26
Temporal Bone: Vascular Tinnitus
William W.M. Lo and M. Marcel Maya
ARTERIAL CAUSES
Atherosclerosis
Fibromuscular Dysplasia
Dissection of the Carotid or Vertebral Artery
Styloid Carotid Compression
Petrous Carotid Aneurysm
Aberrant Carotid Artery
Laterally Displaced Carotid Artery
Persistent Stapedial Artery
Miscellaneous Arterial Anomalies
ARTERIOVENOUS CAUSES
Paraganglioma
Miscellaneous Vascular Head and Neck
Tumors
Paget’s Disease
Tinnitus is a broad and complex subject concerning a
symptom, rather than a syndrome or a disease.1 The
following discussion is confined to tinnitus from vascular
causes.
Tinnitus may be caused by an intrinsic process such as
vestibulocochlear disease, or it may have an extrinsic
muscular or vascular cause.1 Intrinsic tinnitus is subjec-
tive, being audible only to the patient, and extrinsic
tinnitus is often objective, being potentially although not
always audible to the examiner as well as to the patient.
Although muscular tinnitus such as myoclonus of the
palatal muscles or of the tensor tympani muscle can be
pulsatile, it is not usually pulse-synchronous. By com-
parison, vascular tinnitus is always pulse-synchronous, and
it is often a recordable sound audible to the examiner as a
bruit.1 However, whether a vascular tinnitus can be
classified as objective may depend on the thoroughness of
the search, the equipment used, and the level of ambient
noise.2, 3
Tinnitus is a common complaint affecting some 30 to 40
million Americans.4 In the majority of cases, it is subjective
and may be associated with numerous conditions including
conductive or sensorineural hearing loss and brainstem and
cortical lesions.1 When tumor, anomaly, or trauma is the
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Otosclerosis or Otospongiosis
Cerebral Head and Neck Arteriovenous
Malformation
Dural Arteriovenous Fistula
Direct Arteriovenous Fistula
VENOUS CAUSES
Venous Tinnitus in Systemic Conditions
Venous Tinnitis in Intracranial Hypertension
Venous Tinnitus Caused by Transverse Sinus
Stenosis
Venous Tinnitus Associated with a Large or
Exposed Jugular Bulb or Large Emissary
Veins
Idiopathic Venous Tinnitus
RADIOLOGIC INVESTIGATION
suspected cause, the patient usually receives a radiologic
evaluation. However, the majority of tinnitus cases are
caused by Meniere’s disease or syndrome, viropathies,
drugs, allergy, noise, or systemic diseases, and the patients
do not come to the attention of the radiologist.5 Unfortu-
nately, the cause of subjective tinnitus is often unclear, and
effective treatment is lacking.
By contrast, although it is far rarer, objective tinnitus can
usually be traced to a specific cause. In the case of vascular
tinnitus, the radiologist tends to have a more active role in
the diagnosis and treatment of this entity.
The causes of vascular tinnitus may be arterial, arteriove-
nous, or venous (Box 26-1). Some authors believe that
paragangliomas are the most common cause of vascular
tinnitus, but others cite dural arteriovenous fistula (AVF),
idiopathic venous tinnitus, or idiopathic intracranial hyper-
tension as being the most common causes.3, 6–10 The
experience of different authors likely reflects their individ-
ual expertise and referral patterns. Interestingly, in Remley
et al.’s series of 107 patients with pulsatile tinnitus and a
vascular retrotympanic mass, paraganglioma was the most
common cause of subjective tinnitus, while dural and
extracranial AVFs were the most common causes of
objective tinnitus.11
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BOX 26-1
VASCULAR TINNITUS: CAUSES
Arterial
Atherosclerosis
Fibromuscular dysplasia
Arterial dissection
Styloid carotid compression
Petrous carotid aneurysm
Aberrant carotid artery
Laterally displaced carotid artery
Persistent stapedial artery
Miscellaneous arterial anomalies
Arteriovenous (AV)
Paraganglioma (tympanicum, jugulare)
Miscellaneous vascular tumors
Paget’s disease of bone
Otosclerosis or spongiosis
Cerebral AV malformation
Dural sinus AV fistula
Direct AV fistula
Venous
Chronic anemia
Pregnancy
Thyrotoxicosis
Hypertensive patients on vasodilators
Intracranial hypertension
Transverse sinus stenosis
Idiopathic venous tinnitus with or without large or
exposed jugular bulb or large emissary vein
ARTERIAL CAUSES
The arterial causes of tinnitus include abnormalities in
the lumen and abnormalities in the course. Aberrant arteries
are rare but exceedingly important because of the hazards of
mistreatment they invite when mistaken for tumors. They
are discussed in greater detail in Chapter 21.
Atherosclerosis
Atherosclerotic plaques may produce turbulence of
carotid flow and occasionally cause pulsatile tinnitus.
However, in proportion to its high prevalence as a cause of
asymptomatic carotid bruit, atherosclerosis is not a common
cause of symptomatic pulsatile tinnitus.12 This may be
because the stenosis or luminal irregularity usually lies at the
origin of the internal or external carotid artery, distant from
the petrous bone.13 Nonetheless, some cases have been
reported.14–17 In a report of eight patients with objective
tinnitus caused by atherosclerotic carotid artery disease,
tinnitus was the presenting symptom in five; however, no
patient in the series required surgery or angioplasty for relief
of symptoms.15 On rare occasions, contralateral carotid
artery stenosis or occlusion, or stenosis in the proximal
brachiocephalic arteries, have also been reported as causes
of pulsatile tinnitus.18–21 Transluminal angioplasty and
stenting may be performed on those lesions that are not
readily accessible to surgical endarterectomy.22, 23 Trans-
mitted cardiac murmurs have also been implicated.3
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Fibromuscular Dysplasia
Among the stenotic arteries, fibromuscular dysplasia
