Tinnitus: Definitions, Evaluation and Management

Definition

• Perception of sound without an external acoustic stimulus; or
• Perception of a sound produced involuntarily within the body.

Prevalence

• 15–32% of adults have had tinnitus at some point; ~5% are severely disabled by their tinnitus.
• Male/Female ratio ≈ 1; peak incidence at 50–70 years.
• Most patients also have hearing loss; pitch of tinnitus may correlate with pathology.

Classification(s)

By Source

1. Tinnitus generated by para-auditory structures (usually vascular or myoclonic)
2. Tinnitus generated by the peripheral sensorineural auditory system
3. Tinnitus generated by the central sensorineural auditory system

By Audibility

• Subjective: audible only to the patient
• Objective: audible to the examiner

Aetiology

(I) Para‑auditory

Vascular tinnitus

• History of pulsatile tinnitus synchronous with heartbeat; varies with cardiac rate (can confirm with light exercise); audible bruit may be present.

Muscle contraction tinnitus

• Synchronous contractions of muscles of middle ear, Eustachian tube, and palate
• Palatal myoclonus often faster than heart rate (≈60–200/min); can be objectively audible
• TMJ dysfunction may trigger tensor tympani spasm
• Causes include multiple sclerosis, intracranial neoplasm, cerebrovascular disease, or psychogenic
• Myoclonus persists during sleep

External and middle ear tinnitus

• Conductive hearing loss can accentuate perception of pulsatile tinnitus (infection, effusion, cerumen, otosclerosis)
• Cerumen/foreign bodies/hairs on TM can cause tinnitus
• Patulous ET: rushing/blowing sound with respiration (management may include myringotomy with tube, sclerosing/diathermy at orifice)

(II) Peripheral sensorineural tinnitus

Peripheral tinnitus is typically localized to one or both ears (vs central tinnitus perceived all over the head). About 85% of these patients have some degree of hearing loss. Prevalence and severity increase with age.

Proposed pathophysiology

• Altered spontaneous discharge rates of auditory nerve fibers; drugs that increase spontaneous firing (e.g., salicylates) may induce tinnitus
• Reduced efferent inhibition leading to increased afferent firing (e.g., after acoustic trauma or in Ménière’s)
• Decoupling of stereocilia from tectorial membrane (Tonndorf, 1980)
• Abnormal cross-talk or artificial synapses between adjacent auditory nerve fibers (Møller, 1984)
• Abnormal basilar membrane displacement leading to hyperactivity (Eggermont, 1984)
• Damaged outer hair cells with normal inner hair cells (Spoendlin, 1987)
• Chronic tinnitus related to deafferentation of nerve fibers (Tonndorf, 1987)

Common causes

• Noise exposure: most common; typically high-pitched, constant; SNHL often progresses with continued exposure; early 4 kHz “noise notch”
• Presbycusis: high-frequency sloping SNHL, often with high-frequency tinnitus
• Head trauma: tinnitus may be delayed
• Acoustic neuroma: tinnitus in ~10% (may be with/without hearing loss; variable pattern)
• Ménière’s disease: typically low-pitched (≈300 Hz), rumbling, unilateral, often intermittent and more annoying/unstable
• Otosclerosis: tinnitus due to conductive component and/or inner ear involvement; typically low–medium pitch; 70–95% report tinnitus
• Drugs/other: aminoglycosides (high-pitched with drug-induced HL), quinine (rare permanent high-pitched), salicylates (temporary, reversible HL), loop diuretics (can cause “screaming” tinnitus and permanent HL); caffeine, cocaine, marijuana, tobacco; metabolic disease (hyperthyroidism, diabetes); intracranial neoplasms and other CNS lesions (e.g., infections, MS)

(III) Central sensorineural tinnitus

• Often described as occurring “all over the head”
• May persist after labyrinthectomy or VIII nerve section
• Mechanism unknown; possibly changes in firing rates of central inhibitory neurons (e.g., dorsal cochlear nucleus)

Details on Specific Para‑auditory Conditions

Arteriovenous malformations (AVMs)

• Usually present as pulsatile tinnitus; posterior fossa AVMs between branches of occipital artery and transverse sinus are most common
• Carotid–cavernous communications (often post-trauma); bruit is usual; palpable masses may have thrill and be compressible
• Mandibular/maxillary AVMs: loosening teeth, periodontal bleeding, mucosal discoloration; risk of exsanguination during extraction

