ENT : Tinnitus

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Tinnitus - Comprehensive ENT Review

Definition

Tinnitus is the perception of sound in the absence of an external acoustic source. The term derives from the Latin tinnire ("to ring"). It is a symptom, not a disease, and may arise from any level of the auditory pathway.
  • Scott-Brown's Otorhinolaryngology, Vol 2 notes that a completely unambiguous definition remains elusive - some definitions inadvertently include auditory hallucinations of mental illness or exclude certain forms of pulsatile tinnitus where a real intracorporeal sound source exists.

Classification

1. Subjective vs Objective

FeatureSubjectiveObjective
Heard byPatient onlyPatient + examiner (stethoscope / microphone)
Prevalence~98.5% of tinnitusRare (~1.5% at tertiary centres)
SourcesAberrant neural activityMuscular, vascular, joint

2. Pulsatile vs Non-Pulsatile

  • Non-pulsatile: Most common (~90% of ENT referrals). Described as ringing, hissing, buzzing, or roaring. Almost always subjective.
  • Pulsatile: Sound is rhythmic; divided into:
    • Synchronous - in time with the arterial pulse (vascular origin)
    • Non-synchronous - rhythmic but not pulse-synchronous (muscular, e.g., palatal myoclonus)

3. Primary vs Secondary

TypeFeatures
PrimaryNo identifiable cause; may or may not have SNHL
SecondaryIdentifiable underlying cause (auditory or non-auditory)

Epidemiology

  • Prevalence of persistent spontaneous tinnitus: 10.1% of adults (UK MRC study, n = 48,313)
  • ~5% describe it as moderately or severely annoying
  • ~0.5% report severe impact on normal daily life
  • Up to 50 million adults in the USA affected; ~16 million with frequent/chronic tinnitus
  • Only ~20% find it bothersome enough to seek treatment
  • ~28% of acute tinnitus (< 6 months) resolves spontaneously
  • Tinnitus is the most common service-connected disability among US veterans (>1.5 million claims in 2016, costs >$2.75 billion)
  • Cummings Otolaryngology notes 10.6% of adults aged 21-84 report tinnitus of at least moderate severity that interferes with sleep

Etiology / Causes

Auditory Causes

LocationCause
External earCerumen impaction, foreign body, otitis externa
Middle earOtosclerosis, chronic otitis media, ossicular chain disorders
Inner earSNHL, Meniere's disease, noise-induced hearing loss (NIHL), presbycusis, labyrinthitis
RetrocochlearVestibular schwannoma (VS) - tinnitus in 11-63% of VS cases

Causes of Pulsatile Tinnitus (Table 99.2 - Scott-Brown's)

Arterial:
  • Extracranial arteriovenous malformation
  • Dural arteriovenous fistulae
  • Carotid-cavernous fistulae
  • Aneurysm of internal carotid or vertebral artery
  • Fibromuscular dysplasia of ICA
  • ICA dissection
  • Atherosclerosis
  • Vascular anomalies of the ear (persistent stapedial artery, carotid-cochlear dehiscence)
  • Migraine
Venous:
  • Jugular bulb anomalies (high-riding, enlarged, jugular bulb diverticulum)
  • Abnormal condylar/mastoid emissary veins
  • Idiopathic intracranial hypertension (IIH)
Tumours:
  • Paraganglioma (glomus tympanicum, glomus jugulare) - hypervascular
  • Jugular foramen schwannoma
  • Meningioma
Muscular (non-synchronous pulsatile):
  • Palatal myoclonus
  • Stapedial myoclonus
  • Tensor tympani myoclonus
Note: In up to 30% of pulsatile tinnitus cases, no cause is found.

Ototoxic Drugs Causing Tinnitus

  • Salicylates (aspirin - dose-dependent, usually reversible)
  • Quinine and antimalarials
  • Aminoglycoside antibiotics (gentamicin, streptomycin)
  • Platinum-based antineoplastics (cisplatin, carboplatin)
  • Loop diuretics (furosemide - especially with aminoglycosides)
  • NSAIDs (less definitive evidence)

Non-Auditory Causes

  • TMJ dysfunction (one-third of TMJ patients report tinnitus modulation with jaw movement)
  • Cervical spine disorders
  • Idiopathic intracranial hypertension
  • Anaemia, thyroid disorders

Pathophysiology

The pathophysiology of subjective non-pulsatile tinnitus is not fully understood. Several interacting mechanisms have been proposed:

1. Peripheral Mechanisms

  • Cochlear hair cell damage leads to reduced afferent input to the auditory nerve
  • This deafferentation triggers compensatory upregulation of central gain

2. Central Mechanisms

Three main theories:
a) Increased spontaneous activity Damage to the ear reduces activity in the auditory nerve, which in turn downregulates inhibitory processes in higher auditory centers, potentially generating increased spontaneous activity in the auditory cortex perceived as tinnitus.
b) Increased central neural synchrony Spontaneous neural activity in the auditory cortex is normally random; synchronization signals the presence of a sound. Peripheral damage causes spontaneous cortical activity to become pathologically synchronized, generating a false sound percept.
c) Reorganization of the cortical auditory map (tonotopic reorganization) The auditory system is tonotopically organized from cochlea to cortex. Following cochlear damage, neurons that previously received input from damaged regions "retune" to adjacent intact frequencies. This creates over-representation of frequencies bordering the damaged region, with increased neural activity at those frequencies - a proposed substrate for tinnitus.

