylar veins (courses between the superior bulb of the internal jugular
vein and deep cervical vein) and occipital emissary veins (drains from 4.1.2.1. High riding jugular bulb and dehiscent jugular bulb. A high riding
the confluence of the sinuses into the internal vertebral plexus) [12] jugular bulb is a normal variant and a recognised cause of PT, more
which theoretically could transit flow related sounds to the mastoid. 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
4.1.1.3. Venous stenosis. Venous sinus stenosis describes a sudden being posterosuperior to the floor of the internal auditory canal (IAC).
change in venous calibre. This can be intrinsic narrowing due to acute The jugular bulb consequently lies at the level of the basal turn of the
venous sinus thrombosis or due to post thrombotic related fibrosis. cochlea (Fig. 6). The jugular foramen and sigmoid plate are intact with
Venous stenosis can also be secondary to extrinsic compression and no extension into the middle ear cavity. The presence of a high riding
subsequently lead to PT. CT A–V with MPR evaluation can identify jugular bulb is also important to report for surgical planning during a
extrinsic compression of the suprahyoid internal jugular vein (IJV) mastoidectomy. However, given jugular bulb variations are normal
typically caused by the C1 transverse process, styloid process or poste­ variants and hence can be noted incidentally in asymptomatic patients,
rior belly of digastric (Fig. 5) [4]. Elevated intracranial CSF pressure can care must be taken to ensure there are no other causes of PT on the study.
also lead to external compression of the sigmoid and transverse sinuses. A dehiscent jugular bulb, whilst also considered a normal variant,
It has been postulated that this results in turbulent venous flow due to has been associated with PT in the literature [16,18,19]. On CT A–V,
stenosis or periodic narrowing caused by arterial narrowing secondary there is superolateral extension of the jugular bulb through a dehiscent
to pulsating arteries, the affects of which are transmitted to the venous petrous septum of the sigmoid plate and into the middle ear cavity
sinuses across the CSF space [14]. This can then create a vicious feed­ where it can contact the ossicles, restricting their mobility, or invade the
back loop leading to a further increase in intracranial pressure and bony labyrinth leading to conductive hearing loss. This should be
consequently increasing venous narrowing which may present as PT [3, reviewed on high resolution bone windows on CT A–V (Fig. 7). This may
15]. However, narrowing of the venous sinuses, related to contralateral be seen otoscopically as a retrotympanic blue mass. A jugular bulb
dominance, is a common incidental finding. Hence true pathological diverticulum arises as a focal outpouching of the bulb, most commonly
venous stenosis should be considered when there are signs of raised superior and posterior to the IAC, and protrudes into the temporal bone
intracranial pressure/idiopathic intracranial hypertension (IIH), taking (anterior, posterior and medial positions are also possible) [16,20].
into account the laterality of PT and excluding other causes. 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].