(FMD), a segmental nonatheromatous, noninflammatory
angiopathy of unknown etiology, is probably the most
important cause of pulsatile tinnitus.24–30 FMD, seen in
0.5% to 0.6% of carotid angiograms and autopsies, is the
second most common cause of extracranial carotid narrow-
ing.12, 25 It is due to a fibroblastlike transformation of the
smooth muscle cells of the arterial wall in medium-sized
muscular arteries.26 The vertebral and renal arteries may
also be involved, bilaterality is common, and some patients
may have intracranial berry aneurysms.27, 31 Genetic predis-
position may be a factor in this disease.26, 32
Often an incidental angiographic finding, FMD occurs
predominantly in middle-aged women, many of whom are
asymptomatic.25 FMD appears to be more common than
atherosclerosis as a cause of pulsatile tinnitus. This may be
due to the fact that the stenosis in FMD is usually high in the
cervical internal carotid artery at the level of the first and
second cervical vertebrae, and the resultant turbulence is
readily transmitted into the petrous bone.13 Next to cerebral
ischemic or hemorrhagic symptoms (such as headache,
transient ischemic attack, stroke, and subarachnoid hemor-
rhage), pulsatile tinnitus is the most common complaint.33
Among patients with symptoms of carotid FMDs, one third
or more name pulsatile tinnitus as a presenting symptom,
and in some patients this may be the primary complaint (Fig.
26-1).24, 26, 33 Spontaneous dissection (Fig. 26-2B) or
arteriovenous fistulization superimposed on carotid FMD
may also precipitate pulsatile tinnitus, and rarely, vertebral
FMD has caused pulsatile tinnitus.29, 34, 35
The classic angiographic appearance of FMD is the
‘‘string of beads’’ pattern, which is found in 85% of carotid
FMD (Fig. 26-2A).36 The less common patterns are tubular
stenosis and semicircumferential narrowing. The accuracy
of magnetic resonance angiography (MRA) in detecting
FMD (Fig. 26-2) is unclear.7, 37 However, magnetic reso-
nance (MR) imaging has been shown to help distinguish
tubular FMD from arterial dissection and arterial hypo-
plasia.38
Besides surgery and antiplatelet therapy, translu-
minal angioplasty has been successful in treating
FMD.28, 32, 33, 39–42 However, because most patients follow
a benign course, treatment should not be instituted in the
absence of progressive cerebral ischemia unless the patient
feels that the noise is incapacitating.13, 25 A survey for
possible intracranial aneurysm with MRA is strongly
advisable because an associated aneurysm may pose a
greater hazard to the patient than the FMD itself.43 The
differential diagnosis of FMD includes Ehlers-Danlos
syndrome type IV and giant cell and Takayasu’s arteri-
tides.44
Dissection of the Carotid or Vertebral Artery
Dissection of the cervicocephalic arteries may be
spontaneous or traumatic.45 Spontaneous dissections, some-
times after trivial trauma, usually affect one or both of the
cervical internal carotid arteries of a young to middle-aged
adult, and the vertebral artery is occasionally involved.46–49
The etiology of spontaneous dissection is unknown;
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however, angiographic FMD is present in 10% to 15% of the
patients.46
The majority of the patients complain of ipsilateral
headache.46, 49 Other common manifestations are focal
cerebral ischemic symptoms (transient ischemic attack or
stroke), oculosympathetic paresis (partial Horner’s syn-
drome), and bruit.49 Bruits, subjective or objective, are
found in about 40% of the patients (Fig. 26-3).50
The angiographic findings include luminal stenosis,
abrupt reconstitution of the lumen, dissecting aneurysm,
intimal flap, slow flow, occlusion, and distal emboli.51 MR
imaging may show loss of flow void in occlusion and
hyperintense signal from intraluminal hemorrhage.52, 53
MRA, dynamic computed tomography (CT), and ultraso-
nography have all been used for evaluation of cervicocepha-
lic arterial dissection.54–61
Though the efficacy of medical and surgical therapy is
unclear, anticoagulant followed by antiplatelet therapy is
commonly prescribed.49, 53 A persistent dissecting aneu-
rysm discharging emboli may be resected. Nearly all of the
stenoses resolve, but many occlusions do not recanalize, and
further dissections may occur in other cervicocephalic
arteries.48, 49, 51
Styloid Carotid Compression
An elongated styloid process compressing a tortuous
carotid artery has been reported as a cause of pulsatile
tinnitus, but this appears to be a unique case.6
Petrous Carotid Aneurysm
Bruit may be the main complaint of patients with petrous
carotid aneurysms.62, 63 These aneurysms have been suc-
cessfully treated with percutaneous transarterial emboliza-
tion using detachable balloons or with surgical resec-
tion.62, 64
Aberrant Carotid Artery
The aberrant carotid artery is a rare anomaly, and
patients who have one may be seen at almost any
age.65 Some of the patients experience pulsatile tinnitus
and some have conductive hearing loss, but most have
relatively mild symptoms that do not require treatment.65
The aberrant carotid artery is extremely important in that
clinically it simulates a paraganglioma in the middle
ear.65, 66 Many of the cases first reported were diagnosed
after myringotomy or biopsy, often with disastrous con-
sequences such as massive hemorrhage and hemiple-
gia.67, 68 The aberrant artery enters the tympanic cavity
through an enlarged inferior tympanic canaliculus and then
undulates through the middle ear to enter the horizontal
carotid canal through a dehiscence in the carotid plate.65, 69
The ipsilateral ascending carotid canal is absent. CT is
diagnostic (Figs. 26-4A and 26-5A). MRA may be used for
confirmation (Fig. 26-4B) or for detection of a suspected
associated aneurysm (Fig. 26-5B). Angiography is not
necessary.70