3. Tinnitus Models

ModelAuthorsKey Concept
Habituation modelHallam et al. (1984)Tinnitus = neurophysiological disturbance; normally habituated to; fails under high autonomic arousal
Neurophysiological modelJastreboff (1990)Tinnitus involves altered activity in the limbic system, reticular system, and autonomic nervous system beyond the classical auditory pathway - basis for TRT

4. Somatic Tinnitus

A subset in which loudness, laterality, or tonality can be modulated by head/neck maneuvers or stimulation. Mechanism involves synkinesis (aberrant reinnervation after auditory deafferentation). Associated with:
  • TMJ dysfunction
  • Cervical spine pathology
  • Responds to: acupuncture, trigger point therapy, TMJ treatment

5. Typewriter Tinnitus

  • Staccato quality (like typewriter tapping, popcorn popping, Morse code)
  • Intermittent; may be triggered by head movements or sounds
  • May mimic tensor tympani/stapedius spasm or palatal myoclonus
  • Important to differentiate: responds to carbamazepine

Clinical Assessment

History

Key points to elicit:
  • Laterality: unilateral vs bilateral
  • Quality: ringing, buzzing, hissing, roaring, pulsatile, staccato
  • Onset and duration: acute (<6 months) vs chronic
  • Severity and impact: sleep, concentration, emotional wellbeing
  • Associated features: hearing loss, vertigo, aural fullness, otalgia, neurological symptoms
  • Aggravating factors: noise, head position, jaw movement
  • Drug history: ototoxic medications
  • Noise exposure: occupational/recreational
  • Vascular risk factors: hypertension, atherosclerosis

Examination

  • Otoscopy: EAC, TM
  • Auscultation: peri-auricular, neck, chest (for objective tinnitus)
  • Neurological exam: cranial nerve testing (VS, CPA lesion)
  • Head and neck: TMJ palpation, cervical spine
  • Cardiovascular: blood pressure

Investigations

IndicationInvestigation
All patients with tinnitusAudiometry (pure tone audiogram)
Unilateral/asymmetric SNHLMRI internal auditory meati (rule out VS)
Pulsatile tinnitusMRI/MRA, CT angiography, Doppler
Suspected IIHMRI brain, LP for opening pressure
Objective tinnitusTympanometry (myoclonus), auscultation
Metabolic screeningTFTs, FBC (anaemia)
Cummings: Pulsatile tinnitus, unilateral tinnitus, focal neurologic abnormalities, or asymmetric hearing loss all prompt imaging. Routine imaging in all patients with tinnitus is no longer recommended.

Tinnitus Assessment Questionnaires

  • Tinnitus Handicap Inventory (THI) - most widely used in the UK
  • Tinnitus Reaction Questionnaire (TRQ)
  • Tinnitus Functional Index (TFI) - newer, claimed to have several advantages
  • Mini Tinnitus Questionnaire
  • Hospital Anxiety and Depression Scale (HADS) - comorbid depression/anxiety
  • Insomnia Severity Index - comorbid sleep disturbance

Comorbidities

  • Depression and anxiety - frequently coexist; causal direction is often unclear
  • Hyperacusis - 40% of tinnitus patients report some degree of hyperacusis; conversely, 86% of patients with hyperacusis also report tinnitus
  • TMJ dysfunction
  • Insomnia - 10.6% of adults with tinnitus report sleep interference
  • Impaired concentration and work productivity

Management

The principle: no cure for primary subjective non-pulsatile tinnitus exists, but effective therapeutic interventions do. Management is stepped and multidisciplinary.

Step 1 - Treat Underlying Cause (Secondary Tinnitus)

  • Cerumen removal, treatment of OM, otosclerosis surgery
  • Surgical/endovascular treatment of vascular causes
  • Discontinue ototoxic drugs where possible
  • Treat IIH, anaemia, thyroid disease

Step 2 - Patient Education & Reassurance

  • Explanation of the condition is a key initial step
  • RCTs support formal education/information giving as a therapeutic modality
  • Negative counselling ("nothing can be done") is damaging and must be avoided
  • ~28% of acute tinnitus resolves spontaneously - reassurance is appropriate

Step 3 - Audiological Rehabilitation

Hearing aids - indicated when there is associated hearing loss
  • Amplification partially ameliorates tinnitus by increasing background sound
  • Evidence is supportive but limited in quality
Sound therapy / masking devices
  • White noise generators / broadband noise
  • Sound enrichment reduces the contrast between tinnitus and ambient sound
  • Partial masking (not complete suppression) is the preferred approach

