252

Pulsatile Tinnitus

Cathy A. Sila, Anthony J. Furlan, and John R. Little

Pulse-synchronous tinnitus suggests a vascular etiology and is deemed rare by the otologic literature.During the period 1978-1985 we evaluated 20 patients with the sole or initial complaint of pulsatiletinnitus. Fourteen patients had objective pulsatile tinnitus, perceived by the patient and the examineralike, and 6 had subjective pulsatile tinnitus, perceived by the patient only. Angiographic findings inpatients with objective pulsatile tinnitus included dural or pial arteriovenous malformations, occlusivedisease of the intra- or extracranial carotid arteries from atherosclerosis or dissection, panarterialectasia, and venous sinus thrombosis. Most of the patients with subjective pulsatile tinnitus hadnormal evaluations, but other possible causes of subjective pulsatile tinnitus included a carotidocclusion and pseudotumor cerebri. Pulsatile tinnitus is an uncommon symptom produced by avariety of causes. Given the abnormalities present in our series, we would recommend intraarterialdigital subtraction angiography or conventional angiography in the evaluation of objective pulsatiletinnitus and intravenous digital subtraction angiography for subjective pulsatile tinnitus. Increasedintracranial pressure must also be considered. (Stroke 1987; 18:252-256)

TINNITUS may be classified as "subjective",perceived only by the patient, or "objective",perceived by the patient and examiner alike.

When tinnitus is pulse-synchronous, a vascular etiol-ogy is suggested.

The causes and evaluation of pulsatile tinnitus havenot been adequately addressed in the neurologic litera-ture. The otologic literature suggests that objectivetinnitus is uncommon or, when of vascular origin,rare. The most common cause cited is a dural arterio-venous malformation (AVM),12 usually involvingbranches of the external carotid artery (occipital andgreater auricular branches) and the transverse sinus.Other causes include traumatic or spontaneous carot-id-cavernous fistulae,3"3 AVM's of the neck,4-6-7 in-creased intracranial pressure,38 high cardiac outputstates (anemia, thyrotoxicosis, or beri-beri),89 intra-cranial aneurysms,9 vascular tumors of the temporalbone and cerebello-pontine angle,*-* and possibly,asymmetry of the jugular bulbs.l0 There have been fewdocumented cases of objective pulsatile tinnitus as-cribed to ectatic, dissected, stenotic, or occluded cra-niocervical arteries.1416"'2

Subjects and MethodsDuring the period 1978-1985, 20 patients with the

sole or initial complaint of pulsatile tinnitus were iden-tified and reviewed (Table 1). Of these, 14 had audiblebruits about the orbits, cranium, or neck and wereclassified as having objective pulsatile tinnitus. Theremaining 6 had no audible bruits and were classifiedas having subjective pulsatile tinnitus. The group com-prised 15 women aged 26-76 years and 5 men aged41-79 years. The tinnitus lateralized to the left in 10patients, to the right in 5, and was bilateral in 5. Theduration of tinnitus at the time of presentation ranged

From the Cleveland Clinic Foundation, Cleveland, Ohio.Address for reprints: Cathy A. Sila, MD, Department of Neurol-

ogy, Cleveland Clinic, 9500 Euclid Avenue, Cleveland, OH44106.

Received February 19, 1986; accepted July 7, 1986.

from 1 week to 11 years. Nineteen patients had imag-ing of the intracranial and cervical vessels by conven-tional film screen angiography (FSA), intraarterial(IA-DSA), or intravenous digital subtraction angiog-raphy (IV-DSA). The results of angiographic findingsare summarized in Table 2. One patient had only com-puted tomography of the head with and without theadministration of contrast material. Follow-up from 3months to 7 years was obtained for 18 patients. Duringthe follow-up period, pulsatile tinnitus resolved in 5patients, improved in 3, and did not change in 10.

Objective Pulsatile TinnitusOf the 14 patients with objective pulsatile tinnitus, 5

had angiographic demonstration of an ipsilateral duralAVM supplied primarily by branches of the externalcarotid artery and draining into the transverse or lateralvenous sinus. In these patients the bruit localized to theregion of the mastoid (Table 1, Cases 7-11; Figure 1).

Occlusive arterial disease was demonstrated in 4patients (Figure 1). One patient presented to an outsideinstitution for evaluation of pulsatile tinnitus and con-tralateral retro-orbital pain. Examination at that timerevealed an ipsilateral cervical and periauricular bruitas well as a diaphragmatic paralysis and contralateralHomer's syndrome. Angiography revealed marked ta-pering stenosis of the internal carotid arteries (ICA)bilaterally suggesting spontaneous dissections (Figure1). Upon evaluation at our institution 3 months later,his tinnitus and bruits had resolved and an IV-DSAwas normal, documenting the spontaneous resolutionof bilateral carotid dissections (Table 1, Case 4). Threepatients had significant stenosis or occlusion of theICA at the siphon or at the carotid bifurcation (Table 1,Cases 1, 2, 3).