FIGURE 26-1 Fibromuscular dysplasia of the

internal carotid artery. Selective left internal carotid
angiogram. A, Anteroposterior projection. B, Lateral
projection. Critical noncircumferential web-like stenosis
(arrowheads) immediately proximal to an eccentric
diverticulum. The patient’s major complaint was
pulsatile tinnitus in the left ear aggravated by exercise
and sufficient to cause sleeplessness. Symptoms were
promptly relieved by percutaneous transluminal angio-
plasty. (From Hasso AN, Bird CR, Zinke DE, et al.
Fibromuscular dysplasia of the internal carotid artery:
percutaneous transluminal angioplasty. AJNR 1981;2:
175–180.)

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1364 TEMPORAL BONE

FIGURE 26-2 Bilateral carotid fibromuscular dysplasia. MRA 3D time-of-flight technique, maximum intensity
projection. A, Right internal carotid artery shows segmental corrugation at the first and second cervical levels. B,
Left internal carotid artery shows similar irregularity with a superimposed spontaneous carotid dissection (open
arrow). The patient had intermittent right pulsatile tinnitus of gradual onset but no symptoms on the left side. Cranial
MRA also showed an internal carotid bifurcation berry aneurysm. The findings were confirmed by angiography.
(Courtesy of Dr. Fred Steinberg.)

FIGURE 26-3 Spontaneous dissection of a right internal carotid artery. The patient abruptly developed right
pulsatile tinnitus without headache, ischemic symptoms, or Horner’s syndrome. A, MRA 3D time-of-flight
technique, maximum intensity projection. B, MRA individual partition. Arrows point to a false lumen or a dissecting
aneurysm, which contains flowing blood or subacute thrombus.

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 Chapter 26 Temporal Bone: Vascular Tinnitus 1365

FIGURE 26-4 Right aberrant carotid artery. A, High-resolution CT. The arrow indicates an aberrant artery
coursing through the right tympanic cavity to enter the horizontal carotid canal through a dehiscence in the carotid
plate. B, MRA 3D time-of-flight technique, maximum intensity projection, shows the typical sharp bend of a narrow
aberrant artery (arrow) through the tympanic cavity.

