Objective tinnitus …

Douglas J Lanska MD MS MSPH

Neuro-Ophthalmology & Neuro-Otology

Updated 04.30.2024
Released 09.17.2001
Expires For CME 04.30.2027

Objective tinnitus

Author: Douglas J Lanska MD MS MSPH

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Objective tinnitus

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Introduction

Overview

The author explains the clinical presentation, pathophysiology, diagnostic workup, and management of objective tinnitus. Objective tinnitus is a perceived sensation of sound that occurs in the absence of external acoustic stimulation, but it can also be heard by the examiner (eg, by placing a stethoscope over the patient's external auditory canal). Objective tinnitus is much less common than subjective tinnitus, but it often has an identifiable cause and may be curable, whereas subjective tinnitus is often idiopathic and is seldom curable.

Key points

	• Objective tinnitus is a perceived sensation of sound that occurs without external acoustic stimulation, but it can also be heard by the examiner (eg, by placing a stethoscope over the patient's external auditory canal).
	• Objective tinnitus can occur either from the perception of an abnormal somatosound or abnormal perception of a normal somatosound.
	• Objective tinnitus is much less common than subjective tinnitus, but it often has an identifiable cause and may be curable, whereas subjective tinnitus is often idiopathic and is seldom curable.
	• Tinnitus is frequently associated with depression (in up to half of patients), anxiety, and insomnia.
	• Objective tinnitus may be associated with a variety of vascular noises arising from the internal jugular vein or jugular bulb, arteriovenous malformations or fistulas, cavernous hemangiomas, aneurysms, vascular stenoses (particularly of the carotid arteries), vascular tumors, and intracranial hypertension.
	• The cervical venous hum is a common but innocuous murmur that can be heard in the anterior neck and sometimes upper chest and is often mistaken for more sinister sounds. A venous hum is caused by turbulence (ie, disruption of the otherwise smooth laminar flow into turbulent eddies) in the internal jugular vein, which causes the vessel walls to vibrate. This is precipitated or accentuated by turning the head away from the auscultated side.
	• Objective tinnitus associated with a patulous Eustachian tube is synchronous with nasal breathing (usually more marked in the upright position), gradually disappears with lying down, and often transiently abates with sniffing, snorting, or a Valsalva maneuver.
	• Objective tinnitus associated with abnormal clonic muscular contractions of palatal or middle ear muscles may occur as an intermittent series of sharp, regular clicks or with palatal myoclonus as a fairly regular, continuous clicking sound.

Historical note and terminology

Objective tinnitus is a perceived sensation of sound that occurs in the absence of external acoustic stimulation, but it can also be heard by the examiner (eg, by placing a stethoscope over the patient's external auditory canal). Objective tinnitus can occur either from perception of an abnormal somatosound or abnormal perception of a normal somatosound (65). Objective tinnitus is much less common than subjective tinnitus, but it often has an identifiable cause and may be curable, whereas subjective tinnitus is often idiopathic and is seldom curable.

Although pulsatile tinnitus may be objective or subjective, subjective pulsatile tinnitus is not inherently different in terms of likely causes than objective pulsatile tinnitus; therefore, both forms of pulsatile tinnitus are considered in this chapter.

Clinical manifestations

Presentation and course

	• Objective tinnitus is a perceived sensation of sound that occurs without external acoustic stimulation, but it can also be heard by the examiner (eg, by placing a stethoscope over the patient's external auditory canal).
	• Objective tinnitus can occur either from perception of an abnormal somatosound or abnormal perception of a normal somatosound.
	• Objective tinnitus is often rhythmic and may be synchronous with the pulse or respiration.
	• Tinnitus is frequently associated with depression (in up to half of patients) as well as anxiety and insomnia.
	• Objective tinnitus may be associated with a variety of vascular noises arising from the internal jugular vein or jugular bulb, arteriovenous malformations or fistulas, cavernous hemangiomas, aneurysms, vascular stenoses (particularly of the carotid arteries), vascular tumors, and intracranial hypertension.

Key clinical features from the history include the patient’s age, onset (eg, insidious or sudden), duration, temporal pattern (eg, episodic or continuous, progression over time), location (ie, one ear, both ears, or non-localizable), pitch (high or low), amplitude (loud or soft), rhythm (steady, gradually fluctuating, or rhythmic), associated symptoms (eg, hearing loss, aural fullness, otalgia, vertigo, insomnia, anxiety, depression, headache, and neurologic dysfunction), as well as family history, previous head injury, noise exposure, medication use, previous ear infections, and previous ear surgery (26; 113; 80). High-pitched tinnitus may be described as ringing, steam- or wind-like (like steam blowing from a tea kettle), or clicking, whereas low-pitched tinnitus is often roaring, grinding, or like the sound of a seashell held to the ear. Objective tinnitus is often rhythmic and may be synchronous with the pulse or respiration. Tinnitus is generally most apparent and bothersome at night when the masking ambient noise is less.

Tinnitus is frequently associated with depression (in up to half of patients), anxiety, and insomnia. Patients may excessively focus on their tinnitus, with detrimental effects on occupational and social functioning; these patients may rate their tinnitus as louder than nondistressed patients, even though such reports are inconsistent with objective measures of tinnitus loudness using masking (127).

Objective tinnitus may be associated with a variety of vascular noises arising from the internal jugular vein or jugular bulb, arteriovenous malformations or fistulas (30), cavernous hemangiomas, aneurysms, vascular stenoses (particularly of the carotid arteries), vascular tumors, and intracranial hypertension (80). Objective tinnitus from (non-venous) vascular causes is usually harsh and is synchronous with the pulse. Audiometry is generally normal with pulsatile tinnitus, but occasional cases may have associated conductive or sensorineural hearing loss (eg, middle-ear inflammation and semicircular canal dehiscence may be associated with conductive hearing loss) (109); a high-riding jugular bulb, jugular bulb diverticulum, or jugular bulb tumor (typically a glomus jugulare tumor but also rarely a meningioma or lower cranial nerve schwannoma) can erode into the inner ear, involve the ossicular chair, and cause conductive hearing loss (51); microvascular compression of the eighth nerve has been reported to cause pulsatile tinnitus and sensorineural hearing loss). Rarely, iatrogenic surgical complications can produce pulsatile tinnitus with observable movement of the tympanic membrane as with transmission of dural pulsations through leaking cerebrospinal fluid into the mastoid air cells (157; 40).

The cervical venous hum is a common but innocuous murmur that can be heard in the anterior neck and sometimes upper chest; the hum is often mistaken for more sinister sounds, including a carotid bruit, the vascular sounds of an arteriovenous malformation or fistula, or the murmurs of aortic regurgitation, aortic stenosis, or a patent ductus arteriosus (73; 50; 118; 32; 80). Most patients with venous hums are asymptomatic, but occasionally venous hums are the source of disturbing objective tinnitus and sometimes are also associated with conductive or factitious sensorineural hearing loss (due to a masking property of the venous hum) (23; 155; 62; 25; 120; 105; 80). Objective tinnitus associated with a venous hum is a continuous murmur with pulse-synchronous (diastolic) accentuation of variable character from a hum to a musical whistle to a roar. Clinically it is best detected with the bell of a stethoscope, and it is typically loudest beneath the lower lateral border of the sternal attachment of the sternocleidomastoid muscle and just superior to the medial end of the clavicle. It can be unilateral or bilateral, but when unilateral, it is typically present on the right side. It is accentuated by neck extension and turning the head 45 degrees away from the side auscultated, and it is diminished by turning the head toward the side auscultated. Clinically it can be confirmed by elimination of the sound with moderate pressure over the internal jugular vein a few inches above the clavicle with a finger pressed lateral to the thyroid cartilage (which is insufficient to interfere with the carotid artery pulse), and often accentuated with release of this pressure or by pressure on the contralateral internal jugular vein.

Other cranial venous vascular noises with pulsatile tinnitus can result from a high jugular bulb (also referred to as an enlarged jugular bulb or jugular dehiscence) that elevates the floor of the hypotympanum unilaterally and protrudes into the middle ear (instead of lying normally, inferior to the middle ear space separated by a thick area of petrous bone) (03; 53; 44; 51; 80). A dehiscent jugular bulb may be visible as a bluish mass behind the tympanic membrane and can be mistaken for a middle ear mass (03). A dehiscent jugular bulb can produce conductive hearing loss by impeding mobility of the tympanic membrane or ossicular chain (03). It may also pose a risk of severe hemorrhage with myringotomy (03). The tinnitus associated with a high jugular bulb may not be readily appreciated on examination with a regular stethoscope, but a preliminary diagnosis can be made when the tinnitus is eradicated with compression of the ipsilateral jugular vein (53).

