Aetiology
A wide range of diseases can result in tinnitus:[7]
Otological
Neurological, such as multiple sclerosis, head trauma
Metabolic, such as hyperlipidaemia, vitamin B12 deficiency, diabetes mellitus, hyperthyroidism, hypothyroidism
Psychogenic
Vascular disorders, such as arterial bruits, venous hums
Ototoxic medicine, such as aspirin, non-steroidal anti-inflammatory drugs, aminoglycosides, certain narcotics, phosphodiesterase type 5 inhibitors
Other.
Tinnitus has been traditionally classified as subjective and objective. The source of subjective tinnitus is difficult to identify as the sound is heard only by the affected individual. Thus, its severity depends on patient perception.[4][5] In contrast, objective tinnitus sounds can be heard by the examiner. It is the less common form of tinnitus and can occur as a result of perception of sounds produced by neighbouring structures, such as muscular contraction and vascular noise.[4][5] This kind of tinnitus can occur with arteriovenous malformations, anaemia, thyrotoxicosis, middle ear inflammation, vascular neoplasm such as glomus tumour, benign intracranial hypertension, partial stenosis of cervical vessels, and muscle contractions (palatal myoclonus) such as tensor veli palatini or tensor tympani contractions.[13]
More recently, tinnitus has been categorised as primary and secondary, of which primary tinnitus is the most common type.[4][5][14] Primary tinnitus is idiopathic and may be associated with sensorineural hearing loss, whereas secondary tinnitus has an underlying identifiable cause, apart from sensorineural hearing loss.[1][4][5]
Pathophysiology
The pathophysiology of tinnitus is not fully understood but may be divided into conductive, sensorineural, or central processes.[2] The potential mechanism of sound generation leading to tinnitus may be due to changes in spontaneous activity in the auditory nerves that alter the sensitivity of sound detection.[7] Other theories involve hair cell, auditory nerve, and central auditory nervous system participation.
Aberrancies in the form of discordant hair cell function, calcium imbalance, activation of cochlear N-methyl D-aspartic acid receptors, excitatory drift in hair cells, and enhanced glutamate activity in response to hair cell activation due to stress have all been cited as potential causes of tinnitus.[15][16][17][18][19][20][21] Tinnitus-inducing agents cause alterations in outer hair cells and subsequently the basilar membrane, which result in changes of frequency tuning in the cochlea.[7]
Theories involving the auditory nerve include synchronisation of spontaneous activity in auditory nerve fibres due to cross-linking, deafferentation hyperexcitability, temporary abnormal patterns in the spontaneous activity of nerve fibres, and different activity in tonotopically adjacent nerve fibres.[22][23][24][25]
Central auditory involvement has been linked to efferent auditory system abnormalities, increased activity in the dorsal cochlear nucleus, multi-modal networks of neurons, and cortical plasticity.[26][27][28][29][30]
Tinnitus is reported by patients with thyroid disorder, hyperlipidaemia, syphilis, diabetes mellitus, and anaemia. Anaemia and hyperthyroidism cause a hyperdynamic state that can cause pulsatile tinnitus. Severe hypothyroidism, diabetes mellitus, and tertiary syphilis can cause sensorineural hearing loss with associated tinnitus. Hyperlipidaemia can cause an inner ear stroke and sudden hearing loss, which would in turn cause tinnitus.
Classification
Based on origin[2]
1. Conductive: vibrations in the middle ear.
2. Sensorineural: inner and outer hair cells, auditory nerves, and extra sensory structures.
3. Central: aberrant central processing.
Based on symptoms[3]
1. Objective: the patient and the examiner can hear real sounds, such as venous hum or carotid artery bruit. The patient may perceive his or her own pulse or the mechanical sounds of muscle contraction. Usually it is produced by adjacent structures. Use of a Toynbee device can allow the examiner to hear the sound on occasion.
2. Subjective: the patient perceives noise secondary to neural activity or biochemical changes in the peripheral or central auditory systems.
Based on causative factors[1][4][5]
1. Primary: idiopathic origin; may be associated with sensorineural hearing loss.
2. Secondary: has an underlying identifiable cause, apart from sensorineural hearing loss.
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