Tinnitus

What is Tinnitus?

Tinnitus in Elderly People

Tinnitus (ringing in the ear) is a common yet poorly understood disorder.

It is more common in elderly patients reaching peak incidence between the ages of 50 and 70 years. It is estimated from several American studies that between 10 and 15% of men and women aged between 50 and 70 have significant tinnitus. It can vary significantly in severity from being a minor irritation to being a debilitating symptom significantly affecting people’s quality of life.

There is a vast amount of information in the community and on the Internet pertaining to tinnitus so there is enormous pressure on clinicians to “do something” about treating it.


Types of Tinnitus

Tinnitus is classified as subjective if it is audible only to the patient or objective if it is audible to the clinician and or observer.

In terms of severity, tinnitus is classified as:

Mild: if it is only audible when there is no background noise and has minimal impact on quality of life;

Moderate: as above and if audible when there is background noise, is a minor irritation but not a significant impairment on quality of life;

Severe: when it is present all the time with or without background noise, and poses a significant and/or debilitating impact on quality of life.

Subjective Tinnitus: Pathophysiology

Subjective tinnitus can arise from dysfunction within the cochlea, in the vestibulo cochlea nerve, or from the brain stem itself. Subjective tinnitus is nearly always associated with some degree of hearing loss and it is postulated that a process of disinhibition occurs. Under normal circumstances the hair cells in the cochlea have a very low basic resting firing potential which increases dramatically when they are stimulated by the transference of acoustic energy into mechanical energy by the eardrum and the three little bones. It is postulated that in people with subjective tinnitus, a process of disinhibition occurs (often associated with some form of toxic insult to the hair cells be it hypoxic due to decreased or altered blood flow or chemical due to drugs or post trauma). With this process the basic resting firing potential increases significantly and stimulates the cerebral cortex without there being appropriate peripheral source of stimulation. A similar process of disinhibition can occur along the vestibulo cochlea nerve.

A process of cortical, analogous to phantom limb syndrome after amputation, can take place with damage to the cochlea or vestibular nerve and this is postulated as the pathophysiology of central subjective tinnitus.

Objective Tinnitus: Pathophysiology

Tinnitus

Objective tinnitus is often caused by clicking due to spasmodic contraction of the palatal muscles, either the tensor tympani or the stapedius muscle. Occasionally, spontaneous vibration of outer hair cells of the cochlea produces audible sounds and these are known as spontaneous otoacoustic emissions. It is interesting to note that these spontaneous otoacoustic emissions occur more commonly in people with minimal cochlea damage.

Flow murmurs due to narrowing of the common carotid, internal carotid, or vertebro basilar arteries can cause objective pulsatile tinnitus.

Other lesions causing objective pulsatile tinnitus include vascular anomalies such as tumours (like glomus jugulare), valvular heart disease (commonly aortic stenosis), high cardiac output states such as anaemia, hypertension and certain conditions causing turbulent blood flow such as narrowing of the major channels draining the brain and the inner ear.

Eustachian tube dysfunction, most commonly patulous Eustachian tubes is associated with “noise” synchronous with breathing and many patients present with a complaint of tinnitus when in fact, due to patulous Eustachian tubes they are hearing their own respiration.

Other Causes of Tinnitus

Tinnitus may be associated other another pathophysiological processes, common conditions associated with subjective tinnitus that may require treatment include: impacted wax, otitis media, other infectious or inflammatory conditions that affect hearing, Meniere’s disease (which is often associated with low pitch tinnitus) and otosclerosis.

It is imperative to take a drug history as drug induced tinnitus is common and may persist even after medication is stopped.


Tinnitus Assessment

Common Medications associated with Tinnitus:
• Salicylates
• Non-steroidal anitinflammatory drugs
• Aminoglycoside antibiotics
• Loop diuretics
• Chemotherapy agents
• Heavy metals
• Antidepressants
• Quinine
• Quinidine
• Vancomycin
• IVI Erythromycin

Audiological Assessment

A comprehensive audiological assessment is essential. Apart from pure tone threshold testing (air and bone) measures of acoustic impedance (tympanometry and acoustic reflex threshold) speech audiometry and test for frequency matching should be undertaken.

It is important to remember that any asymmetrical sensorineural hearing loss raises the possibility of significant retro cochlea pathology specifically superior vestibular nerve schwannoma and these patients should be appropriately referred to otorhinolaryngological assessment.

Physical Examination

Physical examination should be focused on the head and neck, careful examination of the oral cavity, outer ear, tympanic membrane, middle ear cleft, free field and tuning fork hearing testing, cranial nerve testing particularly the 5th, 7th and 8th cranial nerve, testing of the temperomandibular joints/auscultation over the temperomandibular joints, auscultation over the anterior neck, auscultation of the base of the skull, and auscultation of the heart.

Ancillary Tests

Ancillary tests are appropriate as per physical examination. If a carotid or skull base bruit is found, then Doppler studies and or computerised angiographic evaluation is indicated.

If clinical evidence of temperomandibular joint dysfunction is found, appropriate dynamic imaging of the temperomandibular joint (during opening and closing) is appropriate.

If significant retro cochlea pathology is suspected and/or if cerebral microvasculopathy is suspected, appropriate imaging is magnetic resonance imaging/magnetic resonance angiography (MRI/MRA).


Tinnitus Treatment

Masking

Tinnitus masking involves applying an external source of sound to partially cover up the tinnitus. Masking of tinnitus can be achieved by:

  • Hearing aids
  • Tinnitus masking devices
  • Tinnitus instruments

The phenomenon of residual inhibition involves a process whereby the process of tinnitus is abolished for a process significantly longer than the masking device is applied. Testing for residual inhibition is a good predictive index of the likelihood of success of tinnitus masking devices.

The overall success rate of tinnitus masking devices appears to be around 30%.

Retraining or habituation therapy

These techniques involve processes using specific protocols by which patients can reach a state of being unaware of the process of tinnitus.

Tinnitus retraining is different from masking and is thought to be a reconditioning of connections within subcortical centres.

These techniques involve extensive counselling and the use of binaural broadband noise generators.

Tinnitus habituation requires at least 12 months of treatment and it is recommended that patients continue for an additional 6 to 9 months.

Significant improvement has been reported in up to 70% of patients. Controlled studies are however not available.

Electrical stimulation

Transcutaneous electrical stimulation or direct transtympanic electrical stimulation has been successful in the treatment of tinnitus in about 50% of patients.

Biofeedback

Biofeedback techniques should be considered for patients whose tinnitus is associated with high degrees of anxiety and stress, tension headaches or significant temporomandibular joint dysfunction.


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