Laterally Displaced Carotid Artery
The laterally displaced carotid artery is one that knuckles
into the tympanic cavity through a dehiscence of the bony
carotid canal at the junction between the canal’s vertical and
horizontal segments.71, 72 The artery does not take the long,
narrow detour of an aberrant carotid artery, and it may be
accompanied by an aneurysm. Although even rarer than the
aberrant carotid artery and embryologically different, it does
present the same hazards.
Persistent Stapedial Artery
A persistent stapedial artery large enough to be symptom-
atic is extremely rare. The artery courses from the
infracochlear carotid through the stapedial obturator fora-
men and then enlarges the tympanic facial nerve canal en
route to the middle cranial fossa to terminate as the middle
meningeal artery.69, 73, 74 The facial canal enlargement must
not be mistakenly attributed to a facial nerve tumor.
Characteristically, the ipsilateral foramen spinosum is
absent.73 CT is diagnostic (Fig. 26-6). The persistent
stapedial artery may also accompany an aberrant carotid
artery or a laterally displaced carotid artery, or it may
originate from an ascending pharyngeal artery.69, 72, 75
Miscellaneous Arterial Anomalies
An anomalous artery 0.5 mm in diameter was encoun-
tered in the stria vascularis of the apex of the cochlea at
postmortem histopathology. This anomaly appeared to be
the cause of the patient’s low-tone pulsatile tinnitus.76 Such
a vessel may be detectable with the recently available
high-resolution, heavily T2-weighted, fast spin-echo or
constructive interference steady-state MR imaging. Cross-
compression of the eighth nerve in the cerebellopontine

FIGURE 26-5 Left aberrant carotid artery after needling. A, High-resolution CT shows an aberrant artery
(arrow) coursing through the left tympanic cavity to enter horizontal carotid canal through a dehiscence in the
carotid plate. Note the packing material in the external auditory canal for hemostasis. B, MRA 3D time-of-flight
technique, maximum intensity projection, shows a false aneurysm (arrow) in its intratympanic segment, confirmed
by selective catheter angiography.

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1366 TEMPORAL BONE
FIGURE 26-6 Persistent stapedial artery. A, B, High-resolution CT. The artery in the tympanic cavity through
the stapes is not visualized, but the anterior portion of the tympanic segment of the facial nerve canal is enlarged
(arrow) and the ipsilateral foramen spinosum is absent (arrowhead ). (Courtesy of Dr. David Sobel.)
angle by a persistent trigeminal artery was suggested as a
cause of pulsatile tinnitus, although the evidence was
circumstantial and venous tinnitus was not clearly excluded
in the cases described.77 Anterior communicating artery
berry aneurysm has also been implicated in pulsatile
tinnitus.78 However, in view of the common coexistence of
intracranial berry aneurysms with cervical internal carotid
FMD, unless the latter has been specifically excluded, a
causal relationship should not be assumed.31
ARTERIOVENOUS CAUSES
Arteriovenous (AV) causes include hypervascular tu-
mors, hypervascular bone diseases, and high-flow shunts.
Paraganglioma
Paraganglioma is the second most common tumor of the
temporal bone and the most common in the middle ear.79
Characteristically hypervascular, it is one of the most
common causes of pulsatile tinnitus. Whether involving the
jugular bulb (glomus jugulare or jugulotympanicum) or
confined to the middle ear or mastoid (glomus tympanicum),
the majority of the paragangliomas first appear with pulsatile
tinnitus (see Chapter 25).80 The clinical differentiation
between tympanicum and jugulare tumors is often difficult;
however, CT with bone detail can be used to define the
tumor and differentiate the tympanicum tumors, which
require no angiography and only simple surgery, from the
jugulare tumors, which require MR imaging, angiography,
preoperative embolization, and extensive surgery.81 An MR
venogram (MRV) may also help detect jugular vein
invasion.82 MRA has not been shown to be reliable for
assessment of tumor vascularity.
Miscellaneous Vascular Head and Neck
Tumors
Other vascular tumors in the head and neck, both inside
and outside the temporal bone, have been sporadically
reported as causes of pulsatile tinnitus. These include,
among others, AV malformation, capillary hemangioma,
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cavernous hemangioma, histiocytosis, jugular meningioma,
adenoma, and cholesterol granuloma.6, 11, 83–87
Paget’s Disease
Paget’s disease affects 3% of the population over 40
years of age, men more often than women. The majority of
cases are discovered incidentally.88 Three histologic phases
are recognized: (1) osteoclastic resorption, (2) osteoblastic
regeneration, and (3) ‘‘mosaic’’ bone replacing the original
bone.88 Increase in the size and number of blood vessels and
extensive AV shunting are frequently present.88 In a series
of 165 patients with skull involvement, 31 had tinnitus, 20 of
whom had pulsatile tinnitus.89 Two of the patients in the
series had common carotid flow measurements determined,
and values twice the normal rate were found. Proximal
ligation of the hypertrophic arteries gives only temporary
relief, but experience with transarterial embolization of the
distal vessels does not appear to have been reported.90
Otosclerosis or Otospongiosis
Pulsatile tinnitus has been encountered in a small number
of otosclerotic patients and is attributed to neovasculariza-
tion and arteriovenous microfistulas.3
Cerebral and Head and Neck Arteriovenous
Malformation
Cerebral AV malformations are congenital lesions
consisting of a cluster of nonneoplastic dilated, tortuous
arteries and veins without an intervening arteriole-capillary
bed. Cerebral blood flow through large AV malformations
may be markedly increased.91, 92 The majority of the
patients are young adults who most commonly have
headache, subarachnoid hemorrhage, and seizures.93 Al-
though in one series as many as one third of the patients had
cranial bruit on auscultation, few had pulsatile tinnitus as a
complaint.93 Rarely, cerebral AV malformations may cause
a symptomatic bruit, and in at least one case pulsatile
tinnitus was the primary complaint.94, 95 Because the
symptoms presumably result from high flow through the
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 Chapter 26 Temporal Bone: Vascular Tinnitus 1367

sigmoid and petrosal sinuses, the malformation itself does

not need to be in close proximity to the temporal bone. The
same applies to large extracranial AV malformation in the
head and neck.

