Endovascular treatment of pulsatile tinnitus associated with

transverse sigmoid sinus aneurysms and jugular bulb anomalies

Felipe Padovani Trivelato, João Francisco Santoro Araújo, Rodrigo dos Santos Silva, Marco
Túlio Salles Rezende, Alexandre Cordeiro Ulhôa, and Guilherme Duarte Castro
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Abstract
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Introduction

Pulsatile tinnitus is a rare but very annoying symptom which has several possible causes, including a vascular and a non-vascular origin.1–3 It
may arise in arterial or venous structures, resulting from a turbulent blood flow due to an increase in blood volume or pressure or to changes
in the vessel lumen.4 Some vascular anomalies, such as dural arteriovenous fistulas and transverse sigmoid sinus stenosis, have been
frequently described as an aetiology.5,6

More recently, many authors have reported the association of pulsatile tinnitus with other anomalies of dural venous sinuses and the jugular
bulb, such as diverticula, aneurysms, and a high-riding or laterally placed jugular bulb. In such circumstances, mainly concomitantly with
disabling tinnitus, endovascular treatment has been successfully employed.1–4,7–13

We report an additional case of a patient harbouring a jugular bulb diverticulum (JBD) associated with transverse sigmoid sinus stenosis,
presenting with disabling pulsatile tinnitus. Moreover, we performed a literature review, focused on transverse sigmoid sinus aneurysms
(TSSA) and JBD, aiming to identify possible risk factors for developing the symptoms, as well as the safety and results of endovascular
treatment.

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Case report

A 45-year-old woman presented with a 2-year history of worsening left-side pulsatile tinnitus that recently became incapacitating. ENT
evaluation revealed no abnormalities. Neurological exam was normal. On physical examination, complete resolution of the tinnitus while
compressing the ipsilateral internal jugular vein was noted.

A temporal bone computed tomography (CT) scan showed a high-riding jugular bulb and enlargement of the left jugular foramen, with
erosion of the bony septum (Figure 1). Magnetic resonance angiography revealed hypoplasia of the right transverse sinus and stenosis in a
dominant left transverse sigmoid sinus transition. Digital subtraction angiography (DSA) confirmed these findings (Figure 2).

Figure 1.

Left: A temporal bone CT scan shows a high-riding jugular bulb and enlargement of the left jugular foramen, with erosion of the bony septum. Right: Coronal

contrasted CT scan demonstrates a high-riding jugular bulb.

Figure 2.

(a) and (b): DSA reveals left jugular diverticulum, hypoplasia of the right transverse sinus and stenosis in a dominant left transverse-sigmoid
sinus transition; (c): Control angiogram after left transverse-sigmoid sinus stenting and stent-assisted coiling of jugular diverticulum; (d): cast
of coils and stent.

Considering the intensity of the symptoms, we decided to perform invasive manometry. The patient was placed under dual antiplatelet
therapy (aspirin 100 mg and clopidogrel 75 mg daily) for 5 days before treatment. Under general anaesthesia and heparinization, a diagnostic
catheter was placed into the left internal carotid artery to perform a control angiogram (allowing venous navigation). The venous access
sheath was a construct of 11 F 80 cm length sheath (Arrow, Reading, Pennsylvania) and an 8 F-guiding catheter (Stryker, Kalamazoo,
Michigan). Through the venous access, a 0.027 inch Renegade microcatheter (Boston Scientific, Natick, Massachusetts) over a 0.014 inch
Transend microwire (Stryker, Kalamazoo, Michigan) was navigated across the area of stenosis and placed with the distal tip at the level of
the torcula. Cerebral venous pressure at various locations was measured by attaching a pressure transducer to the microcatheter. Manometry
revealed a gradient of 10 mmHg across the stenosis. Considering the progressive, incapacitating nature of the symptoms, we decided to treat
both conditions, namely sinus stenosis and JBD.

A 9 × 40 mm carotid Wallstent (Boston Scientific, Natick, Massachusetts) was deployed at the level of the transverse sigmoid sinus stenosis.
Post-stent angioplasty was not required. New manometry showed total resolution of the pressure gradient (equal to zero).

After stenting for sinus stenosis, we performed stent-assisted coiling of the JBD, because of the wide neck. A 9 × 30 mm Protegé stent (EV3,
Plymouth, Minnesota) was chosen because of the very acute angle. The JBD was totally occluded with 8 Axium coils (EV3, Plymouth,
Minnesota) (Figure 2). The patient experienced immediate complete regression of the pulsatile tinnitus. After 16 months, she was
asymptomatic and control CT scan showed the cast of coils inside jugular diverticulum (Figure 3).
Figure 3.

Upper and lower: Postoperative CT scan shows cast of coils inside jugular diverticulum.

