Tinnitus: Assessment and Management

Introduction

Tinnitus is the perception of sound in the absence of an external source - typically described as ringing, buzzing, hissing or humming. It is extremely common, affecting around 1 in 8 adults at some point, and for most people it is a benign, self-limiting nuisance rather than a sign of serious disease.¹

The clinical priority is not to eliminate the sound itself, which is not usually possible, but to identify the minority of patients in whom tinnitus is a marker of an underlying condition that needs treatment - an asymmetric hearing loss, a vascular abnormality, or, rarely, a tumour of the auditory nerve.

Classification and pathophysiology

Subjective tinnitus

The great majority of tinnitus is subjective - audible only to the patient, with no identifiable external sound source even on careful examination. It is thought to arise from abnormal neural activity generated when damaged cochlear hair cells reduce normal afferent input, leading to disinhibition and hyperactivity in the central auditory pathways - the brain, in effect, generates phantom sound to compensate for missing input, in a way that parallels phantom limb pain.²

Objective tinnitus

A small minority of cases are objective - a genuine sound generated within the body that can, in principle, also be heard by an examiner (classically with a stethoscope over the neck, orbit or mastoid). This is usually pulsatile, synchronous with the heartbeat, and arises from turbulent blood flow near the ear: causes include arteriovenous malformations, glomus tumours, carotid artery stenosis or dissection, a high-riding or dehiscent jugular bulb, and idiopathic intracranial hypertension (via pulsatile venous sinus flow). Rarer non-vascular objective causes include palatal myoclonus and stapedial or tensor tympani muscle spasm, producing a clicking sound.²

Aetiology

Tinnitus is a symptom rather than a diagnosis, and shares many causes with hearing loss:¹

• Presbycusis and noise-induced hearing loss: the most common associations
• Ear wax or a foreign body occluding the canal
• Meniere's disease: tinnitus with fluctuating hearing loss and vertigo
• Otosclerosis: conductive hearing loss with tinnitus in a younger adult
• Ototoxic drugs: aspirin and other NSAIDs (dose-related and reversible), aminoglycosides, loop diuretics, and platinum-based chemotherapy
• Sudden sensorineural hearing loss: tinnitus is a frequent accompanying symptom and should trigger urgent assessment as described separately
• Vestibular schwannoma: classically unilateral tinnitus with asymmetric sensorineural hearing loss
• Depression and anxiety: strongly associated, and can both cause and be worsened by tinnitus
• Idiopathic: no cause is found in a substantial proportion of patients

Risk factors

• Any cause of hearing loss, particularly noise exposure and presbycusis
• Ototoxic medication use
• Anxiety, depression and high stress levels
• Cardiovascular risk factors for pulsatile tinnitus (hypertension, atherosclerosis)
• Obesity and idiopathic intracranial hypertension for pulsatile tinnitus
• Head injury

Clinical features

Establish the character (ringing, buzzing, hissing, clicking or pulsatile), laterality (unilateral versus bilateral), timing (constant or intermittent) and any triggers. Ask specifically whether the sound is pulsatile and synchronous with the heartbeat, since this single feature reframes the differential towards a vascular cause.¹

Associated symptoms are important: hearing loss, aural fullness and vertigo point towards Meniere's disease; unilateral hearing loss with unsteadiness raises concern for a vestibular schwannoma; headache and visual disturbance with pulsatile tinnitus raise concern for idiopathic intracranial hypertension.

Assess the impact on the patient's life - sleep disturbance, difficulty concentrating, and effect on mood are common and are central to management, since the degree of distress often matters more than the loudness of the tinnitus itself.

Examination

Otoscopy to look for wax, infection or a drum abnormality; formal hearing assessment with Rinne and Weber tests at the bedside. Auscultate over the mastoid, periauricular area, orbit and neck for a bruit if pulsatile tinnitus is reported, and check for a carotid bruit and blood pressure.¹

A full cranial nerve examination, including facial nerve function and testing for nystagmus, is important when a retrocochlear cause is being considered. Fundoscopy for papilloedema is added if idiopathic intracranial hypertension is suspected.

Differential diagnosis

Tinnitus itself is the presenting symptom; the differential lies in identifying its cause, which follows the aetiology list above. The key branch points are whether hearing loss is present and symmetric, and whether the tinnitus is pulsatile.

Investigations

Pure tone audiometry should be arranged for every patient with persistent tinnitus, both to identify any underlying hearing loss and as a baseline. MRI of the internal auditory meatus is indicated for unilateral or markedly asymmetric tinnitus, particularly with asymmetric hearing loss, to exclude a vestibular schwannoma.³

Pulsatile tinnitus warrants vascular imaging - MR or CT angiography/venography, or Doppler ultrasound of the carotids - to look for an arteriovenous malformation, carotid stenosis or dissection, or venous sinus abnormality. Blood pressure, FBC (anaemia can cause a hyperdynamic pulsatile tinnitus) and thyroid function are also reasonable baseline tests.

Management

Treat any identifiable underlying cause first: remove wax, manage Meniere's disease or otosclerosis, stop or switch an ototoxic drug where possible, or refer urgently if a vestibular schwannoma or vascular abnormality is found.¹

When no treatable cause is identified, which is common, management focuses on reducing the impact of the symptom rather than eliminating the sound:

• Sound therapy/masking: background noise (white noise generators, fans, or simply not sitting in silence) reduces the contrast between tinnitus and ambient sound, making it less intrusive
• Hearing aids: where hearing loss coexists, amplification often reduces tinnitus perception as a secondary benefit alongside improving hearing
• Cognitive behavioural therapy (CBT): the best-evidenced psychological intervention, helping patients change their emotional and attentional response to the sound rather than trying to remove it
• Tinnitus retraining therapy: combines directive counselling with sound therapy to promote habituation over time
• Managing sleep, anxiety and depression: actively treating these frequently improves tinnitus distress even without changing the sound itself

There is no medication licensed specifically to cure tinnitus, and drug trials (including antidepressants and anticonvulsants used off-label) have shown limited and inconsistent benefit; treatment is instead directed at coexisting anxiety, depression or insomnia where present.¹ Patients benefit from reassurance that tinnitus is very rarely a sign of serious disease once red flags have been excluded, and from information and support, including from patient organisations such as the British Tinnitus Association.

Complications

• Sleep disturbance and insomnia
• Difficulty concentrating at work or school
• Anxiety and depression, which can form a vicious cycle with the tinnitus itself
• Reduced quality of life in severe, persistent cases
• Missed diagnosis of an underlying treatable cause if red flags are not recognised

Red flags

Prognosis

For most patients, tinnitus either resolves or, more often, becomes less intrusive over time as the brain habituates to the sound, particularly with sound therapy and psychological support. A significant minority experience persistent, bothersome tinnitus that requires ongoing multidisciplinary management, but even in this group, distress and impact on quality of life can usually be substantially reduced even when the perceived sound itself does not disappear.¹