TINNITUS AND TINNITUS MASKERS

MS ENT University Examination — 20 Marks

DEFINITION

CLASSIFICATION

1. By Audibility

2. By Rhythm

3. By Duration

• Transient: Brief episodes, common in normal population
• Persistent: Lasts >5 minutes per episode; clinically significant

EPIDEMIOLOGY

• Prevalence of persistent spontaneous tinnitus in adults: 10.1% (UK MRC Study, n=48,313)
• 5% report it as moderately or severely annoying; 0.5% report severe effect on quality of life
• Prevalence in Italy 14.5%, USA 14.9%, Sweden 15.8%
• 5-year incidence: 5.7%; 10-year incidence: 12.7% (Beaver Dam, Wisconsin)
• Tinnitus increases with age, plateaus around 70 years
• High-frequency hearing loss is the strongest predictor
• Left-sided tinnitus is slightly more common than right (reason unknown)
• 40% of tinnitus patients also have hyperacusis; conversely, 86% of hyperacusis patients have tinnitus

ETIOLOGY / CAUSES

Peripheral (Cochlear/Conductive)

• Noise-induced hearing loss (most common cause)
• Presbycusis (age-related hearing loss)
• Otosclerosis
• Meniere's disease
• Acoustic trauma
• Cerumen impaction, otitis media, otitis externa

Central / Retrocochlear

• Vestibular schwannoma (acoustic neuroma) - tinnitus incidence 11-63% in VS
• Multiple sclerosis
• Brainstem lesions

Vascular (Pulsatile Tinnitus)

Ototoxic Drugs (Important)

• Salicylates (aspirin) - dose-dependent, reversible
• Quinine and antimalarials
• Aminoglycoside antibiotics (gentamicin, streptomycin)
• Platinum-based antineoplastics (cisplatin) - often irreversible
• Loop diuretics (furosemide)

Systemic

• Hypertension, cardiovascular disease
• Anaemia, thyroid disorders
• Temporomandibular joint dysfunction (comorbidity)

PATHOPHYSIOLOGY

Peripheral Theory (Historical)

Central Mechanisms (Current Understanding)

1. Deafferentation / Edge Effect: Hair cell loss at a specific frequency leads to reduced inhibitory input to corresponding central neurons, causing those neurons to fire spontaneously - analogous to phantom limb pain (Flor, 1998).
2. Cortical Map Reorganization: Following peripheral hearing loss, plastic reorganization of the tonotopic map in the auditory cortex occurs; neurons deprived of input are "colonized" by adjacent frequency areas, generating spurious signals perceived as tinnitus.
3. Increased Neural Synchrony: There is abnormal synchronous firing of central auditory neurons. This is the basis for Acoustic CR Neuromodulation therapy.
4. Neurophysiological Model (Jastreboff, 1990): The most influential model. Tinnitus involves altered activity not just in the classical auditory system but also in the limbic system (emotional significance), reticular system (arousal and sleep) and autonomic nervous system. The model explains why identical audiological tinnitus causes mild distress in one patient and severe disability in another - it is the activation of the limbic and autonomic pathways that determines suffering. This is the basis of TRT.
5. Autonomic Arousal Theory: High autonomic arousal prevents the central auditory system from habituating to tinnitus signals - basis for relaxation therapy and CBT.

ASSESSMENT / INVESTIGATION

History

• Character: ringing, hissing, whistling, roaring, pulsatile
• Unilateral vs bilateral vs central (in the head)
• Duration, onset (sudden vs gradual)
• Associated: hearing loss, vertigo, aural fullness (Meniere's triad), ear discharge, headache
• Drug history (ototoxic agents), noise exposure history
• Effect on sleep, concentration, quality of life

Clinical Examination

• Otoscopy (wax, TM perforation, middle ear mass - glomus)
• Auscultation over neck, periauricular, mastoid (objective tinnitus)
• Cranial nerve examination (facial palsy with VS)
• Head and neck examination for vascular tumours