Venous hum

• Results from eddy currents in jugular vein; common in children and some adults
• Attribution to C2 transverse process impinging on jugular vein; less commonly due to AVM or raised ICP
• Loudness increases with increased cardiac output (anemia, thyrotoxicosis, pregnancy)
• May become audible with CHL (reduced environmental noise)

Diagnosis

• Symptoms may be nearly diagnostic
• Decreases with gentle anterior neck pressure (without carotid occlusion) or turning head toward uninvolved side
• Increases with turning head toward involved side, deep breathing, or Valsalva
• Arteriography often required

Management

• Reassurance
• High ligation of jugular vein in selected cases (after angiography confirms contralateral patency)
• Determination of effective ligation level via balloon occlusion during retrograde venogram
• Some may require ablation of transverse sinus; prosthetic device applying gentle constant neck pressure has been described

Muscle contraction tinnitus

• Rapid, repetitive contractions (60–200/min) of palatal and middle ear muscles; persists during sleep, anesthesia, and coma
• Often in younger patients; may coexist with neurologic disorders (e.g., brainstem infarct, MS)
• Audible click may correspond to relaxation/tubal closure

Diagnosis

• Auscultate mastoid, neck, skull, orbit; determine synchrony with pulse
• Palatal observation may suppress myoclonus; tympanometry can demonstrate periodic compliance changes (sawtooth-like)

Management

• Reduce hyperactive motor discharge: phenytoin, valproic acid, carbamazepine; behavioral maneuvers (open mouth, touch palate, water fill, corneal air)
• Reduce symptom impact: section tensor tympani, dislocate TVP tendon/hamulus, hamulus fracture, myringotomy with ventilating tube

Patient Evaluation

A. History

• General health, medications, habits
• Quality: pitch, loudness, location, duration, pattern (constant/pulsatile/intermittent)
• Otologic history: hearing loss, vertigo, otorrhea, fullness, otalgia, infections, trauma, noise exposure, ototoxic drugs
• Aggravating factors: fatigue, stress, sleep disturbance, disability level

Tinnitus Handicap Scale (Kuk; Tyler et al.)

Indicate agreement 0–100 for each statement; subtract 100 from questions 25 and 26; add all and divide by 27.

1. I do not enjoy life because of tinnitus.
2. My tinnitus has gotten worse over the years.
3. Tinnitus interferes with my ability to tell where sounds are coming from.
4. I am unable to follow a conversation during meetings because of tinnitus.
5. Tinnitus causes me to avoid noisy situations.
6. Tinnitus interferes with my speech understanding in a noisy room.
7. I feel uneasy in social situations because of tinnitus.
8. The public does not know about the devastating nature of tinnitus.
9. I cannot concentrate because of tinnitus.
10. Tinnitus creates family problems.
11. Tinnitus causes me to feel depressed.
12. I find it difficult to explain what tinnitus is to others.
13. Tinnitus causes stress.
14. I am unable to relax because of tinnitus.
15. I complain more because of tinnitus.
16. I have trouble falling asleep at night because of tinnitus.
17. Tinnitus makes me feel tired.
18. Tinnitus makes me feel insecure.
19. Tinnitus contributes to a feeling of general ill health.
20. Tinnitus affects the quality of my relationships.
21. Tinnitus has caused a reduction in my speech understanding.
22. Tinnitus makes me feel annoyed.
23. Tinnitus interferes when listening to the television.
24. Tinnitus makes me feel anxious.
25. I think I have a healthy outlook on tinnitus.
26. I have support from my friends regarding my tinnitus.
27. I feel frustrated frequently because of tinnitus.

Quality, Location, Pitch, Loudness

• Descriptors: buzzing, rushing, ringing, roaring, whistling; pulsing/popping suggests vascular or muscular sources but may occur in SN tinnitus
• Perceptual location: one/both ears; back/middle/side/front of head; occasionally externalized
• Pitch matching techniques vary; reliability varies and pitch can fluctuate within/day-to-day
• Loudness matching often 3–4 dB above threshold even when perceived as “very loud”

B. Physical Examination

• General H&N with CNS/CVS focus
• Inspect pinna and canal; TM for masses (e.g., glomus), hemotympanum; note pulsation/paling with pneumatic otoscopy
• Auscultate mastoid, orbit, neck, skull; correlate with pulse; look for palpable thrill
• Assess positional effects (venous hum often modified by neck pressure, Valsalva, head turning)
• Look for AVM signs in mandible/maxilla; consider flexible nasopharyngoscopy for palatal myoclonus
• Assess TMJ; consider sensitive canal microphone amplification for subtle sounds

