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EN4.19 | Tinnitus — SDL Guide

Learning Objectives

Classify tinnitus into subjective/objective and pulsatile/non-pulsatile subtypes
Identify the clinical red flags in tinnitus that mandate urgent investigation
Describe the pathophysiology of tinnitus including the role of central maladaptive plasticity
Outline the investigation strategy, including when to order MRI and CT angiography
Explain the principles of management including tinnitus retraining therapy, CBT, and hearing aids

INSTRUCTIONS

Tinnitus — the perception of sound without an external acoustic stimulus — affects approximately 15% of adults and is severely debilitating in about 2–3%. It is important because it is frequently dismissed as 'just anxiety' or 'normal for your age,' yet it can be the presenting symptom of acoustic neuroma (unilateral tinnitus), Meniere's disease, ototoxicity, or a vascular lesion (pulsatile tinnitus). Learning to identify the red flags that mandate investigation is the essential clinical skill.

References

Dhingra PL — Diseases of Ear, Nose and Throat, 7th ed., Ch. 8 (Tinnitus) (textbook)
Hazarika P — Textbook of Ear Nose Throat and Head & Neck Surgery, 3rd ed. (textbook)
Scott-Brown's Otorhinolaryngology, Head and Neck Surgery, 8th ed., Vol. 3, Ch. 238 (textbook)

Version 2.0 | NMC CBUC 2024

CLINICAL SCENARIO

A 55-year-old retired factory worker presents with a constant high-pitched ringing in both ears for the past 3 years. He attributes it to his years of working on a noisy production line. He is now finding it difficult to sleep and is increasingly anxious about the noise. Meanwhile, a 38-year-old teacher presents with a new pulsatile thumping in her right ear for the past 6 months, which she says matches her heartbeat. She has no hearing loss and no headache. Both have tinnitus — but one needs reassurance and audiological management, while the other needs urgent vascular imaging. Which is which, and why?

WHY THIS MATTERS

Tinnitus — the perception of sound in the ear or head without an external acoustic source — affects approximately 10–15% of the adult population, with severe and debilitating tinnitus (causing significant distress, sleep disruption, difficulty concentrating, and reduced quality of life) in approximately 2–3%. In India, the prevalence is increasing with urbanisation and rising occupational and recreational noise exposure. Tinnitus is important clinically for three reasons: first, it is almost always a symptom rather than a disease in itself, and identifying its underlying cause determines management; second, unilateral tinnitus in a young or middle-aged adult without obvious cause mandates MRI to exclude acoustic neuroma — this is missed too often; and third, pulsatile tinnitus is a vascular symptom until proven otherwise and requires imaging. For the vast majority of patients with bilateral, high-pitched, non-pulsatile tinnitus and a history of noise exposure or age-related hearing loss, tinnitus is the natural consequence of cochlear hair cell damage — but it can still be severely debilitating, and the patient needs a structured management plan rather than dismissal.

RECALL

Recall that the auditory system extends from the cochlear hair cells through the spiral ganglion and cochlear nerve to the cochlear nuclei, inferior colliculus, medial geniculate nucleus, and primary auditory cortex. Normal auditory perception requires continuous processing of afferent signals. When cochlear hair cells are damaged or lost — from noise, ageing, or ototoxicity — the afferent input to the central auditory pathway is reduced or altered. This reduction of peripheral input is thought to unmask or amplify spontaneous activity in the central auditory system, generating the phantom sound perception we call tinnitus. This central auditory neuroplasticity model explains why tinnitus persists even after the ear is anaesthetised or the cochlear nerve is cut in some patients — the tinnitus generator has shifted to the central nervous system.

Clinical Presentation of Tinnitus

Tinnitus presents as a sound perceived in the ear or head that has no external source. The clinical assessment begins with a careful characterisation of the tinnitus — its type, laterality, temporal pattern, quality, and associated symptoms — because these features guide both the diagnostic classification and the investigation plan.

The most important initial question is whether the tinnitus is pulsatile (rhythmic, synchronous with the heartbeat) or non-pulsatile (continuous, intermittent, or tonal without rhythmic beat). This single question divides tinnitus into two fundamentally different pathophysiological categories with different investigation strategies. Pulsatile tinnitus is a vascular symptom until proven otherwise, and its investigation requires vascular imaging. Non-pulsatile tinnitus is much more common and is usually cochlear in origin.

The second important question is whether the tinnitus is unilateral or bilateral. Unilateral tinnitus in a patient without an obvious cause (such as known NIHL or CSOM on that side) is a red flag for acoustic neuroma and mandates MRI with gadolinium. Bilateral tinnitus is much less likely to represent a focal structural pathology.

Clinical classification of tinnitus:

Subjective tinnitus (vast majority): perceived only by the patient; generated in the cochlea, VIII nerve, or central auditory pathway; related to cochlear hair cell dysfunction, sensorineural hearing loss, or central auditory changes.
Objective tinnitus (rare, <5%): audible to the examiner as well as the patient, using auscultation over the ear, mastoid, or neck; indicates a mechanical sound source near the ear.

