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Tinnitus is the hearing of sound when no external sound is present. While often described as a ringing, it may also sound like a clicking, hiss or roaring. Rarely, unclear voices or music are heard. The sound may be soft or loud, low pitched or high pitched and appear to be coming from one ear or both. Most of the time, it comes on gradually. In some people, the sound causes depression, anxiety or interferes with concentration.
Tinnitus is not a disease but a symptom that can result from a number of underlying causes. One of the most common causes is noise-induced hearing loss. Other causes include: ear infections, disease of the heart or blood vessels, Ménière's disease, brain tumors, emotional stress, exposure to certain medications, a previous head injury, and earwax. It is more common in those with depression.
The diagnosis of tinnitus is usually based on the person's description. A number of questionnaires exist that assess how much tinnitus is interfering with a person's life. The diagnosis is commonly assisted with an audiogram and neurological exam. If certain problems are found, medical imaging, such as with MRI, may be performed. Other tests are suitable when tinnitus occurs with the same rhythm as the heartbeat. Occasionally, the sound may be heard by someone else using a stethoscope, in which case it is known as objective tinnitus.
Prevention involves avoiding loud noise. If there is an underlying cause, treating it may lead to improvements. Otherwise, typically, management involves talk therapy. Sound generators or hearing aids may help some. As of 2013, there are no effective medications. It is common, affecting about 10-15% of people. Most, however, tolerate it well with its being a significant problem in only 1–2% of people. The word tinnitus is from the Latin tinnīre which means "to ring".
- 1 Signs and symptoms
- 2 Causes
- 3 Pathophysiology
- 4 Diagnosis
- 5 Prevention
- 6 Management
- 7 Prognosis
- 8 Epidemiology
- 9 See also
- 10 References
- 11 External links
- 12 Further reading
Signs and symptoms
Tinnitus can be perceived in one or both ears or in the head. 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. 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 the latter 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: they are often unable to clearly hear 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 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 condition than loudness or frequency range. Other psychological problems such as depression, anxiety, sleep disturbances and concentration difficulties are common in those with worse tinnitus. 45% of people with tinnitus have an anxiety disorder at some time in their life.
As part of the idea that the central-auditory-system may be implicated into the tinnitus development, serotonin has also been implicated. Indeed, serotonin has been postulated to be involved in plastic changes in the brain. Serotonin re-uptake inhibitors (such as some anti-depressant drugs) have often been used for this reason. However those medications do not benefit in a consistent fashion on non-depressant people.
Psychological research has looked at the tinnitus distress reaction (TDR) to account for differences in tinnitus severity. Research has stigmatized people with severe tinnitus by implying they have 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.
There are two types of tinnitus: subjective tinnitus and objective tinnitus. Tinnitus is usually subjective, meaning that others cannot hear it. Subjective tinnitus has been also called "tinnitus aurium" "nonauditory" and "nonvibratory" tinnitus. Occasionally, tinnitus may be heard by someone else using a stethoscope: in which case, it is objective tinnitus. Objective tinnitus has been called "pseudo-tinnitus" or "vibratory" tinnitus.
Subjective tinnitus is the most frequent type of tinnitus. It can have many possible causes but, most commonly, results from hearing loss. A frequent cause of subjective tinnitus is noise exposure which damages hair cells in the inner ear causing tinnitus. Subjective tinnitus can only be heard by the affected person and is caused by otology, neurology, infection or drugs.
There is a growing body of evidence suggesting that tinnitus is a consequence of neuroplastic alterations in the central auditory pathway. These alterations are assumed to result from a disturbed sensory input, caused by hearing loss. Hearing loss could indeed cause a homeostatic response of neurons in the central auditory system, and therefore cause tinnitus.
Despite the opinion amongst researchers that tinnitus is primarily a central nervous system pathology, there certainly exists a class of people whose tinnitus is peripherally based.
Ototoxic drugs (such as aspirin) can also cause subjective tinnitus, as they may cause hearing loss, or increase the damage done by exposure to loud noise. Those damages can occur even at doses that are not considered ototoxic. Tinnitus 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 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.
