|Classification and external resources|
Tinnitus is not a disease, but a condition that can result from a wide range of underlying causes: neurological damage (multiple sclerosis), ear infections, oxidative stress, foreign objects in the ear, nasal allergies that prevent (or induce) fluid drain, wax 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). However, the most common cause is noise-induced hearing loss.
As tinnitus is usually a subjective phenomenon, it is difficult to measure using objective tests, such as by comparison with noise of known frequency and intensity, as in an audiometric test. The condition is often rated clinically on a simple scale from "slight" to "catastrophic" according to the practical difficulties it imposes, such as interference with sleep, quiet activities, and normal daily activities.
Tinnitus is common: about 20% of people between 55 and 65 years old report symptoms on a general health questionnaire, and 11.8% on more detailed tinnitus-specific questionnaires.
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. Heller and Bergman (1953) conducted a study of 100 tinnitus-free university students placed in an anechoic chamber and found 93% reported hearing a buzzing, pulsing or whistling sound. 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. Cohort studies have demonstrated damage to hearing (among other health effects) from unnatural levels of noise exposure is very widespread in industrialized countries.
For research purposes, the more elaborate Tinnitus Handicap Inventory (THI) is often used. Persistent tinnitus may cause irritability, fatigue, and on occasions, clinical depression and musical hallucinations.
As with all diagnostics, other potential sources of the sounds normally associated with tinnitus should be ruled out. For instance, two recognized sources of very-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.
Objective tinnitus 
In some cases, a clinician can perceive an actual sound (e.g., a bruit) emanating from the patient's ears. 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 or increased blood turbulence near the ear (such as from atherosclerosis or 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.
Subjective tinnitus 
Subjective tinnitus 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:
- Otologic problems and hearing loss:
- conductive hearing loss
- sensorineural hearing loss
- excessive or loud noise
- presbycusis (age-associated hearing loss)
- Ménière's disease
- acoustic neuroma
- mercury or lead poisoning
- ototoxic medications
- chemotherapy and antiviral drugs:
- loop diuretics:
- 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
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 disorder (TMJD or TMD) 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.
Studies by researchers at the University of Western Australia suggest tinnitus is 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. This, in turn, is related to changes in the genes involved in regulating the activity of those nerve cells. This proposed mechanism suggests possible treatments for the condition, involving the normalization or suppression of overactive neural activity through electrical or chemical means.
While most discussions of tinnitus tend to emphasize physical mechanisms, there is strong evidence that the level of an individual's awareness of her or his tinnitus can be stress-related, and so should be addressed by improving the state of the nervous system generally, using gradual, unobtrusive, long-term treatments.
Since some tinnitus mimics electronic sounds, some recent research is focusing on electronics, the prolonged use of cell phones, and other modern electronic devices as possible causes. These findings are consistent with reviews of older research associating tinnitus with prolonged exposure to electromagnetic radiation.
Pediatric tinnitus 
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.
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 he hears. 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 his ear, he 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.
If the attention of a subject is focused on a sample noise, he can often detect it at levels below 5 decibels, which would indicate her tinnitus would be almost impossible to hear. Conversely, if the same test subject is told to focus only on the tinnitus, he will report hearing the sound even when test noises exceed 70 decibels, making the tinnitus louder than a ringing phone. This quantification method suggests subjective tinnitus relates only to what the patient is attempting to hear. Whilst it is tempting to assume patients actively complaining about tinnitus have simply become obsessed with the noise, this is only partially true. The noises are often present in both quiet and noisy environments, and can become quite intrusive to their daily lives. The problem is involuntary; generally, complaining patients simply cannot override or ignore their tinnitus.
Subjective tinnitus may not always be correlated with ear malfunction or hearing loss. Even people with near-perfect hearing may still complain of it.
Measuring tinnitus with 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 About two million Americans are so seriously disturbed by tinnitus that they cannot function on a day-to-day basis. (American Tinnitus Association, 2010).
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 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.
The “Edge Effect” theory has been described by many researchers throughout the literature when discussing tinnitus. As hair cells are lost or damaged, afferent neurons generate auditory sensations at frequencies near the impaired region. This theory possibly explains why tinnitus can be associated with a reflection of hearing loss and why tinnitus can be persistent.
Some researchers believe that spontaneous otoacoustic emissions (SOAEs) may be associated with tinnitus. Processes in the cochlea can cause self oscillation that is perceived as tinnitus, but most studies found that the two phenomena are not related. The evaluation of SOAEs and tinnitus was based on pitch matching and researchers concluded that not enough evidence could be seen to make the conclusion. When the researchers used two specific criteria to evaluate the results, researchers found SOAEs and tinnitus to be related in 2.42% of subjects.