Dural Arteriovenous Fistula

Most if not all dural arteriovenous fistulas (DAVFs) are
acquired.96 The pathogenesis is unclear, but some arise
because of recanalization of a thrombosed dural sinus, with
the transverse, sigmoid, and cavernous sinuses being the
most common sites.97–99 The blood supply may come from
any of the meningeal branches of the external or even of the
internal carotid arteries (Figs. 26-7 to 26-9). Delayed
postoperative DAVFs have been reported after suboccipital
craniotomy.100–102
Accounting for 10% to 15% of all intracranial AV
malformations, DAVFs are rare.103 However, they are a
much more common cause of pulsatile tinnitus than are
cerebral AV malformations, and in the experience of some
clinicians they are the most common cause.6, 10
Nearly all patients with lateral or sigmoid sinus DAVFs,
and some patients with cavernous sinus DAVFs, have pulsa-
tile tinnitus and an audible bruit.98, 101 In more than half of
the patients in a Mayo Clinic series, the tinnitus stabilized or
regressed, and spontaneous closures, usually of small fistu-

FIGURE 26-8 Large DAVF. Selective left external carotid angiogram.

An extensive lesion along the transverse and sigmoid sinuses supplied by
several hypertrophic external carotid branches (arrows) with rapid
drainage down the internal jugular vein (arrowhead ). The patient had
temporary relief of pulsatile tinnitus after surgical ligation and,
subsequently, partial relief of recurrent symptoms after transcatheter
occlusive procedures.

las, also were reported.104–107 On the other hand, aggressive

FIGURE 26-7 Small DAVF. Selective left external carotid angiogram.
A small lesion in the region of the inferior petrosal sinus (arrow) supplied
by the ascending pharyngeal artery. The patient’s pulsatile tinnitus
diminished after a program of self-administered compression.
lesions may cause cerebral ischemic or hemorrhagic events
or chronic increased intracranial pressure.108, 109 The pres-
ence of veno-occlusive disease is a major determinant of the
aggressiveness of a fistula.42, 101, 104, 108
Although selective catheter angiography remains defini-
tive in the evaluation of DAVF, three-dimensional (3D)
time-of-flight MRA, which successfully demonstrated the
fistula site in a series of six of seven cases, is a capable
screening tool.110 Nevertheless, while MR imaging effec-
tively identifies infarct and hemorrhage in patients with
veno-occlusive disease, neither MRA nor MR imaging is
completely reliable in excluding dilated cortical veins,
which is an important determinant for management.110, 111
A variety of treatment methods have been employed
successfully.98, 99, 112 In one series, self-administered exter-
nal compression benefited about half of the patients without
causing complications.99 Patients who gain no relief from
external compression can be treated by embolization with
either isobutyl cyanoacrylate or polyvinyl alcohol sponges.
The most problematic cases can be treated with a
combination of embolization and surgery. In a series of 28
patients treated with these various methods, there were three
strokes but no deaths, and transvenous embolization at the

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1368 TEMPORAL BONE

FIGURE 26-9 DAVF. The patient developed increasing right pulsatile tinnitus of gradual onset over a 2-year
period after head trauma. No basal skull fracture was found on high-resolution CT. A, Gadolinium T1-weighted
image. The long arrow points to the right internal carotid artery; short arrows point to the enlarged right and normal
left ascending pharyngeal arteries. A cluster of serpentine ‘‘flow voids’’ without an associated soft-tissue mass lies
posterior to the right internal carotid and ascending pharyngeal arteries and between the open arrows. B, MRA 3D
time-of-flight technique, maximum intensity projection. The hypertrophic right ascending pharyngeal artery (curved
arrow) and a cluster of dilated vessels (open arrow) lie immediately medial, and a dilated inferior petrosal sinus
(arrow) lies inferior to the right internal carotid artery.