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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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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 the sigmoid sinus, however with dehiscence, flow sounds may be
plate dehiscence and diverticulum formation have been associated with transmitted into the mastoid and cochlea leading to PT (Fig. 8) [26].
PT in up to 20 % of cases [22,23]. These abnormalities are one of the few Extensive pneumatisation of the mastoid segment of the temporal bone
surgically correctable causes of PT with successful resolution of symp­ is thought to amplify this phenomenon [27]. A sigmoid plate divertic­
toms reported post treatment in several studies [23–25]. An intact sig­ ulum is believed to arise from forceful flow in the adjacent sigmoid sinus
moid plate is likely to insulate vibrations from the adjacent flow through 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) cortical bone overlying the sinus or the ‘air on sinus’ sign (mastoid air
[26]. PT is widely thought to result from the consequent turbulent flow cells directly contact the sinus wall) [23]. The affected side and
in the pouch (46). It is more common on the side of the dominant venous maximum diameter of the dehisced segment should be reported because
sinus but with a similar prevalence on both sides in co-dominant systems sigmoid plate dehiscence can also be an incidental finding, hence the
[26,28,29]. size and side affected should be correlated clinically. [31]. A divertic­
On CT A–V, bone window assessment of the sigmoid plate using the ulum can be more readily identified on CT A–V bone windows as an
acquired high resolution bone reformats should be performed, with outpouching from the sigmoid sinus into the mastoid with venous phase
dehiscence/diverticulum more likely noted on the dominant side of enhancement. The AP and transverse circumference on axial images of a
venous outflow and within the lateral wall of the sigmoid plate [28]. On sigmoid plate diverticulum can be measured and reported, aiding sur­
review of the literature, there remains no apparent size classification for gical management.
sigmoid plate dehiscence. Consequently, various studies have used
different criteria to identify dehiscence such as a minimum width of 4.1.2.3. Idiopathic intracranial hypertension. There has been a known
5 mm on 2 consecutive slices [4,30]. Eisemann reported the following association in the literature between IIH and PT [15,32]. The aetiology
criteria as useful in identifying dehiscence/diverticulae: irregularity of is complex; external compression (e.g. styloidogenic, posterior belly of
the bony sigmoid sinus wall, focal thinning of the calvarial cortex digastric or C1 transverse process) with IJV stenosis, dural sinus stenosis
overlying the adjacent sinus wall, absence of the normal thin layer of

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

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

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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 4.1.3.5. Vascular loops. Vascular loops within the cerebellar-pontine
assessing for indirect signs of its existence. This includes absence of the angle (CPA) are common incidental findings [41,42] but are also
foramen spinosum (however this can be a normal finding in 3% of cases another recognised cause of PT [43]. They frequently arise from the
[40] (Fig. 10), subtle enlargement of the anterior tympanic segment of anterior inferior cerebellar artery (AICA) and can contact or compress
the facial nerve canal or an associated aberrant ICA [11]. DSA can be the vestibulocochlear nerve [44]. Reports have suggested that distortion
used for confirmation if required [16]. of the vestibulocochlear nerve at the intrameatal segment towards the
fundus rather than the cisternal segment at the nerve root entry zone
4.1.3.4. Aberrant internal carotid artery. An aberrant ICA is another may result in PT [45] with improvement post surgical treatment [46].
congenital variant which can lead to PT. This vascular anomaly arises Vascular loops can be confidently identified on CT A–V by assessing the
due to absent formation of the extracranial ICA, leading to the devel­ CPA and internal auditory meatus (IAM) in both the axial and coronal
opment of an arterial collateral. This runs horizontally through the planes. However, given these are frequent incidental findings, further
middle ear cavity, entering through an enlarged inferior tympanic characterisation with heavily T2 weighted high resolution MRI IAM
canaliculus, coursing anteriorly across the cochlear promontory, then imaging should be reserved for those cases with vascular loops
entering the carotid canal due to dehiscence of the carotid plate traversing at or near the IAM fundus when no other cause of PT has been
(Fig. 11). The transfer of pulsating sounds by bone conduction to the identified.
inner ear may be the cause of PT. 30 % have a coexisting persistent
stapedial artery [40].

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).

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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.

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

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

11
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.

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

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

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.

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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. European Journal of Radiology 139 (2021) 109722