In 2010, Qasem compared the differences in outer hair cell function in normal hearing patients with and without tinnitus. Distortion product OAEs (DPOAEs) were measured and results showed significant differences between groups at all DPOAE frequencies tested. Researchers concluded that decreased DPOAE amplitude can be seen in tinnitus patients due to the association between tinnitus and reduced outer hair cell movement. This study illustrates that the outer hair cells are related to tinnitus.
Moller studied the effects of tinnitus in relation to compound action potentials (CAP) in 1992. Researchers recorded compound action potential components N1 and N2 and found that the latencies of the responses in the tinnitus patients were similar to patients with no tinnitus. This study concludes that tinnitus effects can not be observed in CAP. The effects of tinnitus on auditory brainstem response (ABR) measures have also been evaluated by many researchers. Auditory pathway plays a role in the emotional and physiological response to tinnitus. Research has shown abnormal ABR results (interwave latency delays) in patients with tinnitus. In 2008, Kehrle used ABR testing to evaluate the auditory nerve and brainstem function of tinnitus patients with normal hearing. Results showed delayed wave latencies and interpeak latencies between the tinnitus and non tinnitus patients. Researchers concluded that latency prolongations of wave I and lengthening of III-V IPL found in this study confirmed the findings in previous research. Maurizi in 1985 used ABRs to evaluate the auditory pathway in patients with tinnitus and concluded that patients with tinnitus had abnormal ABR recordings. Peripheral tinnitus was reduced with residual inhibition and recordings returned to normal. However, this method is not valid for all tinnitus patients due to the many different causes of tinnitus. Gerken in 2001 evaluated the influence of tinnitus on auditory evoked potentials. Results showed delayed ABR wave VII latencies in the tinnitus group and about half of the tinnitus patients had MLR amplitudes that were significantly greater than the control group mean. Researchers concluded the latency differences for wave VII only adds more diversity to research findings and should be included in future research. Large MLR waves seen in the tinnitus group may be caused by unknown smaller factors not accounted for in the study.
Tinnitus and auditory evoked cortical potentials have also been studied. It is important to evaluate the primary auditory cortex in relation to Jastrebroff’s model. “ALRs reflect stimulus properties as well as attention and the psychological state of the subjects, both of which are presumed to contribute to tinnitus” -Kadner (2002). Low and colleagues in 2008 concluded that ALRs can be used to evaluate the effectiveness of therapies used to alleviate tinnitus.
Tinnitus has also been studied in relation to event related potentials. In 1991, Shiraishi and colleagues found that the contingent negative variation (CNV) amplitude was significantly enlarged in tinnitus patients. They also found no effect on the latency and amplitude of the N100 and P300 responses. Attias in 1993, found that the amplitudes of N1, P2, and P3 were reduced, P3 latencies delayed, and N1 and N2 had delayed latencies to non-target stimuli.
In 2008, Delb conducted a study that evaluated tinnitus patients with high and low tinnitus related distress and how they differ in respect to focus levels on the tinnitus. Researchers concluded that patients with different levels of distress have differences in their ability to shift attention.
Elbert in 2004 studied the relation between tinnitus and mismatched negativity (MMN). Researchers recorded MMN potentials at stimulus levels at the edge frequency of the patient’s tinnitus and found differences in the recordings. This finding can be applied to tinnitus treatments to monitor progress and show effectiveness.
Tinnitus and long latency auditory evoked potentials (LLAEPs) have also been researched quite frequently. Alterations of LLAEPs have been seen in individuals with tinnitus and indicate problems in the auditory pathway in the cortex which can be concluded by increased latency values. In 2010, Santos Filha measured LLAEP potentials of tinnitus patients with a history of noise exposure. Researchers concluded that LLAEP shifts occur more often in individuals with tinnitus when compared to the control group.
In conclusion, 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.
Tinnitus and hearing loss can be permanent conditions. If a ringing in the ears is audible following lengthy exposure to a source of loud noise, such as a music concert or an industrial workplace, it means lasting damage may have already occurred.
Prolonged exposure to sound or noise levels as low as 70 dB can result in damage to hearing (see noise health effects). For musicians and DJs, special musicians' earplugs play an important role in preventing tinnitus; they can lower the volume of the music without distorting the sound and can prevent tinnitus from developing in later years. For anyone using loud electrical appliances, such as hair dryers or vacuum cleaners, or who work in noisy environments such as building sites, where earmuffs are impractical, earplugs are also helpful in reducing noise exposure. This is also the case when riding motorcycles, mopeds etc. When operating lawn mowers, hammer drills, grinders, and similar, earmuffs may be more appropriate for hearing protection.
It is also important to check medications for potential ototoxicity. Ototoxicity of multiple medicines can have a cumulative effect, and can greatly 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.
