Tinnitus Retraining Therapy

Article about tinnitus retraining therapy (TRT).


  1. Tinnitus Retraining Therapy (TRT) is strictly based on the neurophysiological model of tinnitus.
  2. Tinnitus is a phantom auditory perception, i.e. perception of tinnitus is not linked to any vibratory activity within the cochlea.
  3. The model postulates that it is necessary to include interconnections within a network of systems in the brain in the study and treatment of tinnitus.
  4. The auditory system, while needed for perception of tinnitus, is secondary for clinically relevant tinnitus (i.e. tinnitus which is bothersome to the extent of requiring treatment).
  5. The limbic and autonomic nervous systems are the main systems responsible for negative tinnitus evoked reactions.
  6. Tinnitus is frequently accompanied by a decreased sound tolerance, consisting of hyperacusis and misophonia.
  7. Hyperacusis results from an increased gain within the auditory pathways and is determined solely by physical characteristics of sound (i.e. its intensity and spectrum).
  8. Misophonia results from enhanced functional connections between the auditory and the limbic and autonomic nervous systems, and reactions occur to specific patterns of sound, with the total spectral energy being secondary or irrelevant.
  9. In misophonia, the meaning of sound and an individual’s past history of encountering it is crucial, with the auditory characteristics of the sound playing a secondary role. 
  10. There are two loops in network processing tinnitus signal: a. High loop, which involves cognitive processing of the signal and which is dominant at the initial stages of tinnitus. b. Low, subconscious loop, which appears to become dominant in chronic tinnitus. Connections within the neural networks that are involved in the adverse effects of tinnitus are governed by the principles of conditioned reflexes.
  11. The primary goal of TRT is habituation of reactions evoked by tinnitus.
  12. Habituation is initiated and further facilitated using the method of modified passive extinction of the conditioned reflexes and involves: a. Teaching/counseling aimed at reclassification of the tinnitus signal to the category of neutral stimuli. b. Sound therapy, which decreases the strength of the tinnitus signal by increasing the level of background neuronal activity in the auditory system achieved by providing an enhanced sound background.
  13. Habituation of perception happens automatically once sufficient level of habituation of reactions is achieved.
  14. Decreased sound tolerance must be treated concurrently with tinnitus.
  15. Different protocols must be used for hyperacusis than for misophonia. 
  16. A specific variant of treatment, related to classifying a patient to one of 5 categories, is determined by the following factors: a. Impact of tinnitus on patients’ lives and/or duration of clinically significant tinnitus. b. The presence of hyperacusis. c. The presence and significance of hearing loss. d. Prolonged exacerbation of tinnitus/hyperacusis by sound.
  17. Misophonia is treated independently by specific protocols concurrently with tinnitus, hyperacusis, and hearing loss.
  18. Results from many centers have confirmed the effectiveness of the tinnitus retraining therapy (TRT) for tinnitus, reporting a success rate of more than 80%.
  19. Specific studies performed to assess the stability of improvement after 3 and 5 years revealed that improvement continues to be present with patients over time. These studies show a trend of continuing improvement, even after ending the treatment.
  20. Prevention of clinically significant tinnitus or potential worsening of already existing tinnitus could be achieved by: a. Avoidance of silence and providing enriched sound environment. b. Avoidance of negative counseling and providing proper information in advance.
  21. Certain populations are at high risk of developing clinically significant tinnitus, such as military personnel, police officers and firefighters, and patients who are going to have ear-related surgery. Providing them with a proper short informational session about tinnitus would significantly decrease the risk of developing bothersome tinnitus. People will still hear tinnitus, but it will not be a problem for them.


  • TRT Tinnitus retraining therapy
  • LDL Loudness discomfort level
  • DDT Discordant dysfunction theory
  • OHC Outer hair cells
  • IHC Inner hair cells
  • REM Real ear measurements

Outline of the Concepts Presented in this Article 

The theoretical ideas and the description of treatments presented in this article propose a different view on the phenomenon of tinnitus and its treatment than those found in the majority of other published hypotheses about tinnitus and descriptions of treatments. Therefore, definitions of tinnitus and decreased sound tolerance (hyperacusis and misophonia), as used in this chapter, will be provided first, followed by a brief outline of the main concepts of the neurophysiological model of tinnitus [1]. Tinnitus Retraining Therapy (TRT) is strictly based on this model and is one of several potential implementations of therapies aimed at habituation of tinnitus. Furthermore, as it is argued in this chapter, tinnitus should not be treated alone, but as one of the components of a more general dysfunction of the auditory system (including hearing loss and decreased sound tolerance), which needs concurrent treatment. Furthermore, the emphasis is on dynamic interaction of the auditory system with other systems in the brain, which is governed by principles of conditioned reflexes, and the role of subconscious pathways is stressed as well. The main goal of TRT is habituation of negative reactions evoked by tinnitus, with habituation of perception occurring as the subsequent, but inevitable, process.

Definitions of Tinnitus and Decreased Sound Tolerance

Tinnitus is defined as a phantom auditory perception, namely perception of sound without corresponding vibratory, mechanical activity in the cochlea [1, 2]. This perception is absolutely real and can be compared to phantom pain and the phantom limb phenomena. There is a tinnitus signal in the form of neural activity somewhere in the brain that is perceived as a sound, thus tinnitus. It is not known exactly where in the brain this occurs, but some studies indicate that the secondary auditory cortex plays an important role in this respect. Understanding the phantom aspect of tinnitus is fundamental for understanding the interaction of tinnitus with external sounds and thus is the basis for the different forms of sound therapies currently in use. Problems can arise from misunderstanding of the role of external sounds on tinnitus, such as when the suppression of tinnitus perception by external sound is called “masking” [3]. Masking represents interaction of two traveling waves at the basilar membrane of the cochlea and therefore exhibits a “V-shaped” masking curve and depends on the phenomenon of the critical band (i.e. it is impossible to mask one sound by a second if there is a sufficient frequency difference between the two sounds). None of these phenomena exists in connection with tinnitus, which can be equally easily suppressed by sounds from wide range of frequencies [4]. Obviously, it is possible to interact with the tinnitus signal, including suppression of the perception that it leads to, but the mechanism is one of interactions between sound-evoked neural activity and the tinnitus-related neuronal activity. Furthermore, it is possible to decrease the strength of the tinnitus signal by increasing the general level of sound-evoked neuronal activity, and thus by decreasing the difference between the tinnitus signal and the background neuronal activity.

Consequently, the author is against classification of tinnitus into “subjective” and “objective” tinnitus and instead supports using the term “somatosound” in place of “objective tinnitus” as well as reserving the term “tinnitus” for what other authors have referred to as “subjective tinnitus.” This terminology is used in this article.

Tinnitus is frequently accompanied by decreased sound tolerance [5–7]. It is possible to identify two components of decreased sound tolerance, hyperacusis and misophonia [7–9]. Results from several centers show that about 25–30% of individuals with tinnitus also have hyperacusis. Results from the Emory Tinnitus & Hyperacusis Center showed that out of 149 consecutive patients, 66% required treatment for decreased sound tolerance and 33% required treatment for hyperacusis while 57% required treatment for misophonia [8]. Most patients with decreased sound tolerance have both hyperacusis and misophonia, contributing to a decreased sound tolerance to different degrees. While these two components evoke a similar extent of behavioral reaction, there are significant differences in the categories of sound which trigger hyperacusis compared with misophonia, and the physiological mechanisms and treatments of hyperacusis and misophonia are distinctively different. Treatments that are effective for hyperacusis are not effective for misophonia, and treatments for misophonia have only limited impact on hyperacusis.

It is characteristic for hyperacusis that the reaction depends exclusively on the physical characteristics of a bothersome sound, such as its energy and frequency spectrum. The meaning of a sound and an individual’s past history are irrelevant. For example, a person may have a strong negative reaction to speech sounds. If this speech signal is recorded, the spectrum is determined, and then the sound is re-synthesized from individual frequencies with randomly assigned phases, this procedure will yield a sound with the identical energy spectrum as the original speech sound; however, this sound will be perceived as a noise without any meaning. A person with hyperacusis will react in the same manner to both such sounds; it is irrelevant whether this sound is familiar to the person or being encountered for the first time. The environment in which this sound is presented (e.g. doctor’s office, home, part of a sound track of a favorite movie) will not affect how a person with hyperacusis reacts to the sound. People with hyperacusis have a tendency to react stronger (or have lower sound tolerance levels) to sound of higher frequencies (e.g. sound of a metal spoon hitting china, washing machines with clicking plates), reflecting the general tendency of high-frequency sound being more bothersome even for individuals who do not have hyperacusis.

It is proposed that the neural mechanisms of hyperacusis involve abnormally high amplification within the auditory system, with only secondary activation of other centers of the brain responsible for negative reactions (i.e. the limbic and autonomic nervous systems). In other words, the activity that occurs within the auditory pathways after stimulation by 80 dB HL sound in a person with hyperacusis would be similar to that occurring in an individual who does not have hyperacusis and is exposed to a much louder sound such as a sound of 120 dB HL. Studies in animals support proposed mechanism [10, 11]; however, lack of an animal model of hyperacusis hinders researchers from performing more specific studies.