Subjective Pulsatile TinnitusOf the 6 patients with subjective tinnitus, 3 could

alleviate the tinnitus by rotating their head to the ipsi-lateral side. One of these patients had pseudotumorcerebri and experienced transient relief from tinnitus

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Sila et al Pulsatile Tinnitus 253

FIGURE 1. Examples of angio graphic lesions causing pulsatile tinnitus, clockwise from top left: a) dural arteriovenous malformationaffecting the transverse sinus, b) carotid siphon stenosis, c) internal carotid artery dissection, d) intrapetrous carotid artery aneurysm(clinical details unavailable).

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254 Stroke Vol 18, No 1, January-February 1987

Table 1.

Case/Age/Sex

1/41/M

2/76/F

3/79/M

4/55/M

5/60/M

6732/F

7/60/F

8/67/F

9/63/F

10/67/F

11/64/M

12/58/F

13/41/F

14/26/F

Duration ofpulsatiletinnitus

at time ofevaluation

6 wk.

6 mo.

11 yr.

1 wk.

3 mo.

lyr .

lyr.

6 mo.

2 mo.

8 mo.

7yr.

3yr.

2yr.

14 mo.

Perceivedlaterality

Bilateral

Left

Left

Right

Right

Bilateral

Left

Right

Right

Left

Bilateral

Right

Left

Bilateral

Aggravatingor

alleviatingfactors

—

f lying onR side

t Valsalva

—

—

—

—

| exercise

| Valsalva4 compressingL-STA

f exercise

Neurological

Bruits

Ocular L>R

Cervical L>R

L ocular, bilateralcervical

R cervical

Bilateral ocular,R mastoid

Bilateral ocularand cranial

L mastoid

R mastoid

R mastoid and cervical

L mastoid

L mastoid, bilateralocular

R cervical, supra-clavicular

L cranial — disappearswith L-STA compression

Bilateral ocularafter exercise,none at rest

examination

Other

—

Mild L central facialweakness

Complete L Homer'sR diaphragm paralysis

4 visual acuity,chronic papilledema

—

—

—

—

4 dexterity L hand

—

15/66/F 2yr. Bilateral

16/49/F17/50/F

18/35/F

19/61/F

20/43/F

lyr .3yr.

6 mo.

1 yr.

18 mo.

LeftLeft

Left

Left

Left

—4 rotate head

to left

4 rotate headto left

1 Valsalva

4 light pres-sure L neck,rotating headto left

Papilledema

after lumbar puncture (Table 1, Case 20). The other 2patients with and 2 patients without postural changeshad normal IV- or IA-DSA's (Table 1, Cases 16-19).

DiscussionGiven the proximity to the auditory apparatus of the

petrous portion of the carotid artery, the sigmoid sinus,and the jugular bulb, it is surprising that pulsatile tinni-tus is not a more common complaint with lesions ofthese vessels. With the symptom of pulsatile tinnitus, avascular anomaly is often suspected. In 1938, Sears9

wrote of intracranial arterial aneurysms that it was"commonly believed and often stated that a bruit audi-

ble to the patient and on auscultation is generally pres-ent in this condition." However, objective tinnitus wasdescribed in only 4 of 22 cases of intracranial aneu-rysm and 1 of 13 cases of "angioma racemosum" byBergstrand et al13 and in 2 of 7 cases of arteriovenousaneurysms by Dalsgaard-Nielsen.14 In a series of 555intracranial aneurysms, only 2 had an intracranialbruit. More recently, pulsatile tinnitus has been recog-nized as a common symptom of dural AVM's. In theseries of Houser et al2 with AVM's affecting the trans-verse dural venous sinus, 10 of 14 patients had objec-tive pulsatile tinnitus.

Occlusive arterial disease is less recognized as a

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Sila el al Pulsatile Tinnitus

Table 1. (continued)

255

Other clinical diagnoses Radiographic findings

Duration offollow-up

sinceevaluation

7 mo.

8 mo.

6 yr.

1 yr.

10 mo.

Vh yr.

12 mo.

11 mo.

4 mo.

3yr.

3 mo.

7yr.

Outcome

Unchanged

Resolved fewweeks afterLCE

Unchanged

Spontaneouslyresolved

Unchanged

Occurs onlywith Valsalva

Unchanged

Spontaneouslyresolved

Unchanged

Softercharacterunchanged

Unchanged

Spontaneouslyresolved

Totalduration of

pulsatiletinnitus

8 mo.

