Tinnitus is the perception of sound — ringing, hissing, buzzing, whistling or humming — in the absence of any external source. It affects around 14% of adults, and about 2% experience it severely enough to significantly affect sleep, concentration, mood and quality of life. Despite being experienced as coming from the ear, tinnitus is generated in the brain's auditory pathways: when input from the cochlea is reduced, usually by hair cell damage from age or noise, the central auditory system compensates by increasing its gain and generates aberrant activity that is perceived as sound. This is why it so often accompanies hearing loss, and why treatments directed at the ear alone rarely help.

Is it true that nothing can be done for tinnitus?

No — and being told this is one of the most damaging things that happens to tinnitus patients. It is true that no treatment reliably eliminates the sound itself, and no drug is recommended for that purpose. But a great deal can be done about the distress and disability, which is what actually causes the suffering. Cognitive behavioural therapy has the strongest evidence of any intervention for reducing tinnitus-related distress. Hearing aids frequently reduce tinnitus prominence in people with hearing loss. Sound enrichment reduces the contrast between the tinnitus and silence. Tinnitus retraining therapy and mindfulness-based approaches help many people. And addressing coexisting insomnia, anxiety and depression often produces the largest single improvement.

When is tinnitus a red flag?

Several patterns require prompt assessment rather than reassurance. Pulsatile tinnitus — a whooshing sound in time with the heartbeat — needs vascular imaging, because causes include dural arteriovenous fistula, carotid stenosis or dissection, glomus tumours and raised intracranial pressure. Unilateral tinnitus, particularly with asymmetric hearing loss, needs an MRI to exclude a vestibular schwannoma. Tinnitus with sudden hearing loss is an emergency — sudden sensorineural hearing loss requires urgent high-dose steroids, ideally within days. Tinnitus with vertigo, neurological signs, headache or visual disturbance requires neurological assessment. And tinnitus accompanied by significant low mood or thoughts of self-harm requires immediate mental health support, since severe tinnitus distress carries real psychological risk.

Does anything make tinnitus worse?

Several things commonly do. Silence — tinnitus is almost always most intrusive in quiet rooms and at night, which is why sound enrichment at bedtime helps so many people, and why total silence should be avoided. Noise exposure — loud noise causes further hair cell damage and often a step-change worsening; hearing protection at concerts, in workplaces and for power tools and shooting is essential. Poor sleep, stress and anxiety amplify the perception through the same limbic pathways that maintain it. Some medicines, including high-dose aspirin, aminoglycoside antibiotics, cisplatin and loop diuretics. And, paradoxically, over-use of earplugs in ordinary quiet environments — a very common self-management strategy — worsens both tinnitus and sound sensitivity over time by further increasing the central gain that causes them.

Can tinnitus be prevented?

To a large extent, yes — because its dominant preventable cause is noise-induced hearing damage, and hair cells do not regenerate in humans. WHO estimates that over a billion young people are at risk of avoidable hearing loss from unsafe listening, and has issued a global standard for safe listening devices alongside the Make Listening Safe initiative. Practical measures: limit personal listening device volume and duration (the commonly used rule is no more than 60% volume for no more than 60 minutes at a time); use properly fitted hearing protection at concerts, in noisy workplaces, when shooting and when using power tools; use noise-cancelling rather than higher volume in noisy environments such as aircraft; and ensure occupational hearing conservation programmes with audiometric surveillance where noise exposure is unavoidable.

How does GMJ News cover tinnitus?

GMJ News covers tinnitus prevalence and central generation mechanisms, the harm of "nothing can be done", CBT as the strongest-evidence intervention, hearing aids and sound enrichment, tinnitus retraining therapy, pulsatile tinnitus red flags and vascular imaging, unilateral tinnitus and vestibular schwannoma, validated outcome measures (THI, TFI), somatic tinnitus modulation, ototoxic drugs and the guidance against routine drug treatment, hyperacusis and the harm of over-protection, and WHO Make Listening Safe noise prevention. Relevant to PHIG's hearing health, occupational health and mental health programmes.

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Tinnitus

GMJ News knowledge hub · last reviewed September 2026 · Georgian Medical Journal

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Tinnitus — the perception of sound in the absence of an external acoustic source — affects approximately 14% of adults worldwide, with around 2% experiencing it severely enough to substantially impair quality of life, sleep, concentration and mental health, and is generated not in the ear but in the central auditory pathways as a maladaptive response to reduced peripheral input — which is why it so commonly accompanies hearing loss and why treatments aimed at the ear alone usually fail (WHO). No drug has been shown to eliminate tinnitus, and patients are frequently told, wrongly and damagingly, that nothing can be done; in reality cognitive behavioural therapy has the strongest evidence base of any intervention for reducing tinnitus-related distress and disability, and hearing aids, sound enrichment and tinnitus retraining therapy all have a role — while pulsatile tinnitus, particularly if unilateral and synchronous with the pulse, is a fundamentally different symptom requiring vascular imaging to exclude dural arteriovenous fistula, carotid stenosis, glomus tumour or idiopathic intracranial hypertension.