Step 4 - Psychological Therapies

Cognitive Behavioural Therapy (CBT)
  • The most evidence-based treatment for bothersome tinnitus
  • Addresses the emotional and attentional response to tinnitus
  • Does not reduce tinnitus loudness but significantly improves quality of life
  • Recommended by multiple guidelines
Tinnitus Retraining Therapy (TRT) - Jastreboff's neurophysiological model
  • Combines directive counselling (demystification) with sound therapy
  • Goal is habituation to the tinnitus signal so it no longer provokes a reaction
  • Long-term efficacy data supportive
Relaxation therapy - based on Hallam's habituation model; reduces autonomic arousal

Step 5 - Pharmacotherapy

No drug is specifically licensed for tinnitus. Evidence base is generally poor.
Drug/ClassEvidence
BetahistineSome evidence in Meniere's-associated tinnitus; not for primary tinnitus
Antidepressants (TCAs, SSRIs)Treat comorbid depression/anxiety; no direct tinnitus benefit
BenzodiazepinesMay reduce anxiety-driven exacerbation; not recommended for routine use (dependence risk)
CarbamazepineEffective for typewriter tinnitus specifically
Intratympanic steroidsSome evidence in acute SNHL-associated tinnitus
Ginkgo bilobaSystematic reviews of RCTs are contradictory; no clear recommendation; avoid with antiplatelet/anticoagulant therapy (risk of hemorrhage)
MelatoninSmall RCTs suggest benefit for tinnitus + insomnia; insufficient evidence for routine use
Vitamins/supplements (B vitamins, magnesium, CoQ10, lipoflavonoids)No evidence to support use
A 2025 network meta-analysis (PMID: 40441764) systematically reviewed pharmacotherapy options for subjective tinnitus.

Step 6 - Neuromodulation / Invasive Options

Transcranial Magnetic Stimulation (rTMS)
  • Repetitive TMS induces neuroplastic changes in cortical excitability
  • Multiple RCTs showed no significant difference in tinnitus severity vs sham
  • Not currently recommended in guidelines
Transcranial Direct Current Stimulation (tDCS)
  • Direct current modulates cortical excitability
  • Early trials; insufficient evidence for routine use
Cochlear implants
  • May dramatically reduce or eliminate tinnitus in profoundly deaf patients
  • A significant side benefit of implantation
Middle ear implants / auditory brainstem implants
  • Role being investigated

Acupuncture

  • Blinded RCTs show no effect vs sham acupuncture for routine tinnitus
  • May have a role in somatic tinnitus subset
  • Current guidelines make no recommendation for or against it

Special Subtypes

Noise-Induced Hearing Loss (NIHL) and Tinnitus

  • 50-70% of persistent tinnitus is associated with NIHL
  • 61% of adolescents after attending concerts report temporary tinnitus
  • Intense sound exposure triggers reactive oxygen/nitrogen species in the cochlea causing hair cell damage
  • NIHL and associated tinnitus are preventable - ear protection is key
  • Periexposure systemic steroids show promise for NIHL; effect on tinnitus unclear
  • Vitamin E and ginkgo biloba have been abandoned (RCTs do not support)

Vestibular Schwannoma (VS)

  • Unilateral tinnitus may be the only presenting symptom of VS
  • Tinnitus incidence with VS: 11-63%
  • Warrants MRI of internal auditory meati (same workup as asymmetric SNHL)

Meniere's Disease

  • Triad of episodic vertigo + SNHL + aural fullness, with tinnitus as a fourth feature
  • Tinnitus is low-frequency and fluctuating initially

Idiopathic Intracranial Hypertension (IIH)

  • Pulsatile tinnitus (often bilateral) is a classic feature
  • Associated with obesity, female sex, papilloedema, headache
  • Treatment of IIH (acetazolamide, weight loss, LP) often resolves tinnitus

Prognosis

  • ~28% of acute tinnitus (<6 months) resolves spontaneously
  • Chronic tinnitus (>6 months) is less likely to resolve completely
  • Effective management reduces distress and improves quality of life even when loudness persists
  • Negative prognostic factors: severe comorbid anxiety/depression, hyperacusis, high tinnitus-related distress scores

2025 Guidelines Update

The VA/DoD Clinical Practice Guideline for Management of Tinnitus (2025) - PMID: 40111327 - provides updated evidence-based recommendations. An umbrella review (PMID: 40712351) synthesizing all tinnitus treatment methods was also published in 2025.
Key current recommendations align with textbook teaching:
  1. CBT is the most evidence-supported intervention for bothersome tinnitus
  2. Hearing amplification when hearing loss is present
  3. Sound therapy for symptom relief
  4. No pharmacotherapy has sufficient evidence for routine recommendation
  5. Routine imaging is not indicated except for pulsatile, unilateral, or neurologically complex cases

Sources: Scott-Brown's Otorhinolaryngology Head & Neck Surgery, Vol 2 | Cummings Otolaryngology Head and Neck Surgery | VA/DoD Clinical Practice Guideline 2025 (PMID: 40111327)
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