Otalgia (Ear Pain)

• Primary (otogenic) otalgia - pain arising from disease within the ear itself
• Secondary (referred) otalgia - pain arising from a remote structure whose sensory nerve supply converges with that of the ear

Sensory Nerve Anatomy - The Basis of Referred Otalgia

Causes of Primary Otalgia

Causes of Referred (Secondary) Otalgia

1. Dental/TMJ (Most Common)

• Pulpitis from dental caries - poorly localised pain via unmyelinated C fibres
• Acute apical periodontitis/abscess - severe throbbing, often poorly localised
• Pericoronitis from impacted/partially erupted wisdom teeth
• TMJ dysfunction syndrome - otalgia reported in 64% of TMJ dysfunction patients; bruxism is a major aetiological factor (>50% of cases); sufferers are more likely female, with elevated psychological stress; masticatory muscle tenderness is the most reliable clinical finding, with lateral pterygoid tenderness in 85%

2. Malignancy (Must Not Be Missed)

• Isolated unilateral otalgia with a normal ear exam should raise suspicion of occult aerodigestive tract malignancy
• Upper aerodigestive tract tumours (oropharynx, tongue base, hypopharynx, larynx) - referred via CN IX and X
• Skull base/petrous temporal bone tumours (adenoid cystic carcinoma most common; also adenocarcinoma, SCC)
• Temporal bone metastases - commonest primary sites: breast, lung, kidney, stomach, prostate; triad of otalgia + periauricular swelling + facial nerve weakness is highly suspicious
• Parotid malignancy, cervical lymph node malignancy, thyroid disease

3. Pharyngeal and Laryngeal Disease

• Tonsillitis, peritonsillar abscess, adenoiditis (via CN IX)
• Carcinoma of tongue base, tonsil, hypopharynx, larynx
• Pharyngitis, laryngitis
• Foreign bodies in throat
• Inflammatory parapharyngeal space lesions

4. Neuralgias (Rare but Important)

• Glossopharyngeal neuralgia - paroxysmal severe pain in throat/tongue base radiating to ear, preauricular area, neck, or EAC; lasts seconds to minutes; vascular compression (usually PICA) at root entry zone is the main cause; first-line treatment is carbamazepine; surgery (microvascular decompression) achieves complete relief in 64-75%
• Geniculate neuralgia (Ramsay Hunt syndrome) - herpes zoster of CN VII; vesicles in EAC/pinna, severe otalgia, facial palsy, sensorineural hearing loss
• Great auricular neuralgia - pain along the cervical plexus territory

5. Cervical Spine Disease

6. Eagle's Syndrome (Stylohyoid Syndrome)

7. Laryngopharyngeal Reflux (LPR)

8. Cardiac Pain

Diagnostic Approach

Key Clinical Clue

Otalgia in the absence of otorrhoea, hearing loss, or otoscopic abnormality while the patient is symptomatic should strongly raise suspicion of secondary (referred) otalgia. - Scott-Brown's

History

• Character, location, radiation, duration, triggers
• Associated otological symptoms: hearing loss, discharge, tinnitus, vertigo
• Associated non-otological symptoms: sore throat, dysphagia, odynophagia, voice change, weight loss, dental pain, jaw click/trismus
• Relevant social history: tobacco and alcohol use (red flags for aerodigestive malignancy)
• Chronic pain history, psychological stressors

Examination

1. Full ear examination - otoscopy, TM inspection
2. Oral cavity and oropharynx - including tongue base, tonsillar fossae
3. Neck - lymphadenopathy, thyroid
4. TMJ and masticatory muscles - palpate lateral and medial pterygoids intraorally
5. Dental inspection - occlusal wear, buccal mucosa scarring (bruxism)
6. Cranial nerve assessment - especially CNs V, VII, IX, X

Investigations

• Dental X-rays, panoramic radiograph if dental/TMJ cause suspected
• Flexible nasendoscopy - to visualise nasopharynx, oropharynx, hypopharynx, larynx
• MRI with gadolinium - for skull base, perineural spread, parapharyngeal lesions
• CT - temporal bone, cervical spine pathology
• If neuralgia suspected: neurology referral for guidance on medical management

