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 (eg, carotid fistula/aneurysm, arteriovenous malformation, dural arteriovenous fistula, stenosis of the sigmoid sinus or carotid artery) or within the middle ear (eg. tensor tympani or stapedius muscle spasm). By definition, the tinnitus is loud enough to be heard by the examiner either with or without a stethoscope to auscultate the mastoid bone. Objective tinnitus is exceedingly rare.
Characteristics
Tinnitus may be described as buzzing, ringing, roaring, whistling, or hissing and is sometimes variable and complex. If the sound perceived by the patient is not synchronous with their heartbeat, it is described as non-pulsatile. 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 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. However, subjective, nonpulsatile tinnitus is far more common in sensorineural hearing loss, occurring in up to 70 to 85% of patients with concurrent sensorineural hearing loss (1).
Objective tinnitus represents actual noise generated by physiologic phenomena occurring near the middle ear that can be heard by the clinician. Usually the noise is pulsatile and 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. Objective tinnitus always warrants further evaluation with diagnostic imaging studies.
Pathophysiology reference
1. Shargorodsky J, Curhan GC, Farwell WR. Prevalence and characteristics of tinnitus among US adults. Am J Med 2010;123(8):711-718. doi:10.1016/j.amjmed.2010.02.015
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
Acoustic trauma (noise-induced sensorineural hearing loss)
Presbycusis (with aging)
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 otitis externa. 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
Cerebral venous sinus stenosis or thrombosis, especially transverse sinus stenosis
Idiopathic intracranial hypertension (usually bilateral pulsatile tinnitus)
Bony dehiscence over the sigmoid sinus or jugular bulb in the middle ear, sigmoid sinus diverticulum
Superior semicircular canal dehiscence
Middle ear fluid can lead to increased transmission of pulsations from the carotid artery or jugular bulb that resolves when the middle ear fluid resolves.
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
Cause | Suggestive Findings | Diagnostic Approach |
|---|---|---|
Subjective tinnitus* | ||
Acoustic trauma (eg, noise-induced hearing loss) | History of occupational or recreational exposure, hearing loss | Audiogram |
Clear history of exposure to increased air or water pressure | Audiogram | |
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 Audiogram |
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) | Tympanometry Audiogram |
Infections (eg, otitis media, labyrinthitis, meningitis, neurosyphilis) | History of infection | History and physical examination alone Sometimes other confirmatory tests (eg, CSF examination for meningitis) Audiogram |
Medications (eg, salicylates; aminoglycosides; loop diuretics; some chemotherapeutic agents, including cisplatin) | Onset of bilateral tinnitus coincident with use of medication Except with salicylates, hearing loss also possible Aminoglycosides also possibly associated with bilateral vestibular loss (eg, dizziness, dysequilibrium) | Audiogram |
Episodic unilateral hearing loss, tinnitus, fullness in the ear, and severe vertigo Typically, fluctuating and eventually permanent low-frequency hearing loss | Audiogram Gadolinium-enhanced MRI to evaluate unilateral sensorineural hearing loss and exclude vestibular schwannoma | |
Obstruction of ear canal (eg, caused by cerumen, foreign body, or otitis externa) | Unilateral, with visible, diagnostic abnormalities on ear examination, including discharge with otitis externa | History and physical examination alone |
Presbycusis (with aging) | Progressive hearing loss, often with family history | Audiogram |
Objective tinnitus† | ||
Unilateral, constant, pulsatile tinnitus Usually no other symptoms May have bruit over skull Physical examination should always include periauricular auscultation | CT, MRI, 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 | MRI Tympanometry |
Turbulent flow in carotid artery or jugular vein | Bruit or venous hum in neck Venous hum that can change (increase or decrease in intensity with ipsilateral jugular vein compression or head rotation | Sometimes history and physical 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) | CT MRI Angiogram (usually done before surgery) Audiogram |
* 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; CT = computed tomography; MRI = magnetic resonance imaging; TM = tympanic membrane; URI = upper respiratory infection. | ||
Evaluation of Tinnitus
History
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 (pulsatile) 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 nerve disorders, including dysfunction of the 8th cranial nerve). 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 (eg, occupational, concerts, firearms), 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 patulous Eustachian tube dysfunction). Medication use should be ascertained, particularly any salicylates, aminoglycosides, or loop diuretics.
Various scoring systems are used to quantify the impact of tinnitus on patients' day to day activities (eg, tinnitus functional index, tinnitus handicap index) (1, 2).
Physical examination
Physical examination focuses on the ear, the nervous system, and auscultation for bruits in the neck and mastoid processes.
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, including Weber and Rinne tests using a 512-Hz tuning fork.
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
Objective tinnitus (that the examiner can hear)
Interpretation of findings
Tinnitus with asymmetric hearing loss may indicate retrocochlear pathology, such as a vestibular schwannoma (benign 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 usually benign but often merits further diagnostic evaluation to exclude serious pathology. 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 medications before onset suggests those factors as the cause.