Sigmoid sinus diverticula and dehiscence can also produce venous vascular noises (110; 94; 42; 86; 125; 56; 63; 128; 153; 154; 158). Although rare, sigmoid sinus diverticulum or dehiscence is an increasingly recognized cause of pulsatile objective tinnitus and is amenable to endovascular or surgical correction (110; 112; 125; 56; 154). These anomalies typically occur in or adjacent to the region of the transverse-sigmoid sinus junction (153), but they are not limited to this position. These dural sinus anomalies are generally seen in obese women in their forties (56; 63; 153) and overlaps of sigmoid sinus diverticula and dehiscence with idiopathic intracranial hypertension have been noted (63). These anomalies are commonly associated with sensorineural hearing loss and aural fullness and may be associated with audible mastoid bruits in about one quarter of affected patients (56).

Objective tinnitus associated with abnormal clonic muscular contractions of palatal or middle ear muscles may occur as an intermittent series of sharp, regular clicks, or with palatal myoclonus as a fairly regular, continuous clicking sound (13; 103; 91; 49; 144; 08; 15; 11; 38; 54; 01; 68; 28; 33; 124; 147; 02). The clicks occur over a wide frequency range in different patients (ie, from 10 to 300 Hz) (85; 145; 129).

There are two distinct forms of palatal myoclonus: (1) symptomatic palatal myoclonus and (2) essential palatal myoclonus (37). Symptomatic palatal myoclonus is associated with brainstem and cerebellar dysfunction, whereas there are no reports of associated neurologic dysfunction or neuropathology associated with essential palatal myoclonus.

Middle ear myoclonus is commonly manifest by objective tinnitus that is characterized as clicking (possibly due to tensor tympani movement) or buzzing (possibly due to stapedius movement), but that has also been described as throbbing, tapping, bubbling, ticking, twitching, blowing, drum-like thumping, crunching, whooshing, or gushing (45; 111; 124). Tinnitus associated with middle ear myoclonus is usually objective (though it may be subjective) and rhythmic; it may be either continuous or intermittent and either unilateral or bilateral (45; 33; 124). Stapedius myoclonus may be precipitated by loud sounds and is often associated with facial nerve pathology (eg, hemifacial spasm and sometimes with Bell palsy) (95), but it may also be associated with clinical expression of diffuse motor unit hyperexcitability (eg, benign fasciculation syndrome) (18). Audiometry is generally normal. Tympanometry may demonstrate rhythmic changes in middle-ear compliance (01). Spontaneous otoacoustic emission testing may demonstrate large emission responses in affected ears (124). Forced eyelid closure syndrome involves an aberrant neural reflex between cranial nerve VII, activating the orbicularis oculi muscle, and cranial nerve V, activating the tensor tympani muscle and causing objective tinnitus with eyelid closure (75).

Objective tinnitus associated with a patulous Eustachian tube may be described variously as a blowing sound, an ocean roar, a low-pitched sound, a flapping sound, or a click (26; 113; 107; 143). It is synchronous with nasal breathing, usually more marked in the upright position, gradually disappears with lying down, and often transiently abates with sniffing, snorting, or a Valsalva maneuver (95; 26; 113; 143). It is more common in women and has been associated with weight loss, oral contraceptive use, pregnancy, and mucosal atrophy (eg, due to atrophic rhinitis or radiotherapy) (95; 113; 107). Physical examination is usually normal, although the tympanic membrane may occasionally move synchronously with respiration (95; 107; 143). Audiometry is normal.

Prognosis and complications

The prognosis depends heavily on the etiology, but many cases of objective tinnitus can be cured with surgery. Tinnitus is frequently associated with depression, anxiety, and insomnia.

Clinical vignette

A 75-year-old man presented with a 2-year history of a pulsatile "squeaking, whooshing" tinnitus in his right ear that caused insomnia (21). A whooshing noise could be auscultated throughout the skull. Carotid duplex studies showed severe bilateral carotid stenosis; an arteriogram demonstrated bilateral 90% stenosis at the origins of the carotid arteries, with ulceration on the left. Staged left-then-right carotid endarterectomies were performed without complication and with resolution of the tinnitus.

Biological basis

	• Objective tinnitus may occur with blood flow through a normal artery near the ear, in conjunction with respiration from a patulous Eustachian tube, with palatal myoclonus, or from vascular abnormalities (eg, venous bruits, arterial bruits, vascular malformations or fistulas, and vascular tumors).
	• Objective tinnitus results from transmission of sounds generated near the ear from respiration, vascular noises, or muscular contractions.

Anatomic localization

Objective tinnitus may occur with blood flow through a normal artery near the ear, in conjunction with respiration from a patulous Eustachian tube, with palatal myoclonus, or from vascular abnormalities (eg, venous bruits, arterial bruits, vascular malformations or fistulas, and vascular tumors) (90).

Pathophysiology

Objective tinnitus results from transmission of sounds generated near the ear from respiration, vascular noises, or muscular contractions. The sounds of respiratory air turbulence may be transmitted to the middle ear by a patulous Eustachian tube. Pulsatile vascular noises occur with blood turbulence. Muscle contractions may be transmitted to the middle ear ossicles via vibrations, or they may induce Eustachian tube opening or closure. Objective tinnitus rarely occurs with high-intensity spontaneous otoacoustic emissions generated within the cochlea (57).

Pulsatile tinnitus may occur because of blood turbulence near areas of arterial narrowing (eg, from atherosclerosis or arterial dissections), near areas of abnormal blood flow (eg, arteriovenous malformations, dural arteriovenous fistulas, carotid-cavernous fistulas, vertebro-vertebral arteriovenous fistulas, aberrant vascular loops, glomus jugulare tumors, sigmoid plates, neovascularization with otosclerosis, Paget disease), by increased blood flow (eg, anemia, thyrotoxicosis, pregnancy, or hypertension treated with agents that lower peripheral vascular resistance, or other causes of high cardiac output), by transmission of heart sounds (eg, aortic stenosis), and as a result of intracranial hypertension (90; 134; 135; 136; 148; 149; 74; 114; 35; 84; 07; 141; 80; 52; 16; 71; 104).

Sigmoid sinus diverticula, jugular diverticula, and dehiscent sigmoid plates may present as pulsatile tinnitus (52; 87; 161; 43; 55; 152). A sigmoid plate is a thin bony plate separating the sigmoid sinus from adjacent structures (eg, the mastoid air cells) or separating a high-riding jugular bulb from the middle-ear cavity. Sigmoid plate dehiscence often involves either the anterolateral aspect of the superior curve or the descending segment of the sigmoid sinus on the side of the dominant lateral sinus, which often coexists with extensive temporal bone pneumatization (52). The similar radiologic prevalence and extent of dehiscent sigmoid plates among different age groups suggest that sigmoid plate dehiscence is more likely to be congenital than acquired (87).

A presumptive “somatosensory pulsatile tinnitus syndrome” has been described in which a high-pitched, cardiac-synchronous pulsatile tinnitus could be suppressed by strong contractions of the neck and jaw muscles (83). Approximately half of the cases are unilateral and half bilateral. Levine and colleagues suggested that this form of tinnitus resulted from “cardiac synchronous somatosensory activation of the central auditory pathway” in which the “cardiac somatosounds” were not suppressed by somatosensory-auditory central nervous system interactions. Whether some of these cases were actually venous hums is not clear.

A venous hum is caused by turbulence (ie, disruption of the otherwise smooth laminar flow into turbulent eddies) in the internal jugular vein, which causes the vessel walls to vibrate (31; 155). This is precipitated or accentuated with turning the head away from the auscultated side as the internal jugular vein is stretched and pulled against the transverse process of the atlas (31) and as the contraction of the ipsilateral sternocleidomastoid muscle (ie, that turns the head to the opposite side) removes pressure on the ipsilateral internal jugular vein and, thus, increases flow on that side (155).

Patients with hydrocephalus or pseudotumor cerebri commonly develop pulsatile tinnitus (138; 137; 133; 134; 121; 102; 150; 82; 146; 156; 12; 80; 151). This occurs in up to 52% of patients with pseudotumor cerebri (150; 151). Pulsatile tinnitus with increased intracranial pressure may result from several (not mutually exclusive) mechanisms: (1) turbulence as blood flows from the hypertensive intracranial vessels to the lower-pressure jugular bulb (96; 97); (2) augmentation of venous and cerebrospinal fluid pulsations because the accompanying arteriolar dilation allows a greater transmission of the arterial pulse (03); and (3) transmission of systolic CSF pulsations to the walls of the venous sinuses, which in turn produces turbulent flow in the sinuses (133; 146; 12; 134). The noise may be unilateral because of asymmetries of jugular vein flow (96; 97; 146), with the bruit occurring on the side of greatest jugular vein flow (96; 97). It is attenuated by maneuvers that decrease jugular vein flow (eg, jugular vein compression ipsilateral to the tinnitus, Valsalva, and turning the head) (97; 133; 134; 146; 12). It also remits transiently with lumbar puncture or permanently with definitive treatment of intracranial hypertension (eg, with shunting, or with suboccipital decompression in cases of hydrocephalus due to type I Arnold Chiari malformation) (133; 134; 146; 156).

