|Classification and external resources|
Tinnitus // or //; from the Latin word tinnītus meaning "ringing" is the perception of sound within the human ear ("ringing of the ears") when no external sound is present. Despite the origin of the name, "ringing" is only one of many sounds the person may perceive.
Tinnitus is not a disease, but a condition that can result from a wide range of underlying causes. The most common cause is noise-induced hearing loss. Other causes include neurological damage (multiple sclerosis), ear infections, oxidative stress, emotional stress, foreign objects in the ear, nasal allergies that prevent (or induce) fluid drain, earwax build-up, and exposure to loud sounds. Withdrawal from benzodiazepines may cause tinnitus as well. Tinnitus may be an accompaniment of sensorineural hearing loss or congenital hearing loss, or it may be observed as a side effect of certain medications (ototoxic tinnitus).
There are two main types of tinnitus, subjective tinnitus and objective tinnitus. Tinnitus is usually a subjective phenomenon, such that it cannot be objectively measured. The condition is often rated clinically on a simple scale from "slight" to "catastrophic" according to the difficulties it imposes, such as interference with sleep, quiet activities, and normal daily activities. Subjective tinnitus has been also called "tinnitus aurium" "nonauditory" and "nonvibratory" tinnitus, objective tinnitus "pseudo-tinnitus" or "vibratory" tinnitus.
If there is an underlying cause, treating it may lead to improvements. Otherwise typically management involves talk therapy. As of 2013, there are no effective medications. It is common, affecting about 10-15% of people. Most however tolerate it well, with it being a significant problem in only 1-2% of people.
- 1 Signs and symptoms
- 2 Causes
- 3 Pathophysiology
- 4 Diagnosis
- 5 Prevention
- 6 Management
- 7 Prognosis
- 8 Epidemiology
- 9 Research
- 10 Children
- 11 See also
- 12 References
- 13 External links
- 14 Further reading
Signs and symptoms
Tinnitus can be perceived in one or both ears or in the head. It is usually described as a ringing noise, but in some patients, it takes the form of a high-pitched whining, electric buzzing, hissing, humming, tinging or whistling sound, or as ticking, clicking, roaring, "crickets" or "tree frogs" or "locusts (cicadas)", tunes, songs, beeping, sizzling, sounds that slightly resemble human voices or even a pure steady tone like that heard during a hearing test, and in some cases, pressure changes from the interior ear. It has also been described as a "whooshing" sound because of acute muscle spasms, as of wind or waves. Tinnitus can be intermittent, or it can be continuous, in which case it can be the cause of great distress. In some individuals, the intensity can be changed by shoulder, head, tongue, jaw, or eye movements.
Most people with tinnitus have some degree of hearing loss, in that they are often unable to hear clearly external sounds that occur within the same range of frequencies as their "phantom sounds". This has led to the suggestion that one cause of tinnitus might be a homeostatic response of central dorsal cochlear nucleus auditory neurons that makes them hyperactive in compensation to auditory input loss.
The sound perceived may range from a quiet background noise to one that can be heard even over loud external sounds. The specific type of tinnitus called pulsatile tinnitus is characterized by one hearing the sounds of one's own pulse or muscle contractions, which is typically a result of sounds that have been created from the movement of muscles near to one's ear, changes within the canal of one's ear or issues related to blood flow of the neck or face.
There has been little research on the course of tinnitus, and most research has been retrospective. An Australian study of participants aged 49–97 years found that 35% of participants reported that their tinnitus was present all the time and 4% rated their tinnitus as annoying. Findings from a retrospective National Study of Hearing found that for 25% of people surveyed, the perceived volume of their tinnitus increased over time, while for 75% it did not. The rate of annoyance decreased for 31% of people from onset of tinnitus to the middle time. A study of the natural history of tinnitus in older adults found that for women, tinnitus increased for 25%, decreased in 58%, leaving 17% unchanged. The study found that for men, tinnitus increased in 8%, decreased in 39%, leaving 53% unchanged. Information about the course of tinnitus would benefit from prospective studies investigating change over time as these studies may potentially be more accurate.
Tinnitus annoyance is more strongly associated with psychological symptoms than acoustic characteristics. Other psychological problems such as depression, anxiety, sleep disturbances and concentration difficulties are common in those with worse tinnitus.
Subjective tinnitus is the most frequent type of tinnitus. It can have many possible causes, but most commonly results from otologic disorders – the same conditions that cause hearing loss. The most common cause is noise-induced hearing loss, resulting from exposure to excessive or loud noises. Tinnitus, along with sudden onset hearing loss, may have no obvious external cause. Ototoxic drugs can cause subjective tinnitus either secondary to hearing loss or without hearing loss and may increase the damage done by exposure to loud noise, even at doses that are not in themselves ototoxic.
