Tinnitus

Condition

The perception of phantom sound in the head or ears without a corresponding external acoustic source. Common — adult prevalence estimates range 11.9–30.3% depending on the diagnostic criteria applied — at least two-thirds of Australians report noticing tinnitus at some point in their lives. A multifactorial condition, brought on by factors including age, noise exposure, ototoxic medications, vascular problems, genetic predisposition, temporomandibular disorders (see TMJ Dysfunction), or as a consequence of other disease (e.g. Ménière’s disease).

Tinnitus is usefully classified along two axes. Subjective (only the patient can hear it — the great majority of cases) vs objective (the examiner can also hear it too, e.g. TMJ crepitus, a vascular bruit). Primary (idiopathic, with or without symmetrical sensorineural hearing loss) vs secondary (a specific identifiable underlying cause, which is what most of this page’s assessment is aimed at excluding or confirming). Pulsatile tinnitus — a regular, pulse-synchronous sound — is a separate descriptive category that can be subjective or objective and always warrants its own work-up (see Assessment). Duration is further split into acute (<6 months) and chronic (>6 months), which affects how proactively bothersome tinnitus needs managing.

Common ototoxic medications: aminoglycosides (amikacin, gentamicin, neomycin), macrolides (azithromycin, clarithromycin, erythromycin), vancomycin; antimalarials (chloroquine, mefloquine, quinine); platinum- based chemotherapy (carboplatin, cisplatin); loop diuretics (furosemide); NSAIDs (including high-dose aspirin/salicylates); tricyclic antidepressants. Effects can be temporary (NSAIDs, diuretics, quinine) or permanent (aminoglycosides, platinum-based drugs). Other reversible secondary causes worth actively excluding: cerumen impaction, otitis externa/media, otosclerosis, and cholesteatoma.

Assessment

History: onset, laterality, pulsatile vs non-pulsatile character, associated hearing loss/vertigo/aural fullness, noise exposure history, medication review (ototoxic drugs above), and impact on sleep/mood/ concentration. Whether the tinnitus is bothersome is itself a key history point — separate from its cause, it determines how actively a GP needs to manage it. Anxiety and depression are common comorbidities and worth screening for, given the demonstrated link between tinnitus distress and psychological disorder.

Examine the ear (otoscopy, wax/foreign body), assess for conductive vs sensorineural hearing loss (Weber/Rinne — see Presentation: Loss of Hearing), and consider TMJ and cervical spine as contributing sources. Auscultate the head and neck (carotid, periauricular regions) if pulsatile tinnitus is reported. Pulsatile tinnitus warrants specific investigation for a vascular cause (arteriovenous malformation, glomus tumour, carotid stenosis, idiopathic intracranial hypertension) — refer for imaging/ENT assessment. Unilateral tinnitus, especially with asymmetric hearing loss, warrants investigation for acoustic neuroma (vestibular schwannoma).

Audiometry (pure tone audiogram + tympanogram) is recommended for all patients presenting with tinnitus, not only those who also report hearing loss — a large proportion have some degree of measurable loss even when unreported. Conductive hearing loss on audiometry almost always points to a secondary, often reversible cause; sensorineural loss may be primary or secondary. Imaging (CT temporal bone or MRI of the cerebellopontine angle/internal acoustic meatus) is not routine, but is indicated for: unilateral tinnitus, pulsatile tinnitus (CT angiography), asymmetric sensorineural hearing loss (≥10 dB difference between ears at three or more frequencies — MRI to exclude vestibular schwannoma), a focal neurological deficit, or suspected otosclerosis. Sudden-onset sensorineural hearing loss accompanying tinnitus needs urgent ENT referral and prompt steroid therapy — don’t wait on imaging to act.

Management

Address modifiable contributors first: review and, where possible, stop/substitute ototoxic medications; manage underlying otological conditions (wax, otitis media/externa, otosclerosis); smoking cessation is a specific, evidence-supported recommendation for tinnitus patients, though it’s inconsistently offered in primary care. If, after this work-up, tinnitus is primary and not bothersome, reassurance alone is appropriate.

Dietary factors — what the evidence actually supports:

• Dietary supplements are ineffective and should not be recommended for tinnitus.
• No supporting evidence for the commonly-advised caffeine or dietary salt restriction in tinnitus management — these are widely given but not evidence-based recommendations.
• Very weak evidence that overall diet quality affects tinnitus symptoms (some population-level association between a healthier diet pattern and lower persistent-tinnitus incidence) — not strong enough to base specific dietary prescriptions on, but general healthy-eating advice (as for any patient) is reasonable.

Drug therapy has little role. GPs should avoid prescribing antidepressants, anticonvulsants or anxiolytics for tinnitus itself — there is no evidence for effectiveness and they carry adverse effects. Betahistine, despite being widely prescribed for tinnitus, has no demonstrated benefit: a Cochrane review of five randomised trials (303–305 participants) found no difference in tinnitus loudness, symptom severity, or side effects between betahistine and placebo — evidence quality ranged from moderate to very low, but there is no signal of benefit to act on. Complementary medicines likewise have no supporting evidence.

Multidisciplinary management for troublesome persistent tinnitus: hearing aids (if hearing loss present — amplification can reduce tinnitus prominence); sound therapy/masking; cognitive behavioural therapy; psychoeducational counselling; neuromodulation (specialist-led). Of these, cognitive behavioural therapy has the best evidence base: a Cochrane review (28 trials, 2,733 participants) found low-to-moderate certainty evidence that CBT reduces the negative impact of tinnitus on quality of life at end of treatment compared with no intervention, audiological care, tinnitus retraining therapy, or other active treatments, with few or no adverse effects — though whether the benefit persists beyond treatment end is uncertain, as no included trial followed patients past 12 months.

Refer to audiology/ENT for persistent, bothersome tinnitus, especially if pulsatile, unilateral, or associated with asymmetric hearing loss.