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David M. Kaylie

, MS, MD, Duke University Medical Center

Last full review/revision Mar 2021| Content last modified Mar 2021
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Tinnitus is a noise in the ears. It is experienced by 10 to 15% of the population.

Subjective tinnitus is perception of sound in the absence of an acoustic stimulus and is heard only by the patient. Most tinnitus is subjective.

Objective tinnitus is uncommon and results from noise generated by structures near the ear. Sometimes the tinnitus is loud enough to be heard by the examiner.


Tinnitus may be described as buzzing, ringing, roaring, whistling, or hissing and is sometimes variable and complex. Objective tinnitus typically is pulsatile (synchronous with the heartbeat) or intermittent. Tinnitus is most noticeable in quiet environments and in the absence of distracting stimuli and, thus, frequently seems worse at bedtime.

Tinnitus may be intermittent or continuous. Continuous tinnitus is at best annoying and is often quite distressing. Some patients adapt to its presence better than others; depression occasionally results. Stress generally exacerbates tinnitus.

Pathophysiology of Tinnitus

Subjective tinnitus is thought to be caused by abnormal neuronal activity in the auditory cortex. This activity results when input from the auditory pathway (cochlea, auditory nerve, brain stem nuclei, auditory cortex) is disrupted or altered in some manner. This disruption may cause loss of suppression of intrinsic cortical activity and perhaps creation of new neural connections. Some believe the phenomenon is similar to the development of phantom limb pain after amputation. Conductive hearing loss (eg, caused by cerumen impaction, otitis media, or eustachian tube dysfunction) may also be associated with subjective tinnitus, by altering sound input to the central auditory system.

Objective tinnitus represents actual noise generated by physiologic phenomena occurring near the middle ear. Usually the noise comes from blood vessels, either normal vessels in conditions of increased or turbulent flow (eg, caused by atherosclerosis) or abnormal vessels (eg, in tumors or vascular malformations). Sometimes muscle spasms or myoclonus of palatal muscles or muscles in the middle ear (stapedius, tensor tympani) cause clicking sounds.

Etiology of Tinnitus

Causes may be considered by whether they cause subjective or objective tinnitus (see table Some Causes of Tinnitus).

Subjective tinnitus

Subjective tinnitus may occur with almost any disorder affecting the auditory pathways.

The most common disorders are those that involve sensorineural hearing loss, particularly

Infections and central nervous system lesions (eg, caused by tumor, stroke, multiple sclerosis) that affect auditory pathways also may be responsible.

Disorders causing conductive hearing loss also may cause tinnitus. These include obstruction of the ear canal by cerumen, a foreign body, or external otitis. Otitis media, barotrauma, eustachian tube dysfunction, and otosclerosis may also be associated with tinnitus.

Temporomandibular joint dysfunction may be associated with tinnitus in some patients.

Objective tinnitus

Objective tinnitus usually involves noise from vascular flow, which causes an audible pulsating sound synchronous with the pulse. Causes include

  • Turbulent flow through the carotid artery or jugular vein

  • Highly vascular middle ear tumors

  • Dural arteriovenous malformations (AVMs)

Muscle spasms or myoclonus of palatal muscles or those of the middle ear (stapedius, tensor tympani) may cause perceptible noise, typically a rhythmic clicking. Such spasms may be idiopathic or caused by tumors, head trauma, and infectious or demyelinating diseases (eg, multiple sclerosis). Palatal myoclonus causes visible movement of the palate, tympanic membrane, or both that coincides with tinnitus.


Some Causes of Tinnitus


Suggestive Findings

Diagnostic Approach*

Subjective tinnitus†

Acoustic trauma (eg, noise-induced hearing loss)

History of occupational or recreational exposure, hearing loss

Clinical examination alone

Clear history of exposure

Clinical examination alone

Central nervous system tumors (eg, vestibular schwannoma, meningioma) and lesions (eg, caused by multiple sclerosis or stroke)

Unilateral tinnitus and often hearing loss

Sometimes other neurologic abnormalities

Gadolinium-enhanced MRI

Drugs (eg, salicylates; aminoglycosides; loop diuretics; some chemotherapeutic drugs, including cisplatin)

Onset of bilateral tinnitus coincident with use of drug

Except with salicylates, hearing loss also possible

Aminoglycosides also possibly associated with bilateral vestibular loss (eg, dizziness, dysequilibrium)