Subjective tinnitus is also a side effect of some medications, such as aspirin, and may also result from an abnormally low level of serotonin activity. It is also a classical side effect of quinidine, a Class IA anti-arrhythmic. Over 260 medications have been reported to cause tinnitus as a side effect. In many cases, however, no underlying physical cause can be identified.
Tinnitus can also occur due to the discontinuation of therapeutic doses of benzodiazepines. It can sometimes be a protracted symptom of benzodiazepine withdrawal and may persist for many months.
Causes of subjective tinnitus include:
- ear problems and hearing loss:
- conductive hearing loss
- sensorineural hearing loss
- neurologic disorders:
- other causes:
- tension myositis syndrome
- hypertonia (muscle tension)
- thoracic outlet syndrome
- Lyme disease
- sleep paralysis
- glomus tympanicum tumor
- anthrax vaccines which contain the anthrax protective antigen
- Some psychedelic drugs can produce temporary tinnitus-like symptoms as a side effect
- benzodiazepine withdrawal
- nasal congestion
- intracranial hyper or hypotension caused by, for example, encephalitis or a cerebrospinal fluid leak
In some cases, tinnitus is generated by a self sustained oscillation within the ear. This oscillation most often can be heard or measured as a sound outside the ear. This is called objective tinnitus. Objective tinnitus can arise from muscle spasms that cause clicks or crackling around the middle ear. Some people experience a sound that beats in time with the pulse (pulsatile tinnitus, or vascular tinnitus). Pulsatile tinnitus is usually objective in nature, resulting from altered blood flow, increased blood turbulence near the ear (such as from atherosclerosis, venous hum, but it can also arise as a subjective phenomenon from an increased awareness of blood flow in the ear. Rarely, pulsatile tinnitus may be a symptom of potentially life-threatening conditions such as carotid artery aneurysm or carotid artery dissection. Pulsatile tinnitus may also indicate vasculitis, or more specifically, giant cell arteritis. Pulsatile tinnitus may also be an indication of idiopathic intracranial hypertension. Human ears generate their own noises, called spontaneous otoacoustic emissions (SOAEs) that can be measured outside the ear and form beats with and lock into external tones. The majority of the people are unaware of their SOAEs; portions of 1-9% however perceive an SOAE as an annoying tinnitus.
One of the possible mechanisms relies on otoacoustic emissions. The inner ear contains thousands of minute inner hair cells with stereocilia which vibrate in response to sound waves, and outer hair cells which convert neural signals into tension on the vibrating basement membrane. The sensing cells are connected with the vibratory cells through a neural feedback loop, whose gain is regulated by the brain. This loop is normally adjusted just below onset of self-oscillation, which gives the ear spectacular sensitivity and selectivity. If something changes, it is easy for the delicate adjustment to cross the barrier of oscillation, and tinnitus results. Exposure to excessive sound kills hair cells, and studies have shown as hair cells are lost, different neurons are activated, activating auditory parts of the brain and giving the perception of sound.
Another possible mechanism underlying tinnitus is damage to the receptor cells. Although receptor cells can be regenerated from the adjacent supporting Deiters cells after injury in birds, reptiles, and amphibians, in mammals it is believed they can be produced only during embryogenesis. Although mammalian Deiters cells reproduce and position themselves appropriately for regeneration, they have not been observed to transdifferentiate into receptor cells except in tissue culture experiments. Therefore, if these hairs become damaged, through prolonged exposure to excessive sound levels, for instance, then deafness to certain frequencies results. In tinnitus, they may relay information that an externally audible sound is present at a certain frequency when it is not.
The mechanisms of subjective tinnitus are often obscure. While it is not surprising that direct trauma to the inner ear can cause tinnitus, other apparent causes (e.g., temporomandibular joint dysfunction and dental disorders) are difficult to explain. Research has proposed there are two distinct categories of subjective tinnitus: otic tinnitus, caused by disorders of the inner ear or the acoustic nerve, and somatic tinnitus, caused by disorders outside the ear and nerve, but still within the head or neck. It is further hypothesized somatic tinnitus may be due to "central crosstalk" within the brain, as certain head and neck nerves enter the brain near regions known to be involved in hearing.