Many treatments for tinnitus have been claimed, with varying degrees of statistical reliability:
- Gamma knife radiosurgery (glomus jugulare)
- Shielding of cochlea by teflon implant
- Botulinum toxin (palatal tremor)
- Clearing ear canal (in the case of earwax plug)
- Using a neurostimulator
- Drugs and nutrients
- Melatonin (especially for those with sleep disturbance)
- Lidocaine injection into the inner ear was found to suppress the tinnitus for 20 minutes, according to a Swedish study.
- Older benzodiazepines, e.g. diazepam, are sometimes used for tinnitus; however, there are significant risks associated with the long-term use of benzodiazepines.
- Tricyclics (amitriptyline, nortriptyline) in small doses
- Avoidance of caffeine, nicotine, or salt can reduce symptoms, but, tinnitus can also be induced by reducing caffeine and/or smoking.
- The consumption of alcohol has been found to both increase and decrease the severity of tinnitus. Therefore, alcohol's effect on the severity of tinnitus is dependent on the causes of the individual's affliction, and cannot be considered a treatment.
- Zinc supplementation (where serum zinc deficiency is present)
- Etidronate or sodium fluoride (otosclerosis)
- Lignocaine or anticonvulsants (usually in patients responsive to white noise masking)
- Vitamin combinations (lipoflavonoid)
- Electrical stimulation
- Transcranial magnetic stimulation or transcranial direct current stimulation
- Transcutaneous electrical nerve stimulation
- Direct stimulation of auditory cortex by implanted electrodes
- Berthold Langguth, a German neurologist, would apply an electric or magnetic current for stimulation over the head of the patient to reduce the ringing sound. Dirk De Ridder, a Belgian neurosurgeon, implanted electrodes to the brain of sufferers to normalise overactive neurons. Cambridge University scientists also found lidocaine, an anaesthetic, reduces the sound in 2/3 of patients for 5 minutes, but it needs another drug to suppress its dangerous effects.
- Vagus nerve stimulation
- External sound
- Low-pitched sound treatment has shown some positive, encouraging results.
- Tinnitus masker (white noise, or better 'shaped' or filtered noise)
- Tinnitus retraining therapy
- Auditive stimulation therapy (music therapy)
- Auditive destimulation therapy (also called "notched music" therapy) uses individually designed music with the patients' favorite music altered to remove the musical tones that match the aural frequencies associated with their tinnitus. The removal of these tones alleviates the tinnitus by destimulating brain activity for these specific frequencies.
- Compensation for lost frequencies by use of a hearing aid.
- Ultrasonic bone-conduction external acoustic stimulation
- Avoidance of outside noise (exogenous tinnitus)
- Psychological treatment
Psychological mechanisms and treatment 
The typical course of tinnitus involves habituation over time; however, research shows that those seeking treatment tend to display less habituation function than controls.
Recent psychological research on tinnitus focuses on the Tinnitus Distress Reaction (TDR) to account for differences in tinnitus severity. Studies have demonstrated that tinnitus annoyance is more strongly associated with psychological symptoms than acoustic characteristics. Several robust psychological findings have demonstrated comorbidity of psychological complaints of depression, anxiety, sleep disturbances and concentration difficulties with increased tinnitus severity.
Several personality characteristics, such as neuroticism, anxiety sensitivity, and catastrophic thinking predispose increased TDR and maladaptive coping skills. Further, evidence from biochemical studies of patients with distressing tinnitus and psychological disturbances demonstrated some evidence of altered serotonin function that is consistent with studies that linked non-habituation processes with increased negative perceptions and tinnitus annoyance; Simpson and Davies 2000). 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.
Misinterpretation of symptoms as threatening and debilitating triggers avoidance and safety behaviours, including sound and social avoidance, which maintain symptoms. This self-perpetuating pattern impairs daily functioning, leading to greater isolation and increased symptom awareness, impedes concentration and prevents engagement in activities that challenge maladaptive beliefs, resulting in a vicious cycle that further decreases cognitive ability to manage symptoms.
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. 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. The recently developed Tinnitus Functional Index (TFI) is the only measure specifically developed to detect treatment-induced changes.
In the treatment of tinnitus-related distress, studies have focused on the efficacy of cognitive-behavioural therapy (CBT), relaxation training, and mindfulness-based interventions. Two systematic reviews, using stringent inclusion criteria, and meta-analyses have been conducted on studies undertaken between 1995 and 2010. Only cognitive-behavioural studies are numerous enough to perform meta-analysis. Face-to-face therapist-delivered treatments with individual or group formats demonstrate greatest main effects in improving tinnitus-related distress, anxiety and depression. Internet-based CBT interventions provide mixed results, with some studies showing no improvements to anxiety and depression as well as higher attrition rates and smaller main effects than face-to-face treatments.