Audiological Investigations

1. Pure tone audiogram (PTA) - mandatory for ALL patients with tinnitus
2. Tympanometry - middle ear function
3. Tinnitus-specific tests:
   • Tinnitus pitch matching: patient matches their tinnitus to a test tone; majority ~4 kHz
   • Tinnitus loudness matching: almost always only 5-10 dB above threshold (SL); this is important - subjectively loud tinnitus is objectively very quiet
   • Minimum masking level (MML): lowest level of broad-band noise that just masks the tinnitus
   • Residual inhibition test: after 1 minute of masking sound at 10 dB above MML, degree and duration of tinnitus suppression is measured
   • Loudness Discomfort Level (LDL): important for hyperacusis assessment
4. Speech audiometry, OAEs, ABR - as clinically indicated

Questionnaires (Validated)

• Tinnitus Handicap Inventory (THI) - most widely used
• Tinnitus Reaction Questionnaire
• Beck Depression/Anxiety inventories (comorbidity screening)

Imaging

• MRI with gadolinium - investigation of choice for unilateral tinnitus, asymmetric SNHL, suspected VS
• CT temporal bone - for bony lesions, otosclerosis
• CT angiography / MR angiography - for pulsatile tinnitus (paraganglioma, AVM, fistula)
• Doppler ultrasound - carotid disease

MANAGEMENT

A. General Principles (Counselling and Education)

• Reassurance and demystification: explaining that tinnitus is not life-threatening, not a sign of mental illness, and does not generally worsen
• Avoidance of silence (promotes tinnitus awareness)
• Avoidance of further noise exposure, ototoxic drugs
• Treatment of any underlying identifiable cause (e.g. wax removal, treating otitis media, correcting anaemia)

B. Sound Therapy (Including Masking)

1. Tinnitus Maskers

• Introduced by Vernon in the 1970s; based on earlier work of Goodhill, Saltzman and Ersner (1947)
• Principle: "By amplification, much outside sound is enabled to reach the cochlea, crowding out and masking the patient's head noises" (Saltzman & Ersner)
• A tinnitus masker is a device - resembling a hearing aid - that generates broad-band noise (white/pink noise) to mask the tinnitus perception
• Residual inhibition: after cessation of masking sound, tinnitus may remain suppressed for seconds to minutes; clinically useful as a test of response, but rarely lasting enough to be of standalone therapeutic value
• Important finding (Feldman's experiments): tinnitus suppression is based on neuronal suppression, NOT acoustic masking at the basilar membrane; there is no critical band phenomenon, no "V"-shaped masking curve around tinnitus pitch - tinnitus is equally suppressible by sounds of a wide frequency range; even contralateral masking can be effective
• Masker-hearing aid combinations: for patients with both tinnitus and hearing loss

Types of Masker Devices:

• Pink noise (environmental sound masking) and relaxation CDs: widely used but evidence limited
• Vernon claimed tinnitus "maskable in 95% of tinnitus patients" - not confirmed by other groups
• Continuous use of maskers for >6 months: some benefit in subgroup of patients; not superior to placebo in some trials
• Occlusive hearing aids can worsen tinnitus by acting as earplugs - important caution

C. Tinnitus Retraining Therapy (TRT)

• Developed by Jastreboff based on his neurophysiological model (1990)
• Two components:
  1. Directive counselling: reclassification of tinnitus signal from "threatening" to "neutral" by retraining the limbic and autonomic systems
  2. Sound therapy: low-level broadband noise (sub-masking level, NOT masking) via wearable sound generators to reduce the contrast between tinnitus and background noise and promote habituation
• Goal: habituation of reactions to tinnitus (primary goal) and ultimately habituation of perception (final goal)
• TRT sound generators are set below MML (unlike maskers which are set AT or above MML) - this is a fundamental difference from masking
• Success rate: 82% significant reduction in THI at 12 months (Jastreboff, 2007)
• Randomized study (Henry et al., 2006): TRT superior to masking therapy
• Herraiz et al.: 82% improvement with TRT vs waiting-list control; more severe tinnitus paradoxically responded better