fistula site may be indicated in some patients.42, 99, 112 yielded better results with far less mortality than excision.118
Surgical excision with packing of the sinus, now out of Some groups, however, maintain that the variability in
favor, also produced excellent results in most of the patients, degrees of sinus occlusion is a progressive process in
but in a series of 27 patients there were two deaths by DAVFs, and hence that all such lesions should be treated.119
exsanguination.98
An analysis of 205 patients with DAVFs by Cognard et
al. has shown that five angiographic patterns of venous Direct Arteriovenous Fistula
drainage are highly predictive of the clinical course of the
fistulas.113 These patterns, with subtypes, form valuable Direct AV fistulas (AVFs) occur most often in the
guidelines for management. In essence, in the presence of vertebral artery, but they may also involve the internal
antegrade dural sinus flow, only 1 of 84 patients developed carotid artery or a branch of the external carotid artery. In the
intracranial hypertension and none experienced aggressive experience of some clinicians they are usually due to trauma,
symptoms. Thus, such fistulas may be considered benign, but in the experience of others they are more often
and the patients should be treated only if incapacitated by spontaneous.42, 120 The vertebral artery in its course through
their tinnitus. They may be monitored annually with the foramen transversarum from C6 through C2 is closely
Doppler studies for flow and should be reevaluated upon
change of symptoms. In the presence of retrograde dural
sinus flow, 8 of 27 patients developed intracranial hyperten-
sion; arterial embolization should be done in these patients
to reduce flow and venous hypertension. With the develop-
ment of retrograde leptomeningeal venous drainage (Fig.
26-10), hemorrhage and focal neurologic deficits occur;
thus, occlusion or at least suppression of the leptomeningeal
drainage by arterial embolization becomes mandatory. If
necessary, transvenous occlusion or surgical resection of the
sinus should be considered. Direct drainage of a fistula into
the cortical veins carries an extremely high risk of
hemorrhage and demands complete occlusion by any and all
means.113 Based on similar observations, Borden et al.
proposed a simpler classification of three drainage pat-
terns.114, 115
Recently, Davies et al. validated the value of both the
Cognard and Borden classifications for predicting develop-
ment of symptoms. They also confirmed that low-grade FIGURE 26-10 Large DAVF. Superselective occipital angiogram
shows rapid antegrade drainage into the sigmoid sinus and down the
lesions tended to remain benign or resolve, while high-grade internal jugular vein, and retrograde leptomeningeal reflux into the
lesions tended to result in poor outcomes without therapeutic anastomotic lateral mesencephalic vein (arrowhead ), a risk factor for
embolization and/or surgery.116–118 Surgical disconnection intracranial hemorrhage not apparent on MRA.