It is characteristic for misophonia that the adverse reactions occur due to specific patterns of sound, with the sound’s spectrum being secondary or irrelevant. The meaning of a sound and the past history of an individual encountering it is crucial. Sounds, which in the past have been associated with something negative (e.g. discomfort, pain, or other situations associated with strong negative emotions), will trigger misophonic negative reactions. Basically, the mechanism of misophonia involves the creation of a conditioned reflex linking specific patterns of a sound to negative reinforcement. Significant hyperacusis, even present for a short period of time, will automatically create misophonia, because exposure to the sound will create discomfort/pain and it will consequently provide the negative reinforcement associated with the sound. Once this reflex is created, it will persist, even when hyperacusis ceases to exist.

For example, in a situation such as the one described above, a person with misophonia may react very strongly to normal speech but show no reaction to re-synthesized speech sounds that seem like meaningless noise. People who have misophonia may exhibit strong reactions to soft sounds (e.g. sounds of eating or speech of certain people) while not having problems with even very loud sounds. Many individuals with misophonia react to sounds “louder than” a certain level, yielding Loudness Discomfort Levels (LDL) determined for pure tones following the shape of audiogram and being better for frequencies where hearing loss exists [8, 12].

The auditory system is perfectly normal in persons with pure misophonia; however, selective connections from the auditory system to the limbic and autonomic nervous systems for specific patterns of sound are abnormally activated or enhanced. Functional properties of these connections are governed by principles of conditioned reflexes. Consequently, the strength of the reactions they cause depends on the strength of the reinforcement, and the sound level plays a secondary role.

Sounds-evoking misophonic reactions do not have to be unpleasant on their own, but it will be sufficient that the individual who has misophonia identify sounds, exposure to which enhances tinnitus for some time. These sounds will be associated with an increased emotionally negative status, caused by enhancement of tinnitus which will be sufficient to create a conditioned reflex arc evoking misophonic reaction to these sounds, even at lower levels than that needed to increase tinnitus loudness.

Physiological Basis for Tinnitus-Induced Negative Reactions

It is crucial to distinguish between mechanisms involved in the generation of tinnitus perception and mechanisms involved in tinnitus-evoked negative reactions. Most individuals who have tinnitus are just experiencing a sound sensation, without any problems related to it. Only about 20% of people with tinnitus have negative reactions evoked by tinnitus. It is interesting that the psychoacoustic characteristics of tinnitus in these two subpopulations are undistinguishable and not related to the severity of the tinnitus as it is experienced by the people who have the bothersome tinnitus.

These observations indicate that there are different mechanisms involved in the generation of the neural signal that causes tinnitus perception, and other mechanisms responsible for evoking negative reactions to this signal. Recognition of this distinction is important, and by aiming treatments at the mechanism of tinnitusinduced negative reactions, it should be possible to remove the problems of the tinnitus without trying to remove tinnitus perception. In the past, most research and treatment attempts were aimed at removing, or at least decreasing tinnitus perception. These approaches were not particularly successful and so far we do not have any reliable method that would make it possible to achieve this goal. Notably, decrease of tinnitus perception does not automatically translate into decrease of tinnitus severity, and actually there is no relation between tinnitus loudness match and the perceived severity of the tinnitus [13].

Analysis of the negative effects of tinnitus on individuals provides information about which system in the brain may be involved in this process. It is possible to distinguish between two main categories of negative effects: (1) physiological responses to tinnitus (e.g. anxiety, depression, sleep problems, increased stress level) and (2) behavioral responses and consequences (e.g. attention and concentration problems, decreased joy of life, and affected life activities such as social interactions, work impairment, family problems). Two major systems in the brain are involved in generating the negative effects of tinnitus, namely the limbic and autonomic nervous systems, which interact with many other systems such as the prefrontal cortex, thalamus, reticular formation, and cerebellum playing some role as well. It has been proposed that it is necessary to include these systems in the analysis of the generation of tinnitus and a person’s reaction to the tinnitus and its treatment [1, 12].

The Neurophysiological Model of Tinnitus

The basic concept of the neurophysiological model of tinnitus is that it is necessary to include variety of systems in the brain in study and treatment of tinnitus [1, 12]. The auditory system, while needed for perception of tinnitus, plays a secondary role for clinically relevant tinnitus (i.e. tinnitus which is bothersome to the extent of requiring treatment). In the past, studies and treatments of tinnitus have tended to be cochleocentric. The neurophysiological model of tinnitus proposed earlier [1] and outlined here shifts the attention away not only from the cochlea but also from the auditory nervous system. The main focus of the model can be envisioned in a form of a diagram, first published in late 1990s [14] (Picture 1).

tinnitus treatment picture - the neurophysiological model of tinnitus

Picture 1 The neurophysiological model of tinnitus

This concept is currently generally accepted and it is believed that any valid neurophysiological model of tinnitus must include several different systems in the brain to represent mechanisms of tinnitus and to be useful in the treatment of tinnitus.

According to their model, the tinnitus signal – the generation of which is typically linked to the periphery of the auditory system – is detected and processed by subconscious centers of the auditory pathways and finally interpreted at the highest level of the auditory system (probably the secondary auditory cortices). If a person just perceives tinnitus without having a negative reaction induced by it, the tinnitus signal may be constrained within the auditory pathways. If, however, this activity spreads to the limbic and autonomic nervous systems by activation of specifically the sympathetic part of the autonomic system, it evokes several negative reactions such as annoyance, anxiety, and panic and triggers survival reflexes resulting in a decreased ability to enjoy life activities. This last mentioned effect has a profound impact on a person’s life by depriving an individual of positive aspects of life which may push a person into depression [12]. The model shown in  Picture 1 has been described in detail already [15–23] and only the main aspects are outlined in this text.

Two Loops

All the systems in the brain are interconnected and work in the dynamic balance scenario, i.e. if a connection is frequently active it becomes stronger, if it is not activated it gradually becomes weaker. This feature is reflected in the diagram of the model (Picture 1), with the main systems mutually interconnected. It was postulated that tinnitus as a problem results mainly from over-activation of the sympathetic part of the autonomic system [1, 19, 22]. It is, therefore, important to analyze pathways involved in tinnitus-related activation of these systems. Firstly, it should be noted that continuous activation of the connections illustrated in Picture 1 causes their strengthening and yields stronger activation of the limbic and autonomic nervous systems by the same tinnitus signal according to the general rules of neural plasticity. Secondly, increased activation of the limbic and autonomic nervous systems occurs via reciprocal connections (feedback) and causes increased activity in the system from which the initial signal was coming. For example, autonomic system activation via a backward feedback can increase the activity in the limbic system, in cognitive brain areas, as well as auditory system. Therefore, the term “loop” is used instead of the term “connections” to emphasize the feedback aspects of the interaction between the different systems.

The tinnitus signal activates the limbic and autonomic nervous systems via two such loops. The upper one (“high loop”) (named the “high route” by LeDoux [24], involves conscious areas of the cerebral cortex, involves perception, evaluation, verbalization, conscious associations, and fears. This loop is crucial in the initial stage of developing clinically significant tinnitus. The second, lower (“low loop”, named the “low route” by LeDoux [24], involves subconscious centers in the brain. It branches from the auditory system at the level of extralemniscal subnuclei of the medial geniculate body, reaching the lateral nucleus of amygdala and, via other parts of the limbic system, reaches centers of the autonomic nervous system. Documented connections link the amygdala with the inferior colliculus, and therefore both connections (from auditory system to limbic system and back) are included in the diagram. The importance of these connections described in the model has been documented [25–27].

Both high and low loops contribute to the final activation of the autonomic nervous system and the negative reactions evoked by tinnitus. High loop is dominant in the acute stage of tinnitus development, but once tinnitus reaches a chronic stage, the subconscious becomes more important or even dominant. The analysis of results from over 300 patients with chronic tinnitus revealed that the proportion of time when patients are aware of tinnitus and subjectively ranked tinnitus loudness does not contribute significantly to tinnitus severity [28]. These results argue strongly against the dominant role of the conscious, high loop, because then tinnitus awareness and tinnitus loudness would be expected to be highly significant factors. These findings have a profound implication on tinnitus treatment.

Conditioned Reflexes

The connections between the brain systems involved in processing the tinnitus signal are governed by principles of conditioned reflexes. The tinnitus signal in the auditory pathways acts as a conditioning stimulus, which, via one or more reflex arc, activates the limbic and autonomic nervous systems and thereby evokes negative reactions. Several different scenarios may create these conditioned reflexes. The most common is the situation of “negative counseling,” i.e. a person is told something which links tinnitus with a threatening, unpleasant, or dangerous situation such as “nothing can be done, you will have tinnitus up to the end of your life, you need to learn to cope with it, and we need to do a brain scan just to eliminate the possibility of a brain tumor.” An extreme example of such negative counseling is when a patient is told that he/she has tinnitus because “he/she has a bad brain.” The negative counseling provides a reinforcement which creates a conditioned reflex arc causing the tinnitus signal to subsequently evoke strong reactions of the limbic and autonomic nervous systems, causing physiological and behavioral reactions.

Another common scenario occurs when a person with tinnitus is under strong emotionally negative stress, such as during retirement, divorce, or from nonrelated health problems. Indeed, a study ranking ordered factors present when a person’s tinnitus became a clinical problem revealed that there was no auditory-related factor in the top 10 most frequent situations [29]. While noise exposure is regarded a frequent cause of the appearance of tinnitus perception, it is not the case for emergence of tinnitus as a problem. Non-bothersome tinnitus may be present for years, and only when it becomes associated with something negative does it become a problem. It should be noted that no causal link is necessary for the creation of a conditioned reflex of any kind, but a close temporal association of a conditioning signal and reinforcement is sufficient to create the reflex.