Key messages

~14% of adults — generated centrally, not in the ear

Tinnitus affects approximately 14% of adults worldwide, with around 2% experiencing it severely enough to substantially impair quality of life, sleep, concentration and mental health. Critically, the sound is generated in the CENTRAL auditory pathways, not the ear: reduced peripheral input (usually from cochlear hair cell loss) triggers maladaptive increases in central gain, aberrant neural synchrony and cross-modal reorganisation. This explains why treatments aimed at the ear alone usually fail, and why cutting the auditory nerve does not abolish tinnitus.

"Nothing can be done" is false and harmful — CBT has the strongest evidence

Patients are still routinely told nothing can be done, which is both inaccurate and damaging: it removes hope, prevents referral and worsens distress. No drug eliminates the tinnitus percept — but cognitive behavioural therapy has the strongest evidence base of any intervention for reducing tinnitus-related DISTRESS, disability and quality-of-life impact (Cochrane; NICE; multiple guidelines). The therapeutic target is the reaction to the sound, not the sound itself — and the reaction is what actually causes the suffering.

Pulsatile tinnitus is a different symptom requiring imaging

Pulsatile tinnitus — a rhythmic whooshing synchronous with the heartbeat — is NOT ordinary tinnitus and must not be managed with reassurance and sound therapy. It signals turbulent flow or a vascular abnormality and requires investigation, particularly if unilateral, objective (audible to the examiner), or associated with headache, visual symptoms or a bruit. Causes: dural arteriovenous fistula; carotid stenosis or dissection; glomus tympanicum or jugulare (paraganglioma — may be visible as a red retrotympanic mass); idiopathic intracranial hypertension (obese young women, headache, papilloedema); sigmoid sinus diverticulum or dehiscence; AVM. Investigation: MRI/MRA or CT angiography of the head and neck.

Hearing aids and sound enrichment treat the underlying deprivation

Because tinnitus arises from reduced auditory input, restoring input helps. Hearing aids in patients with coexisting hearing loss frequently reduce tinnitus prominence — both by amplifying environmental sound that masks it and by reducing the central gain that generated it. Sound enrichment (broadband noise, environmental sound, low-level music, bedside sound generators) reduces the contrast between the tinnitus and silence — hence the near-universal observation that tinnitus is worst in quiet rooms and at night. Total silence should be avoided. Cochlear implantation frequently reduces tinnitus in profoundly deaf patients.

Screen for hearing loss, mental health and sleep — not just the ear

Every patient with tinnitus needs: pure tone audiometry (coexisting hearing loss is present in the majority and is directly treatable); screening for depression, anxiety and suicidal ideation (tinnitus-related distress carries measurable psychological morbidity, and severe tinnitus is associated with increased suicide risk); and assessment of sleep, since insomnia both worsens and is worsened by tinnitus. Also review ototoxic and tinnitus-associated medication: aminoglycosides, cisplatin, loop diuretics, high-dose salicylates and quinine. Unilateral tinnitus with asymmetric sensorineural hearing loss requires MRI to exclude vestibular schwannoma.

Noise exposure prevention is the main population-level lever

The dominant preventable cause of both hearing loss and tinnitus is noise — occupational (industry, construction, agriculture, military) and recreational (personal listening devices, concerts, motorsport, shooting). WHO estimates over one billion young people are at risk of avoidable hearing loss from unsafe listening practices, and has issued the WHO-ITU global standard for safe listening devices and the Make Listening Safe initiative. Hearing protection, sound level limits, exposure duration limits, and personal device volume monitoring are the interventions. Once hair cells are lost they do not regenerate in humans — prevention is the only cure currently available.

Key statistics

~14%

of adults worldwide experience tinnitus; ~2% severely

JAMA Neurol/WHO

CBT

strongest evidence of any intervention for tinnitus-related distress and disability

Cochrane/NICE

Pulsatile

tinnitus requires vascular imaging — a different symptom with treatable structural causes

AAO-HNS

>1 billion

young people at risk of avoidable hearing loss from unsafe listening practices

WHO

Asymmetric

unilateral tinnitus with asymmetric hearing loss requires MRI to exclude vestibular schwannoma

AAO-HNS/NICE

No drug

has been shown to eliminate tinnitus — guidelines advise against routine drug treatment

AAO-HNS/NICE

Tinnitus interventions — evidence for reducing distress and disability

Source: NICE/AAO-HNS/Cochrane. Interventions target the reaction and the underlying hearing loss, not the percept itself.