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surrounded by a venous plexus and is thus prone to develop
AVFs when subjected to penetrating trauma (Fig. 26-11).
Stab and bullet wounds are the most common causes.121
Iatrogenic causes include direct vertebral puncture for
angiography and anterior cervical discectomy.122, 123 Spon-
taneous development occurs in neurofibromatosis 1 and
FMD, as well as without specific underlying disease.124–126
Tinnitus is the usual complaint in patients with vertebral
AVF, and endovascular occlusion is the treatment of
choice.120, 127
Traumatic AVF of the internal carotid artery usually
develops in the cavernous sinus, where it is closely
surrounded by a venous plexus.128 Spontaneous carotico-
cavernous fistulas may occur in fibromuscular dysplasia,
Ehlers-Danlos syndrome, or neurofibromatosis.1, 35, 42, 129
Ophthalmic symptoms and signs and pulsatile tinnitus are
present in most of the patients. For vertebral AVFs,
transarterial balloon embolization is the treatment of choice.
Scalp AVFs also may cause pulsatile tinnitus.42, 130, 131
VENOUS CAUSES
Laminar flow is silent, and turbulent flow creates noise.
When the noise exceeds the masking capability of the ear, it
FIGURE 26-11 Vertebral AV fistula. Selective innominate angiogram
(right posterior oblique projection). The right vertebral artery (arrow) is
larger than the right carotid (curved arrow). A fistula (open arrow) at the
C3-4 level drains promptly into the surrounding venous plexus. The patient
developed pulsatile tinnitus 3 months after suffering a stab wound in the
neck. Symptoms were promptly relieved by transcatheter ballon occlusion.
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#7210 @sunultra1/raid/CLS_books/GRP_gordon/JOB_som/DIV_ch26
Chapter 26 Temporal Bone: Vascular Tinnitus 1369
becomes venous tinnitus to the patient and may be audible to
the examiner as a continuous bruit.132 A venous bruit is
usually heard around the ear. It should be distinguished from
a venous hum, which can be elicited over the lower jugular
vein in about half of normal subjects and in 80% of pregnant
women.133
Venous tinnitus is invariably heard on the side of the
dominant jugular vein.8, 134, 135 Because the jugular fossa is
larger on the right twice as often as it is on the left, it follows
that the majority of venous tinnitus is heard on the
right.8, 134, 136
Venous tinnitus is heard as a continuous murmur
accentuated in systole. It is abolished by light pressure on
the ipsilateral jugular vein and is accentuated by pressure on
the contralateral vein. The symptom decreases when the
head is rotated toward the involved side, and it increases
when the head is turned away. Depending on its severity,
venous tinnitus may or may not be audible to the examiner.8
Venous Tinnitus in Systemic Conditions
Venous tinnitus may be heard in conditions of hyperdy-
namic systemic circulation such as chronic anemia, preg-
nancy, and thyrotoxicosis.132, 134, 137, 138 Hypertensive pa-
tients taking an angiotensin-converting enzyme inhibitor or
a calcium channel blocker to reduce peripheral vascular
resistance may rarely experience pulsatile tinnitus as a side
effect.15 Venous tinnitus in systemic conditions disappears
as the underlying condition resolves.
Venous Tinnitus in Intracranial Hypertension
Headaches and blurring of vision are the predominant
symptoms of intracranial hypertension, but venous tinnitus
may also be a symptom.139, 140 The pathogenesis of tinnitus
in intracranial hypertension is unknown, but it is clearly and
directly related to cerebrospinal fluid (CSF) pressure, and
compression of dural sinuses by transmitted intracranial
arterial pulsations has been postulated to be the mecha-
nism.15 Drainage of CSF by lumbar puncture promptly
relieves the tinnitus.
Occasionally, pulsatile tinnitus can be a prominent
symptom of intracranial hypertension resulting from a
variety of causes.42, 141, 142 These include aqueductal steno-
sis, Chiari I malformation and pneumocephalus.143, 144 In
some cases of idiopathic intracranial hypertension (IIH),
also called benign intracranial hypertension and pseudotu-
mor cerebri syndrome, it can be the presenting symptom or
even the only symptom.140, 142, 145, 146
IIH is a syndrome characterized by increased intracranial
pressure without focal neurologic signs, except for an
occasional sixth nerve palsy.139 The diagnosis is made by
exclusion of lesions such as hydrocephalus, mass, chronic
meningitis, dural sinus thrombosis, and hypertensive and
pulmonary encephalopathy.
Patients suffering from pulsatile tinnitus from IIH tend to
be young, obese women.139, 141 In Sismanis et al.’s series of
31 patients, tinnitus was unilateral in 27 and bilateral in 4
and was also objective in 27 and subjective in 4.141 On
the CT and MR imaging scans performed to rule out
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1370 TEMPORAL BONE
other causes of intracranial hypertension, more than half
of the patients showed an empty sella or small ven-
tricles.141, 144, 147 A subsequent report by Sismanis and
Smoker noted that papilledema was present in only 16 of 42
patients with CSF pressure over 200 mm Hg.3
The treatment must be directed to the underlying cause of
the intracranial hypertension. In the case of IIH, acetazol-
amide, furosemide, and weight reduction are usually
effective. Cases refractory to medical management may
necessitate subarachnoid peritoneal shunting.139–142
Venous Tinnitus Caused by Transverse Sinus
Stenosis
Venous tinnitus resulting from transverse sinus stenosis
independent of DAVF is a diagnosis thus far seldom
made.7, 148, 149 Little information exists in the literature with
regard to its etiology, natural history, or treatment. When
warranted by incapacitating symptoms, transvenous stenting
has been successfully performed.149 True stenosis should
be differentiated from arachnoid granulations in a dural
sinus.150 When there is unilateral transverse sinus thrombo-
sis, the shifting of all of the blood flow to the contralateral
side appears to be the cause of the contralateral pulsatile
tinnitus.
Venous Tinnitus Associated with a Large or
Exposed Jugular Bulb or Large Emissary Veins
Venous tinnitus has often been encountered in as-
sociation with a large, high, or exposed jugular
bulb.134, 135, 137, 151 In view of the fact that the jugular bulb
rises above the inferior tympanic annulus in 6% of the
population and rises above the inferior border of the round
window in 25%, and that venous tinnitus is much rarer, a
high or large bulb in itself is not likely to be the cause of
venous tinnitus.152, 153 However, a large, high, or exposed