The neurophysiological model described above and presented in simplified form in Picture 1 predicts that a combination of rapid appearance of tinnitus together with high-level emotional stress is particularly effective in evoking clinically significant tinnitus. Indeed, bothersome tinnitus is evoked typically as a result of sudden hearing loss or when tinnitus starts at a specific time when a person is in the state of highly negative emotions due to sudden hearing loss. Consequently, clinically significant tinnitus can be expected to be more prevalent in professions where there is a combination of a high level of noise, particularly impulsive noise (e.g. gun fire) with a high level of negative emotional stress. Policeman, firefighters, and soldiers are typical examples of members of such professions.

This prediction has been confirmed by the fact that tinnitus occurs in a high rate (49%) of soldiers returning from Iraq and Afghanistan who were exposed to blast noise, the occurrence of which is even higher than the reported proportion of soldiers with blastinduced hearing loss (25%) (see Chap. 67). This unfortunate issue has significant financial connotations, as the American Veterans Administration spent $1.1 billion in 2009 (doubling from $540 million spent in 2006) on compensation for tinnitus alone, with the expected compensation for tinnitus reaching $2.3 billion by 2014 [30]. Since impulse noise can evoke hyperacusis and misophonia, in addition to tinnitus, adding significant problems for the Veterans health care system that must be taken care of in the near future and which will persist for many years to come (untreated clinically significant tinnitus tends to be stable for many years and untreated misophonia tends to worsen with time).

Once the reflex is established, a negative reaction can be evoked without a negative reinforcement, which means that while general health may improve and work problems may be resolved, a person’s tinnitus will keep evoking negative reactions. One of the reasons is that a tinnitus-evoked negative reaction acts as the reinforcement to the reflex arc that has been created and which causes these negative reactions. This aspect of tinnitus explains the low rate of spontaneous recovery, since clinically significant tinnitus is constantly present and that it evokes constant negative reactions, passive extinction of this reflex will not occur and it may actually cause further reinforcement of the reflex arc that causes the negative reactions.

Tinnitus Treatments

There are different methods in use for treatment of tinnitus, and before discussing TRT, it may be useful to briefly discuss some of these other main treatments for tinnitus. Traditionally, the goal has been to eliminate the tinnitus source and tinnitus perception, thus, aiming at achieving a cure of the tinnitus. So far, however, this goal is rarely achieved. Many treatments, typically aimed at the cochlea by delivering drugs directly to the cochlea or through the middle ear, have been tried, and some studies of the outcome of such treatments are currently in progress. Another traditional approach for treatment of tinnitus has been aimed at eliminating tinnitus perception. Suppression of tinnitus perception by external sound, labeled “masking,” has been widely promoted. This approach has not been as successful as hoped, with reported effectiveness from zero [31] to 60% [32]. Recently, “masking” has been re-defined as use of any sound which provides some immediate relief for tinnitus [33]. This approach has shown some effectiveness [34, 35], but it is not clear if it is better that any other type of sound therapy.

Different investigators have used the term “masking” in different ways to describe tinnitus suppression. Auditory masking results from interaction between two traveling waves on the basilar membrane of the cochlea, and as such exhibits phenomena of “critical band” and “V-shaped suppression curve.” None of this is true for tinnitus, it is possible to suppress tinnitus perception equally easy by sound of any frequency, and there is lack of significant dependence on the intensity of the sounds needed to suppress tinnitus from a frequency of the tone [4]. These findings support the hypothesis that tinnitus is a phantom auditory perception without any correspondence to the vibratory activity within the cochlea.

Another approach to suppress tinnitus perception that has been described makes use of electrical stimulation of the cochlea/auditory nerve or, recently, electrical stimulation of the auditory cortex [36–39]. In the case of the auditory cortex, in addition to direct electrical stimulation, Transcranial Magnetic Stimulation (TMS) has been used [40–42]. In TMS, impulses of a very strong magnetic field are applied locally to the skull and the induced electrical current stimulates the cerebral cortex. All these attempts to treat patients with tinnitus were partially successful, with an average rate of about 50%. These methods are now under further investigation.

Different classes of treatment have been aimed at decreasing tinnitus-evoked reactions by improving coping strategies, modifying an individual’s thinking about tinnitus, or by using psychotropic drugs to attenuate activity of the limbic system [12, 43–46]. Psychological approaches have shown effectiveness in the range of 50%, while so far none of the drugs tested have shown significantly positive effects.

Last, but not least, a variety of sound therapies based on the concept of attenuating tinnitus or making it less noticeable have been described [33, 47–51]. These treatments have shown some effectiveness, but for most of these methods lack of systematic, independent studies have made it impossible to accurately assess their efficacy. Recently, the concept of using sounds where the energy at frequencies around the pitch of a person’s tinnitus were eliminated has been reintroduced [52]. The use of such sounds is based on the hypothesis that utilizing the mechanism of lateral inhibition in the auditory cortex would suppress tinnitus. Lateral inhibition, which occurs commonly in the brain and reflects situation that stimulation of one neuron, is frequently accompanied by inhibition of nearby neurons [12, 53]. In the case of the auditory system, which exhibits tonotopic organization, stimulation with a given frequency can inhibit neurons that respond best to nearby frequencies. Specifically, in case of tinnitus, it has been postulated that by removing the music’s frequencies around a person’s tinnitus pitch, the neurons in this range will be inhibited due to activation of neurons which respond best to nearby frequencies.

Treatments Aimed at Habituation of Reactions to Tinnitus and Its Perception

The above outlined treatments aim at removing or attenuating source of tinnitus signal, or at alleviation reactions evoked by tinnitus. The neurophysiological model of tinnitus suggests another possible direction for treatment, namely the possibility of blocking the spread of the tinnitus signal to other than auditory regions of the brain, particularly to the limbic and autonomic nervous systems. If such treatment is successful, a person may still perceive their tinnitus, but tinnitus will not bother her/him. This process is called habituation of tinnitus-evoked reactions. Notably, once sufficient level of habituation of reactions is achieved, habituation of perception automatically follows and a person is aware of tinnitus for smaller and smaller proportions of time as the brain automatically habituates all stimuli that are not important [12]. As a result, an individual with tinnitus changes from being a sufferer to becoming a member of the population of people with tinnitus who experience it, but are not bothered by it. It is important to note that this treatment will not work when attempts have been made to first induce habituation of perception. Any method yielding habituation of tinnitus may be labeled Tinnitus Habituation Therapy [54].

According to the model outlined in Picture 1, habituation of reactions will occur when all connections carrying the tinnitus signal to the limbic and autonomic nervous systems are attenuated and preferably blocked - Picture2. Proper counseling can relatively easily modify the functional connections from the cognitive areas down to the limbic and autonomic nervous systems. Retraining subconscious connections between the auditory system and the limbic and autonomic nervous systems, however, is more complex and difficult to accomplish. Counseling alone will not work, and it is necessary to utilize methods appropriate for retraining the conditioned reflexes.

From the time of Pavlov, it is well known that a conditioned reflex created by exposing a person many times to a sensory stimulus spontaneously undergoes extinction if reinforcement is not given (e.g. using the classical example of the Pavlovian dog, the bell keeps ringing but food is no longer given). This process is known as passive extinction of conditioned reflexes or habituation of reaction [12, 55, 56]. While effective in many situations, this technique cannot be applied in its original form to tinnitus, because the tinnitus signal and its perception are constant and cannot be eliminated. Reinforcement is provided by reactions of the limbic and autonomic nervous systems and, consequently, is constant and cannot be blocked. To solve the problem, the author proposed a modified version of passive extinction of conditioned reflexes using a simultaneous decrease of the sensory signal and reinforcement with these changes maintained for some time (corresponding to the ringing of the Pavlov bell being softer and less food given). This process should be effective, but it requires more time than classical passive extinction. In the case of tinnitus, it requires that the strength of the tinnitus signal is decreased, with a decrease of the strength of negative reactions happening at the same time. These interventions must be carried on for some time to obtain good results.

Tinnitus Retraining Therapy and Its Clinical Goals

TRT is a specific implementation of general Tinnitus Habituation Therapy, which utilizes counseling to decrease tinnitus-evoked reactions and sound to decrease the strength of the tinnitus signal. The primary goal of TRT is to achieve habituation of tinnitus evoked negative reactions and remove the effect of tinnitus on patients’ lives. As pointed out above, once habituation of reactions has been at least partially achieved, habituation of perception automatically occurs without the need of any additional action. At the end of a successful treatment, people are not bothered by tinnitus (or bothered very little), even when perceiving it, and tinnitus has no impact on their lives. Additionally, their awareness of tinnitus typically drops to 5 or 10% of their waking time.

Counselling: Habituation cannot be achieved to stimuli indicating danger or are threatening and is achieved with difficulty to stimuli that evoke strong emotional reactions (negative or positive). Therefore, the primary role of counseling in TRT is to achieve reclassification of tinnitus to a category of neutral stimuli. This is achieved by intensive teaching about mechanisms of the tinnitus origin and its benign nature (as perception), which nevertheless may evoke strong negative reactions affecting patients’ lives. Patients typically have many incorrect concepts about tinnitus and, at the same time, tinnitus remains a mystery for them. Therefore, demystification of tinnitus and providing patients with solid knowledge is important.