Objective tinnitus associated with clonic muscular contractions has been variously attributed to transmission of muscular vibrations to middle ear structures and to sounds generated by secondary closing or opening of the Eustachian tube (115; 91; 79; 54); sophisticated observations with sonotubometry, however, have localized the clicking sounds associated with palatal myoclonus to opening of the Eustachian tube, presumably with release of sound energy as the surface tension holding the tube closed is suddenly broken (139). Symptomatic palatal myoclonus is usually attributed to a lesion in the Guillain-Mollaret triangle (ie, between the dentate nucleus, the inferior olive, and the red nucleus); the cause is typically vascular, but less commonly multiple sclerosis, head trauma, syphilis, electric shock, and other causes may be responsible. These lesions produce hypertrophic degeneration of the inferior olive and secondary rhythmic, synchronized discharges that act on a variety of brainstem motor nuclei, causing nystagmus, palatal contractions, extrapalatal tremors (eg, of the chin and platysma), and rarely ear clicks. Essential palatal myoclonus is less well understood but is thought to result from a distinct brainstem oscillator that stimulates the trigeminal motor nucleus, causing rhythmic contraction of the tensor veli palatini muscle, Eustachian tube opening, and ear clicks (37).

Differential diagnosis

Associated or underlying disorders

Unilateral pulsatile tinnitus is by far the most common type of objective tinnitus, but it may also be subjective. Usually, it is a benign symptom resulting from normal vascular sounds, possibly exacerbated by anxiety, insomnia, caffeine, or exercise. Pulsatile tinnitus, however, can be a symptom of a more serious problem, such as an arteriovenous malformation, carotid-cavernous fistula, aneurysm, vascular stenosis, arterial dissection, vascular tumor, or intracranial hypertension. Pulsatile tinnitus may occur with otosclerosis or Paget disease, apparently because of neovascularization and the formation of arteriovenous fistulae within the temporal bone (134). Pulsatile tinnitus following head trauma may indicate a traumatic arteriovenous malformation, carotid-cavernous fistula, or carotid dissection. Although vascular loops in contact with the eighth cranial nerve are considered a normal variant, individuals with unilateral hearing loss are twice as likely to have such loops in the symptomatic ear than in the asymptomatic ear; individuals with pulsatile tinnitus were 80 times more likely to have a contacting vascular loop on the symptomatic side than individuals with nonpulsatile tinnitus (24).

A venous hum is a normal finding in the vast majority of cases (73) and can be detected by appropriate examination in almost all children between ages 1 and 15 years (50) and 25% to 50% of older adults (73; 50; 06). Less commonly, it may occur or be accentuated (to the point where it is symptomatic) in pregnancy and various disease states (eg, anemia, aortic insufficiency, thyrotoxicosis, intracranial arteriovenous malformations that produce increased cerebral blood flow, or high cardiac output states as with fever, dialysis patients with anemia and arteriovenous fistulas, or pulmonary or other arteriovenous fistulas) (23; 73; 118; 59; 60; 61; 22; 32; 155; 62; 131; 117). Venous hums may be bilateral with hyperdynamic cardiac states (59) and may be associated with cranial or orbital bruits if the underlying cause of a secondary venous hum is an intracranial arteriovenous malformation (59).

Tinnitus synchronous with respiration suggests a patulous Eustachian tube. Rhythmic tinnitus may also occur with clonic muscular contractions, especially with palatal myoclonus, but also reportedly with spasm of the tensor veli palatini muscle, the levator veli palatini muscle, the tensor tympani muscle, or the stapedius muscle (89; 113; 54). Rarely, popping sounds may occur with mucous bubbling through a tympanic membrane perforation (29).

Diagnostic workup

	• Clinical examination of patients with any form of tinnitus should include funduscopy, otoscopy, tests of hearing, neurologic examination, auscultation for objective tinnitus (eg, by placing a regular or electronic stethoscope over the patient's external auditory canal, orbit, cranium, and neck), observation for palatal myoclonus, palpation of the neck or oral cavity for masses, examination of the temporomandibular joint, and audiometry.
	• Audiometry is often normal in patients with objective tinnitus but may show conductive, sensorineural, or mixed hearing loss.
	• In patients with pulsatile tinnitus, clinical evaluation should include assessment of vascular risk factors, funduscopy to exclude papilledema, otoscopy to exclude a retrotympanic mass (eg, glomus jugulare tumor), assessment of the effect of jugular bulb pressure on the tinnitus, auscultation for cranial and carotid bruits, and examination for evidence of occlusive vascular disease elsewhere in the body.
	• Further diagnostic studies can include CT of the head or temporal bones, MRI of the head, carotid ultrasound, CT angiography and venography, magnetic resonance angiography and venography, conventional angiography, and lumbar puncture.

Clinical examination of patients with any form of tinnitus should include funduscopy, otoscopy, tests of hearing, neurologic examination, auscultation for objective tinnitus (eg, by placing a regular or electronic stethoscope over the patient's external auditory canal, orbit, cranium, and neck), observation for palatal myoclonus, palpation of the neck or oral cavity for masses, examination of the temporomandibular joint, and audiometry (80). Otoscopy can identify impacted cerumen, a perforated eardrum, middle ear fluid, cholesteatoma, glomus jugulare tumors, and other masses. Auscultation is performed by listening with a regular or electronic stethoscope over the patient's external auditory canal, orbit, cranium, and neck. If objective tinnitus is identified, it should be timed relative to the pulse and respiration. A venous hum may be eliminated by turning the head to the same side, with Valsalva, or by gentle temporary pressure on the neck that occludes the jugular vein but not the carotid artery.

Audiometry is often normal in patients with objective tinnitus but may show conductive, sensorineural, or mixed hearing loss (80). Spontaneous otoacoustic emission testing may demonstrate large emission responses in affected ears of patients with middle ear myoclonus (124). Tympanometry may demonstrate oscillations with a glomus jugulare tumor, a carotid bruit, a patulous Eustachian tube, stapedius muscle myoclonus, or palatal myoclonus (20; 54). In glomus jugulare tumor and carotid bruit, the oscillations are synchronous with the pulse. In contrast, with a patulous Eustachian tube, the oscillations are synchronous with respiration, and palatal myoclonus causes small amplitude, high-frequency oscillations that are not synchronous with either the pulse or respiration. Carotid artery pressure will eliminate the oscillations if they are transmitted from a carotid stenosis. Brainstem auditory evoked potential studies can help assess retrocochlear lesions. Rhythmic ambient pressure tympanometry wave patterns can be seen with various temporal bone pathologies that present with objective tinnitus, including superior semicircular canal dehiscence, sigmoid sinus dehiscence, internal carotid artery dehiscence, glomus tumor, and encephalocele; about 90% of individuals found to have rhythmic waves showed a radiographic finding on computed tomography temporal bone imaging associated with the objective tinnitus (126).

In patients with pulsatile tinnitus, clinical evaluation should include assessment of vascular risk factors, funduscopy to exclude papilledema, otoscopy to exclude a retrotympanic mass (eg, glomus jugulare tumor), assessment of the effect of jugular bulb pressure on the tinnitus, auscultation for cranial and carotid bruits, and examination for evidence of occlusive vascular disease elsewhere in the body (80).

Further diagnostic studies can include CT of the head or temporal bones, MRI of the head, carotid ultrasound, CT angiography and venography, magnetic resonance angiography and venography, conventional angiography, and lumbar puncture (93; 135; 80; 100). Head MRI with gadolinium enhancement should be obtained in patients with unexplained unilateral tinnitus (with or without hearing loss), and in patients with hearing loss suspicious for retrocochlear pathology (135). Identification of a jugular bulb abnormality on MRI should prompt CT and vestibular-evoked myogenic potential (VEMP) testing to evaluate for inner ear erosion or dehiscence into the vestibular aqueduct or posterior semicircular canal (51). Thin-slice, high-resolution CT venography is recommended to evaluate sigmoid plate dehiscence (161). Suspected carotid stenosis can be imaged with duplex ultrasonography or MR, CT, or conventional angiography. In patients with evidence of increased intracranial pressure (eg, headache and papilledema), CT or MRI should be performed to exclude a mass lesion; in addition, lumbar puncture should be performed if there is communicating hydrocephalus and no mass lesion on brain imaging. In obese, middle-aged women with pulsatile tinnitus but without idiopathic intracranial hypertension, high-resolution temporal bone CT can identify sigmoid sinus diverticula or dehiscence, which can be confirmed with angiography (112; 86; 56; 128; 153); important imaging characteristics include a dehiscent sigmoid plate and extensive temporal bone pneumatization (86). Angiography or magnetic resonance venography may be helpful if dural sinus thrombosis is suspected. In patients with a retrotympanic lesion otoscopy, it is important to distinguish an aberrant carotid artery, abnormal jugular bulb, and glomus jugulare tumor; CT of the temporal bones is recommended (134; 135), but head CT, MRI, MRA, CT angiography, and conventional angiography may also be helpful. As noted above, a tympanogram may demonstrate oscillations synchronous with the pulse.