It may be caused by increased neural activity in the auditory brainstem where the brain processes sounds, causing some auditory nerve cells to become overexcited. The basis of this theory is most people with tinnitus also have hearing loss, and the frequencies they cannot hear are similar to the subjective frequencies of their tinnitus. Models of hearing loss and the brain support the idea a homeostatic response of central dorsal cochlear nucleus neurons could result in them being hyperactive in a compensation process to the loss of hearing input.
The basis of quantitatively measuring tinnitus relies on the brain’s tendency to select out only the loudest sounds heard. Based on this tendency, the amplitude of a patient's tinnitus can be measured by playing sample sounds of known amplitude and asking the patient which they hear. The volume of the tinnitus will always be equal to or less than that of the sample noises heard by the patient. This method works very well to gauge objective tinnitus (see above). For example: if a patient has a pulsatile paraganglioma in their ear, they will not be able to hear the blood flow through the tumor when the sample noise is 5 decibels louder than the noise produced by the blood. As sound amplitude is gradually decreased, the tinnitus will become audible, and the level at which it does so provides an estimate of the amplitude of the objective tinnitus.
Objective tinnitus, however, is quite uncommon. Often patients with pulsatile tumors will report other coexistent sounds, distinct from the pulsatile noise, that will persist even after their tumor has been removed. This is generally subjective tinnitus, which, unlike the objective form, cannot be tested by comparative methods. However, pulsatile tinnitus can be a symptom of intracranial vascular abnormalities, and should be evaluated for bruits by a medical professional with auscultation over the neck, eyes, and ears. If the exam reveals a bruit, imaging studies such as transcranial doppler (TCD) or magnetic resonance angiography (MRA) should be performed.
The accepted definition of chronic tinnitus, as compared to normal ear noise experience, is five minutes of ear noise occurring at least twice a week. However, people with chronic tinnitus often experience the noise more frequently than this, and can experience it continuously or regularly, such as during the night, when there is less environmental noise to mask the sound.
Assessment of psychological processes related to tinnitus involves measurement of tinnitus severity and distress (i.e. nature and extent of tinnitus-related problems), measured subjectively by validated self-report tinnitus questionnaires. These questionnaires measure the degree of psychological distress and handicap associated with tinnitus, including effects on hearing, lifestyle, health and emotional functioning. A broader assessment of general functioning, such as levels of anxiety, depression, stress, life stressors and sleep difficulties is also important in the assessment of Tinnitus due to higher risk of negative well-being across these areas, which may be affected by and/or exacerbate the Tinnitus symptoms for the individual. Overall, current assessment measures are aimed to identify individual levels of distress and interference, coping responses and perceptions of tinnitus in order to inform treatment and monitor progress. However, wide variability, inconsistencies and lack of consensus regarding assessment methodology is evidenced in the literature, limiting comparison of treatment effectiveness. Developed to guide diagnosis or classify severity, most tinnitus questionnaires have also been shown to be treatment-sensitive outcome measures.
Auditory evoked response
Tinnitus is the description of a noise inside a person’s head in the absence of auditory stimulation. The noise can be described in many different ways, but the most common description of the tinnitus is a pure tone sound. Tinnitus affects one third of adults at some time in their lives, whereas ten to fifteen percent are disturbed enough to seek medical evaluation.
Tinnitus can be classified as either subjective or objective. Objective tinnitus can be detected by other people and is usually caused by myoclonus or a vascular condition. Subjective tinnitus can only be heard by the affected person and is caused by otology, neurology, infection, or drugs. A frequent cause of subjective tinnitus is noise exposure which damages hair cells in the inner ear causing tinnitus. Tinnitus can be associated with many emotions. It is best illustrated by Jastreboff’s Neurophysiological model.
Tinnitus can be evaluated with most auditory evoked potentials; however results may be inconsistent. Results must be compared to age and hearing matched control subjects to be reliable. This inconsistently reported may be due to many reasons: differences in the origin of the tinnitus, ABR recording methods, and selection criteria of control groups. Since research shows conflicting evidence, more research on the relationship between tinnitus and auditory evoked potentials should be carried out before these measurements are used clinically.
Other potential sources of the sounds normally associated with tinnitus should be ruled out. For instance, two recognized sources of high-pitched sounds might be electromagnetic fields common in modern wiring and various sound signal transmissions. A common and often misdiagnosed condition that mimics tinnitus is radio frequency (RF) hearing, in which subjects have been tested and found to hear high-pitched transmission frequencies that sound similar to tinnitus.
Avoidance of potentially ototoxic medicines. Ototoxicity of multiple medicines can have a cumulative effect, and can increase the damage done by noise. If ototoxic medications must be administered, close attention by the physician to prescription details, such as dose and dosage interval, can reduce the damage done.