The modified method of passive extinction requires a decrease of the strengths of both the activation of the limbic and the autonomic nervous systems and the tinnitus signal. It is impossible to modify the activity of the subconscious low loop that connects information from the thalamus to the limbic system directly [12], but it is possible to attenuate and finally remove the contribution of cognitive components (the high loop). As both the high and low loops contribute to the final activation of the limbic and autonomic nervous systems, it is possible to achieve a decrease of activation of the limbic system by removing or at least decreasing the transmission and processing of tinnitus signals in the high loop, thus removing its contribution.

Picture 2 Habituation of reactions (HR) and habituation of perception (HP) 

By reclassifying tinnitus to the category of neutral stimuli, showing its benign character, providing explanation about its origin and mechanisms, pointing out that the patients have “a proper reaction but to an improper stimulus,” and answering questions, etc., it is possible to eliminate transmission of the tinnitus signal in the high loop in a relatively short time.

Another, more general mechanism of attenuation of the effects of the high loop in tinnitus is based on the fact that people react stronger to unknown dangers than to even significant dangers which are known. Therefore, once patients are able to predict the behavior of their tinnitus (e.g. typical increase of the tinnitus when in quiet places or in a stressful situation) and their own reactions to it, they may still be annoyed and bothered by their tinnitus, but to a smaller extent.

Even complete abolishment of tinnitus signal processing and transmission in the high loop is not sufficient to remove negative reactions evoked by tinnitus because the low loop remains fully active and unchanged.

The negative reaction to a person’s tinnitus will undergo gradual extinction as the result of this modified method of passive extinction, but the process will be slower than eliminating processing and transmission of tinnitus signals in the high loop. Nevertheless, on average, patients show clear improvement after just one month of TRT treatment. This observation has been recently collaborated by reports from other centers [57, 58].

The counselling/teaching session is crucial for achieving high effectiveness of the TRT treatment. Without it, sound therapy will have some positive effect, as well as using some general counseling, but the effectiveness of such treatments is clearly lower [34] because they will not eliminate processing and transmission of the tinnitus signal in the high loop, and patients will still have negative cognitive association with tinnitus.

Sound therapy: In principle, many different methods may be used to decrease the tinnitus signal (e.g. drugs, electrical stimulation, TMS), but in practice, the use of sound is simple and can be easily controlled and adapted to the needs of an individual patient. Sound therapy utilizes the principle that the strength of the neuronal signal within the brain is based on the contrast principle, thus the difference of the signal is from background sound or background neuronal activity. Therefore, the strength of the tinnitus signal can be deceased by systematically increasing the background neuronal activity within the auditory pathways. This can be achieved by enhancing background sound levels to which patients are exposed, thereby affecting the perception of the tinnitus.

Specifics regarding the implementation of sound therapy, including use of sound generators, combination instruments, and hearing aids, have been described in detail elsewhere [5, 8, 15, 59]. It is crucial to remember the basic rule for its successful implementation: “Never use sound as a part of sound therapy, which would create annoyance or discomfort for any reason.” Use of a sound which would evoke any negative reactions would activate the limbic and autonomic nervous systems, worsening the situation and making habituation more difficult to achieve. Other recommendations, which are helpful while less critical, include the use of sound enrichment preferably all the time, 24/7, use more than one type of sound source (e.g. sound generators and tabletop sound machines) and preferentially use nature sounds in the background. Music is typically used in the basic protocol for misophonia [8, 12].

Decreased Sound Tolerance

Tinnitus is typically accompanied by decreased sound tolerance, both hyperacusis and misophonia. Results from many centers indicate that hyperacusis coexists with tinnitus in 25–30% of people who seek help for their tinnitus. Data indicate that misophonia is present in about 60% of the patients treated [8]. Proper diagnosis and treatment of decreased sound tolerance and its components is crucial for successful outcome of tinnitus treatment. Hyperacusis is relatively easy to treat with the desensitization protocol [12], and typically it can be attenuated or eliminated within a couple of months of treatment. Treatment of misophonia is much more complex and lengthy and requires specific protocols. This reflects the fact that the same neuronal networks are involved in tinnitus and misophonia, and consequently, treatment of misophonia takes a similar amount of time as treatment of tinnitus. Methods used for successful treatment of hyperacusis are not effective for treatment of misophonia.

The situation is further worsened by the fact that the presence of tinnitus frequently induces or enhances misophonia, as patients dislike and start to avoid sounds in general, which makes their tinnitus worse (or patients think that this is happening). Last, but not least, misophonia tends to trigger the tensor tympani syndrome (fullness in the ears, pain, feeling of pulsation, vestibular problems, headaches, etc.) [60], which may become a significant, or even a dominant problem.

Severe decreased sound tolerance is more debilitating than severe or even catastrophic tinnitus and can totally disable people. Without adequate treatment of decreased sound tolerance, and particularly misophonia, the effectiveness of tinnitus treatment becomes substantially decreased.

On the positive side, TRT is very effective for treatment of both hyperacusis and misophonia, and it is possible to achieve a cure in most patients, which means total elimination of hyperacusis and misophonia. Another positive aspect is that after successful treatment of misophonia, the tensor tympani syndrome disappears as well, and that tinnitus, if still bothersome, typically also improves.

Outline of Treatment by TRT

Patient Evaluation

In evaluation of patients with tinnitus and decreased sound tolerance, the detailed initial interview is crucial for the diagnosis. We are using a structured interview for initial and follow-up visits conducted with help of specific forms [61, 62] (see Appendix A). While information provided by this interview gives good insight into many aspects of tinnitus including its severity, the Tinnitus Handicap Inventory (THI) is used as well to assess tinnitus severity in a more formal manner [63, 64].

An audiological evaluation includes a pure-tone audiogram (up to 12 kHz), determination of pure-tone Loudness Discomfort Levels (LDL) (measured for all frequencies evaluated in the audiogram), evaluation of speech discrimination, and high-frequency resolution Distortion Product Otoacoustic Emission (DPOAE) (10 points per octave, frequency range of f2 from 1 to 10 kHz), all are tests that are needed for evaluation of patients for treatment using TRT. Audiogram and speech discrimination scores show the patient’s hearing ability. LDLs are crucial in assessing decreased sound tolerance, and DPOAE is extremely helpful during counseling, particularly when Discordant Dysfunction Theory (DDT) is used [1, 12, 65]. This theory postulates that the tinnitus signal originates from the regions of the basilar membrane where there is decreased activity of Outer Hair Cells (OHC) while Inner Hair Cells (IHC) are functional. Measurements of tinnitus pitch and loudness match are performed as well, but these results have no impact on diagnosis or treatment. Determination of Minimal Masking Levels (MML) is done for research purposes.

The acoustic reflexes and reflex decay are not a part of routine evaluation. They are not necessary or sufficient to determine presence of vestibular schwannoma (if it is suspected). Since most patients with tinnitus have decreased sound tolerance, the exposure to loud sounds (which are necessary for testing the acoustic middle-ear reflexes) may cause worsening of the symptoms and make subsequent interaction with patients more difficult.


The following information is used for diagnosis and categorizing the patients’ category and variant of TRT treatment in TRT which should be used.

Impact of Tinnitus on Patients’ Lives and/or the Duration of Clinically Significant Tinnitus

This information provides insight regarding the strength of neuronal connections in the network processing the tinnitus signal. If tinnitus has a low severity, the connections are likely to be weak because it has been shown that tinnitus severity does not depend on the loudness to which a patient matches his/her tinnitus, and it is as well established that the strength of reactions that occurs through activation of conditioned reflexes depends primarily on the strength of the reinforcement; the strength of the conditioned stimulus plays a limited role. Therefore, weak reactions indicate weak strength of the connections in the neural networks involved in causing the tinnitus-evoked reactions. If an individual’s tinnitus is very recent (a few weeks), these connections have not had enough time to become permanent, which would make it easier to modify them. In this connection, it should be noted that the duration of the symptoms regards clinically significant tinnitus and not the duration of the tinnitus perception as such. Tinnitus may be perceived for many years, without bothering a person, before suddenly becoming a problem.


Presence of hyperacusis imposes some constraints on the use of sound therapy, including the allowed category of protocols for misophonia. The differentiation between hyperacusis and misophonia is complex, but a detailed interview, together with a comparison of the shape of a person’s audiogram and that of the LDLs, typically provides enough information to make this distinction [8]. A positive diagnosis of hyperacusis requires that the average LDL is less than about 90 dB. A low value of the LDL does not prove the presence of hyperacusis, however, because a low value of LDLs may be due to misophonia. The behavioral reactions evoked by hyperacusis and misophonia are identical, thus they cannot be used for differentiation either. Detailed interview with attention paid to sounds evoking negative reactions is necessary for differentiation of hyperacusis form misophonia and assign their relative contribution to decreased sound tolerance. If both hyperacusis and misophonia are present together and hyperacusis is treated successfully, but misophonia is not treated and disappears, misophonia typically may be enhanced, and at the behavioral level, no improvement in the patient’s condition is achieved.