In patients with rhythmic tinnitus from palatal myoclonus, the key to diagnosis is to recognize the palatal contractions. Pressing a finger on the affected side of the palate in the direction of the Eustachian tube opening can temporarily cease tinnitus, even while the muscular contractions continue.

In patients with tinnitus synchronous with nasal breathing, a suspected patulous Eustachian tube can be confirmed by temporary resolution of tinnitus with the head recumbent or with sniffing, snorting, or Valsalva maneuver (95; 26). As noted above, a tympanogram may also demonstrate oscillations synchronous with respiration (20).

Management

	• Symptomatic treatment of the tinnitus, as well as treatment of any associated depression, anxiety, and insomnia, can be helpful, even if the associated tinnitus cannot be eliminated.
	• Masking is generally attempted ipsilaterally and contralaterally. A variety of management actions can assist with masking, including removal of ear wax, nighttime use of a bedside radio (possibly with a pillow speaker) tuned between stations, white noise generators, white noise tapes, tapes of "ocean surf," a hearing aid, tinnitus masking devices, and "tinnitus instruments" (which combine a masking device and a hearing aid).
	• Drug therapies have not been successful to date for long-term tinnitus reduction.
	• Pulsatile tinnitus related to vascular pathology may also respond to surgery or endovascular approaches.

Symptomatic treatment of the tinnitus, as well as treatment of any associated depression, anxiety, and insomnia, can be helpful, even if the associated tinnitus cannot be eliminated (80). Symptomatic treatment of tinnitus can include reassurance, various psychological treatments (eg, supportive psychotherapy, biofeedback, hypnosis) (05), habituation therapy (67), masking techniques (127; 47), drugs, electrical stimulation, and, rarely, surgery (09). The most widely employed treatments include reassurance, masking techniques, and various drugs, but many patients receive little apparent benefit from these (80). Biofeedback does not reduce tinnitus loudness, but it may reduce muscular tension and anxiety, may facilitate coping with the tinnitus, and may be better accepted by patients than psychological counseling (05; 113). Tinnitus retraining or habituation therapy utilizing a multidisciplinary treatment team is expensive and not widely available but shows promise (135; 10). Electrical stimulation with a cochlear implant or with transtympanic stimulation of the cochlea has been helpful in some patients, but this invasive approach needs further testing before it can be generally advocated.

Removal of ear wax may help some patients with tinnitus, partly because it increases ambient sound and assists with masking, and partly because ear wax on the tympanic membrane can produce tinnitus through local effects on the conduction pathway. For patients who are particularly bothered by tinnitus at night, a bedside radio (possibly with a pillow speaker) tuned between stations can provide effective masking and allow them to get to sleep. White noise generators or recordings of white noise or "ocean surf" produce similar results. Similarly, a hearing aid may improve hearing and communication and decrease tinnitus by amplifying ambient sound and providing some masking. Tinnitus masking devices can be worn like a hearing aid, and "tinnitus instruments" combine a masking device and a hearing aid. Masking is generally attempted ipsilaterally and contralaterally. Unfortunately, the long-term efficacy of tinnitus masking units is, at best, variable; in some studies, efficacy was poor (127; 47; 26; 113); in a large observational study of tinnitus masking, two thirds of patients achieved at least partial relief, but only 6% achieved complete relief (127), whereas results in one small, randomized trial were no better than placebo (47). In some patients, a high level of masking is required (ie, above 10 dB), and the patient finds the masking signal too distracting (20). In others, bilateral tinnitus is not relieved with masking devices, or the application of bilateral masking devices makes it difficult for patients to hear environmental sounds (20).

Many investigators have evaluated a range of drugs in the hope that a long-acting oral medication could be found that was effective in treating tinnitus (101). In particular, numerous anticonvulsants have been tried (98), including carbamazepine (92), phenytoin, barbiturates, benzodiazepines (81; 101; 72), and sodium valproate (99). Other agents purported to be effective include nortriptyline (142) and melatonin (119). All of these agents provide, at best, modest relief in subsets of patients; drug therapies generally have not been successful for long-term tinnitus reduction (101; 20; 58). Clinical trials of pharmacologic agents have had significant deficiencies; methodologically improved studies are needed, using specific etiologic groups and appropriate controls with subjective and objective psychophysical measurements (101).

Symptomatic secondary venous hums may resolve with treatment of the underlying condition (62); other cases have been effectively treated by an external device to compress the internal jugular vein (23), by mastoidectomy (41), or by internal jugular vein ligation (155; 17; 62; 25; 70; 120; 105; 04). Similarly, pulsatile tinnitus resulting from an abnormal jugular bulb may be cured with jugular vein ligation (53). Internal jugular vein ligation typically results in immediate and permanent relief of the pulsatile tinnitus associated with venous hums or a high jugular bulb; however, there is a theoretical risk of precipitating a venous hum on the opposite side because of the increased contralateral flow postsurgically. Angiography is recommended before internal jugular vein ligation to exclude other vascular pathology and to ensure normal venous drainage on the opposite side. Surgical reconstruction of the middle ear floor under local anesthesia can be effective for patients with incapacitating tinnitus due to dehiscent middle ear floor from a high-riding jugular bulb, but there is a risk of sigmoid sinus thrombosis (44).

Total resection of jugular foramen tumors, including most commonly glomus jugulare tumors but also meningiomas and lower cranial nerve schwannomas, can be a curative treatment, but there is a significant frequency (approximately 20%) of new lower cranial nerve deficits with surgery (48). Subtotal removal may be required to preserve cranial nerve function, vital vascular structures, and the brainstem, in which case postoperative radiotherapy is used to control residual tumor (48).

Other forms of pulsatile tinnitus related to vascular pathology may also respond to surgery or endovascular approaches (80). For example, pulsatile tinnitus resulting from carotid stenosis may be cured with carotid endarterectomy (88; 21; 108; 77; 132), carotid ligation (21), or angioplasty and stenting (46; 132). Ipsilateral carotid endarterectomy is effective for treatment of vascular pulsatile tinnitus caused by proximal atherosclerotic carotid artery disease (over 90% cure rate), whereas distal lesions have been treated by stenting, though with less effectiveness (132).

Pulsatile tinnitus from sigmoid sinus and jugular bulb pathology, such as diverticula, aneurysms, and dehiscence, is a rare, but largely treatable condition using sigmoid sinus wall reconstruction/resurfacing, endovascular intervention, and cardiac U-clip techniques (152; 106; 158). Pulsatile tinnitus caused by transverse and sigmoid sinus dural arteriovenous fistulas has been cured endovascularly with transarterial or transvenous embolization (130; 36; 78) or with surgery (34; 152); pulsatile tinnitus associated with a transverse-sigmoid sinus aneurysm has been cured with an endovascularly placed stent (160). A spontaneous carotid-jugular fistula has been cured with endovascular embolization (69). Pulsatile tinnitus associated with sigmoid sinus diverticula or dehiscence can be treated with endovascular or surgical procedures, including transmastoid reconstruction of the sigmoid sinus or just soft tissue resurfacing (110; 112; 125; 56; 153; 76; 159; 152; 106).

Pulsatile tinnitus caused by hydrocephalus or pseudotumor cerebri remits transiently with lumbar puncture or permanently with definitive treatment of intracranial hypertension (eg, with shunting or with suboccipital decompression in cases of hydrocephalus due to type I Arnold Chiari malformation) (96; 133; 134; 146; 156; 39). Jugular venous compression may alleviate the bruit and pulsatile tinnitus but further elevate intracranial pressure, so jugular vein ligation is contraindicated in the setting of increased intracranial pressure (96). Based on an uncontrolled case series, venous sinus stenting appears to be an effective treatment for pulsatile tinnitus in patients with intracranial hypertension and significant venous sinus stenosis (14).