D. Cognitive Behavioural Therapy (CBT)

• Most evidence-based psychological intervention for tinnitus
• Targets the emotional and cognitive response to tinnitus, not the tinnitus itself
• Reduces anxiety, depression, catastrophizing, and sleep disturbance related to tinnitus
• Evidence: Level 1 Cochrane reviews support CBT for reducing tinnitus distress

E. Pharmacological Treatment

• Antidepressants (tricyclics - amitriptyline; SSRIs): help patients cope; small benefit; Harrison's notes antidepressants are beneficial post-masking
• Anxiolytics (benzodiazepines): short-term use only; not recommended long-term
• Betahistine: used in Meniere's disease-associated tinnitus
• Ginkgo biloba: mixed evidence; used empirically; not superior to placebo in large trials
• Intravenous lidocaine: temporarily suppresses tinnitus; not practical for long-term use; basis for sodium channel modulator research
• No role for antihistamines or vasodilators in idiopathic tinnitus

F. Novel and Emerging Therapies

1. Acoustic CR Neuromodulation: four tones above/below tinnitus frequency to disrupt pathological neural synchrony; initial promise but Phase III RCT failed to show benefit over placebo
2. Sound therapy with vagus nerve stimulation (VNS): paired sound + VNS to reverse cortical reorganization; early-phase animal studies promising; human trials underway
3. Bimodal neuromodulation (Mute Button): acoustic + electrical stimulation of trigeminal fibres in tongue; early-stage evidence
4. Transcranial magnetic stimulation (TMS): targets auditory cortex; some evidence but inconsistent results
5. Deep brain stimulation, cochlear implants: for refractory tinnitus; cochlear implants effectively abolish tinnitus in profoundly deaf patients

G. Surgical Treatment

• Surgical treatment is generally reserved for tinnitus with a specific treatable cause:
  • Stapedectomy in otosclerosis relieves tinnitus in ~70% of cases
  • Surgical correction of vascular anomalies (paraganglioma resection, fistula repair)
  • Cochlear implantation in severe SNHL/deafness
  • Microvascular decompression of auditory nerve (controversial)
• Destructive procedures (cochlear nerve section) do NOT reliably cure tinnitus - reinforces the central origin of persisting tinnitus

PULSATILE TINNITUS - SPECIAL NOTE

• Examination: auscultate over neck, mastoid, eye; check BP
• Carotid bruit, neck mass
• Objective: audible with stethoscope over mastoid (dural AVF, high-riding JB)
• Compressibility: tinnitus reduces with ipsilateral carotid compression (vascular source)
• Up to 30% of pulsatile tinnitus remains idiopathic after full investigation

SUMMARY TABLE: MASKING vs. TRT

IMPORTANT EXAM POINTS (VIVA PEARLS)

1. Tinnitus loudness is almost always only 5-10 dB SL despite being subjectively described as very loud - this is a classic MCQ/viva point.
2. Feldman's finding: Tinnitus suppression is neuronal, not acoustic; no V-shaped masking curve; contralateral masking can be as effective as ipsilateral.
3. Residual inhibition: suppression of tinnitus after masking stops, lasting seconds to minutes; useful diagnostic test but not a treatment.
4. TRT uses sub-masking levels - this differentiates it from masking therapy.
5. Cochlear nerve section does NOT cure tinnitus - evidence that the generator is central.
6. Unilateral tinnitus = must exclude vestibular schwannoma (MRI with gadolinium).
7. Most common cause: noise-induced hearing loss and presbycusis.
8. Salicylate tinnitus: dose-dependent, bilateral, high-pitched, fully reversible on stopping aspirin.
9. Objective pulsatile tinnitus heard by examiner = glomus tumour until proven otherwise.
10. Jastreboff's neurophysiological model - cornerstone of modern tinnitus understanding and management.