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Tinnitus

The perception of sound without an external acoustic source. It affects 10 to 15 percent of adults, with 1 to 2 percent experiencing severe distress and functional impairment. Distress correlates poorly with loudness and strongly with attention, emotional response and insomnia, which is why treatment targets the reaction rather than the sound.

Classification

  • Subjective tinnitus, audible only to the patient, accounting for well over 95 percent.
  • Objective tinnitus, generated by a real acoustic source within the body and potentially audible to the examiner. This group contains the treatable and the dangerous causes.

Mechanism of subjective tinnitus

Cochlear damage reduces afferent input in specific frequency bands. Central auditory structures respond with increased spontaneous firing, increased neural synchrony and tonotopic map reorganisation, generating a percept. Limbic and autonomic networks including the amygdala, anterior cingulate and insula determine whether that percept is ignored or becomes distressing, which explains why two patients with identical audiograms have completely different disability.

Causes to identify

  • Sensorineural: presbycusis, noise induced loss, ototoxicity, sudden loss, Ménière disease, vestibular schwannoma.
  • Conductive: wax, otitis media with effusion, otosclerosis, tympanic perforation.
  • Pulsatile arterial: atherosclerotic carotid stenosis, fibromuscular dysplasia, carotid or vertebral dissection, dural arteriovenous fistula, arteriovenous malformation, glomus tumours, aberrant internal carotid artery, persistent stapedial artery, hyperdynamic states from anaemia, thyrotoxicosis and pregnancy.
  • Pulsatile venous: idiopathic intracranial hypertension, sigmoid sinus diverticulum and dehiscence, high riding jugular bulb, venous sinus stenosis.
  • Somatosounds: palatal myoclonus producing a clicking tinnitus, middle ear myoclonus of tensor tympani and stapedius, and patulous Eustachian tube producing breath synchronous sound with autophony.
  • Drugs: salicylates, quinine, aminoglycosides, loop diuretics, platinum agents, some antidepressants.
  • Temporomandibular joint dysfunction and cervical spine disorders, which produce somatic tinnitus modulable by jaw or neck movement.

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Continue reading · Surgery

Nasal Polyps

Benign oedematous outgrowths of sinonasal mucosa arising most often from the ethmoid sinuses and prolapsing into the middle meatus and nasal cavity. They are a manifestation of chronic rhinosinusitis rather than a disease in themselves, and their presence defines the polyp phenotype of chronic rhinosinusitis.

Prevalence and associations

Around 1 to 4 percent of the general population. Associations that must be actively sought:

  • Asthma in 40 to 65 percent of polyp patients.
  • Aspirin exacerbated respiratory disease, comprising asthma, polyps and nonsteroidal anti inflammatory drug sensitivity, in around 10 percent. This subgroup has more aggressive disease, higher recurrence and a distinct treatment pathway.
  • Cystic fibrosis, which must be excluded in every child with nasal polyps, where the prevalence of polyps is 20 to 50 percent. Polyps in a child are cystic fibrosis until proven otherwise.
  • Primary ciliary dyskinesia.
  • Allergic fungal rhinosinusitis.
  • Eosinophilic granulomatosis with polyangiitis.
  • Non steroidal exacerbated disease and, in some series, allergic rhinitis, though the association with atopy is weaker than commonly assumed.

Pathology

Polyps are oedematous stroma with a loose extracellular matrix, sparse blood vessels and glands, and dense inflammatory infiltrate. In Western populations the infiltrate is predominantly eosinophilic with type 2 cytokines interleukin 4, 5 and 13, local immunoglobulin E production frequently against Staphylococcus aureus superantigens, and reduced tissue plasminogen activator with excess fibrin deposition producing the characteristic oedema. In East Asian populations a higher proportion are neutrophilic with a type 1 or type 3 profile, which is less corticosteroid responsive.

The critical rule on laterality

Bilateral polyps are inflammatory disease. Unilateral polyps are a neoplasm until proven otherwise and require imaging and histology in every case. The differential includes inverted papilloma, juvenile nasopharyngeal angiofibroma in an adolescent male, antrochoanal polyp, squamous cell carcinoma, adenocarcinoma, olfactory neuroblastoma, lymphoma, melanoma, encephalocele and meningocele. Never remove a unilateral nasal mass in clinic without imaging, since biopsy of an encephalocele or an angiofibroma has catastrophic consequences.

Antrochoanal polyp: a solitary polyp arising from the maxillary sinus, passing through an accessory ostium and extending posteriorly into the choana and nasopharynx. It occurs in younger patients, is unilateral, is not associated with eosinophilic disease, and does not respond to steroid. Treatment is complete surgical removal including the maxillary antral origin, since incomplete removal causes recurrence.