Palatal myoclonus has anecdotally been reported to respond to 5-hydroxytryptophan, anticholinergic drugs, clonazepam (08), sodium valproate (15), barbiturates, phenytoin, and carbamazepine (116), but results with these agents are inconsistent at best (37). Several surgical procedures to treat the associated tinnitus have also been reported with variable results, including sectioning the stapedius or tensor tympani muscles (85; 64; 124), operating on the levator palatini muscle to maintain a permanently open Eustachian tube (85), Eustachian tube obliteration (37), and middle ear aeration with tympanostomy tubes (79; 107). In some cases, surgical procedures have made the patients worse. Psychotherapy, application of cocaine to the nasopharynx (115), otic ganglion blockade with anesthetic agents, stimulation of the corneal reflex, acupuncture, hypnosis, relaxation exercises, and other approaches have also been tried without much success. Patients may receive some benefit from tinnitus masking (122). Injections of clostridium botulinum toxin into the levator veli palatini and tensor veli palatini muscles may be the most useful approach to suppressing the tinnitus associated with palatal myoclonus and essential palatal tremor (122; 123; 19; 27; 140; 33). The most common side effects of clostridium botulinum treatment are paresis-induced Eustachian tube obstruction and velopharyngeal weakness, with nasal regurgitation and dysphagia (122; 19); tympanostomy tube placement can relieve discomfort associated with Eustachian tube dysfunction, and careful titration can minimize side effects (19).

In patients with objective tinnitus resulting from middle ear myoclonus, the response to middle ear muscle tendon lysis is variable (despite prior expectations that such treatment should be definitive) (45; 66; 111). Forced eyelid closure syndrome has been successfully treated with intrapalatal botulinum toxin (75).