The Presence and Significance of Hearing Loss

Approximately 70–80% of individuals with tinnitus have some degree of hearing loss, which is typically less than 60 dB HL in the frequency range up to 8 kHz. It is important to consider whether such hearing loss has any impact on a person’s everyday life. The same degree of hearing loss can be of large significance to one person (e.g. professions requiring communication in noise or musicians) while having no significance to another (e.g. farmers). A factor to consider when evaluating a person’s hearing is whether the hearing loss is accompanied by a “strain to hear” in everyday life because this increases the severity of tinnitus. Only after all these factors have been taken into consideration can a patient be classified as having hearing loss of significance for treatment of tinnitus. It should be noted that a patient’s subjective awareness of her/his hearing loss has little relevance because patients often do not acknowledge mild or even significant hearing loss.

Prolonged Exacerbation of Tinnitus/Hyperacusis by Sound

Over 50% of patients report that their tinnitus becomes worse for some time after exposure to sound (loud, moderate, or even soft). This time is in the range of minutes to hours for most individuals with tinnitus and typically affects hyperacusis or misophonia more than tinnitus. Some patients report that the effect persists through the next day, even after a good night’s sleep, or it may even last several days. This observation can be due to two scenarios and has profound impact on the diagnosis and treatment:

  1. it may involve functional plastic changes in the nervous system that occurs as the “kindling” or “wind up” phenomenon
  2. strong misophonia.

“Kindling” is a term from the field of epilepsy that describes the phenomenon that may occur when a weak stimulus that initially does not evoke a seizure evokes epileptic seizures after being presented repeatedly over several weeks.

The “Wind-up” phenomenon is a term from the field of chronic pain and describes the situation when the second presentation of a painful stimuli causes a stronger reaction than caused by the first presentation or when a stimulus presented for a limited time (e.g. a few minutes) is not inducing pain; when its duration is longer, it becomes painful. This is similar to what occurs when a sound, which initially is without any effect causes a worsening of tinnitus or hyperacusis after the sound has been presented for a longer period of time. These phenomena are particularly observed in people with certain medical problems, such as after head injury, brain surgery, Lyme disease, or symptoms associated with hormonal changes (for instance, during menopause).

In the past, it has not been appreciated that perception of prolonged sounds can often cause misophonia, causing elements of phonophobia to become worse. People with tinnitus may become afraid that exposure to sound may cause their hyperacusis or tinnitus to become permanently worse and by paying extra attention to such problems and avoiding sounds (using ear protection) can enhance tinnitus and hyperacusis/misophonia or cause prolongation of an initial worsening. The experience of treating patients with tinnitus has shown that most incidences of worsening were due to the development of misophonia; only a few people have had indications that the worsening had a medical basis. Nevertheless, when medical reasons are reported by a patient, it should be considered.

Categories of Tinnitus

Five categories of patients are proposed on the basis of the factors listed above [12, 22, 66], and specific variant of TRT treatment has been associated with each one of these categories. These categories, listed below, provide general directions, and the borders between them are not sharp. While the categorization forms a continuum that provides some general guidelines that can help in avoiding some mistakes in the treatment, there is a certain degree of overlap between neighboring categories. For example, patients can be categorized as C 2/3 or 3/2 in case of coexisting hearing loss (category 2) and hyperacusis (category 3), depending on which problem is dominant. If ear-level instrumentation is used, it should be aimed at preserving or restoring symmetrical stimulation of the auditory pathways. Consequently, most of those who use instruments use these bilaterally, with exception being for cases with no hearing in one ear.

Misophonia may be present or absent in all these categories since treatment of misophonia is different from treatment of hyperacusis and tinnitus and can be conducted simultaneously with treatments aimed at the patient’s tinnitus and their hyperacusis. Consequently, misophonia is not included as a discriminating factor in the categorization. A detailed description of the categories and associated variants of treatments has been presented earlier [7, 19].

In the following, each one of the 5 categories is described as well as the methods in which patients with each category are treated using proper variant of TRT method.

Category 0

This category of patients is characterized by a low degree of severity (or hyperacusis) or a short duration of the problem. An abbreviated version of counseling is conducted providing basic information aimed at reclassification of tinnitus into a category of neutral stimuli, furthermore, following the principle that the problem should not be presented, so that it gives an impression that it could be worse than the patient reports (e.g. patients are not told that tinnitus or decreased sound tolerance can be debilitating and push them into depression or suicide!). All the remaining 4 categories have higher severity tinnitus and/or hyperacusis as well as potentially having tinnitus of a longer duration.

Treatment of patients with this category of tinnitus consists of providing basic information about sound therapy, with a short discussion about enrichment from environmental sounds by using sound machines producing nature sounds, or by using other sound sources. The benefit from the principle “Avoid Silence” during the treatment is pointed out. Ear-level instrumentations (e.g. sound generators) are typically not needed in this category, but such devices may anyhow be beneficial. However, as they are not essential for a successful outcome of the treatment and due to financial reasons, they are not recommended.

While an initial visit is typically sufficient to achieve noticeable improvement in this category of patients, a short follow-up visit or telephone call at 1, 3, and 6 months after treatment is worthwhile. Patients who are not improving should be reassessed and, if needed, have more extensive counseling, and recommendation of an ear-level instrumentation should be considered.

Category 1

Patients with this category of tinnitus have significant tinnitus, without hyperacusis, but misophonia may also be present. There is no significant hearing loss, and there is no sound-induced prolonged worsening of tinnitus (except when induced by misophonia). The treatment involves full counseling focused on the patient’s tinnitus, with omitted elements related to hyperacusis.

Sound generators are recommended as part of the therapy, providing well-controlled sound delivery. The sound level is typically determined by the level that evokes annoyance, and only in some patients it is possible to reach the sound level where the patient can perceive their tinnitus and the external sounds as separate entities, but with both sounds start to mix or blend together (the “mixing point”).

Formally, this is the level where partial suppression (“partial masking”) starts to occur. Reaching the mixing point is not important for successful outcome of the treatment. In fact, pushing patients toward reaching the mixing point at the expense of going above the level evoking annoyance or discomfort is counterproductive and works against facilitation of habituation. Sound levels which are low should be avoided, however, because of the effect of stochastic resonance will enhance a person’s tinnitus and work against its habituation [67, 68]. Real Ear Measurements (REM) are highly recommended as a part of fitting an in-the-ear device and are repeated at follow-up visits.

Category 2

The characteristic feature of this category of patients is the presence of significant hearing loss as defined above. Full counseling is performed with stressing matters that are related to hearing loss. Combination instruments (a combination of an independently controlled sound generator and hearing aid in one shell) are preferable for sound therapy to be used in conjunction with enrichment of environmental sounds, as recommended for other categories. If such devices cannot be used due to technical or financial issues, the focus should be on achieving sufficient enrichment of background sounds, typically including the use of tabletop sound machines, with increased stimulation of the auditory system further enhanced by hearing aids. Fitting and use of hearing aids is specific for individuals with tinnitus and different than for people without tinnitus [59, 69].

Sound generators alone are not used for this category of patients, as they would make the understanding of speech even more difficult. Such devices would make tinnitus worse due to an increase in the strain to hear and understand speech.

Category 3

The characteristic feature of this category of tinnitus is a presence of significant hyperacusis that must be treated first. Full counseling is performed, stressing issues related to hyperacusis (e.g. both peripheral and central mechanisms controlling amplification within the auditory pathways are explained). Sound generators are always recommended for sound therapy in patients without hearing loss. Combination instruments are used in patients with hearing loss with stress in the initial stage on sound generators (and low amplification of hearing aid part) followed by second stage when amplification is increased. In both stages, sound generator and hearing aids parts are used concurrently. When combination instruments cannot be utilized, a two-stage procedure may be considered: the first stage with use of sound generators and in the second stage, they are replaced by hearing aids. In this scenario, patients need to be counseled properly to ensure that they expect and accept increased impairment of understanding of speech while using sound generators during the first stage of treatment. Patients should not use these devices when speech communication is essential. Another option is to make use of enrichment of sound background for treatment of hyperacusis before proceeding to the stage in the treatment where hearing aids are used. As hyperacusis is relatively easy to treat and the treatment is fast, this approach may be considered as well.

Combination instruments are the most versatile earlevel instruments for tinnitus treatment and, in theory, they can be used in about 80% of all patients. Technical limitations of currently available instruments as well as their high costs hinder their general use. Another significant aspect is that they require a specific fitting, and lack of proper theoretical and technical know-how by the people who do the fitting results in a high return rate of such instruments. In our experience, we have excellent results with the use of combination instruments and very few were returned.

It should be noted that the presence or absence of misophonia is irrelevant for treatment of patients with this category, which has hyperacusis present. If misophonia is present, it may be treated in the same way as described for the other categories of tinnitus, and for example patients with tinnitus and misophonia will be classified as category 1 with misophonia. Therefore, the presence of decreased sound tolerance is not sufficient to classify patient as belonging to category 3; presence of hyperacusis is required. If misophonia is present in this category, due to presence of hyperacusis, certain restrictions are imposed on the type of protocol that can be used for the treatment of misophonia. Note that the basic features of the protocol for misophonia can be used even for patients with severe hyperacusis [8, 19].

Category 4

The characteristic feature of the tinnitus in this category is a prolonged exacerbation of the patients’ worst problem; typically, hyperacusis that may last at least after a good night’s sleep and does not result from misophonia. If there are medical problems involved that cannot be treated medically, such as from the effect of brain injury after car accidents, blast injuries from military operations, or brain operations, the treatment is highly individualized and difficult. Checking for the presence of Lyme disease may be worthwhile, because it has been reported that hyperacusis is present in 48% of Lyme disease cases [70]. If Lyme disease is the base of the problem, treatment for Lyme disease with antibiotics could be helpful even regarding the tinnitus.