at a multidisciplinary team meeting can provide insight into the clinical [19] S. Koesling, P. Kunkel, T. Schul, Vascular anomalies, sutures and small canals of the
temporal bone on axial CT, Eur. J. Radiol. 54 (2005) 335–343.
significance and relevance of any incidental ‘soft’ radiologic findings
[20] H.K. El-Kashlan, H.A. Arts, S. Gebarski, Jugular diverticulum: clinical significance,
and normal variants, which may not be implicated in the patient’s PT. Otolaryngol. Head Neck Surg. 122 (4 April) (2000) 575–576, https://doi.org/
10.1067/mhn.2000.104640.
[21] T. Gejrot, Retrograde jugulography in the diagnosis of abnormality of the superior
6. Conclusion
bulb of the internal jugular vein, Acta Otolaryngol. 57 (1964) 177–180.
[22] D.E. Mattox, P. Hudgins, Algorithm for evaluation of pulsatile tinnitus, Acta
There are many recognized causes of pulsatile tinnitus and they can Otolaryngol. 128 (2008) 427Y31.
be broadly classified as vascular and non-vascular causes. CT A–V pro­ [23] D.J. Eisenman, Sinus wall reconstruction for sigmoid sinus diverticulum and
dehiscence: a standardized surgical procedure for a range of radiographic findings,
vides a quick, single ‘one catch’ imaging technique which can reliably Otol. Neurotol. 32 (2011) 1116Y9.
detect almost all causes of PT including those that are harmful and [24] R. Zeng, G.P. Wang, Z.H. Liu, X.H. Liang, P.F. Zhao, Z.C. Wang, S.S. Gong, Sigmoid
treatable. A reporting checklist, supported by the relevant clinical in­ sinus wall reconstruction for pulsatile tinnitus caused by sigmoid sinus wall
dehiscence: a single-center experience, PLoS One 11 (10 October) (2016)
formation, allows a comprehensive and methodical approach in e0164728, https://doi.org/10.1371/journal.pone.0164728, 13.
reporting this examination. [25] A.C. Wang, A.N. Nelson, C. Pino, P.F. Svider, R.S. Hong, E. Chan, Management of
sigmoid sinus associated pulsatile tinnitus: a systematic review of the literature,
Otol. Neurotol. 38 (10 December) (2017) 1390–1396, https://doi.org/10.1097/
Declaration of Competing Interest MAO.0000000000001612.
[26] Z. Liu, C. Chen, Z. Wang, S. Gong, J. Xian, Y. Wang, X. Liang, X. Ma, Y. Li, Sigmoid
There are no conflicts of interest to declare. sinus diverticulum and pulsatile tinnitus: analysis of CT scans from 15 cases, Acta
Radiol. 54 (7) (2013) 812–816, https://doi.org/10.1177/0284185113481698.
Epub 2013 Apr 30. PMID: 23550183.
Acknowledgements [27] L. Zhaohui, Sigmoid sinus diverticulum and pulsatile tinnitus: analysis of CT scans
from 15 cases, Acta radiol. 54 (2013) 812–816, https://doi.org/10.1177/
0284185113481698.
I would like to thank Mr. Sachin Samji, CT superintendent radiog­ [28] P. Zhao, H. Lv, C. Dong, Y. Niu, J. Xian, Z. Wang, CT evaluation of sigmoid plate
rapher, for his advice and expertise pertaining to the pulsatile tinnitus dehiscence causing pulsatile tinnitus, Eur Radio 26 (2016) 9–14, https://doi.org/
protocol utilised in our institution. 10.1007/s00330-015-3827-8.
[29] A. Grewal, H. Kim, R. Comstock, F. Berkowitz, H.J. Kim, A. Jay, Clinical
There has been no external funding. presentation and imaging findings in patients with pulsatile tinnitus and sigmoid
sinus Diverticulum/Dehiscence, Otology & Neurotol. Am. Otological Soc. Am.
References Neurotol. Soc. Euro. Acad. Otology Neurotol. 35 (2013), https://doi.org/10.1097/