References

01: Abdul-Baqi KJ. Objective high-frequency tinnitus of middle-ear myoclonus. J Laryngol Otol 2004;118:231-3. PMID 15068524
02: Acosta RM, Saro-Buendía M, García LT, Antonia M, Vernetta CP. Objective tinnitus secondary to palatal tremor: two case reports. Int Tinnitus J 2022;25(2):129-32. PMID 35239294
03: Adler JR, Ropper AH. Self-audible venous bruits and high jugular bulb. Arch Neurol 1986;43:257-9. PMID 3947273
04: Al Turki S, Al-Kohlani H, Shabra S. Venous hum tinnitus. Int J Angiol 2003;12:32-3.
05: Andersson G, Lyttkens L. A meta-analytic review of psychological treatments for tinnitus. Br J Audiol 1999;33:201-10. PMID 10509855
06: Appleyard WJ, Joseph M. Innocent heart murmurs in children. A survey of 119 patients. Practitioner 1976;217:783-6. PMID 995834
07: Armstrong RJ, Downer J, Evans N, Anslow P, Ebers FC. Teaching neuroimages: Headache with pulsatile tinnitus. Neurology 2011;76(17):e82. PMID 21518994
08: Bakheit AM, Behan PO. Palatal myoclonus successfully treated with clonazepam. J Neurol Neurosurg Psychiatry 1990;53:806. PMID 2246666
09: Baloh RW. Dizziness, hearing loss, and tinnitus. Philadelphia: FA Davis, 1998.
10: Berry J, Gold SL, Frederick EA, Gray WC, Staecker H. Patient-based outcomes in patients with primary tinnitus undergoing tinnitus retraining therapy. Arch Otolaryngol Head Neck Surg 2002;128:1153-7. PMID 12365886
11: Bertholon P, Convers P, Antoine JC, et al. Objective tinnitus associated with essential laryngeal myoclonus: report of two cases. Mov Disord 2002;17:218-20. PMID 11835471
12: Biousse V, Newman NJ, Lessell S. Audible pulsatile tinnitus in idiopathic intracranial hypertension. Neurology 1998;50:1185-6. PMID 9566427
13: Bjork H. Objective tinnitus due to clonus of the soft palate. Acta Otolaryngol Suppl 1954;116:39-45. PMID 13188659
14: Boddu S, Dinkin M, Suurna M, Hannsgen K, Bui X, Patsalides A. Resolution of pulsatile tinnitus after venous sinus stenting in patients with idiopathic intracranial hypertension. PLoS One 2016;11(10):e0164466. PMID 27768690
15: Borggreve F, Hageman G. A case of idiopathic palatal myoclonus: treatment with sodium valproate. Eur Neurol 1991;31:403-4. PMID 1756767
16: Breda MS, Amorim J, Rocha J, Dias L. Vertebro-vertebral fistula presenting as a pulsatile tinnitus. BMJ Case Rep 2018;2018. PMID 29437736
17: Brennan FJ, Salerno TA. Surgical treatment of symptomatic cervical venous hum. J Thorac Cardiovasc Surg 1981;81:135-6. PMID 7453215
18: Brigo F, Storti M, Lochner P, Nardone R. Transitory stapedial myoclonus in a patient with benign fasciculation syndrome. J Laryngol Otol 2013;127(6):605-6. PMID 23480624
19: Bryce GE, Morrison MD. Botulinum toxin treatment of essential palatal myoclonus tinnitus. J Otolaryngol 1998;27:213-6. PMID 9711516
20: Campbell K. Audiologic assessment and management of tinnitus. In: Essential audiology for physicians. San Diego: Singular Publishing Co, 1998:167-77.
21: Carlin RE, McGraw DJ, Anderson CB. Objective tinnitus resulting from internal carotid artery stenosis. J Vasc Surg 1997;25:581-3. PMID 9081143
22: Cartlidge NE, Ayyar DR, Lee M. Intracranial A-V malformation associated with cranial bruit and cervical venous hum. Postgrad Med J 1970;46:726-8. PMID 5492708
23: Cary FH. Symptomatic venous hum. Report of a case. N Engl J Med 1961;264:869-70. PMID 13691212
24: Chadha NK, Weiner GM. Vascular loops causing otological symptoms: a systematic review and meta-analysis. Clin Otolaryngol 2008;33(1):5-11. PMID 18302544
25: Chandler JR. Diagnosis and cure of venous hum tinnitus. Laryngoscope 1983;93:892-5. PMID 6865626
26: Ciocon JO, Amede F, Lechtenberg C, Astor F. Tinnitus: a stepwise workup to quiet the noise within. Geriatrics 1995;50:18-25. PMID 7835722
27: Conill Tobias N, de Paula Vernetta C, García Callejo FJ, Marco Algarra J. Objective tinnitus from palatal myoclonus. Use of botulinum toxin: a case report. Acta Otorrinolaringol Esp 2012;63(5):391-2. PMID 21513907
28: Costa de Araujo P, Savage J. Objective tinnitus from middle ear myoclonus. Arch Otolaryngol Head Neck Surg 2012;138(4):421. PMID 22508628
29: Cox LC, MacDonald CB. Patient with audible popping sounds emanating from the ear canal. J Am Acad Audiol 1995;6:261-3. PMID 7620205
30: Cui B, Wang H, Zhou Y, Liang Z. Multiple dural arteriovenous fistulas presenting as objective pulsatile tinnitus and evaluated using four-dimensional contrast-enhanced MR angiography. Ear Nose Throat J 2024;103(4):219-21. PMID 34643457
31: Cutforth R, Wiseman J, Sutherland RD. The genesis of the cervical venous hum. Am Heart J 1970;80:488-92. PMID 5471210
32: Danahy DT, Ronan JA Jr. Cervical venous hums in patients on chronic hemodialysis. N Engl J Med 1974;291:237-9. PMID 4834753
33: Dang J, Liu YC. Treatment of objective tinnitus with transpalatal Botox(®) injection in a pediatric patient with middle ear myoclonus: a case report. Int J Pediatr Otorhinolaryngol 2019;116:22-4. PMID 30554701
34: de Paula Lucas C, Prandini MN, Spelle L, Piotin M, Mounayer C, Moret J. Parallel transverse-sigmoid sinus harboring dural arteriovenous malformation. How to differentiate the pathological and normal sinus in order to treat and preserve patency and function. Acta Neurochir (Wien) 2010;152(3):523-7. PMID 19517058
35: De Ridder D, De Ridder L, Nowe V, Thierens H, Van de Heyning P, Moller A. Pulsatile tinnitus and the intrameatal vascular loop: why do we not hear our carotids. Neurosurgery 2005;57:1213-7. PMID 16331169
36: Delgado F, Muñoz F, Bravo-Rodríguez F, Jurado-Ramos A, Oteros R. Treatment of dural arteriovenous fistulas presenting as pulsatile tinnitus. Otol Neurotol 2009;30(7):897-902. PMID 19730142
37: Deuschl G, Mishke G, Schenck E, Schulte-Monting J, Lucking CH. Symptomatic and essential rhythmic palatal myoclonus. Brain 1990;113:1645-72. PMID 2276039
38: Deuschl G, Wilms H. Clinical spectrum and physiology of palatal tremor. Mov Disord 2002;17(Suppl 2):S63-6. PMID 11836758
39: Digre KB. Idiopathic intracranial hypertension headache. Curr Pain Headache Rep 2002;6:217-25. PMID 12003693
40: Doshi K, Anari S, Carrie S. Objective pulsatile tinnitus: a video clip demonstration of the condition. Laryngoscope 2006;116(10):1926. PMID 17003696
41: Duvillard C, Ballester M, Redon E, Romanet P. Pulsatile tinnitus cured by mastoidectomy. Ann Otol Rhinol Laryngol 2004;113:730-3. PMID 15453531
42: Eisenman DJ. Sinus wall reconstruction for sigmoid sinus diverticulum and dehiscence: a standardized surgical procedure for a range of radiographic findings. Otol Neurotol 2011;32(7):1116-9. PMID 21799456
43: Eisenman DJ, Raghavan P, Hertzano R, Morales R. Evaluation and treatment of pulsatile tinnitus associated with sigmoid sinus wall anomalies. Laryngoscope 2018;128 Suppl 2:S1-S13. PMID 29756346
44: El-Begermy MA, Rabie AN. A novel surgical technique for management of tinnitus due to high dehiscent jugular bulb. Otolaryngol Head Neck Surg 2010;142(4):576-81. PMID 20304281
45: Ellenstein A, Yusuf N, Hallett M. Middle ear myoclonus: two informative cases and a systematic discussion of myogenic tinnitus. Tremor Other Hyperkinet Mov (N Y) 2013;3. PMID 23610741
46: Emery DJ, Ferguson RD, Williams JS. Pulsatile tinnitus cured by angioplasty and stenting of petrous carotid artery stenosis. Arch Otolaryngol Head Neck Surg 1998;124:460-1. PMID 9559697
47: Erlandsson S, Ringdahl A, Hutchins T, Carlsson SG. Treatment of tinnitus: a controlled comparison of masking and placebo. Br J Audiol 1987;21:37-44. PMID 3828583
48: Fayad JN, Keles B, Brackmann DE. Jugular foramen tumors: clinical characteristics and treatment outcomes. Otol Neurotol 2010;31(2):299-305. PMID 19779386
49: Fitzgerald DC. Palatal myoclonus--case report. Laryngoscope 1984;94:217-9. PMID 6694495
50: Fowler NO, Gause R. The cervical venous hum. Am Heart J 1964;67:135-6. PMID 14110654
51: Friedmann DR, Le BT, Pramanik BK, Lalwani AK. Clinical spectrum of patients with erosion of the inner ear by jugular bulb abnormalities. Laryngoscope 2010;120(2):365-72. PMID 19924772
52: Geng W, Liu Z, Fan Z. CT characteristics of dehiscent sigmoid plates presenting as pulsatile tinnitus: a study of 23 patients. Acta Radiol 2015;56(11):1404-8. PMID 25422514
53: Golucke PJ, Panetta T, Sclafani S, Varughese G. Tinnitus originating from an abnormal jugular bulb: treatment by jugular vein ligation. J Vasc Surg 1987;6:248-51. PMID 3625880
54: Golz A, Fradis M, Martzu D, Netzer A, Joachims HZ. Stapedius muscle myoclonus. Ann Otol Rhinol Laryngol 2003;112(6):522-4. PMID 12834120
55: Gozen ED, Erdur ZB, Karaman E, Yener M, Kizilkiliç O. A rare cause of objective tinnitus: jugular diverticulum. J Craniofac Surg 2018;29(3):e300-2. PMID 29420384
56: Grewal AK, Kim HY, Comstock RH 3rd, Berkowitz F, Kim HJ, Jay AK. Clinical presentation and imaging findings in patients with pulsatile tinnitus and sigmoid sinus diverticulum/dehiscence. Otol Neurotol 2014;35(1):16-21. PMID 24005164
57: Guinchard AC, Ghazaleh N, Saenz M, et al. Study of tonotopic brain changes with functional MRI and FDG-PET in a patient with unilateral objective cochlear tinnitus. Hear Res 2016;341:232-9. PMID 27663095
58: Hannan SA, Sami F, Wareing MJ. Tinnitus. BMJ 2005;330(7485):237. PMID 15677658
59: Hardison JE. Cervical venous hum. A clue to the diagnosis of intracranial arteriovenous malformations. N Engl J Med 1968;278:587-90. PMID 5637756
60: Hardison JE. The cervical venous hum: a help and a hindrance. [Editorial] N Engl J Med 1975a;292:1239-40. PMID 1128577
61: Hardison JE. Cervical venous hum in hyperthyroidism. N Engl J Med 1975b;293:360. PMID 1128577
62: Hardison JE, Smith RB 3rd, Crawley IS, Battey LL. Self-heard venous hums. JAMA 1981;245:1146-7. PMID 7463641
63: Harvey RS, Hertzano R, Kelman SE, Eisenman DJ. Pulse-synchronous tinnitus and sigmoid sinus wall anomalies: descriptive epidemiology and the idiopathic intracranial hypertension patient population. Otol Neurotol 2014;35(1):7-15. PMID 24270723
64: Hazell JW. Tinnitus. II. Surgical management of conditions associated with tinnitus and somatosounds. J Otolaryngol 1990;19:6-10. PMID 2179577
65: Hertzano R, Teplitzky TB, Eisenman DJ. Clinical evaluation of tinnitus. Neuroimaging Clin N Am 2016;26(2):197-205. PMID 27154603
66: Hidaka H, Honkura Y, Ota J, Gorai S, Kawase T, Kobayashi T. Middle ear myoclonus cured by selective tenotomy of the tensor tympani: strategies for targeted intervention for middle ear muscles. Otol Neurotol 2013;34(9):1552-8. PMID 24232057
67: House JW. Treatment of severe tinnitus with biofeedback training. Laryngoscope 1978;88:406-12. PMID 628294
68: Howsam GD, Sharma A, Lambden SP, Fitzgerald J, Prinsley PR. Bilateral objective tinnitus secondary to congenital middle-ear myoclonus. J Laryngol Otol 2005;119(6):489-91. PMID 15992481
69: Huang CF. Pulsatile tinnitus from a spontaneous carotid-jugular fistula: case report. Neurologist 2009;15(6):335-7. PMID 19901713
70: Hvidegaard T, Brask T. Objective venous tinnitus: a case report. J Laryngol Otol 1984;98:189-91. PMID 6693821
71: In 't Veld M, Fronczek R, de Laat JA, Kunst HPM, Meijer FJA, Willems PWA. The incidence of cranial arteriovenous shunts in patients with pulsatile tinnitus: a prospective observational study. Otol Neurotol 2018;39(5):648-53. PMID 29561378
72: Johnson RM, Brummett R, Schleuning A. Use of alprazolam for relief of tinnitus: a double-blind study. Arch Otolaryngol Head Neck Surg 1993;119:842-5. PMID 8343245
73: Jones FL Jr. Frequency, characteristics and importance of the cervical venous hum in adults. N Engl J Med 1962;267:658-60. PMID 14452256
74: Jun BH, Choi IS, Lee GJ. Pulsatile tinnitus alleviated by contralateral neck compression: a case report. Auris Nasus Larynx 2003;30(1):89-91. PMID 12589858
75: Kaffenberger TM, Mandal R, Schaitkin BM, Hirsch BE. Palatal botulinum toxin as a novel therapy for objective tinnitus in forced eyelid closure syndrome. Laryngoscope 2017;127(5):1199-201. PMID 27717035
76: Kim CS, Kim SY, Choi H, et al. Transmastoid reshaping of the sigmoid sinus: preliminary study of a novel surgical method to quiet pulsatile tinnitus of an unrecognized vascular origin. J Neurosurg 2016;125(2):441-9. PMID 26745481
77: Kirkby-Bott J, Gibbs HH. Carotid endarterectomy relieves pulsatile tinnitus associated with severe ipsilateral carotid stenosis. Eur J Vasc Endovasc Surg 2004;27:651-3. PMID 15121118
78: Kirsch M, Liebig T, Kühne D, Henkes H. Endovascular management of dural arteriovenous fistulas of the transverse and sigmoid sinus in 150 patients. Neuroradiology 2009;51(7):477-83. PMID 19352640
79: Kwee HL, Struben WH. Tinnitus and myoclonus. J Laryngol Otol 1972;86:237-41. PMID 5014915
80: Lanska DJ. Disorders of the special senses in the elderly. In: Nair A, Sabbagh M, editors. Geriatric neurology. Chichester, West Sussex, UK: John Wiley & Sons, 2014:396-459.**