Subsequent randomised controlled trials provide burgeoning support for mindfulness-based interventions. Single session psychoeducation reduces tinnitus-related negative emotions and ruminations, and effects are maintained with mindfulness, but not relaxation training. No significant differences in treatment effectiveness were found when eight-week, manualised, Internet-based CBT and Acceptance and Commitment Therapy (ACT) were compared. Both treatments yielded significant improvements in tinnitus-related stress and impact, as well as in anxiety and depression.
Importantly, evidence suggests that CBT may not improve some wider impacts of tinnitus (e.g. social impacts) when these are assessed. Manualised treatments, without individual attention to client problems, likely limit the foci and impact of intervention. This underscores the importance of comprehensive individualised biopsychosocial assessments, a multi-disciplinarian approach and responsive treatment plans.
A number of tinnitus-specific CBT treatments have been developed with varying degrees of focus on cognitive and behavioural elements. However, the specific change mechanisms are not yet fully understood. These treatments use a variety of CBT strategies. Components common to most of them include psycho-education, cognitive restructuring, management of avoidance, relaxation training, use of positive or calming imagery, sleep hygiene, sound enrichment and coping strategies.
The prognosis of tinnitus presumably depends on the type and severity of the cause, but is unpredictable.
In one study of young men with tinnitus caused by gunshots (acute acoustic trauma), approximately 35% of the cases reported tinnitus subsiding between three and six months after the trauma, with approximately 10% of the participants seeing the complete disappearance of the tinnitus.
Notable individuals 
||This list of "famous" or "notable" persons has no clear inclusion or exclusion criteria. Please help to define clear inclusion criteria and edit the list to contain only subjects that fit those criteria. (June 2012)|
Notable individuals with tinnitus include:
- Richard Attenborough
- Igor Balis
- Thomas Bangalter
- Jeff Beck
- Ludwig van Beethoven
- Peter Brown
- Bilinda Butcher
- Gerard Butler
- Louis-Ferdinand Celine
- Eric Clapton
- Graham Cole
- Phil Collins
- Charles Darwin (see Charles Darwin's illness)
- John Densmore
- Al Di Meola
- Danny Elfman
- John Entwistle
- Till Fellner
- Noel Gallagher 
- Paul Gilbert
- Gary Glitter
- Vincent van Gogh
- Francisco de Goya
- Charlie Haden
- Ayumi Hamasaki
- Sam Harris
- James Hetfield
- Adolf Hitler
- Howard Hughes
- Joey Jordison
- Garrison Keillor
- Myles Kennedy
- Anthony Kiedis
- Steve Kilbey
- David Letterman
- Huey Lewis
- Rush Limbaugh
- Arjen Anthony Lucassen
- Martin Luther
- Chris Martin
- Steve Martin
- Joseph Mawle
- Martin McGuinness
- Stephin Merritt
- Roger Miller
- William Magin
- Liza Minnelli
- Derek Mooney
- Leonard Nimoy
- Ozzy Osbourne
- Andy Partridge
- Tim Powles
- Ian Punnett
- Tony Randall
- Ronald Reagan
- Trent Reznor
- Peter Robinson
- Mick Ronson
- Francis Rossi
- Neal Schon
- Robert Schumann
- William Shatner
- Alan Shepard
- Kevin Shields
- Paul Simon
- Bedřich Smetana
- Vivian Stanshall
- Jack Straw
- Barbra Streisand
- Peter Stringfellow
- Tom Tancredo
- Louis Tomlinson
- Pete Townshend
- Alex Trebek
- KT Tunstall
- Lars Ulrich
- Ville Valo
- Neil Young
See also 
|Wikimedia Commons has media related to: Tinnitus|
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- "Tinnitus". Deafness Research UK. London, UK: Deafness Research UK. 22 October 2012. Retrieved 2 November 2012. Information about Tinnitus and the latest research work being done
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Further reading 
- 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)
- Soleymani, Teo; Pieton, David; Pezeshkian, Patrick; Miller, Patrick; Gorgulho, Alessandra A; Pouratian, Nader; De Salles, Antonio A.F. (29 October 2011). "Surgical approaches to tinnitus treatment: A review and novel approaches". Surgical Neurology International (Mumbai, India: MedKnow) 2 (1): 154. doi:10.4103/2152-7806.86834. ISSN 2152-7806. OCLC 767649631. PMC 3228384. PMID 22140639. Retrieved 5 November 2012.
- Tyler, Richard S. (2000). Tinnitus Handbook. A Singular audiology textbook. San Diego, CA, USA: Singular Publishing Group. ISBN 9781565939226. OCLC 471533235.