Glossary of key terms

Subjective vs objective tinnitus
Audiology/ENTSubjective tinnitus (the vast majority): audible only to the patient; generated by central auditory pathway activity; typically associated with hearing loss; described as ringing, hissing, buzzing, whistling or cicada-like. Objective tinnitus (rare but important): a real acoustic phenomenon that can in principle be heard by the examiner with a stethoscope or Toynbee tube — caused by vascular turbulence (bruit, dural AV fistula, glomus tumour), or by muscular phenomena such as palatal myoclonus (rhythmic clicking from soft palate muscle contraction) or middle ear myoclonus (stapedius or tensor tympani). Objective tinnitus always warrants investigation and frequently has a specific, treatable cause.

Tinnitus Functional Index and THI
Outcome measurementValidated questionnaires quantify tinnitus impact and are essential for tracking treatment response, since the loudness of the percept correlates poorly with the suffering it causes. Tinnitus Handicap Inventory (THI, 25 items, 0-100): grades 1-5 from slight to catastrophic; widely used and translated. Tinnitus Functional Index (TFI, 25 items): designed specifically to be responsive to treatment change, with eight subscales (intrusiveness, sense of control, cognition, sleep, auditory, relaxation, quality of life, emotional). A reduction of around 13 points on the TFI is generally taken as clinically meaningful. Using a validated instrument at baseline and follow-up is the single most useful practical step in structuring tinnitus care.

Tinnitus retraining therapy (TRT)
AudiologyBased on Jastreboff's neurophysiological model, TRT combines: (1) directive counselling — a detailed explanation of the mechanism designed to reclassify the tinnitus signal as neutral rather than threatening, thereby breaking the limbic and autonomic reinforcement loop; and (2) sound therapy — continuous low-level broadband sound, set at a level that does not mask the tinnitus but reduces the contrast against silence, promoting habituation. Treatment is delivered over 12-24 months. Evidence is positive but methodologically weaker than for CBT, and the counselling component is likely to account for much of the effect. The core insight — that the distress is driven by the meaning attached to the sound, not the sound's acoustic properties — is clinically valuable regardless of the specific protocol used.

Somatosensory and somatic tinnitus
Neuro-otologyA substantial minority of patients can modulate the loudness or pitch of their tinnitus by jaw movement, neck movement, or firm pressure on the head, neck or jaw — somatic tinnitus. This reflects convergence of somatosensory input from the trigeminal and cervical systems onto the dorsal cochlear nucleus. Clinically important because it identifies patients in whom temporomandibular disorder or cervical spine dysfunction is contributing, and in whom treating that contributor (dental or TMD management, physiotherapy, postural correction) may improve the tinnitus. Always ask specifically whether jaw or neck movement changes the sound — patients rarely volunteer it.

Drugs and tinnitus
PharmacologyDrug causes and associations to review in every patient: aminoglycosides (gentamicin, amikacin — cochleotoxic and vestibulotoxic, dose- and duration-related, may be irreversible); platinum chemotherapy (cisplatin especially — cumulative and permanent); loop diuretics at high dose or rapid infusion (usually reversible); high-dose salicylates and NSAIDs (classically reversible); quinine and chloroquine; macrolides at high dose. Conversely, no drug is licensed or recommended for tinnitus itself: guidelines (NICE, AAO-HNS) specifically advise AGAINST routine use of antidepressants, anticonvulsants, anxiolytics and betahistine for tinnitus alone. Antidepressants are indicated only where there is comorbid depression or anxiety, which should be treated on its own merits.

Hyperacusis and misophonia
AudiologyFrequently coexist with tinnitus and are commonly missed. Hyperacusis: abnormal intolerance of ordinary environmental sounds at levels comfortable to others, with genuine discomfort or pain — driven by increased central auditory gain. Management is sound desensitisation with graded exposure, NOT ear protection: routine use of earplugs in everyday quiet environments worsens hyperacusis by further increasing central gain, and this common self-management strategy must be actively discouraged (protection remains appropriate for genuinely loud exposure). Misophonia: strong emotional and autonomic reactions (anger, disgust, anxiety) to specific trigger sounds, often human-generated such as chewing or breathing — a distinct condition responding to CBT-based approaches rather than audiological treatment.

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