MAO.0b013e31829ab6d7.
[30] J.A. Lansley, W. Tucker, M.R. Eriksen, P. Riordan-Eva, S.E.J. Connor, Sigmoid sinus
[1] M.L. Kircher, R.T. Standring, J.P. Leonetti, Neuroradiologic assessment of pulsatile
diverticulum, dehiscence, and venous sinus stenosis: potential causes of pulsatile
tinnitus, Otolaryngol. Head Neck Surg. 139 (Suppl) (2008) 144.
tinnitus in patients with idiopathic intracranial hypertension? Am. J. Neuroradiol.
[2] A. Sismanis, Pulsatile tinnitus, Otolaryngolic Clin. North Am. 36 (2 April) (2003)
38 (9 September) (2017) 1783–1788, https://doi.org/10.3174/ajnr.A5277.
389–402.
[31] C. Dong, P. Zhao, Z. Liu, W. Xu, H. Lv, S. Pang, Z. Wang, Association between the
[3] E. Hofmann, R. Behr, T. Neumann-Haefelin, K. Schwager, Pulsatile tinnitus:
extent of sigmoid sinus dehiscence and an occurrence of pulsatile tinnitus: a
imaging and differential diagnosis, Arztebl. Int. 110 (26) (2013) 451–458, https://
retrospective imaging study, Clin. Radiol. 71 (9) (2016) 883–888.
doi.org/10.3238/arztebl.2013.0451.
[32] A. Rohr, L. Dörner, R. Stingele, R. Buhl, K. Alfke, O. Jansen, Reversibility of venous
[4] P. Mundada, A. Singh, R. Lingam, CT arteriography and venography in the
sinus obstruction in idiopathic intracranial hypertension, Am. J. Neuroradiol. 28 (4
evaluation of pulsatile tinnitus with normal otoscopic examination, Laryngoscope
April) (2007) 656–659.
125 (2014), https://doi.org/10.1002/lary.25010.
[33] S.R. Dashti, P. Nakaji, Y.C. Hu, D.F. Frei, A.A. Abla, T. Yao, D. Fiorella,
[5] H.G.J. Kortman, E.J. Smit, M.T.H. Oei, R. Manniesing, M. Prokop, F.J.A. Meijer,
Styloidogenic jugular venous compression syndrome: diagnosis and treatment: case
4D-CTA in neurovascular disease: a review, AJNR Am. J. Neuroradiol. 36 (2015)
report, Neurosurgery 70 (3 March) (2012) E795–E799, https://doi.org/10.1227/
1026–1033.
NEU.0b013e3182333859.
[6] S. Joert, S.A.H. Pegge, S.C.A. Steens, H.P.M. Kunst, F.J.A. Meijer, Pulsatile
[34] H. Suzuki, J. Takanashi, K. Kobayashi, K. Nagasawa, K. Tashima, Y. Kohno, MR
Tinnitus: Differential Diagnosis and Radiological Work up, Curr. Radiol. Rep. 5 (1)
imaging of idiopathic intracranial hypertension, Am. J. Neuroradiol. 22 (1
(2017) 5, https://doi.org/10.1007/s40134-017-0199-7.
January) (2001) 196–199.
[7] M. Shweel, B. Hamdy, Diagnostic utility of magnetic resonance imaging and
[35] D. de Ridder, D. Menovsky, P. van de Heyning, An otoneuro - surgical approach to
magnetic resonance angiography in the radiological evaluation of pulsatile
non-pulsatile and pulsatile tinnitus, B-ENT. 3 (Suppl 7) (2007) 79–86.
tinnitus, Am. J. Otolaryngol. 34 (6) (2013) 710–717.
[36] S.D. Sharma, C. Offiah, M. Williams, J. Williams, N. Patel, Pulsatile tinnitus: a
[8] G. Madani, S.E.J. Connor, Imaging in pulsatile tinnitus, Clin. Radiol. 64 (3 March)
review, BENT 13 (2017) 251–257.
(2009) 319–328, https://doi.org/10.1016/j.crad.2008.08.014. Epub 2008 Nov 5.
[37] E. Hofmann, R. Behr, T. Neumann-Haefelin, K. Schwager, Pulsatile Tinnitus:
[9] A. Krishnan, D.E. Mattox, A.J. Fountain, P.A. Hudgins, CT Arteriography and
imaging and differential diagnosis, Arztebl. Int. 110 (26 June) (2013) 451–458,
Venography in Pulsatile Tinnitus: Preliminary Results, Am. J. Neuroradiol. 27 (8
https://doi.org/10.3238/arztebl.2013.0451. Epub 2013 Jun 28.
September) (2006) 1635–1638.