Discussion

Tinnitus is a common condition that can be divided simply into non-pulsatile or pulsatile.8 A pulsatile pattern suggests a vascular cause, and
nonpathological causes include an aberrant internal carotid artery, a high or dehiscent jugular bulb or a jugular megabulb deformity.1 On the
other hand, pathological causes of pulsatile tinnitus include intracranial hypertension, tumours, dural arteriovenous fistulas, carotid artery
stenosis and venous sinus stenosis.1,8,11

Pulsatile tinnitus is likely of arterial origin when it worsens with gentle compression of the ipsilateral internal jugular vein, whereas it is
likely of venous origin if improves with such compression or with head rotation in the direction of the tinnitus, as both manoeuvres decrease
the jugular flow.2,3

More rarely, TSSA and JBD have been described as a cause of tinnitus. Furthermore, pulsatile tinnitus can become a very incapacitating
symptom and a therapeutic challenge. In such circumstances, endovascular treatment has shown to be a valid alternative. 1–4,7–13

Our literature search yielded 13 patients harbouring TSSA or JBD submitted to endovascular treatment (Table 1). Eight patients had TSSA
and five patients JBD. All patients presented with disabling pulsatile tinnitus. There were 11 women (84.6%) and two men. The mean age of
these patients was 43 years (range 24–71 years). Eight (61.5%) lesions were located at the right side and five at the left side. In all detailed
cases the dominant sinus was involved. Associated sinus stenosis was present in three cases (23%).

Table 1.

Summary of patients harbouring TSSA or JBD submitted to endovascular treatment *.

Author, Age, Venous Side Dominant EVT Associated Complication Follow-up

year sex lesion sinus anomaly

Houdart 33, TSS Left Yes Coiling None None 8 months –

et al., F aneurysm asymptomatic
2000

Sanchez 54, TSS Left Yes SAC None Cerebellar 12 months –

et al., M aneurysm ischemia asymptomatic
2002

Zenteno 38, TSS Left Yes SAC (2 None None 6 months –

et al., F aneurysm steps)+ asymptomatic
2004

Yoon 33, JBD Right Yes SAC None None 15 months –

et al., F asymptomatic
2008

Gard 48, TSS Left Yes Coiling None None 12 months –

et al., F aneurysm asymptomatic
2009

Mehanna 46, TSS Right Yes BAC None None 12 months –

et al., F aneurysm 90%
 Author, Age, Venous Side Dominant EVT Associated Complication Follow-up
year sex lesion sinus anomaly

2010 improvement

Park 31, TSS Right Yes Coiling None None 22 months –

et al., F aneurysm asymptomatic
2011

Signorelli 59, JBD Right Yes Stenting SS stenosis None 18 months –

et al., F asymptomatic
2012

Lenck 28, TSS Right Yes Coiling None None 7 year –

et al., F aneurysm asymptomatic
2012

Hitier 24, JBD Right NM SAC None None 24 months –

et al., M asymptomatic
2013

61, JBD Right NM SAC None None 12 months –

F tinnitus stable,
vertigo
improvement

Franco 59, TSS Right Yes Stenting SS stenosis None 6 months –

et al., F aneurysm asymptomatic
2012
 Author, Age, Venous Side Dominant EVT Associated Complication Follow-up
year sex lesion sinus anomaly

Current 45, JBD Left Yes SAC SS stenosis None 16 months –

case F asymptomatic

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*
All patients presenting with disabling pulsatile tinnitus.

+Surgical approach to stent placement (paratorcular burr hole).

TSS: transverse sigmoid sinus; JBD: jugular bulb diverticulum; EVT: endovascular treatment; SAC: stent-assisted coiling; BAC: balloon-assisted coiling; SS:
sigmoid sinus; NM: not mentioned.

Regarding endovascular treatment, six patients were submitted to stent-assisted coiling, four patients to simple coiling, two patients to sole
stenting and one patient to balloon-assisted coiling. A patient with a TSSA treated with stent-assisted coiling experienced a cerebellar
ischemia. On follow-up, nine patients were asymptomatic and two patients improved.

It is believed that venous sinus stenosis and a high-riding jugular bulb with diverticulum are associated with turbulent blood flow near the
middle ear, and therefore are responsible for objective pulsatile tinnitus.2,4,6,7 The fact that in 84.6% of patients the lesion is located in the
dominant sinus strengthens this theory. So, it is very reasonable to treat these patients, performing venous sinus stenting and JBD coiling, in
order to restore blood flow inside the sinus and avoid the transmission of pulse wave toward the middle ear. A pressure gradient of >8 mmHg
has been described as a cutoff between normal and abnormal.14

Endovascular treatment has been shown to be very safe. Only one (7.7%) complication was observed. Since the dominant sinus is involved,
in the majority of cases, it is mandatory to preserve its patency during treatment.

Although extremely rare, jugular diverticulum and TSSA should be considered as causes of pulsatile tinnitus. Tinnitus resolution with
jugular vein compression is an important diagnostic clue, and may be a positive predictive factor of therapeutic success. Therefore,
endovascular treatment should be offered to patients presenting with disabling tinnitus.

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Funding

This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.

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Conflict of interest

The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

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