6 mo.

17 yr.

1 wk.

13 mo.

AYiyr.

18 mo.

11 mo.

12 mo.

10 yr.

3'/2 yr.

Syr.

HTN, DM, ASHD/CABG, smoking

HTN, ASHD, stroke 3 yr and 6 yr

prior, ankylosing spondylitis

HTN, ASHD, PVD, smoking,increased lipids

HTN

HTN, + serology tx 8 yr. prior

Complex partial seizures

DM, R cerebral TIA 8 mo. prior

HTN

HTN, ASHD, breast cancer

ASHD/CABG

IA-DSA: 90% L carotid siphon stenosis

IA-DSA: 99% L-ICA stenosis, minimal

irregularity R-ICA bifurcation

FSA: R-ICA occlusion, 30% L carotidsiphon stenosis

FSA: Bilateral carotid dissectionsIV-DSA: 3 mo. later — normal

FSA: Pan-arterial ectasia intra-and extracranially

FSA: Thrombosis sagittal and R lateralvenous sinuses

FSA: L dural AVM of transverse sinus

FSA: R dural AVM of transverse sinus

FSA: R dural AVM of transverse sinus

FSA: L dural AVM of transverse sinus

IV-DSA: L dural AVM of transverse sinus

FSA: Large R parietal AVM

CT with/without: normal

IV-DSA, CT with: normal 3 mo. Unchanged •17 mo.

ASHD, smoking

Migraine

MVP

HTN, L frontal calvarialhemangioma resected 1 yr. prior

Pseudotumor cerebri, HTN, DMobesity

IA-DSA: L-ICA occlusion, collateralsthrough L-ECA

CT, IA-DSA: normal

IV-DSA: normal

IV-DSA: normal

IV-DSA: normal

5 mo.

7yr.

9 mo.

6 mo.

Intermittent

Unchanged

Unchanged

Spontaneouslyresolved

1 Vi yr.

10 yr.

15 mo

15 mo

CT, IV-DSA: normal 3 mo. Unchanged 21 mo.

cause of subjective or objective pulsatile tinnitus. In1931, Hamburger3 reported a case of an elderly womanwith angina pectoris and head noises who had subcla-vian and bilateral carotid bruits. No angiography wasperformed. He presumed that murmurs from athero-matous carotid arteries were being conducted to theskull, a concept perhaps first introduced by Jacobson15

in 1882. Hentzer's4 study of patients with objectivevascular tinnitus included 2 patients, 1 with an "ICAatheroma" whose tinnitus resolved after endarterec-tomy and 1 with an "ICA stricture" whose tinnitusspontaneously disappeared after a few months. Hol-gate et al6 described 1 patient with pulsatile tinnitus

who had an ICA stenosis, a contralateral carotid occlu-sion, and a persistent primitive hypoglossal artery. Hebelieved that each of the angiographic findings couldbe causes of pulsatile tinnitus.

In our series, 4 patients had occlusive disease of thecarotid arteries consisting of high-grade extra- or intra-cranial internal carotid stenoses or internal carotid oc-clusions. In 3 of these 4 patients the occlusive diseasewas atherosclerotic in nature, and these patients alsohad evidence of coronary artery disease and other riskfactors for vascular disease. The patients with arterialectasia and carotid dissections had no risk factors forvascular disease.

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256 Stroke Vol 18, No 1, January-February 1987

Table 2. Angiographic Results in 19 Patients with PulsatileTinnitus

Classification

Objective pulsatile tinnitus

Normal

AVMdural (transverse sinus) (n = 5)pial (parietal cortex) (n = 1)

Occlusive arterial diseaseipsilateral siphon stenosis (n = 1)ipsilateral carotid stenosis (n = 1)contralateral carotid occlusion (n = 1)bilateral carotid dissections in = 1)

Pan-arterial ectasia

Venous sinus thrombosis

TOTAL

Subjective pulsatile tinnitus

Normal

Ipsilateral carotid occlusion

Pseudotumor cerebri

TOTAL

Numberof patients

1

6

4

1

1

13

41

1

6

Pulsatile tinnitus is a common symptom in extra-cranial carotid artery dissections.1 Although estimatedto be the major complaint in 4% and an associatedcomplaint in 35% of patients, its significance has beenoverlooked. The complex of sudden pulsatile tinnitusin association with neck or face pain, Homer's syn-drome, and symptoms of cerebral ischemia is highlysuggestive of extracranial carotid artery dissection.