Red Flags in Otalgia

Management Principles

• Treat the underlying cause
• For TMJ dysfunction: conservative first - splints, physiotherapy, NSAIDs, dietary modification; psychological assessment for stress/bruxism
• For neuralgias: first-line is carbamazepine; surgical microvascular decompression for refractory cases
• For otitis externa/media: topical/systemic antibiotics as appropriate
• Unexplained otalgia persisting despite normal ENT examination mandates thorough investigation to exclude malignancy

Tinnitus

Classification

By Audibility

By Temporal Pattern

Epidemiology and Risk Factors

• Noise exposure - the most important modifiable risk factor; noise-induced hearing loss significantly raises tinnitus risk
• Age-related hearing loss (presbycusis) - the most common associated pathology
• Drugs (ototoxic):
  • Salicylates (aspirin) - often dose-dependent and reversible
  • Quinine
  • Aminoglycoside antibiotics
  • Platinum-based antineoplastics (cisplatin)
• Specific ear diseases: Meniere's disease, otosclerosis, vestibular schwannoma ("syndromic tinnitus")
• Comorbidities: depression, anxiety (40% comorbidity - cause and effect are bidirectional), hyperacusis (40% of tinnitus patients have some degree of hyperacusis; conversely, 86% of patients with hyperacusis also have tinnitus), TMJ dysfunction

Pathophysiology

• Ignition site - where the initial aberrant signal is generated (often peripheral - cochlea/auditory nerve)
• Promotion - central auditory processing that transforms the signal into a perceptible, potentially distressing sound

Peripheral Mechanisms

1. Discordant hair cell damage - outer hair cells (more vulnerable to noise, aminoglycosides) are lost while inner hair cells remain; the unsupported tectorial membrane sags and depolarises inner hair cells continuously
2. Calcium channel dysfunction - salicylates and quinine alter intracellular calcium in cochlear hair cells
3. Glutamate excitotoxicity - excess glutamate activates AMPA and NMDA receptors at inner hair cells; massive NMDA receptor activation is toxic to auditory nerve fibres

Central Mechanisms

1. Loss of inhibition - cochlear damage reduces afferent activity, which downregulates inhibitory processes in higher auditory centres, increasing spontaneous cortical activity
2. Increased neural synchrony - peripheral damage causes random spontaneous cortical activity to become synchronized, mimicking a sound signal
3. Cortical map reorganisation - tonotopic reorganisation leads to over-representation of frequencies adjacent to damaged cochlear areas, generating increased neural activity at those frequencies

Neurophysiological Model (Jastreboff, 1990)

Causes

Non-Pulsatile Tinnitus

Pulsatile Tinnitus

Pulsatile tinnitus always warrants investigation - it may indicate a treatable or dangerous vascular lesion.

Assessment

History

• Character: pitch, quality (ringing, hissing, clicking, pulsatile), unilateral or bilateral
• Duration, onset (sudden vs. gradual), fluctuating or constant
• Associated symptoms: hearing loss, vertigo, aural fullness, discharge
• Noise exposure history, drug history
• Psychological impact: sleep disturbance, anxiety, depression
• Impact on daily life - use validated tools:
  • Tinnitus Handicap Inventory (THI) - most widely used outcome measure
  • Hospital Anxiety and Depression Scale (HADS)
  • Insomnia Severity Index

Examination

• Otoscopy - middle/external ear disease
• Auscultation over ear, neck, orbit - for objective/vascular tinnitus
• Cranial nerve assessment
• Neck examination
• Somatic manoeuvres - ask if tinnitus changes with jaw movement, neck position (somatic modulation suggests central involvement)

Investigations

• Pure tone audiogram - mandatory; most patients have hearing loss even if subtle; high-frequency testing may detect loss at >8 kHz
• Tympanometry - middle ear pathology
• MRI with gadolinium - indicated for unilateral tinnitus with or without SNHL to exclude vestibular schwannoma
• MRA/CT angiography - for pulsatile tinnitus to exclude vascular lesions
• Blood tests - FBC, TFTs, lipids if systemic cause suspected

Management

1. Explanation and Reassurance

2. Hearing Aids

• When tinnitus is associated with aidable hearing loss, hearing amplification is the primary intervention
• Amplifying external sounds masks tinnitus and reduces the central gain that drives it
• Indirect benefits: improved communication reduces stress and anxiety that exacerbate tinnitus

3. Sound Therapy / Masking

• Broadband noise generators worn in the ear ("white noise generators") or environmental sound enrichment
• Aims to reduce the contrast between tinnitus and background sound
• Classical tinnitus maskers (designed to completely mask tinnitus) have largely been superseded by partial maskers and sound enrichment