[38] Y. Shimizu, M. Yagi, Pulsatile tinnitus and carotid artery dissection, Auris Nasus
[10] D.R. Friedmann, J. Eubig, M. McGill, S.B. Babb, B.K. Pramanik, A.K. Lalwani,
Larynx 45 (1 Febuary) (2018) 175–177, https://doi.org/10.1016/j.
Development of the jugular bulb: a radiologic study, Otol. Neurotol. 32 (2011)
anl.2016.12.004.Epub2017Jan23.
1389–1395.
[39] J.R. Austin, D.R. Maceri, Anterior communicating artery aneurysm presenting as
[11] B.L. Koch, B.E. Hamilton, P.A. Hudgins, H.R. Harnsberger, Diagnostic Imaging:
pulsatile tinnitus, ORL J. Otorhinolaryngol. Relat. Spec. 55 (1) (1993) 54–57.
Head and Neck, 3rd ed., Elsevier, Philadelphia, 2016.
[40] L.E. Ginsberg, S.W. Pruett, M.Y. Chen, A.D. Elster, Skull base foramina of the
[12] Y. Pekçevik, P. Rıdvan, Why should we report posterior fossa emissary veins?
middle cranial fossa: reassessment of normal variation with high resolution CT,
Diagn. Interv. Radiol. 20 (1) (2014) 78–81, https://doi.org/10.5152/
AJNR 15 (2) (1994) 238–291.
dir.2013.13203.
[41] A.E. Makins, T.P. Nikolopoulos, C. Ludman, G.M. O’Donoghue, Is there a
[13] S.H. Lee, S. Kim, K.Y. Sung, E.C. Nam, Pulsatile tinnitus caused by a dilated
correlation between vascular loops and unilateral auditory symptoms?
mastoid emissary vein, J. Korean Med. Sci. 28 (2013) 628–630, https://doi.org/
Laryngoscope 108 (1998) 1739–1742.
10.3346/jkms.2013.28.4.628.
[42] B. Schick, D. Brors, O. Koch, M. Schäfers, G. Kahle, Magnetic resonance imaging in
[14] A. Sismanis, Otologic manifestations of benign intracranial hypertension
patients with sudden hearing loss, tinnitus and vertigo, Otol. Neurotol. 22 (2001),
syndrome: diagnosis and management, Laryngoscope 97 (8 pt 2 suppl 42) (1987)
808–1.
1–17.
[43] N.A. Ramly, A.R. Roslenda, A. Suraya, A. Asma, Vascular loop in the
[15] J. Ding, J. Guan, X. Ji, R. Meng, Cerebral venous sinus stenosis may cause
cerebellopontine angle causing pulsatile tinnitus and headache: a case report, Excli
intracranial arterial hypoperfusion, Clin. Neuroradiol. 30 (2 June) (2020)
J. 13 (2014) 192–196.
409–411, https://doi.org/10.1007/s00062-019-00833-w.
[44] H.N. Kim, Y.H. Kim, I.Y. Park, G.R. Kim, I.H. Chung, Variability of the surgical
[16] S. Vattoth, R. Shah, J.K. Curé, A compartment-based approach for the imaging
anatomy of the neurovascular complex of the cerebellopontine angle, Ann. Otol.
evaluation of tinnitus, Am. J. Neuroradiol. 31 (2 Febuary) (2010) 211–218,
Rhinol. Laryngol. 99 (4 Pt 1 April) (1990) 288–296, https://doi.org/10.1177/
https://doi.org/10.3174/ajnr.A1704.
0003489490099004.
[17] R. Hourani, J. Carey, D.M. Yousem, Dehiscence of the jugular bulb and vestibular
[45] V. Nowé, D. De Ridder, P.H. Van de Heyning, X.L. Wang, J. Gielen, J. Van
aqueduct: findings on 200 consecutive temporal bone computed tomography scans,
Goethem, O. Ozsarlak, A.M. De Schepper, P.M. Parizel, Does the location of a
J. Comput. Assist. Tomogr. 29 (5 September-October) (2005) 657–662, https://doi.
vascular loop in the cerebellopontine angle explain pulsatile and non-pulsatile
org/10.1097/01.rct.0000175499.34213.5d.
tinnitus? Eur. Radiol. 14 (2004) 2282–2289.
[18] M.A. El-Begermy, A.N. Rabie, A novel surgical technique for management of
tinnitus due to high dehiscent jugular bulb, Otolaryngol. Head Neck Surg. 142 (4
April) (2010) 576–581, https://doi.org/10.1016/j.otohns.2009.12.007.