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Factors associated with tinnitus include:
- ear problems and hearing loss:
- conductive hearing loss
- sensorineural hearing loss
- neurologic disorders:
- metabolic disorders:
- psychiatric disorders
- other factors:
- 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
Objective tinnitus can be detected by other people and is usually caused by myoclonus or a vascular condition. In some cases, tinnitus is generated by a self-sustained oscillation within the ear. This is called objective tinnitus which can arise from muscle spasms around the middle ear. Homeostatic control mechanisms exist to correct the problem within a minute after onset and is normally accompanied by a slight reduction in hearing sensitivity followed by a feeling of fullness in the ear.
Objective tinnitus can most often can be heard as a sound outside the ear, as spontaneous otoacoustic emissions (SOAEs) that can form beats with and lock into external tones. The majority of the people are unaware of their SOAEs; whereas portions of 1-9% perceive a SOAE as an annoying tinnitus.
Pulsatile tinnitus can be a symptom of intracranial vascular abnormalities and should be evaluated for bruits. Some people experience a sound that beats in time with their 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.
One of the possible mechanisms relies on otoacoustic emissions. The inner ear contains tens of 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, then, tinnitus results. Exposure to excessive sound kills hair cells and studies have shown that, 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, it is believed that, in mammals, 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 over-excited. 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.
Even when tinnitus is the primary complaint, audiological evaluation is usually preceded by examination by an ENT to diagnose treatable conditions like middle ear infection, acoustic neuroma, concussion, otosclerosis, etc.
Evaluation of tinnitus will include a hearing test (audiogram), measurement of acoustic parameters of the tinnitus like pitch and loudness, and psychological assessment of comorbid conditions like depression, anxiety, and stress that are associated with severity of the tinnitus.
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.
Since most persons with tinnitus also have hearing loss, a pure tone hearing test resulting in an audiogram may help diagnose a cause, though some persons with tinnitus do not have hearing loss. An audiogram may also facilitate fitting of a hearing aid in those cases where hearing loss is significant. The pitch of tinnitus is often in the range of the hearing loss. A hearing aid boosting the attentuated frequencies may at least partly mask tinnitus by raising the background level of sound in the tuned frequency range.
Acoustic qualification of tinnitus will include measurement of several acoustic parameters like pitch, or frequency in cases of monotone tinnitus, or frequency range and bandwidth in cases of narrow band noise tinnitus, loudness in dB above hearing threshold at the indicated frequency, mixing-point, and minimum masking level. In most cases, tinnitus pitch or frequency range is between 5000 Hz and 8000 Hz, and loudness less than 10 dB above the hearing threshold.[medical citation needed]
Another relevant parameter of tinnitus is residual inhibition, the temporary suppression and/or disappearance of tinnitus following a period of masking. The degree of residual inhibition may indicate how effective tinnitus maskers would be as a treatment modality.
An assessment of hyperacusis, a frequent accompaniment of tinnitus, may also be made. The measured parameter is Loudness Discomfort Level in dB, the subjective level of acute discomfort at specified frequencies over the frequency range of hearing. This defines a dynamic range between the hearing threshold at that frequency and the loudnes discomfort level. A compressed dynamic range over a particular frequency range is associated with subjectve hyperacusis. Normal hearing threshold is generally defined as 0–20 decibels (dB). Normal loudness discomfort levels are 85–90+ dB, with some authorities citing 100 dB. A dynamic range of 55 dB or less is indicative of hyperacusis.
The condition is often rated on a scale from "slight" to "catastrophic" according to the effects it has, such as interference with sleep, quiet activities and normal daily activities. In an extreme case a man committed suicide after being told there was no cure.
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 are 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 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 inconsistent reporting 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.
Several medicines have ototoxic effects, and can have a cumulative effect that 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.
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) also shows promise in the treatment of tinnitus. Relaxation techniques may also be useful. A clinical protocol called Progressive Tinnitus Management for treatment of tinnitus has been developed by the United States Department of Veterans Affairs.
As of 2014[update] there were no medications effective for tinnitus. 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. Steroids injections into the middle ear also do not seem to be effective.
The use of sound therapy by either hearing aids or tinnitus maskers helps the brain ignore the specific tinnitus frequency. Although these methods are poorly supported by evidence, there are no negative effects. 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.
While there is no cure, most people with tinnitus get used to it over time; for a minority, it remains a significant problem.
Tinnitus affects 10–15% of people. About a third of North Americans over 55 experience tinnitus. 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 is commonly thought of as a symptom of adulthood, and is often overlooked in children. Children with hearing loss have a high incidence of tinnitus, even though they do not express the condition or its effect 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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|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. External link in
- 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, 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.