4. Cognitive Behavioural Therapy (CBT)

• The best-evidenced psychological treatment for tinnitus distress
• Does not eliminate the tinnitus perception but changes the patient's emotional and attentional response to it
• Addresses catastrophic thinking, avoidance behaviours, sleep hygiene
• Cochrane reviews support CBT for improving quality of life and reducing tinnitus distress

5. Tinnitus Retraining Therapy (TRT)

• Combines directive counselling (demystifying tinnitus) with long-term sound therapy
• Based on Jastreboff's neurophysiological model - promotes habituation at limbic and autonomic levels
• Evidence: superior to tinnitus masking alone in one RCT (Cochrane review); widely used but requires a rigorous, time-intensive protocol

6. Drug Treatments

• Antidepressants (tricyclics/SSRIs) - may help patients tolerate tinnitus and treat comorbid anxiety/depression but do not directly alter tinnitus perception
• Benzodiazepines - reduce tinnitus distress short-term but addiction risk limits use
• Betahistine - used in Meniere's-associated tinnitus; limited evidence for idiopathic tinnitus
• Carbamazepine - for rare cases of typewriter tinnitus (CN VIII irritation)
• Intratympanic steroids/glutamate antagonists - investigated for acute-onset tinnitus (e.g., following sudden SNHL); a small therapeutic window may exist; intratympanic dexamethasone showed no advantage over placebo in the only placebo-controlled RCT
• Esketamine (intratympanic NMDA antagonist) - under investigation in multinational trials at the time of publication

7. Electromagnetic/Neuromodulation Therapies

• Repetitive transcranial magnetic stimulation (rTMS) - Cochrane review finds very limited support for low-frequency rTMS
• Vagus nerve stimulation paired with sound - early-phase studies only; insufficient evidence
• Acoustic CR Neuromodulation - an RCT failed to show significant benefit

8. Treatment of Underlying Cause

• Otosclerosis: stapedectomy generally improves associated tinnitus
• Vestibular schwannoma: management per tumour protocol; tinnitus may persist post-surgery
• Meniere's disease: diuretics, low-salt diet, betahistine, intratympanic gentamicin/steroids
• Cerumen impaction: microsuction/syringing
• Ototoxic drugs: withdraw or substitute where possible
• Pulsatile tinnitus: directed at vascular cause (embolisation, surgery, IIH treatment)

Recent Evidence Update

Summary Table: Tinnitus at a Glance

Allergic Rhinitis (AR)

Classification

By Temporal Pattern

ARIA Classification (Clinically Preferred)

Local Allergic Rhinitis (LAR)

Predisposing Factors

• Atopy - AR occurs in atopic individuals; strongly associated with asthma (up to 50% of AR patients have asthma; 70-80% of asthmatics have AR), atopic dermatitis, food allergy, urticaria
• Family history of allergic disease
• Female sex, particulate air pollution, maternal tobacco smoking
• "Allergic march" - AR often precedes asthma development; allergen immunotherapy reduces asthma risk by ~40%
• Climate change - earlier tree pollination, prolonged ragweed season (delayed first frost); elevated CO₂ increases pollen production

Pathophysiology

Phase 1 - Sensitisation

1. Inhaled allergen deposited on nasal mucosa; mucosal enzymes digest outer coat releasing protein allergens
2. Mucosal epithelial cells secrete TSLP → maturation of dendritic cells into TH2-promoting subtypes
3. Antigen-presenting cells (macrophages, dendritic cells, Langerhans cells) process and present allergen to CD4+ T cells → TH2 polarisation
4. TH2 cells secrete IL-4, IL-13 → B cell class switching → plasma cells produce allergen-specific IgE
5. IgE binds high-affinity FcεRI receptors on mast cells and basophils → sensitisation complete

Phase 2a - Early-Phase Response (within 5-15 minutes of re-exposure)

• Cross-linking of IgE on mast cells triggers degranulation
• Released preformed mediators: histamine, heparin, tryptase
• Newly synthesised mediators: PGD₂, leukotrienes LTC₄, LTD₄, LTE₄, platelet-activating factor (PAF)
• Symptoms: sneezing, rhinorrhoea, nasal pruritus, conjunctival itching (histamine-dominant)
• PGD₂ attracts eosinophils and basophils; leukotrienes cause nasal congestion and increased vascular permeability