bulb may indeed provide an environment conducive to the
production of venous tinnitus. Furthermore, if a high bulb is
exposed by dehiscence of the jugular plate and becomes
visible as a bluish retrotympanic mass, it may be mistaken
for a tumor.65, 154, 155
A laterally placed sigmoid sinus has been reported to be
associated with pulsatile tinnitus.156 Large emissary veins,
probably of an incidental nature, may be seen in patients
with venous tinnitus.157, 158
Venous tinnitus associated with a large, high, or exposed
jugular bulb or a large emissary vein is essentially idiopathic
venous tinnitus and can be managed similarly. Venous
tinnitus associated with an exposed bulb has been success-
fully treated using a septal cartilage homograft over the
dehiscent plate, but most patients do not require treat-
ment.159 Surgical lowering of the jugular bulb has been
performed for high bulbs thought to be causing Meniere’s
disease and pulsatile tinnitus.160
Below the skull base, venous tinnitus can occur with an
enlarged retromandibular vein and other vascular malforma-
tions in the periauricular region.
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#7210 @sunultra1/raid/CLS_books/GRP_gordon/JOB_som/DIV_ch26
Idiopathic Venous Tinnitus
After exclusion of all specific causes, some cases of
venous tinnitus remain unexplained and hence idiopathic.
These cases usually involve women who are otherwise
healthy, most of whom require only explanation and
reassurance.8, 135 The symptoms often resolve spontane-
ously.14
If the noise is truly intolerable, an external prosthetic
clamp may be tried, and ligation of the vein under local
anesthesia promptly relieves the symptom.6, 132, 134 As an
option, the optimal level of ligation may be tested by
transvenous balloon occlusion; however, recurrences after
ligation have been reported on the same or the contralateral
side.14, 134
Moreover, jugular ligation risks causing intracranial
hypertension. If it is to be attempted at all, IIH must first be
excluded by lumbar puncture, contralateral venous drainage
must be established and transverse sinus stenosis excluded
by angiography or MRV, and an exposed jugular bulb must
be excluded by otoscopy or high-resolution CT. In the
absence of adequate contralateral drainage, jugular ligation
may cause intracranial hypertension.161 In the presence of
dehiscence of the jugular plate, jugular ligation may cause
herniation of the bulb into the middle ear. In such rare cases,
a sigmoid-jugular bypass may be applied with or without
jugular ligation.8
RADIOLOGIC INVESTIGATION
It is clear from the foregoing discussion that the causes of
vascular tinnitus are diverse and numerous. To some
patients, the symptom may be a mere nuisance; to others, it
may herald a life-threatening disease. The natural history of
the disease in different patients with the same diagnosis can
vary widely. Management can also be complex, with some
conditions requiring medical treatment, some requiring
surgical treatment, some requiring endovascular treatment,
some requiring a combination of treatments, and some
requiring only explanation and reassurance with no other
treatment.
The proper choice of imaging procedures is best tailored
to the clinical findings of the patient.3 Reliance on imaging
procedures alone may cause failure to reach a diagnosis
in some 40% of cases.7 Direct communication with the
referring clinician should be established, and, if necessary,
the patient should be examined by the radiologist. The
following imaging guidelines are suggested:
1. In the presence of a visible intratympanic or retrotym-
panic mass, noncontrast high-resolution CT is clearly
the first examination of choice.162 If an arterial
anomaly, exposed jugular bulb, or intratympanic
tumor is found, usually no further imaging is
necessary. If destruction of the jugular plate suggests a
glomus jugulare (jugulotympanicum) tumor, MR
imaging or postcontrast CT may be done, followed by
angiography, and, if indicated, a balloon occlusion test
and preoperative embolization. An MRV with source
images may be used in cases in which jugular vein
invasion is questionable (see Fig. 25-74).82
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2. When the tinnitus can be abolished by light pressure
over the ipsilateral internal jugular vein, it is
presumably of venous origin.3 Systemic diseases,
intracranial hypertension, and lateral sinus stenosis
become the major considerations. Noncontrast MR
imaging (to survey the brain) and an MRV (to define
the posterior fossa dural sinuses, to confirm ipsilateral
dominance, and to establish contralateral drainage in
case of intervention) should suffice in most cases.
Unless dural sinus angioplasty or stenting is indicated,
patients in this group will rarely need angiography.
3. When a systolic bruit or machinery murmur is audible
over the head or neck, indicating the presence of a
stenotic artery or an arteriovenous shunt, MRA of the
neck and head and noncontrast MR imaging of the
head (to evaluate ischemic and hemorrhagic changes)
will most likely yield a diagnosis.7 If MRA fails to
show a small fistula, gadolinium-enhanced MRA may
be attempted.110 Although MRA is less definitive than
catheter angiography, the information that it provides
can be most helpful for discussion and planning with
the patients. If indicated, conventional angiography
may then follow.
As currently performed, MRA appears to be at least
as accurate as ultrasonography in the evaluation of ca-
rotid bifurcation stenosis.163 In addition, it allows
evaluation of the upper cervical arteries and surveying
for possible intracranial aneurysm in the same proce-
dure.164 CT angiography based on helical CT may be
used for patients unable to undogo MR imaging.
4. If none of the aforementioned findings is present, the
search is likely to be more difficult and the yield from
imaging is likely to be low.7 Nevertheless, significant
lesions may still be detected by imaging.7 Thus, MR
imaging/MRA/MRV should be done to exclude
intracranial abnormalities, high and deep-seated ca-
rotid stenosis or aneurysm, and dural sinus stenosis.
Still, mild changes of FMD and small DAVFs may
escape detection. High-resolution CT should be used
to detect Paget’s disease of the temporal bone,
cochlear otospongiosis, and deep-seated tumors in the
temporal bone. If these studies show no abnormality,
the probability of significant disease becomes mini-
mal. The benefit and risks of angiography must then
be weighed carefully against the severity of the
patient’s symptoms.
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