Red flags in tinnitus history:
- Unilateral tinnitus without obvious cause → MRI to exclude acoustic neuroma
- Pulsatile tinnitus → vascular imaging (MRI/MRA/CT angiography)
- Tinnitus with sudden hearing loss → SSNHL emergency protocol
- Tinnitus with vertigo and low-frequency hearing loss → Meniere's disease
- Tinnitus after starting a new drug (especially aminoglycosides, cisplatin) → ototoxicity — stop/review drug

Anatomy and Pathophysiology

The pathophysiology of tinnitus is multifactorial and not fully understood, but the dominant model — supported by neuroimaging and electrophysiological studies — is that most subjective tinnitus arises from maladaptive central auditory plasticity triggered by peripheral cochlear damage. This central origin explains several otherwise puzzling clinical observations: why tinnitus often persists even after the damaged ear is removed, why it cannot be fully suppressed by masking, and why psychological factors (anxiety, depression, sleep deprivation) significantly modulate its perceived severity.

The peripheral trigger is typically loss or dysfunction of cochlear outer hair cells — from noise damage, ageing, ototoxicity, or other causes. Outer hair cells are the active amplifiers of the cochlea; their loss reduces afferent input from specific frequency regions (most commonly the high-frequency basal turn). The central auditory pathway, deprived of normal input from these frequency channels, undergoes compensatory changes — neurons in the cochlear nucleus, inferior colliculus, and auditory cortex representing the deafferented frequencies increase their spontaneous firing rate and expand their receptive fields. This central hyperactivity is perceived as the phantom sound — tinnitus.

Pulsatile tinnitus has a different mechanism. Here, a real turbulent or rhythmic mechanical sound is transmitted to the cochlea. Sources include:
- Vascular turbulence: atherosclerotic narrowing of the carotid artery, arteriovenous malformation (AVM), glomus tumour (paraganglioma of the middle ear or jugular foramen — presents as a red-blue pulsating mass behind the TM)
- Increased flow states: anaemia, thyrotoxicosis, pregnancy (high cardiac output states producing audible venous hum)
- Venous hum: turbulent flow in the sigmoid sinus or jugular bulb — often worsened on turning the head or compressing the jugular vein
- Palatal myoclonus and tensor tympani myoclonus: rhythmic contractions of muscles near the Eustachian tube producing a clicking sound

The physical examination of a patient with pulsatile tinnitus should include auscultation over the ipsilateral periauricular region, mastoid, and neck for a bruit, and otoscopy to look for a vascular middle ear mass (glomus tympanicum — red-blue pulsating mass behind the TM).

SELF-CHECK

A 52-year-old woman presents with a 4-month history of pulsatile tinnitus in the right ear, synchronous with her heartbeat. She has no hearing loss. On otoscopy there is a reddish pulsating mass visible through the intact right tympanic membrane. The most likely diagnosis is:

A. Acute otitis media with pus behind the eardrum

B. Glomus tympanicum tumour (middle ear paraganglioma)

C. Benign paroxysmal positional vertigo

D. Wax impaction against the eardrum

Reveal Answer

Answer: B. Glomus tympanicum tumour (middle ear paraganglioma)

A red-blue pulsating mass visible through the intact tympanic membrane combined with pulsatile tinnitus is pathognomonic of a glomus tympanicum tumour — a paraganglioma arising from the middle ear. The pulsation is synchronous with the heartbeat because the tumour is highly vascular. AOM would show a red, bulging, opaque TM without a visible mass. BPPV does not cause tinnitus or a mass. Wax produces an opaque TM canal obstruction without a pulsating mass. Glomus tympanicum should never be biopsied in the clinic — it is extremely vascular and would cause catastrophic haemorrhage.

Investigations

The investigation of tinnitus is guided by the clinical classification — the specific features of the history (unilateral vs bilateral, pulsatile vs non-pulsatile, associated hearing loss, duration) determine which investigations are necessary. In most patients with bilateral high-pitched tinnitus and documented SNHL from noise or ageing, extensive investigation is not needed. The investigations below are structured by the clinical question they answer, ordered from the most basic (audiometry for all) to the most specialist (vascular imaging for pulsatile tinnitus).

1. Audiometry (all patients with tinnitus):
Pure-tone audiometry identifies and quantifies any associated hearing loss. The audiometric pattern provides strong clues to aetiology: bilateral high-frequency SNHL with a 4 kHz notch = NIHL; low-frequency fluctuating SNHL = Meniere's; unilateral high-frequency SNHL with rollover = acoustic neuroma retrocochlear pattern. Speech audiometry and rollover testing may suggest retrocochlear pathology.

2. Tympanometry:
Rules out middle ear pathology (effusion, perforation). A type As tympanogram suggests otosclerosis as a cause; type B with flat curve suggests effusion.

3. Otoacoustic emissions (OAEs):
Absent OAEs confirm outer hair cell damage; present OAEs with absent ABR would suggest retrocochlear pathology.

4. Tinnitus matching (pitch and loudness matching):
Used in specialist tinnitus clinics to quantify the pitch (most commonly matches to 3–8 kHz) and loudness of the tinnitus. Patients often perceive their tinnitus as much louder than it actually is — the matched loudness is typically only 5–10 dB above their hearing threshold, which can be reassuring when explained.

5. MRI with gadolinium (IAC sequences):
Indicated for: unilateral tinnitus without obvious cause; unilateral SNHL; abnormal ABR; or pulsatile tinnitus (to exclude vascular mass, AVM, glomus jugulare). This is the most important investigation to not miss in unilateral tinnitus.

6. CT angiography / MRA (magnetic resonance angiography):
Indicated specifically for pulsatile tinnitus to image the carotid arteries, jugular bulb, sigmoid sinus, and intracranial vasculature.