Results of TRT

TRT works independent of the cause of the tinnitus, and the habituation of the reaction to the tinnitus occurs outside the central auditory pathways. Therefore, the etiology of tinnitus is irrelevant, and TRT can be successfully used for any type of tinnitus, e.g. bilateral, unilateral, continuous, or intermittent, as well as for somatosounds. This prediction from the neurophysiological model of tinnitus has been confirmed by results of clinical studies. The results of our past studies showed significant improvement in over 80% of the patients with noteworthy improvement as observed after about 12 months after the beginning of the therapy disregarding the etiology of tinnitus [23, 71]. Recent results of studies of over 300 patients treated in the Emory Tinnitus & Hyperacusis Center showed statistically significant improvement after only 3 months of TRT treatment, with further improvement occurring when the treatment was continued [15, 72].

Results of open studies reported from various centers using TRT also consistently showed significant improvement in over 80% of the patients who were treated [57, 73–87].

The results of a 5-year follow-up study showed that TRT had a high degree of effectiveness in treatment of patients with tinnitus and hyperacusis and that the improvement is persistent [88]. A recently published study evaluated the effects of 18 months of TRT treatment (and the following 18 months without continuing the treatment) [89]. Results immediately following the treatment show a high level of statistically significant improvement which persisted for the 18 months after the study’s treatment completion. Moreover, the proportion of patients reporting disappearance of their tinnitus-evoked difficulties while attempting to relax and concentrate and reporting problems with sleep, social interaction, and work increased continuously after treatment completion [89].

Of interest are also reports presenting results of a systematic randomized study, which showed that TRT is not only highly effective in general but is also effective for patients with severe symptoms typically reported to be particularly difficult to treat using other approaches [34, 35]. Interestingly, there was no indication of the results reaching a plateau after the 18 months the treatment, suggesting the possibility for achieving even better results with further continuation of the treatment.

Prevention and Early Treatment

Tinnitus and decreased sound tolerance present a big problem once they are established. Obviously, prevention of the occurrence of bothersome tinnitus, or treatment at the very early stage of tinnitus, would have a significant impact on the extent of problems created by tinnitus in the general population. Unfortunately, tinnitus prevention is an area that has been largely ignored. The neurophysiological model as described earlier [1, 17, 19, 90–92] and outlined in this article provides guidelines for prevention of the appearance of clinically significant tinnitus and indicates how to achieve relief of problems related to tinnitus shortly after they appear [19].

Avoidance of Silence and Providing an Enriched Sound Environment

The vast majority of patients at the Emory Tinnitus & Hyperacusis Center and at University of Maryland  in Baltimore describe the initial appearance of their tinnitus occurred during a period where they were in a silent environment. Experiments have documented that it is possible to evoke tinnitus perception in most people after a few minutes in a quiet environment [93–95]. If a person is in a negative emotional state while perceiving tinnitus, it may lead to development of conditioned reflexes producing tinnitus-evoked negative reactions. Exposure to sound, particularly by being in an environment enriched by natural sounds or sounds generated by tabletop machines, music players, etc., decreases the probability of bothersome tinnitus materializing.

The neurophysiological model of tinnitus developed by the author and described earlier [1, 17, 19, 90–92] predicts that if a person is exposed to an enriched sound environment shortly after the occurrence of tinnitus perception due to any reason (e.g. explosion or exposure to another damaging sound), it will decrease the probability of development of clinically significant tinnitus or, if it does occur, exposure to sound will increase the likelihood of habituation of the tinnitus. Neuronal connections responsible for the tinnitus-evoked reactions will then not have enough time to become permanent, and it is easier to retrain them if tinnitus is treated early after its occurrence. This prediction has support from the results of both clinical studies and recent experiments on animals, showing that it is possible to prevent or reverse the reorganization of cortical maps that have been induced by sound overexposure by providing animals with an enriched sound environment [96, 97].

It is obvious that avoidance of excessive noise, which may cause damage to the cochlea or other changes in the auditory system, is recommended; however, recommendations given to patients with tinnitus frequently result in overprotection and have the opposite effect. The phenomenon of auditory toughening (i.e. increased resistance of the cochlea to damage and protection against loud, damaging sound offered by pre-exposure to moderate to loud sound) [98–100], is not appreciated in general and even more in case of hyperacusis and tinnitus.

Sound exposure is necessary for keeping normal gain in the auditory nervous system; if it does not receive enough sound input, the gain increases and contributes to the development of tinnitus and/or hyperacusis. The experience from treating patients with tinnitus and animal experiments is that both overexposure to sound and overprotection from sound can be harmful. This message needs to be strongly emphasized in both public and professional health education. Exposure to appropriate forms of sound should be promoted as an integral part of our life that is essential for personal well-being.

Avoidance of Negative Counselling and Providing Proper Information in Advance

Negative counselling frequently provided by health care professionals, patient support groups, and the Internet can trigger mechanism that can create clinically significant tinnitus and make existing tinnitus worse. Health professionals should be alerted to the danger of such negative counselling that is offered to people with tinnitus. Instead, the general population should be educated with correct and basic knowledge about tinnitus, pointing out that there is much that can be done to alleviate the harm from tinnitus and that there is a high likelihood of successful treatment and of decreased sound tolerance (hyperacusis and misophonia). The most frequent issues related to negative counselling (e.g. “nothing can be done, let’s take a brain scan to exclude a brain tumor”) should be properly presented, so that the effect of negative counselling a person may receive is eliminated or at least prevented from having any profound effect.

Such education is particularly important for individuals who have a high risk of acquiring tinnitus, such as soldiers. For example, a huge amount of suffering and money would be spared if all soldiers going into combat situations undergo just one thoughtfully prepared 1–2-h educational session. Identification of other high-risk populations (e.g. police officers, firefighters, construction workers, and patients before any type of ear operation) and providing them with proper education would be highly beneficial as well.


TRT is a specific implementation of the Tinnitus Habituation Therapy, which utilizes teaching/counseling to reclassify tinnitus into the category of neutral stimuli, and sound therapy to decrease the tinnitus related neuronal activity (tinnitus signal) within the brain. As a result of TRT, habituation of both a person’s reactions evoked by the tinnitus and its perception occurs. TRT is strictly based on the neurophysiological model of tinnitus developed by Jastreboff [1, 19, 22] (outlined in Picture 1), which stresses the necessity of including a network of interaction between many different systems in the brain in models of tinnitus and hyperacusis. From the beginning, the model stressed that the auditory system plays a secondary role [19]. Emphasis instead is placed on structures involved in evoking tinnitus-induced negative reactions, mainly but not exclusively, the limbic and autonomic nervous systems.

TRT has been used clinically for treatment of tinnitus and decreased sound tolerance since 1988. The method of TRT underwent many modifications since its first description, and the method does not have a stagnant protocol but continues to evolve on the basis of information gathered from both treatment of patients and animal research findings. While the main features and assumptions of TRT remained the same, implementation of TRT has changed substantially regarding both the counseling part and sound therapy. In counseling, main changes included introduction of the concept of misophonia, the emphasis on conditional reflexes, subconscious processing of information, and on direct teaching about using a modified version of passive extinction of conditioned reflexes. The use of sound therapy has also undergone changes from the introduction of specific protocols for misophonia, changing the parameters for the sound stimulation from the use of levels, which could evoke annoyance or discomfort, to the use of lower levels. These modifications resulted in a significant reduction of the time needed to achieve improvement in the patients’ problems, from 1 year to 1 month.

Results from many tinnitus treatment centers show that TRT causes noticeable improvements or cures in and above 80% of patients with any type of tinnitus. Notably, refined counseling and sound therapy increased the effectiveness of TRT in treatment of decreased sound tolerance, so that it now becomes possible to achieve complete elimination (cure) in most patients. 

Appendix A: Forms for Structured Initial and Follow-up Interviews

Form 1: Tinnitus/Hyperacusis initial interview form   

Form 2: Tinnitus/Hyperacusis follow-up interview form 


1. Jastreboff PJ (1990) Phantom auditory perception ( tinnitus): mechanisms of generation and perception. Neurosci Res 8:221–254

2. Jastreboff PJ (1995) Tinnitus as a phantom perception: theories and clinical implications. In: Mechanisms of Tinnitus. Vernon J, Møller AR, editors Boston, London: Allyn & Bacon, pp 73–94

3. Vernon J (1977) Attemps to relieve tinnitus. J Am Audiol Soc 2:124–131

4. Feldmann H (1971) Homolateral and contralateral masking of tinnitus by noise-bands and by pure tones. Audiology 10:138–144

5. Jastreboff PJ, Jastreboff MM (2007) Tinnitus and decreased sound tolerance: theory and treatment. In: Clinical otology. Huges G, Pensak M, editors, 3rd ed. New York: Thieme Medical Publishers, Inc.