Phase 2b - Late-Phase Response (4-8 hours later)

• Recruited inflammatory cells: eosinophils, basophils, neutrophils, monocytes, CD4+ T lymphocytes
• Cytokine amplification sustains and prolongs inflammation
• Symptoms: predominantly nasal blockage, mucus hypersecretion, nasal hyperresponsiveness
• Priming effect: repeated allergen exposure lowers the threshold for subsequent responses ("priming phenomenon")
• Chronic inflammation → nasal hyperresponsiveness to non-specific stimuli (cold air, smoke, strong smells)

Consequences of Chronic Inflammation

• Swelling of turbinates obstructs sinus ostia → secondary sinusitis
• Obstruction of Eustachian tube → middle ear dysfunction, otitis media with effusion
• Olfactory cleft inflammation → hyposmia/anosmia
• Systemic effects: fatigue, malaise, sleep disturbance, impaired cognition

Clinical Features

Symptoms

• Cardinal nasal symptoms: sneezing (often paroxysmal), rhinorrhoea (clear, watery), nasal obstruction, nasal pruritus (most specific for allergic aetiology)
• Ocular symptoms: pruritus, lacrimation, conjunctival injection and oedema (allergic conjunctivitis)
• Palatal/pharyngeal pruritus ("itchy palate" - very characteristic)
• Ear symptoms: eustachian tube dysfunction (popping, clicking), otalgia
• Postnasal drip → throat clearing, snorting, cough
• Systemic: malaise, fatigue, irritability, sleep disturbance, snoring
• Pollen-food allergy syndrome (oral allergy syndrome): oropharyngeal pruritus after ingesting plant-based foods cross-reactive with pollen allergens

Signs

• Pale, boggy nasal mucosa with oedematous turbinates
• Conjunctival congestion and oedema
• Allergic shiners - dark infraorbital circles from venous stasis
• Allergic salute - transverse nasal crease from habitual upward nose rubbing
• Pharynx generally unremarkable

Diagnosis

Clinical Diagnosis

Allergy Testing

Important: A positive allergy test alone does NOT confirm AR - clinical correlation is mandatory. SPT positivity prevalence exceeds 50% in the US population, far exceeding clinical allergy prevalence.

Management

1. Allergen Avoidance

• Identify and reduce exposure to specific triggers
• Dust mite measures: impermeable mattress/pillow covers, hot washing, HEPA vacuuming, reduced humidity
• Pollen: close windows during peak season, sunglasses outdoors, shower after outdoor exposure
• Pet avoidance: most effective measure, though dander persists months after pet removal
• Cockroach: pest control, food storage, fixing water leaks

2. Pharmacotherapy

Updated ARIA-EAACI 2024-2025 Recommendations (Evidence Hierarchy)

• INCS + INAH combination > INAH or INCS alone (strongest recommendation)
• INCS > INAH alone (recommended)
• Intranasal decongestants: short-term use only (rhinitis medicamentosa risk with >5-7 days use)

• INCS > oral antihistamine (OAH) for nasal symptoms
• OAH > leukotriene receptor antagonist (LTRA) for AR
• OAH > ocular antihistamine (OcAH) for ocular symptoms
• Do NOT add LTRA to OAH (no added benefit)

Drug Classes in Detail

3. Allergen-Specific Immunotherapy (AIT) - Disease-Modifying Treatment

• Subcutaneous immunotherapy (SCIT): injections of escalating allergen doses over 3-5 years; requires clinic visits; risk of systemic reactions
• Sublingual immunotherapy (SLIT): tablets or drops taken daily at home; lower systemic reaction risk; growing evidence base

• Desensitisation of mast cells/basophils (upregulation of H2 receptor)
• Shift from TH2 to Treg dominance (IL-10, TGF-β mediated peripheral tolerance)
• Increase in allergen-specific IgG4 (blocking antibody) and gradual decrease in specific IgE
• Induction of FoxP3+/CD25+ Treg cells

• Moderate-severe AR inadequately controlled by pharmacotherapy
• Patient preference to reduce long-term medication
• Prevention of asthma development
• Monosensitisation or clearly dominant allergen

4. Biologic Therapies

• Dupilumab (anti-IL-4Rα): targets IL-4/IL-13 signalling; licensed for chronic rhinosinusitis with nasal polyps; growing evidence in AR
• Omalizumab (anti-IgE): for severe persistent AR

Complications

Latest Guidelines Highlight