15
R. Kumar et al. European Journal of Radiology 139 (2021) 109722

[46] D. De Ridder, L. De Ridder, V. Nowé, H. Thierens, P. Van de Heyning, A. Møller, [58] T.R. Beijer, E.J. van Dijk, J. de Vries, S.E. Vermeer, M. Prokop, F.J. Meijer, 4D-CT
Pulsatile tinnitus and the intrameatal vascular loop: why do we not hear our angiography differentiating arteriovenous fistula subtypes, Clin. Neurol.
carotids? Neurosurgery 57 (2005) 1213–1217. Neurosurg. 115 (8) (2013) 1313–1316.
[47] A.E. Conlin, E. Massoud, E. Versnick, Tinnitus: identifying the ominous causes, [59] M.A. Steiner, M. Khan, B.B. May, B. Schlakman, V. Vijayakumar, Giant recurrent
CMAJ. 183 (18) (2011) 2125–2128, https://doi.org/10.1503/cmaj.091521. glomus jugulotympanicum with intracranial, extracranial, and nasophayngeal
[48] M.C. Chen, W.Y. Chung, C.B. Luo, H.M. Wu, Arteriovenous malformation in the extension: the imaging role in clinical management, Radiol. Case Rep. 4 (4) (2015)
parotid region presenting as pulsatile tinnitus: a case report, Head Neck 32 (2009) 314, https://doi.org/10.2484/rcr.v4i4.314. Published 2015 Nov 6.
262–267, https://doi.org/10.1002/hed.21063. [60] K. Kumar, R. Ahmed, B. Bajantri, A. Singh, H. Abbas, E. Dejesus, R.R. Khan,
[49] M.C. Chen, C.W. Lin, Facial arteriovenous malformation with pulsatile tinnitus: a M. Niazi, S. Chilimuri, Tumors presenting as multiple cranial nerve palsies, Case
potentially curable cause of chronic insomnia, Short Commun. Neuropsychiatry 8 Rep. Neurol. 9 (1 April) (2017) 54–61, https://doi.org/10.1159/000456538, 3.
(2) (2018). [61] K.Y. Lee, Y.W. Oh, H.J. Noh, Y.J. Lee, H.S. Yong, E.Y. Kang, K.A. Kim, N.J. Lee,
[50] H.J. Woo, S.Y. Song, Y.D. Kim, C.H. Bai, Arteriovenous malformation of the Extra-adrenal paragangliomas of the body: imaging features, AJR Am. J.
external ear: a case report, Auris Nasus Larynx 35 (4) (2008) 556–558. Roentgenol. 187 (2 August) (2006) 492–504, https://doi.org/10.2214/
[51] D. Waldvogel, P.H. Mattle, M. Sturzenegger, G. Schroth, Pulsatile tinnitus–a review AJR.05.0370. PMID: 16861555.
of 84 patients, J. Neurol. 245 (1998) 137–142. [62] A.B. Rao, K.K. Koeller, C.F. Adair, Paragangliomas of the head and neck:
[52] Y.H. An, S. Han, M. Lee, J. Rhee, O.K. Kwon, G. Hwang, Y.Bae C.Jung, G. An, radiologic-pathologic correlation. From the archives of the Armed Forces Institute
K. Lee, J.W. Koo, J.J. Song, Dural arteriovenous fistula masquerading as pulsatile of Pathology, Radiographics 19 (6) (1999) 1605–1632, https://doi.org/10.1148/