6. Jastreboff PJ, Jastreboff MM (2004) Decreased sound tolerance. In: Tinnitus: theory and management. Snow JB, editor Hamilton, London: BC Decker, pp 8–15

7. Jastreboff PJ, Jastreboff MM (2003) Tinnitus and hyperacusis. In: Ballenger’s otorhinolaryngology head and neck surgery. Snow JB, Jr., Ballenger JJ, editors16th ed. Hamilton, Ontario, Canada: BC Decker, pp 456–475

8. Jastreboff MM, Jastreboff PJ (2002) Decreased sound tolerance and tinnitus retraining therapy (TRT). Aust N Z J Audiol 21(2):74–81

9. Jastreboff MM, Jastreboff PJ (2001) Component of decreased sound tolerance: hyperacusis, misophonia, phonophobia. ITHS News Lett 2(Summer 2001):5–7

10. Boettcher FA, Salvi RJ (1993) Functional changes in the ventral cochlear nucleus following acute acoustic overstimulation. J Acoust Soc Am 94:2123–2134

11. Gerken GM (1993) Alteration of central auditory processing of brief stimuli: a review and a neural model. J Acoust Soc Am 93:2038–2049

12. Jastreboff PJ, Hazell JWP (2004) Tinnitus retraining therapy: implementing the neurophysiological model. Cambridge: Cambridge University Press

13. Monzani D, Genovese E, Marrara A et al (2008) Validity of the Italian adaptation of the Tinnitus Handicap Inventory; focus on quality of life and psychological distress in tinnitus-sufferers. Acta Otorhinolaryngol Ital 28(3): 126–134

14. Jastreboff PJ (1999) The neurophysiological model of tinnitus and hyperacusis. In: Proceedings of the sixth international tinnitus seminar, 1999, Cambridge, UK. Hazell JWP, editor London, UK: THC; pp 32–38

15. Jastreboff PJ (2007) Tinnitus retraining therapy. Prog Brain Res 166:415–423

16. Jastreboff PJ, Jastreboff MM (2006) Tinnitus retraining therapy: a different view on tinnitus. ORL J Otorhinolaryngol Relat Spec 68(1):23–29

17. Jastreboff PJ (2004) The neurophysiological model of tinnitus. In: Tinnitus: theory and management. Snow JB, editor Hamilton, London: BC Decker; pp 96–106

18. Jastreboff PJ (2004) Tinnitus retraining therapy. In: Tinnitus: theory and management. Snow JB, editor Hamilton, London: BC Decker; pp 295–309

19. Jastreboff PJ, Hazell JWP (2004) Tinnitus retraining therapy: implementing the neurophysiological model. Cambridge: Cambridge University Press

20. Jastreboff PJ, Jastreboff MM (2003) Tinnitus retraining therapy for patients with tinnitus and decreased sound tolerance. Otolaryngol Clin North Am 36(2):321–336

21. Jastreboff PJ, Jastreboff MM (2001) The neurophysiological model of tinnitus and its practical implementation: Current status. In: Advances in Otolaryngology-Head and Neck Surgery, vol 15. Myers EN, Bluestone CD, Brackman DE, Krause CJ, Tutchko MJ, editors St. Louis: Mosby, pp 135–147

22. Jastreboff PJ (2000) Tinnitus habituation therapy (THT) and tinnitus retraining therapy (TRT). In: Tinnitus handbook. Tyler R, editor San Diego: Singular, Thomson Learning; pp 357–376

23. Jastreboff PJ, Jastreboff MM (2000) Tinnitus retraining therapy (TRT) as a method for treatment of tinnitus and hyperacusis patients. J Am Acad Audiol 11(3):156–161

24. LeDoux JE (1992) Brain mechanisms of emotion and emotional learning. Curr Opin Neurobiol 2(2):191–197

25. Woodson W, Farb CR, LeDoux JE (2000) Afferents from the auditory thalamus synapse on inhibitory interneurons in the lateral nucleus of the amygdala. Synapse 38(2): 124–137

26. Farb CR, LeDoux JE (1997) NMDA and AMPA receptors in the lateral nucleus of the amygdala are postsynaptic to auditory thalamic afferents. Synapse 27(2):106–121

27. Marsh RA, Fuzessery ZM, Grose CD, Wenstrup JJ (2002) Projection to the inferior colliculus from the basal nucleus of the amygdala. J Neurosci 22(23):10449–10460

28. Jastreboff PJ (2008) The role of subconscious pathways in tinnitus and decreased sound tolerance. Nineth International Tinnitus Seminar, Goeteborg, Sweden

29. Hazell JWP, McKinney CJ (1996) Support for a neurophysiological model of tinnitus. In: Proceedings of the Fifth International Tinnitus Seminar, 1995, Portland, OR, U.S.A. Vernon JA, Reich G, editors Portland, OR: American Tinnitus Association; pp 51–57

30. (2010) http://www.ata.org/advocacy/tool-kit

31. Erlandsson S, Ringdahl A, Hutchins T, Carlsson SG (1987) Treatment of tinnitus: a controlled comparison of masking and placebo. Br J Audiol 21:37–44

32. Vernon JA, Meikle MB (2000) Tinnitus masking. In: Tinnitus Handbook. Tyler R, editor San Diego: Singular, Thomson Learning; pp 313–356

33. Henry JA, Schechter MA, Zaugg TL et al (2006) Outcomes of clinical trial: tinnitus masking vs. tinnitus retraining therapy. JAAA 17(2):104–132

34. Henry JA, Schechter MA, Zaugg TL et al (2006) Outcomes of clinical trial: tinnitus masking versus tinnitus retraining therapy. J Am Acad Audiol 17(2):104–132

35. Henry JA, Schechter MA, Zaugg TL et al (2006) Clinical trial to compare tinnitus masking and tinnitus retraining therapy. Acta Otolaryngol Suppl 556:64–69

36. De Ridder D, De MG, Verstraeten E et al (2006) Primary and secondary auditory cortex stimulation for intractable tinnitus. ORL J Otorhinolaryngol Relat Spec 68(1):48–54

37. Rubinstein JT, Tyler RS, Johnson A, Brown CJ (2003) Electrical suppression of tinnitus with high-rate pulse trains. Otol Neurotol 24(3):478–485

38. Dauman R (2000) Electrical stimulation for tinnitus supression. In: Tinnitus handbook. Tyler R, editor San Diego: Singular, Thomson Learning; pp 377–398

39. Dobie RA (1999) A review of randomized clinical trials in tinnitus. Laryngoscope 109(8):1202–1211

40. Rossi S, De CA, Ulivelli M et al (2007) Effects of repetitive transcranial magnetic stimulation on chronic tinnitus. A randomised, cross over, double blind, placebo-controlled study. J Neurol Neurosurg Psychiatry 78(8):857–863

41. Langguth B, Zowe M, Landgrebe M et al (2006) Transcranial magnetic stimulation for the treatment of tinnitus: a new coil positioning method and first results. Brain Topogr 18(4): 241–247

42. Langguth B, Hajak G, Kleinjung T, Pridmore S, Sand P, Eichhammer P (2006) Repetitive transcranial magnetic stimulation and chronic tinnitus. Acta Otolaryngol Suppl 556:102–104

43. Wilson PH (2006) Classical conditioning as the basis for the effective treatment of tinnitus-related distress. ORL J Otorhinolaryngol Relat Spec 68(1):6–11

44. Henry JL, Wilson PH (2001) Psychological management of chronic tinnitus: a cognitive-behavioral approach. Boston: Allyn & Bacon

45. Dobie RA (2004) Clinical trials and drug therapy for tinnitus. In: Snow JB (ed) Tinnitus: theory and management. BC Decker, Hamilton, London, pp 266–277

46. Dobie RA (1999) A review of randomized clinical trials in tinnitus. Laryngoscope 109(8):1202–1211

47. Jastreboff MM (2007) Sound therapies for tinnitus management. In: Tinnitus: pathophysiology and treatment. Langguth B, Hajak G, Kleinjung T, Cacace A, Møller A, editors Elsevier, Amsterdam, pp 449–454

48. Nickel AK, Hillecke T, Argstatter H, Bolay HV (2005) Outcome research in music therapy: a step on the long road to an evidence-based treatment. Ann N Y Acad Sci 1060: 283–293

49. Herraiz C, Diges I, Cobo P, Plaza G, Aparicio JM (2006) Auditory discrimination therapy (ADT) for tinnitus managment: preliminary results. Acta Otolaryngol Suppl 556:80–83

50. Davis P, Paki B, Hanley P (2007) Neuromonics tinnitus treatment: third clinical trail. Ear Hearing 28(2):242–259

51. Jastreboff PJ, Jastreboff MM (2009) The role of hearing aids in tinnitus management. In: Hearing aid book. Derebery J, Luxford W editors Plural Publishing, San Diego, CA, pp 119–131

52. Okamoto H, Stracke H, Stoll W, Pantev C (2010) Listening to tailor-made notched music reduces tinnitus loudness and tinnitus-related auditory cortex activity. Proc Natl Acad Sci U S A 107(3):1207–1210

53. Gerken GM (1996) Central tinnitus and lateral inhibition: an auditory brainstem model. Hearing Res 97:75–83

54. Jastreboff PJ (2000) Tinnitus Habituation Therapy (THT) and Tinnitus Retraining Therapy (TRT). In: Tinnitus Handbook. Tyler R, editor San Diego: Singular, Thomson Learning; pp 357–376