If there is an underlying cause, treating it may lead to improvements. Otherwise the primary treatment for tinnitus is talk therapy and sound therapy with there being little support for medications.
The best supported treatment for tinnitus is a type of counseling called cognitive behavioral therapy (CBT) which can be delivered via the internet or in person. It decreases the amount of stress those with tinnitus feel. These benefits appear to be independent of any effect on depression or anxiety in an individual. Acceptance and Commitment Therapy (ACT) is also demonstrating promise in Tinnitus treatment. Relaxation techniques may also be useful. A program has been developed by the United States Department of Veterans Affairs.
There are no medications as of 2014 that are effective for tinnitus and thus none is recommended. There is not enough evidence to determine if antidepressants or acamprosate is useful. While there is tentative evidence for benzodiazepines, it is insufficient to support usage. Anticonvulsants have not been found to be useful.
The use of sound therapy by either hearing aids or tinnitus maskers help the brain ignore the specific tinnitus frequency. Although these methods are poorly supported by evidence, there are no negative effects which makes them a reasonable option. There is some tentative evidence supporting tinnitus retraining therapy. There is little evidence supporting the use of transcranial magnetic stimulation. It is thus not recommended.
Ginkgo biloba does not appear to be effective. Tentative evidence supports zinc supplementation and in those with sleep problems, melatonin. The American Academy of Otolaryngology, however, recommends against melatonin and zinc.
Tinnitus is present in 10-15% of people.
As of 2013 many potential treatments are being investigated. Recent psychological research on tinnitus focuses on the Tinnitus Distress Reaction (TDR) to account for differences in tinnitus severity. Research has stigmatized patients with severe tinnitus by implying they suffer from personality disorders, such as neuroticism, anxiety sensitivity, and catastrophic thinking, which all predispose increased TDR. These findings suggest that at the initial perception of tinnitus, conditioning links tinnitus with negative emotions, such as fear and anxiety from unpleasant stimuli at the time. This enhances activity in the limbic system and autonomic nervous system, thus increasing tinnitus awareness and annoyance.
Tinnitus is commonly thought of as a symptom of adulthood; this may be why tinnitus in children is generally overlooked. Children with hearing loss have a high incidence of tinnitus, even though they do not express that they have tinnitus and the effect it has on their lives. Children do not generally report tinnitus spontaneously and their complaints may not be taken seriously. Among those children who do complain of tinnitus, there is an increased likelihood of associated otological or neurological pathology such as migraine, juvenile Meniere’s disease or chronic suppurative otitis media. Its reported prevalence varies from 12% to 36% in children with normal hearing thresholds and up to 66% in children with a hearing loss and approximately 3-10% of children have been reported to be troubled by tinnitus.
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About 75% of new cases are related to emotional stress as the trigger factor rather than to precipitants involving cochlear lesions.
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|Wikimedia Commons has media related to Tinnitus.|
- Baguley, David; Andersson, Gerhard; McFerran, Don; McKenna, Laurence (March 2013) . Tinnitus: A Multidisciplinary Approach (2nd ed.). Indianapolis, IN, USA: Wiley-Blackwell. ISBN 978-1-4051-9989-6. LCCN 2012032714. OCLC 712915603.
- Hogan, Kevin; Battaglino, Jennifer (May 2010) . Tinnitus: Turning the Volume Down (Revised & Expanded ed.). Eden Prairie, MN, USA: Network 3000 Publishing. ISBN 9781934266038. OCLC 779877737.
- Langguth, B.; Hajak, G.; Kleinjung, T.; Cacace, A.; Møller, A.R., eds. (December 2007). Tinnitus : pathophysiology and treatment. Progress in brain research 166 (1st ed.). Amsterdam ; Boston: Elsevier. ISBN 9780444531674. LCCN 2012471552. OCLC 648331153. Archived from the original on 2007. Retrieved 5 November 2012.
- Møller, Aage R; Langguth, Berthold; Ridder, Dirk et al., eds. (2011). Textbook of Tinnitus. New York, NY, USA: Springer. doi:10.1007/978-1-60761-145-5. ISBN 9781607611448. LCCN 2010934377. OCLC 695388693, 771366370 and 724696022. Archived from the original on 2011. Retrieved 5 November 2012. (subscription required)
- Tyler, Richard S. (2000). Tinnitus Handbook. A Singular audiology textbook. San Diego, CA, USA: Singular Publishing Group. ISBN 9781565939226. OCLC 471533235.