Investigations

Audiometric evaluation

• Pure tone air/bone, SRT and discrimination, reflexes (including decay), impedance/tympanometry
• Tympanometry may show negative pressure or periodic fluctuations (myoclonus/pulsations)
• ABR if retrocochlear pathology suspected
• Tinnitus matching: pitch/loudness, masking, residual inhibition (often 25–45 seconds); many match at ~3–4 dB SL; 50% single tone vs narrow-band noise (3–5 kHz)

Masking

• ~90% have complete masking with tone/noise → shared neural channels somewhere in CNS
• Feldmann patterns: Congruence, Distance, Persistence, Convergence, Divergence
• Psychoacoustic tuning curves (PTC) often abnormal; suggest multiple possible origins
• Noises of different bandwidths assess frequency resolution; careful spectrum tailoring may be helpful
• Ipsilateral vs contralateral masking and central masking considerations; note contralateral “unmasking reveal” phenomenon
• Adaptation: tinnitus may reappear during continuous masking; postmasking residual inhibition common

Spontaneous otoacoustic emissions

Indicate active cochlear mechanisms; relationship to tinnitus unclear.

Auditory brainstem response

Minimal differences between tinnitus and non-tinnitus groups when matched for hearing loss have been reported.

Laboratory studies

For sensorineural tinnitus to evaluate HL sources: FBC, ESR, EUC, UA, TFTs, glucose tolerance, syphilis serology, ANA, lupus prep, rheumatoid factor, complements.

Radiologic evaluation

• CT/MRI for neoplasms and soft‑tissue lesions
• Angiography/contrast CT/MRA/MRV when vascular etiology suspected
• Arteriography often used to delineate feeders and tumor extent

Management

A. Surgical therapy

• Most effective for para‑auditory tinnitus: correct vascular abnormalities (e.g., jugular ligation, AVM embolization, glomus resection); TVP section, myringotomy + tube, ostium sclerosis for patulous ET/palatal myoclonus
• Sensorineural tinnitus: variable benefit; best results in otosclerosis surgery (≈75% improve); variable outcomes with nerve sections; cochleovestibular procedures with mixed results

B. Medication

• Anticonvulsants: carbamazepine (some benefit); primidone/phenytoin less favorable; limited by side effects
• Anti-arrhythmics/Local anesthetics: IV lidocaine can transiently reduce tinnitus in many; oral analogs (e.g., tocainide) limited by side effects; flecainide disappointing overall
• Vasodilators: niacin and others generally of limited value
• Antidepressants: helpful with comorbid depression; possible neuronal effects
• Benzodiazepines: oxazepam/clonazepam have shown benefit in some patients

C. Masking

• Patients often self‑mask with fans, water, radio static
• Hearing aids: first‑line in hearing‑impaired; amplify ambient sounds and improve speech understanding
• Tinnitus maskers: dedicated noise generators; or combination devices (aid + masker)
• Use lowest effective settings to avoid potential noise‑induced damage; noise spectrum need not be centered on tinnitus frequency
• Ear selection individualized; many can be masked equally well bilaterally

D. Biofeedback

Can reduce anxiety/stress and improve coping; reported improvement in many who complete training.

E. Miscellaneous

• Electrical stimulation: extra- and intra‑cochlear approaches variably reduce tinnitus during stimulation; effects may not persist and can worsen post‑stimulation; destructive DC currents damage hair cells/spiral ganglion; select cochlear implant recipients report relief while device is active
• Acupuncture: no benefit over placebo
• Hypnotherapy: useful adjunct to relaxation in some
• Allergy/Diet: uncertain

F. Counselling (Key points)

• Tinnitus is common and usually associated with benign disease
• It may increase over time; coping strategies and protection are important
• Maintain a log of triggers; emphasize ear/noise protection
• Patients with Ménière’s may have greater difficulty coping

Bibliography

• Cummings, C. Otolaryngology. Vol. IV. Ch. 172. pp. 3201‑3217.
• English, G.M. Otolaryngology. Vol. I. Ch. 53.
• Fortnum, H.M., and Coles, R.R.A. Trial of Flecainide in the Management of Tinnitus. Clinical Otolaryngology. 1991. 16:93‑96.
• Glasscock, M.E., et al. Retrolabyrinthine vs. Retrosigmoid Vestibular Nerve Section. Otolaryngology Head Neck Surg. 1991. 104:88‑95.
• Paaske, P.B., et al. Zinc in the Management of Tinnitus. Ann Otol Rhinol Laryngol. 1991. 100:647‑649.