tinnitus: radiologic assessment and clinical implications, Sci. Rep. 6 (2016) 36601, radiographics.19.6.g99no251605.
https://doi.org/10.1038/srep36601. [63] K.S. Caldemeyer, V.P. Mathews, B. Azzarelli, R.R. Smith, The jugular foramen: a
[53] K.B. Remley, W.E. Coit, H.R. Harnsberger, W.R. Smoker, J.M. Jacobs, E.B. Mclff, review of anatomy, masses, and imaging characteristics, RadioGraphics 17 (1997)
Pulsatile tinnitus and the vascular tympanic membrane: CT,MR,and angiographic 1123–1139.
findings, Radiology 174 (2 Febuary) (1990) 383–389, https://doi.org/10.1148/ [64] A.C. Silva, J.M. Evans, A.E. McCullough, M.A. Jatoi, H.E. Vargas, A.K. Hara, MR
radiology.174.2.2296650. imaging of hypervascular liver masses: a review of current techniques,
[54] I.G. Padilha, F.T. Pacheco, A.I.R. Araujo, R.H. Nunes, C.E. Baccin, M.L.M. Conti, A. Radiographics 29 (2) (2009) 385–402.
C.M. Maia Jr., A.J.D. Rocha, Tips and tricks in the diagnosis of intracranial dural [65] K. Song, K.W. Park, J.H. Heo, I.C. Song, Y.H. Park, J.W. Choi, Clinical
arteriovenous fistulas: a pictorial review, J. Neuroradiol. 47 (5 September) (2020) characteristics of temporal bone metastases, Clin. Exp. Otorhinolaryngol. 12 (1)
369–381, https://doi.org/10.1016/j.neurad.2019.06.004. (2019) 27–32, https://doi.org/10.21053/ceo.2018.00171.
[55] J. Narvid, CT angiography as a screening tool for dural arteriovenous fistulas in [66] N. Deggouj, S. Castelein, J.M. Gerard, M. Decat, M. Gersdorff, Tinnitus and
patients with pulsatile tinnitus: feasibility and test characteristics, Am. J. otosclerosis, BENT 5 (4) (2009) 241–244.
Neuroradiology. 32 (3) (2011) 446–453. [67] A.P. Escoda, P.N. Baudin, P. Mora, M. Cos, J.H. Ganan, J.A. Narvaez, C. Aguilera,
[56] B.J. Kwon, MR imaging findings of intracranial dural arteriovenous fistulas: C. Majos, Imaging of skull vault tumors in adults, Insights Imaging 11 (2020) 23,
relations with venous drainage patterns, Am. J. Neuroradiology. 26 (10) (2005) https://doi.org/10.1186/s13244-019-0820-9.
2500–2507. [68] I. Mitra, M. Duraiswamy, J. Benning, H.M. Joy, Imaging of focal calvarial lesions,
[57] C. Deuschl, S. Göricke, C. Gramsch, N. Özkan, G. Lehnerdt, O. Kastrup, Clin. Radiol. 71 (2016) 389–398.
A. Ringelstein, I. Wanke, M. Forsting, M. Schlamann, Value of DSA in the [69] I. Mackenzie, C. Young, W.D. Fraser, Tinnitus and Paget’s disease of bone,
diagnostic workup of pulsatile tinnitus, PLoS One 10 (2 Febuary) (2015) e0117814, J. Laryngol. Otol. 120 (2006) 899–902. Epub 2006 Sep 29.
https://doi.org/10.1371/journal.pone.0117814, 17.

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