81: Lechtenberg R, Schulman A. Benzodiazepines in the treatment of tinnitus. J Laryngol Otol 1984;(Suppl)9:271-6.
82: Lee AG. Pulsatile tinnitus as a presenting symptom of pseudotumor cerebri. J Otolaryngol 1996;25:203-4. PMID 8783088
83: Levine RA, Nam EC, Melcher J. Somatosensory pulsatile tinnitus syndrome: somatic testing identifies a pulsatile tinnitus subtype that implicates the somatosensory system. Trends Amplif 2008;12(3):242-53. PMID 18632767
84: Libman R, Johnson A. Pulsatile tinnitus from a redundant arterial loop. Neurology 2006;66:1687. PMID 16769941
85: Litman RS, Hausman SA. Bilateral palatal myoclonus. Laryngoscope 1982;92:1187-9. PMID 7132522
86: Liu Z, Chen C, Wang Z, et al. Sigmoid sinus diverticulum and pulsatile tinnitus: analysis of CT scans from 15 cases. Acta Radiol 2013;54(7):812-6. PMID 23550183
87: Liu Z, Li J, Zhao P, et al. Sigmoid plate dehiscence: congenital or acquired condition? Eur J Radiol 2015;84(5):862-4. PMID 25660638
88: Louwrens HD, Botha J, Van Der Merwe DM. Subjective pulsatile tinnitus cured by carotid endarterectomy: a case report. S Afr Med J 1989;75:496-7. PMID 2727831
89: Lyons GD, Melancon BB, Kearby NL, Zimny M. The otologic aspects of palatal myoclonus. Laryngoscope 1976;86:930-5. PMID 933688
90: Mackenzie I. The intracranial bruit. Brain 1955;78(3):350-68. PMID 13269596
91: MacKinnon DM. Objective tinnitus due to palatal myoclonus. J Laryngol Otol 1968;82:369-74. PMID 5653249
92: Mardini MK. Ear-clicking “tinnitus” responding to carbamazepine. N Engl J Med 1987;317:1542. PMID 3683492
93: Marsot-Dupuch K. Pulsatile and nonpulsatile tinnitus: a systematic approach. Semin Ultrasound CT MR 2001;22:250-70. PMID 11451099
94: Mattox DE, Hudgins P. Algorithm for evaluation of pulsatile tinnitus. Acta Otolaryngol 2008;128(4):427-31. PMID 18368578
95: McCurdy JA Jr. Tinnitus. In: Taylor RB, editor. Difficult diagnosis. Philadelphia: WB Saunders, 1985:505-12.
96: Meador KJ, Stefadouros M, Malik AJ, Swift TR. Self-heard venous bruit due to increased intracranial pressure. Lancet 1982;1:391. PMID 6120362
97: Meador KJ, Swift TR. Tinnitus from intracranial hypertension. Neurology 1984;34:1258-61. PMID 6540416
98: Melding PS, Goodey RJ. The treatment of tinnitus with oral anticonvulsants. J Laryngol Otol 1979;93:111-22. PMID 429894
99: Menkes DB, Larson PM. Sodium valproate for tinnitus. J Neurol Neurosurg Psychiatry 1998;65:803. PMID 9810969
100: Mundada P, Singh A, Lingam RK. CT arteriography and venography in the evaluation of pulsatile tinnitus with normal otoscopic examination. Laryngoscope 2015;125(4):979-84. PMID 925379666
101: Murai K, Tyler RS, Harker LA, Stouffer JL. Review of pharmacologic treatment of tinnitus. Am J Otol 1992;13(5):454-64. PMID 1359790
102: Murphy TP. Otologic manifestations of pseudotumor cerebri. J Otolaryngol 1991;20:258-61. PMID 1920579
103: Myrhaug H. Clicking ear and pharyngeal tic associated with functional disturbances of the jaw. Acta Otolaryngol 1964;12 (Suppl 188):430-3. PMID 14146707
104: Narsinh KH, Hui F, Saloner D, et al. Diagnostic approach to pulsatile tinnitus: a narrative review. JAMA Otolaryngol Head Neck Surg 2022;148(5):476-83. PMID 35201283
105: Nehru VI, al-Khaboori MJ, Kishore K. Ligation of the internal jugular vein in venous hum tinnitus. J Laryngol Otol 1993;107:1037-8. PMID 8288976
106: Newberry I, Highland J, DeTorres A, Gurgel R. Transmastoid hydroxyapatite resurfacing for sigmoid sinus wall anomalies causing pulsatile tinnitus. Ann Otol Rhinol Laryngol 2021;130(8):885-91. PMID 33412915
107: Ng SK, van Hasselt CA. Images in clinical medicine. Patulous eustachian tube. N Engl J Med 2005;353(6):e5. PMID 16093458
108: Norman LV, West PB, Perry PM. Unilateral pulsatile tinnitus relieved by contralateral carotid endarterectomy. J R Soc Med 1999;92:406-7. PMID 10656006
109: Ogutha J, Page NC, Hullar TE. Postpartum vertigo and superior semicircular canal dehiscence syndrome. Obstet Gynecol 2009;114(2 Pt 2):434-6. PMID 19622951
110: Otto KJ, Hudgins PA, Abdelkafy W, Mattox DE. Sigmoid sinus diverticulum: a new surgical approach to the correction of pulsatile tinnitus. Otol Neurotol 2007;28(1):48-53. PMID 17195746
111: Park SN, Bae SC, Lee GH, et al. Clinical characteristics and therapeutic response of objective tinnitus due to middle ear myoclonus: a large case series. Laryngoscope 2013;123(10):2516-20. PMID 23918695
112: Park YH, Kwon HJ. Awake embolization of sigmoid sinus diverticulum causing pulsatile tinnitus: simultaneous confirmative diagnosis and treatment. Interv Neuroradiol 2011;17(3):376-9. PMID 22005703
113: Peifer KJ, Rosen GP, Rubin AM. Tinnitus: etiology and management. Clin Geriatric Med 1999;15:193-204. PMID 9855667
114: Pelkonen O, Tikkakoski T, Luotonen J, Sotaniemi K. Pulsatile tinnitus as a symptom of cervicocephalic arterial dissection. J Laryngol Otol 2004;118:193-8. PMID 15068515
115: Pulec JL, Simonton KM. Palatal myoclonus: a report of two cases. Laryngoscope 1961;71:668-71. PMID 13738441
116: Rahko T, Hakkinen VX. Carbamazepine in the treatment of objective myoclonus tinnitus. J Laryngol Otol 1979;93:123-7. PMID 429895
117: Reimold SC, Rutherford JD. Valvular heart disease in pregnancy. N Engl J Med 2003;349:52-9. PMID 12840093
118: Rivin AU. The neck venous hum in adults. Calif Med 1966;105:102-3. PMID 5946546
119: Rosenberg SI, Silverstein H, Rowan PT, Olds MJ. Effect of melatonin on tinnitus. Laryngoscope 1998;108:305-10. PMID 9504599
120: Rothstein J, Hilger PA, Boies LR Jr. Venous hum as a cause of reversible factitious sensorineural hearing loss. Ann Otol Rhinol Laryngol 1985;94:267-8. PMID 4014948
121: Round R, Keane JR. The minor symptoms of increased intracranial pressure: 101 patients with benign intracranial hypertension. Neurology 1988;38:1461-4. PMID 2970600
122: Saeed SR, Brookes GB. The use of clostridium botulinum toxin in palatal myoclonus. A preliminary report. J Laryngol Otol 1993;107:208-10. PMID 8509697
123: Saeed SR, Brookes GB. Palatal myoclonus affected by neck posture. J Laryngol Otol 1996;110:207. PMID 8729517
124: Salehi PP, Kasle D, Torabi SJ, Michaelides E, Hildrew DM. The etiology, pathogeneses, and treatment of objective tinnitus: unique case series and literature review. Am J Otolaryngol 2019;40(4):594-7. PMID 30981445
125: Santa Maria PL. Sigmoid sinus dehiscence resurfacing as treatment for pulsatile tinnitus. J Laryngol Otol 2013;127(Suppl 2):S57-9. PMID 23595093
126: Sayyid ZN, Thai A, Swanson A, Hosseini DK, Fitzgerald MB, Ma Y, Vaisbuch Y. Rhythmic wave patterns on ambient pressure tympanometry in patients with objective tinnitus-associated pathologies. Otol Neurotol 2020;41(3):e404-11. PMID 31868782
127: Schleuning AJ, Johnson RM, Vernon JA. Evaluation of a tinnitus masking program: a follow-up study of 598 patients. Ear Hear 1980;1:71-4. PMID 7372020
128: Schoeff S, Nicholas B, Mukherjee S, Kesser BW. Imaging prevalence of sigmoid sinus dehiscence among patients with and without pulsatile tinnitus. Otolaryngol Head Neck Surg 2014;150(5):841-6. PMID 24468899
129: Seidman MD, Arenberg JG, Shirwany NA. Palatal myoclonus as a cause of objective tinnitus: a report of six cases and a review of the literature. Ear Nose Throat J 1999;78:292-7. PMID 10224704
130: Shah SB, Lalwani AK, Dowd CF. Transverse/sigmoid sinus dural arteriovenous fistulas presenting as pulsatile tinnitus. Laryngoscope 1999;109:54-8. PMID 9917041
131: Shiota T, Sakamoto T, Amano K, et al. [Venous hum and innominate vein flow velocity in chronic anemia: a pulsed Doppler echocardiographic study.] J Cardiol 1989;19:885-92. PMID 2701742
132: Singh DP, Forte AJ, Brewer MB, Nowygrod R. Bilateral carotid endarterectomy as treatment of vascular pulsatile tinnitus. J Vasc Surg 2009;50(1):183-5. PMID 19446986
133: Sismanis A. Otologic manifestations of benign intracranial hypertension syndrome: diagnosis and management. Laryngoscope 1987;97(Suppl 42):1-17. PMID 3302575
134: Sismanis A. Pulsatile tinnitus: a 15-year experience. Am J Otol 1998;19:472-7. PMID 9661757
135: Sismanis A. Tinnitus. Curr Neurol Neurosci Rep 2001;1:492-9. PMID 11898561
136: Sismanis A. Pulsatile tinnitus. Otolaryngol Clin North Am 2003;36(2):389-402. PMID 12856306
137: Sismanis A, Butts FM, Hughes GB. Objective tinnitus in benign intracranial hypertension syndrome: an update. Laryngoscope 1990;100:33-6. PMID 2293699
138: Sismanis A, Hughes GB, Abedi E, Williams GH, Isrow LA. Otologic symptoms and findings of the pseudotumor cerebri syndrome: a preliminary report. Otolaryngol Head Neck Surg 1985;93:398-402. PMID 3927238
139: Slack RW, Soucek SO, Wong K. Sonotubometry in the investigation of objective tinnitus and palatal myoclonus: a demonstration of Eustachian tube opening. J Laryngol Otol 1986;100:529-31. PMID 3701200
140: Slengerik-Hansen J, Ovesen T. Botulinum toxin treatment of objective tinnitus because of essential palatal tremor: a systematic review. Otol Neurotol 2016;37(7):820-8. PMID 27273401
141: Song YS, Yuan YY, Wang GJ, Dai P, Han DY. Aberrant internal carotid artery causing objective pulsatile tinnitus and conductive hearing loss. Acta Otolaryngol 2012;132(10):1126-30. PMID 22779753
142: Sullivan M, Katon W, Russo J, Dobic R, Sakai C. A randomized trial of nortriptyline for severe chronic tinnitus: effects on depression, disability, and tinnitus symptoms. Arch Intern Med 1993;153:2251-9. PMID 8215728
143: Takasaki K, Kumagami H, Umeki H, Enatsu K, Takahashi H. The patulous Eustachian tube complicated with amyotrophic lateral sclerosis: a video clip demonstration. Laryngoscope 2008;118(11):2057-8. PMID 18695625
144: Toland AD, Porubsky ES, Coker NJ, Adams HG. Velo-pharyngo-laryngeal myoclonus: evaluation of objective tinnitus and extrathoracic airway obstruction. Laryngoscope 1984;94:691-5. PMID 6717228
145: Tomkinson A, Craven C, Brown MM. Palatal myoclonus affected by neck position. J Laryngol Otol 1995;109:61-2. PMID 7876742
146: Trullen JP, Cervera C, Andre MV. Tinnitus as the first clinical manifestation of hydrocephalus. J Am Geriatr Soc 1996;44(1):103-4. PMID 8537582
147: Viola P, Pisani D, Pullano SA, et al. Objective bilateral tinnitus from palatal nystagmus. Audio and video features of a rare case of palatal myoclonus. Am J Otolaryngol 2020;41(6):102739. PMID 32993860
148: Vories A, Liening D. Spontaneous dissection of the internal carotid artery presenting with pulsatile tinnitus. Am J Otolaryngol 1998;19:213-5. PMID 9617936
149: Waldvogel D, Mattle HP, Sturzenegger M, Schroth G. Pulsatile tinnitus--a review of 84 patients. J Neurol 1998;245:137-42. PMID 9553842
150: Wall M, George D. Idiopathic intracranial hypertension: a prospective study of 50 patients. Brain 1991;114:155-80. PMID 1998880
151: Wall M, Kupersmith MJ, Kieburtz KD, et al. The idiopathic intracranial hypertension treatment trial: clinical profile at baseline. JAMA Neurol 2014;71(6):693-701. PMID 24756302
152: Wang AC, Nelson AN, Pino C, Svider PF, Hong RS, Chan E. Management of sigmoid sinus associated pulsatile tinnitus: a systematic review of the literature. Otol Neurotol 2017;38(10):1390-6. PMID 29135862
153: Wang GP, Zeng R, Liu ZH, et al. Clinical characteristics of pulsatile tinnitus caused by sigmoid sinus diverticulum and wall dehiscence: a study of 54 patients. Acta Otolaryngol 2014;134(1):7-13. PMID 24032538
154: Wang GP, Zeng R, Ma XB, Liu ZH, Wang ZC, Gong SS. Surgical treatment of pulsatile tinnitus caused by the sigmoid sinus diverticulum: a preliminary study. Medicine (Baltimore) 2015;94(21):e882. PMID 26020395
155: Ward PH, Babin R, Calcaterra TC, Konrad HR. Operative treatment of surgical lesions with objective tinnitus. Ann Otol Rhinol Laryngol 1975;84:473-82. PMID 1155883
156: Wiggs WJ Jr, Sismanis A, Laine FJ. Pulsatile tinnitus associated with congenital central nervous system malformations. Am J Otol 1996;17:241-4. PMID 8723955
157: Xenellis J, Nikolopoulos TP, Felekis D, Tzangaroulakis A. Pulsatile tinnitus: a review of the literature and an unusual case of iatrogenic pneumocephalus causing pulsatile tinnitus. Otol Neurotol 2005;26:1149-51. PMID 16272933
158: Xing Y, Gao S, Zhou Y, et al. Surgical treatment of pulsatile tinnitus related to the sigmoid sinus. J Otol 2023;18(1):21-5. PMID 36820162
159: Zeng R, Wang GP, Liu ZH, et al. Sigmoid sinus wall reconstruction for pulsatile tinnitus caused by sigmoid sinus wall dehiscence: a single-center experience. PLoS One 2016;11(10):e0164728. PMID 27736970
160: Zenteno M, Murillo-Bonilla L, Martinez S, et al. Endovascular treatment of a transverse-sigmoid sinus aneurysm presenting as pulsatile tinnitus. J Neurosurg 2004;100:120-2. PMID 14743922
161: Zhao P, Lv H, Dong C, Niu Y, Xian J, Wang Z. CT evaluation of sigmoid plate dehiscence causing pulsatile tinnitus. Eur Radiol 2016;26(1):9-14. PMID 25991486