Clinical examination alone

Eustachian tube dysfunction

Often prolonged decreased hearing, preceding URIs, problems clearing ears with air travel or other pressure change

Severe allergies can worsen symptoms

Unilateral or bilateral (often one ear more of a problem than the other)


Infections (eg, otitis media, labyrinthitis, meningitis, neurosyphilis)

History of infection

Clinical examination alone

Sometimes other confirmatory tests (eg, CSF examination for meningitis)

Episodic unilateral hearing loss, tinnitus, fullness in the ear, and severe vertigo

Typically, fluctuating and eventually permanent low-frequency hearing loss

Vestibular testing

Gadolinium-enhanced MRI to evaluate unilateral sensorineural hearing loss and rule out vestibular schwannoma

Obstruction of ear canal (eg, caused by cerumen, foreign body, or external otitis)

Unilateral, with visible, diagnostic abnormalities on ear examination, including discharge with external otitis

Clinical examination alone

Presbycusis (with aging)

Progressive hearing loss, often with family history

Clinical examination alone

Objective tinnitus‡

Dural arteriovenous malformations

Unilateral, constant, pulsatile tinnitus

Usually no other symptoms

May have bruit over skull

Physical examination should always include periauricular auscultation

CT, MR, or conventional angiogram

Myoclonus (palatal muscles, tensor tympani, stapedius)

Irregular clicking or mechanical-sounding noise

Possibly other neurologic symptoms (eg, of multiple sclerosis)

Movement of the palate, TM, or both seen on examination when symptomatic



Turbulent flow in carotid artery or jugular vein

Bruit or venous hum in neck

Venous hum possibly ceasing with jugular vein compression or head rotation

Sometimes clinical examination alone

Sometimes CT venography and CT angiography

Vascular middle ear tumors (eg, glomus tympanicum, glomus jugulare)

Unilateral, constant, pulsatile tinnitus

Sometimes bruit on auscultation of ear

Tumor usually visible behind TM as a very erythematous, sometimes pulsatile mass, which may blanch (on pneumatoscopy)



Angiogram (usually done before surgery)

* Clinical examination is always done but is mentioned in this column only when that can be the sole means of diagnosis.

† Typically a constant tone and accompanied by some degree of hearing loss. All patients with subjective tinnitus should have audiometry.

‡ Typically intermittent or pulsatile.

CSF = cerebrospinal fluid; TM = tympanic membrane; URI = upper respiratory infection.

Evaluation of Tinnitus


History of present illness should note duration of tinnitus, whether it is in one or both ears, and whether it is a constant tone or intermittent. If intermittent, the clinician should determine whether it is regular and whether it is about the rate of the pulse or sporadic. Any exacerbating or relieving factors (eg, swallowing, head position) should be noted. Important associated symptoms include hearing loss, vertigo, ear pain, and ear discharge.

Review of systems should seek symptoms of possible causes, including diplopia and difficulty swallowing or speaking (lesions of the brain stem) and focal weakness and sensory changes (peripheral nervous system disorders). The impact of the tinnitus on the patient also should be assessed. Whether the tinnitus is sufficiently distressing to cause significant anxiety, depression, or sleeplessness should be noted.

Past medical history should ask about risk factors for tinnitus, including exposure to loud noise, sudden pressure change (from diving or air travel), history of ear or central nervous system infections or trauma, radiation therapy to the head, and recent major weight loss (risk of eustachian dysfunction). Drug use should be ascertained, particularly any salicylates, aminoglycosides, or loop diuretics.

Physical examination

Physical examination focuses on the ear and the nervous system.

The ear canal should be inspected for discharge, foreign body, and cerumen. The tympanic membrane should be inspected for signs of acute infection (eg, redness, bulging), chronic infection (eg, perforation, cholesteatoma), and tumor (red or bluish mass). A bedside hearing test should be done.

Cranial nerves, particularly vestibular function (see Dizziness and Vertigo), are tested along with peripheral strength, sensation, and reflexes. A stethoscope is used to listen for vascular noise over the course of the carotid arteries and jugular veins and over and adjacent to the ear.