In 1902, Mann16 demonstrated that head rotationdecreased the venous return from the ipsilateral side ofthe brain and increased the flow in the contralateraljugular vein. The presumed mechanism was a "prop-ping open" of the contralateral jugular vein andsqueezing of the ipsilateral jugular vein by their re-spective sternocleidomastoid muscles. Graf et al17 de-scribed this characteristic relation of head position totinnitus intensity in his patients with "essential tinni-tus"; turning the head toward the side of the tinnitus, orthe "negative sternocleid position," decreased the tin-nitus. This prompted many theories of turbulence inthe area of the jugular bulb producing pulsatile tinnitusas well as surgical procedures designed to decreasejugular venous flow, primarily by jugular vein liga-tion. Hardison et al18 reported lasting relief from tinni-tus with jugular vein ligation in 1 patient although inHentzer's4 series, only 1 of 3 patients treated similarlyhad lasting relief. Given the benign prognosis of pulsa-tile tinnitus of presumed venous origin, jugular veinligation is seldom indicated.

In summary: Pulsatile tinnitus is an uncommoncomplaint produced by a variety of causes. When the

pulsatile tinnitus is objective, an angiographic abnor-mality is usually demonstrated; and given the nature ofthe lesions in our series, we recommend that IA-DSAor conventional angiography be done. A mastoid bruitsuggests a dural AVM involving the transverse sinus,and additional selective injections of the external ca-rotid artery may be necessary. In our series, occlusiveatherosclerotic disease of the ICA was a commoncause of pulsatile tinnitus, particularly when it wasobjective and associated with risk factors for athero-sclerosis.

Patients with subjective pulsatile tinnitus are morelikely to have a normal angiographic study. The etiol-ogy of the tinnitus is presumed to be turbulence withinthe venous system, especially when it is affected byalterations in head position. However, since 1 of ourcases with subjective pulsatile tinnitus had an ipsilater-al carotid occlusion, we recommend evaluation ofthese patients with IV-DSA or noninvasive tests.

References1. Goodhill V: A tinnitus identification test. Arm Olol Rhinol

Laryngol 1952;61:778-7882. Houser OW, Campbell JK, Campbell RJ, Sundt TM: Arterio-

venous malformation affecting the transverse dural venous si-nus — An acquired lesion. Mayo Clin Proc 1979;54:651—661

3. Hamburger LP: Head murmurs. Am J Med Sci 1931;181:756-768

4. HentzerE: Objective tinnitus of the vascular type. Ada Otolar-yngol (Stockh) 1968;66:273-281

5. Russell EJ, Huckman M, Rosenberg M: Sudden onset of head-ache, proptosis and roaring tinnitus in a hypertensive 60 yearold woman. JAMA 1983;249:3223-3224

6. Holgate RC, Wortzman G, Noyek AM, Makerewicz L,Coaters RM: Pulsatile tinnitus: The role of angiography. JOtolaryngol 1977;6:49-62

7. Lechtenberg R, Shulman A: The neurologic implications oftinnitus. Arch Neurol 1984;41:718-721

8. Meador KJ, Swift TR: Tinnitus from intracranial hypertension.Neurology 1984;34:1258-1261

9. Sears WG: Head noises and cranial bruits. Guy Hosp Rep1938;88:3O8-319Adler JR, Ropper AH: Self-audible venous bruits and highjugular bulb. Arch Neurol 1986;43:257-259Hart RG, Easton JD: Dissections of cervical and cerebral arter-ies. Neurologic Clinics 1983; 1:155—182Nevins MA, Lyon LJ, Kim JM: Multiple arterial abnormalitiespresenting as pulsatile tinnitus. J Med Soc NJ 1978;75:467^70Bergstrand H, Olivecrona H, Tflnnis W: Gef&ssmissbildungenund Gefftssgeschwutste des Gehirns. Leipzig, 1936Dalsgaard-Nielsen T: Studies on intracranial vascular sounds.Acta Physiol Scand 1939;14:69Jacobson L: Arch Ohrenh 1882; 19:42

16. Mann: Ueber den Mechanismus der Blutbewegung in der Venajugularis. Int Z Ohrenh 1902;40:354

17. Graf W, Moller T, Mannheimer E: The continuous murmur.Acta Med Scand (Suppl) 1947;196:167-191Hardison JE, Smith RB III, Crawley IS, Battey LL: Self-heardvenous hums. JAMA 1981;245:1146-1147

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11

12

13

14

15

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KEY WORDS • pulsatile tinnitus • IA-DSA • IV-DSAincreased intracranial pressure • carotid dissection

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C A Sila, A J Furlan and J R LittlePulsatile tinnitus.

Print ISSN: 0039-2499. Online ISSN: 1524-4628 Copyright © 1987 American Heart Association, Inc. All rights reserved.

is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231Stroke doi: 10.1161/01.STR.18.1.252

1987;18:252-256Stroke. 

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