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Objective tinnitus

Differential Diagnosis

unilateral pulsatile tinnitus
venous hum
arteriovenous malformation
carotid-cavernous fistula
aneurysm
- vascular stenosis
- vascular tumor
- intracranial hypertension
- otosclerosis
- Paget disease
- head trauma
- patulous Eustachian tube
- clonic muscular contractions
- palatal myoclonus

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- Subjective tinnitus
- Sudden deafness
- Vestibular schwannoma

Objective tinnitus …

Objective tinnitus

Introduction

Overview

Key points

Historical note and terminology

Clinical manifestations

Presentation and course

Prognosis and complications

Clinical vignette

Biological basis

Anatomic localization

Pathophysiology

Epidemiology

Differential diagnosis

Associated or underlying disorders

Diagnostic workup

Management

References

Contributors

Author

Patient Profile

ICD & OMIM codes

This is an article preview.
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to access the full version.

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Also in This Category

Third nerve palsy

Nystagmus

Brain death/death by neurologic criteria

Hepatic encephalopathy

Cervical spondylotic myelopathy

Bowel dysfunction in neurologic disorders

Coma due to primary brainstem and diencephalic lesions

Giant cell arteritis

Objective tinnitus

Introduction

Overview

Key points

Historical note and terminology

Clinical manifestations

Presentation and course

Prognosis and complications

Clinical vignette

Biological basis

Anatomic localization

Pathophysiology

Epidemiology

Differential diagnosis

Associated or underlying disorders

Diagnostic workup

Management

References

Contributors

Author

Patient Profile

ICD & OMIM codes

This is an article preview. Start a Free Account to access the full version.

Questions or Comment?

Also in This Category

Third nerve palsy

Nystagmus

Brain death/death by neurologic criteria

Hepatic encephalopathy

Cervical spondylotic myelopathy

Bowel dysfunction in neurologic disorders

Coma due to primary brainstem and diencephalic lesions

Giant cell arteritis

This is an article preview.
Start a Free Account
to access the full version.