55. Tinnitus (2009) In: Encyclopedia of neuroscience. Squire LR, editor Oxford Academic Press, pp 1001–1008

56. Okamoto H, Stracke H, Stoll W, Pantev C (2010) Listening to tailor-made notched music reduces tinnitus loudness and tinnitus-related auditory cortex activity. Proc Natl Acad Sci U S A 107(3):1207–1210

57. Ito M, Soma K, Ando R (2009) Association between tinnitus retraining therapy and a tinnitus control instrument. Auris Nasus Larynx 36(5):536–540

58. Hatanaka A, Ariizumi Y, Kitamura K (2008) Pros and cons of tinnitus retraining therapy. Acta Otolaryngol 128(4): 365–368

59. Jastreboff PJ, Jastreboff MM (2009) The role of hearing aids in tinnitus management. In: Hearing aid book. Derebery J, Luxford W editors Plural Publishing, San Diego, CA, pp 119–131

60. Impedance fluctuation and a “Tensor Tympani Syndrome”. 79 Sep 25; Lisbon: Universidad Nova de Lisboa Ed Penha & Pizarro; 1979, Ref ID: 8065

61. Henry JA, Jastreboff MM, Jastreboff PJ, Schechter MA, Fausti SA (2003) Guide to conducting tinnitus retraining therapy initial and follow-up interviews. J Rehabil Res Dev 40(2):157–177

62. Jastreboff MM, Jastreboff PJ (1999) Questionnaires for assessment of the patients and treatment outcome. In: Proceedings of the Sixth International Tinnitus Seminar, 1999, Cambridge, UK. Hazell JWP, editor London, UK: THC, pp 487–490

63. Newman CW, Sandridge SA, Jacobson GP (1998) Psychometric adequacy of the Tinnitus Handicap Inventory (THI) for evaluating treatment outcome. J Am Acad Audiol 9(2):153–160

64. Newman CW, Wharton JA, Jacobson GP (1995) Retest stability of the tinnitus handicap questionnaire. Ann Otol Rhinol Laryngol 104:718–723

65. Jastreboff PJ, Hazell JWP (1998) Treatment of tinnitus based on a neurophysiological model. In: Tinnitus: treatment and relief. Vernon J, editor Allyn & Bacon, pp 201–216

66. Jastreboff PJ (1999) Categories of the patients and the treatment outcome. In: Proceedings of the Sixth International Tinnitus Seminar, 1999, Cambridge, UK. Hazell JWP, editor London, UK: THC, pp 394–398

67. Jastreboff PJ, Jastreboff MM (2000) Potential impact of stochastic resonance on tinnitus and its treatment. Assoc Res Otolaryngol 23:5542

68. Jastreboff PJ, Jastreboff MM (2009) Tinnitus and decreased sound tolerance. In: Ballenger’s Otorhinolaryngology Head and Neck Surgery. Ballenger JJ, Snow JB, Ashley WP, editors17 ed. San Diego: Singular Publishing, pp 351–362

69. Sheldrake JB, Jastreboff MM (2004) Role of hearing aids in management of tinnitus. In: Tinnitus: Theory and Management. Snow JB, editor Hamilton, London: BC Decker, pp 312–315

70. Nields JA, Fallon BA, Jastreboff PJ (1999) Carbamazepine in the treatment of Lyme disease-induced hyperacusi. J Neuropsychiatry Clin Neurosci 11(1):97–99

71. Jastreboff PJ, Gray WC, Gold SL (1996) Neurophysiological approach to tinnitus patients. Am J Otol 17:236–240

72. Jastreboff PJ, Jastreboff MM (2009) Tinnitus and decreased sound tolerance. In: Ballenger’s Otorhinolaryngology Head and Neck Surgery. Ballenger JJ, Snow JB, Ashley WP, editors17 ed. San Diego: Singular Publishing, pp 351–362

73. McKinney CJ, Hazell JWP, Graham RL (1999) An evaluation of the TRT method. In: Proceedings of the Sixth International Tinnitus Seminar, 1999, Cambridge, UK. Hazell JWP, editor London, UK: THC, pp 99–105 596 P.J. Jastreboff

74. Sheldrake JB, Hazell JWP, Graham RL (1999) Results of tinnitus retraining therapy. In: Proceedings of the Sixth International Tinnitus Seminar, 1999, Cambridge, UK. Hazell JWP, editor London, UK: THC, pp 292–296

75. Bartnik G, Fabijanska A, Rogowski M (2001) Effects of tinnitus retraining therapy (TRT) for patients with tinnitus and subjective hearing loss versus tinnitus only. Scand Audiol Suppl (52):206–208

76. Bartnik G, Fabijanska A, Rogowski M (1999) Our experience in treatment of patients with tinnitus and/or hyperacusis using the habituation method. In: Proceedings of the Sixth International Tinnitus Seminar, 1999, Cambridge, UK. Hazell JWP, editor London, UK: THC, pp 415–417

77. Heitzmann T, Rubio L, Cardenas MR, Zofio E (1999) The importance of continuity in TRT patients: Results at 18 months. In: Proceedings of the Sixth International Tinnitus Seminar, 1999, Cambridge, UK. Hazell JWP, editor London, UK: THC, pp 509–511

78. Mazurek B, Fischer F, Haupt H, Georgiewa P, Reisshauer A, Klapp BF (2006) A modified version of tinnitus retraining therapy: observing long-term outcome and predictors. Audiol Neurootol 11(5):276–286

79. Herraiz C, Larrea JL (2004) Implementation of habituation theory to pulsatile somato-sounds (tinnitus): the heart valve prosthesis sound model]. Acta Otorrinolaringol Esp 55(2): 49–54

80. Mazurek B, Fischer F, Haupt H, Georgiewa P, Reisshauer A, Klapp BF (2006) A modified version of tinnitus retraining therapy: observing long-term outcome and predictors. Audiol Neurootol 11(5):276–286

81. Madeira G, Montmirail C, Decat M, Gersdorff M (2007) TRT: results after one year treatment. Rev Laryngol Otol Rhinol (Bord) 128(3):145–148

82. Hatanaka A, Ariizumi Y, Kitamura K (2008) Pros and cons of tinnitus retraining therapy. Acta Otolaryngol 128(4): 365–368

83. Molini E, Faralli M, Calenti C, Ricci G, Longari F, Frenguelli A (2010) Personal experience with tinnitus retraining therapy. Eur Arch Otorhinolaryngol 267:51–56

84. Seydel C, Haupt H, Szczepek AJ, Klapp BF, Mazurek B (2010) Long-term improvement in tinnitus after modified tinnitus retraining therapy enhanced by a variety of psychological approaches. Audiol Neurootol 15(2):69–80

85. Herraiz C, Hernandez FJ, Plaza G, De los SG (2005) Longterm clinical trial of tinnitus retraining therapy. Otolaryngol Head Neck Surg 133(5):774–779

86. Proceedings of the Sixth International Tinnitus Seminar, 1999, Cambridge, UK. (1999) London, UK: THC

87. Baracca GN, Forti S, Crocetti A et al (2007) Results of TRT after eighteen months: our experience. Int J Audiol 46(5):217–222

88. Lux-Wellenhof G, Hellweg FC (2002) Longterm follow up study of TRT in Frankfurt. In: Proceedings of the Seventh International Tinnitus Seminar. Patuzzi R, editor Perth, Australia: The University of Western Australia, pp 277–279

89. Forti S, Costanzo S, Crocetti A, Pignataro L, Del BL, Ambrosetti U (2009) Are results of tinnitus retraining therapy maintained over time? 18-month follow-up after completion of therapy. Audiol Neurootol 14(5):286–289

90. Jastreboff PJ (1999) The neurophysiological model of tinnitus and hyperacusis. In: Proceedings of the Sixth International Tinnitus Seminar, 1999, Cambridge, UK. Hazell JWP, editor London, UK: THC, pp 32–38

91. Jastreboff PJ, Hazell JW, Graham RL (1994) Neurophysiological model of tinnitus: dependence of the minimal masking level on treatment outcome. Hear Res 80(2): 216–232

92. Jastreboff PJ, Hazell JWP (1993) A neurophysiological approach to tinnitus: clinical implications. Br J Audiol 27:1–11

93. Heller MF, Bergman M (1953) Tinnitus in normally hearing persons. Ann Otol 62:73–93

94. Tucker DA, Phillips SL, Ruth RA, Clayton WA, Royster E, Todd AD (2005) The effect of silence on tinnitus perception. Otolaryngol Head Neck Surg 132(1):20–24

95. Del BL, Forti S, Ambrosetti U et al (2008) Tinnitus aurium in persons with normal hearing: 55 years later. Otolaryngol Head Neck Surg 139(3):391–394

96. Eggermont JJ (2006) Cortical tonotopic map reorganization and its implications for treatment of tinnitus. Acta Otolaryngol Suppl (556):9–12

97. Norena AJ, Eggermont JJ (2006) Enriched acoustic environment after noise trauma abolishes neural signs of tinnitus. Neuroreport 17(6):559–563

98. Hamernik RP, Qiu W, Davis B (2003) Cochlear toughening, protection, and potentiation of noise-induced trauma by non-Gaussian noise. J Acoust Soc Am 113(2):969–976

99. Niu X, Tahera Y, Canlon B (2004) Protection against acoustic trauma by forward and backward sound conditioning. Audiol Neurootol 9(5):265–273

100. Niu X, Canlon B (2002) Protective mechanisms of sound conditioning. Adv Otorhinolaryngol 59:96–105