Red flags

The following findings are of particular concern:

  • Bruit, particularly over the ear or skull

  • Accompanying neurologic symptoms or signs (other than hearing loss)

  • Unilateral tinnitus

Interpretation of findings

In some cases, tinnitus may indicate retrocochlear pathology, such as an vestibular schwannoma (benign but invasive tumor originating from the vestibular portion of the 8th cranial nerve in the internal auditory canal).

It is important to note whether the tinnitus is unilateral because vestibular schwannomas may manifest only with unilateral tinnitus. This diagnosis is more likely if there is also unilateral sensorineural hearing loss or asymmetric hearing loss with worse hearing in the ear with tinnitus.

It also is important to distinguish the uncommon cases of objective tinnitus from the more common cases of subjective tinnitus. Tinnitus that is pulsatile or intermittent is almost always objective (although not always detectable by the examiner), as is that associated with a bruit. Pulsatile tinnitus is nearly always benign. Continuous tinnitus is usually subjective (except perhaps for that caused by a venous hum, which may be identified by presence of a bruit and often by a change in tinnitus with head rotation or jugular vein compression).

Specific causes can often be suspected by findings on examination (see table Some Causes of Tinnitus). In particular, exposure to loud noise, barotrauma, or certain drugs before onset suggests those factors as the cause.


All patients with tinnitus should be referred for comprehensive audiologic evaluation to determine the presence, degree, and type of hearing loss.

In patients with unilateral tinnitus and hearing loss, vestibular schwannoma should be ruled out by gadolinium-enhanced MRI. In patients with unilateral tinnitus and normal hearing and physical examination, MRI is not necessary unless tinnitus persists > 6 months.

Other testing depends on patient presentation (see table Some Causes of Tinnitus).

Patients with visible evidence of a vascular tumor in the middle ear require CT, gadolinium-enhanced MRI, and referral to a subspecialist if the diagnosis is confirmed.

Patients with pulsatile, objective tinnitus and no ear abnormalities on examination or audiology require further investigation of the vascular system (carotid, vertebral, and intracranial vessels). The usual test sequence is to begin with CT angiography (CTA). However, because CTA is not very sensitive for dural AVMs, many clinicians then consider doing an MR angiogram or conventional arteriogram. Because dural AVMs are rare, the significant risks of arteriography must be weighed against the potential benefit of diagnosis and treatment (with embolization) of this vascular anomaly.

Patients who report hearing clicking sounds in one or both ears should be evaluated for the presence of objective tinnitus. This evaluation may be done by auscultation using a stethoscope or with tympanometry to identify clonus of the tensor tympani, stapedius, and/or palatal muscles. Palatal myoclonus should be visible on physical exam of the oral cavity.

Treatment of Tinnitus

Treatment of the underlying disorder may lessen tinnitus. Correcting hearing loss (eg, with a hearing aid) relieves tinnitus in about 50% of patients.

Because stress and other mental factors (eg, depression) can exacerbate symptoms, efforts to recognize and treat these factors may help. Many patients are reassured by learning that their tinnitus does not represent a serious medical problem. Tinnitus also can be worsened by caffeine and other stimulants, so patients should try eliminating use of these substances.

Although no specific medical or surgical therapy is available, many patients find that background sound masks the tinnitus and may help them fall asleep. Some patients benefit from a tinnitus masker, a device worn like a hearing aid that provides a low-level sound that can cover up the tinnitus. Tinnitus retraining therapy, offered by programs that specialize in tinnitus treatment, are helpful for some patients. Electrical stimulation of the inner ear, as with a cochlear implant, occasionally reduces the tinnitus but is appropriate only for patients who are profoundly deaf.

Geriatrics Essentials

One out of 4 people > 65 years have significant hearing impairment. Because tinnitus is common among people with sensorineural hearing loss, tinnitus is a common complaint among older patients.

Key Points

  • Subjective tinnitus is caused by an abnormality somewhere in the auditory pathway.

  • Objective tinnitus is caused by an actual noise produced in a vascular structure near the ear.

  • Loud noise, aging, Meniere disease, and drugs are the most common causes of subjective tinnitus.

  • Unilateral tinnitus with hearing loss or dizziness/dysequilibrium warrants gadolinium-enhanced MRI to rule out vestibular schwannoma.

  • Any tinnitus accompanied by a neurologic deficit should prompt neurologic evaluation.

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