Testing
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, a posterior fossa or internal auditory canal lesion, such as vestibular schwannoma or meningioma, should be excluded 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 tinnitus require further investigation of the vascular system (carotid, vertebral, and intracranial vessels). The preferred initial test is usually CT angiography (CTA) of the head and neck, which should include arterial and venous phase images and bony reconstructions. These image sequences can readily identify arterial causes of pulsatile tinnitus (eg, carotid stenosis or aneurysm), venous causes (eg, transverse or sigmoid sinus stenosis, jugular bulb diverticulum), or combined arteriovenous causes such as arteriovenous malformations or dural arteriovenous fistulae, while the bone images can reveal bony etiologies of pulsatile tinnitus (eg, missing or deficient bone over the sigmoid sinus or jugular bulb, superior semicircular canal dehiscence). If CTA reveals concern for aneurysm, dural arteriovenous fistulae, or arteriovenous malformation, digital subtraction angiography (DSA) should be obtained. If the CTA is normal but the index of suspicion for a dural AV fistula or AVM remains high (eg, objective pulsatile tinnitus can be auscultated in the neck or over the mastoid process), DSA should still be obtained. Despite high sensitivity for detecting the aforementioned "must not miss" diagnoses, in approximately 20% of patients with pulsatile tinnitus, CTA will fail to identify an etiology (3). In this circumstance, additional imaging with an MR angiogram/venogram should be considered (4). If CTA reveals any concern for pathology of the middle or inner ear, temporal bone, or skull base, a contrast-enhanced MRI of the internal auditory canals and skull base is required.
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 examination of the oral cavity.
Evaluation references
1. Meikle MB, Henry JA, Griest SE, et al: The tinnitus functional index: development of a new clinical measure for chronic, intrusive tinnitus [published correction appears in Ear Hear 2012 May;33(3):443]. Ear Hear 2012;33(2):153-176. doi:10.1097/AUD.0b013e31822f67c0
2. Newman CW, Jacobson GP, Spitzer JB: Development of the Tinnitus Handicap Inventory. Arch Otolaryngol Head Neck Surg 1996;122(2):143-148. doi:10.1001/archotol.1996.01890140029007
3. Formeister EJ, Xiao G, Clark J, et al: Combined Arterial and Venous Phase Computed Tomographic Imaging of the Skull Base in Pulsatile Tinnitus. Otol Neurotol 2022;43(9):1049-1055. doi:10.1097/MAO.0000000000003672
4. Abdalkader M, Nguyen TN, Norbash AM, et al: State of the Art: Venous Causes of Pulsatile Tinnitus and Diagnostic Considerations Guiding Endovascular Therapy. Radiology 300(1):2-16, 2021. doi: 10.1148/radiol.2021202584
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. Some hearing aids have programmable tinnitus masking sounds that reduce tinnitus as measured with a self-reported scale (1).
Because stress and other mental health concerns (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, some patients benefit from simple tinnitus masking using white noise that provides a low-level sound that can cover up the tinnitus. Tinnitus retraining therapy may help some patients (2). Electrical stimulation of the inner ear, as with a cochlear implant, is highly effective at reducing tinnitus, with > 85% of patients who are profoundly deaf and treated with a cochlear implant reporting complete or partial tinnitus suppression (3).
A bimodal neural stimulation device is an another approach that appears to improve patient-reported subjective scores in approximately 80% of patients with moderate to severe tinnitus (4). This device provides simultaneous electrical stimulation to the tongue with a customized tinnitus masking program played into the ears.
Treatment references
1. Sanders PJ, Nielsen RM,Jensen JJ, Searchfield GD. Hearing aids with tinnitus sound support reduce tinnitus severity for new and experienced hearing aid users. Frontiers in Audiology and Otology 2023;1 doi: 10.3389/fauot.2023.1238164
2. Cima RF, Maes IH, Joore MA, et al. Specialised treatment based on cognitive behaviour therapy versus usual care for tinnitus: a randomised controlled trial. Lancet 2012;379(9830):1951-1959. doi:10.1016/S0140-6736(12)60469-3
3. Peter N, Liyanage N, Pfiffner F, Huber A, Kleinjung T. The Influence of Cochlear Implantation on Tinnitus in Patients with Single-Sided Deafness: A Systematic Review. Otolaryngol Head Neck Surg 2019;161(4):576-588. doi:10.1177/0194599819846084
4. Boedts M, Buechner A, Khoo SG, et al. Combining sound with tongue stimulation for the treatment of tinnitus: a multi-site single-arm controlled pivotal trial. Nat Commun 2024;15(1):6806. doi:10.1038/s41467-024-50473-z
Geriatrics Essentials: Tinnitus
Close to 40% of people between 60 and 69 years have hearing impairment (1). Because tinnitus is common among people with sensorineural hearing loss, tinnitus is common among older patients.
Geriatrics essentials reference
1. Hoffman HJ, Dobie RA, Losonczy KG, Themann CL, Flamme GA. Declining Prevalence of Hearing Loss in US Adults Aged 20 to 69 Years. JAMA Otolaryngol Head Neck Surg 2017;143(3):274-285. doi:10.1001/jamaoto.2016.3527
Key Points
Subjective tinnitus is caused by an abnormality somewhere in the auditory pathway.
Objective tinnitus is usually caused by an actual noise produced in a vascular structure near the ear.
Loud noise, aging, Meniere disease, migraines, and medications are the most common causes of subjective tinnitus.
Unilateral tinnitus with hearing loss or dizziness/dysequilibrium warrants gadolinium-enhanced magnetic resonance imaging to exclude a posterior fossa or internal auditory canal lesion.
Any tinnitus accompanied by a neurologic deficit should prompt neurologic evaluation.
