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Based on the observations of several hundred patients with decreased sound tolerance the existence of unrecognized earlier auditory disorder with distinctive and different from hyperacusis characteristics has been identified. Patients with this disorder exhibited negative emotional and autonomic reactions evoked by a specific for a given patient patterns of sound. Consequently, the name "misophonia" for this previously not described disorder and its definition based on data gathered from our patients was proposed in 2001. Furthermore, clinical observations pointed out that misophonia requires a different approach for diagnosis and treatment than hyperacusis. Although the proposed definition was independent of the etiology of misophonia, nevertheless, on the basis of analysis of its features, including reported reactions to bothersome sounds ("misophonic triggers") it was possible to propose potential mechanisms of misophonia and the neurophysiologi-cal model for both misophonia and hyperacusis. The model postulates that a key characteristic of misophonia is the formation of inappropriate, pattern-specific subconscious connections between the auditory system and other systems of the brain, particularly with the limbic and autonomic nervous systems. These connections are governed by the principles of conditioned reflexes. Notably, the brain systems and connections involved in misophonia are the same as in the case of tinnitus. However, in the case of tinnitus the abnormal neuronal activity is generated within the auditory pathways and spreads to other systems in the brain, while in case of misophonia normal sound-evoked activity which is the same as in case of subjects without misophonia, is spreading and incorrectly activates various systems in the brain, yielding emotional and autonomic reactions to misophonic triggers. The mechanism of hyperacusis is based on abnormally increased gain within the subconscious part of the auditory pathways. This yields a high level of neuronal activity, equivalent to activity evoked by much stronger sound in normal subjects. The activation of the other systems in the brain is a consequence of spreading this abnormally enhanced sound-evoked activity by normally functioning neuronal connections from the auditory to other systems in the brain. In misophonia sound-evoked signals within the auditory pathways are normal, but incorrect pattern-specific connections yield abnormally strong activations of various systems in the brain. [ABSTRACT FROM AUTHOR]

Hyperacusis and misophonia are subcategories of decreased sound tolerance. They may occur individually, but frequently they take place concurrently. In both disorders people exhibit reduced tolerance to sounds normally not bothersome for the average listener and reactions to bothersome sounds are very similar, even identical. However, there are distinctive differences between these conditions which are essential in their differential diagnosis and their treatments. Detailed patients' interview is necessary, with questions focusing on description of bothersome sounds, situations associated with sound, reactions to sound, and how they affect everyday activities, identifying pleasant sounds and other factors influencing the responses to bothersome sounds. Reactions to sound of hyperacusis patients depend predominantly on physical characteristics of the sound, particularly to sound energy (linked to its intensity). The meaning of the sound is irrelevant as well who/what produces it and in which environment. The loud-ness discomfort levels (LDLs) are lower than normal average value of 100 dB HL and they are typically below 80 dB HL. Unfortunately, low values of LDLs cannot be used as a proof of hyperacusis presence as low values can be due to misopho-nia as well. It is postulated that the problems experienced by patients arise from abnormal amplification of sound-evoked activity within the auditory system, with other systems in the brain activated only as secondary consequence. In misopho-nia sound evoked activity within the auditory system is normal, but improper connections between the auditory system and other systems in the brain develop at subconscious level as a result of temporal association of the presence of miso-phonic triggers with negative emotional or physical situation. The values of LDLs can be from as low as 20 dB HL to 120 dB HL and cannot be used to diagnose the presence of misophonia. Detailed patients' interview is essential. Desensitization with the variety of sounds has been proposed and successfully used to reverse abnormal gain within the auditory pathways and by this treat hyperacusis for many years already. The sounds and the protocols of their use are modified to follow guidelines of the neurophysiological model. The advice about the use of sound is combined with counseling focusing on explanation of mechanisms of hyperacusis. For misophonia treatment based on passive and active extinction of subconscious conditioned reflexes is implemented, with stress on the principle of complex conditioned stimuli and on involvement of generalization principle. Detailed counseling, tailored to the case of a specific patient, is crucial to achieve a successful outcome of the treatment. The treatments for hyperacu-sis and misophonia are distinctively different and treatment for hyperacusis is not successful for misophonia and treatment for misophonia has limited effectiveness for hyperacusis. Analysis of over 200 patients with decreased sound tolerance showed an over 80% success rate of significant improvement. [ABSTRACT FROM AUTHOR]

Misophonia is present when negative reactions occur to a sound that has a specific for a given person pattern and/or meaning. The extent of the reaction can vary from mild to extremely strong. The strength of the reaction often depends on the situation in which the sound is presented. Misophonia develops, and is most frequently observed, in children and teenagers, however it affects people of all ages. While the concept of misophonia was proposed in 2001, recently it become the subject of intense discussion by various professionals. Audiologists, psychologists, neurologists, psychiatrists, and occupational therapists propose contrasting models of misophonia and different approaches to help those who suffer because of it. Misophonia reflects an enhanced functional connection between the auditory and the limbic and autonomic nervous systems. As such, there is close analogy between tinnitus and misophonia and both phenomena share the same neuronal networks. Notably, tinnitus is accompanied by misophonia in about 60% of our tinnitus patients. Specifically adjusted tinnitus treatment, Tinnitus Retraining Therapy (TRT) is beneficial for misophonic patients. Moreover, our clinical observation has demonstrated that if misophonia coexists with tinnitus, the treatment of misophonia is crucial to achieve a successful outcome for tinnitus therapy. The behavioral reactions to sound observed in misophonia and hyperacusis are alike, however their mechanisms and treatments are very different. Therefore, it is crucial to distinguish misophonia from hyperacusis as the treatment that is effective for hyperacusis is unsuccessful for misophonia, and the treatment for misophonia has a limited impact on hyperacusis. Loudness Discomfort Levels (LDLs) for pure tone alone cannot help to discriminate misophonia from hyperacusis and therefore specific and detailed interview is essential. Stress is placed on identifying sounds and situations that evoke a patients negative reactions, as well as sounds that are well-tolerated, to determine whether there are any discrepancies between the patient's reaction and the sound's intensity. Patients with misophonia react to specific patterns of sound, and the intensity of the sound is secondary. Misophonia can be successfully treated with TRT. We published the results of TRT treatment for 184 consecutive patients with misophonia and showed an 83% success rate. Treatment consists of intensive counseling and specific sound therapy protocols. Ear level sound generators are frequently recommended as a part of sound therapy. While they are not essential for a successful outcome, sound generators facilitate process of recovery. The most advanced protocol utilizes the principle of complex conditioning stimuli. It combines offensive sounds with positive reinforcement, achieved by introducing sounds and other sensory signals or environments that have a highly positive connotation to the patient. Subsequently, the strength of positive reinforcement is gradually decreased (e.g., by decreasing the level of positive sound). The length of treatment for misophonia is similar to the length of tinnitus treatment. Typically, patients notice some improvement in 3 months, and see further improvement with continuation of treatment. Most patient achieve a significant, positive outcome during the 9 to 18 months of treatment. In some cases, it is possible to achieve a cure for misophonia. [ABSTRACT FROM AUTHOR]

There is growing agreement that patient' problems with tinnitus are not due to tinnitus perception per se, but to negative reactions to tinnitus. Patients' complaints include decreased ability to enjoy life's activities as well as difficulty concentrating, relaxing and sleeping. Tinnitus patients frequently experience anxiety, depression and panic. Two methods have been shown to be effective in the managements of tinnitus: Cognitive Behavioral Therapy (CBT) and Tinnitus Retraining Therapy (TRT). The main premise of CBT is that thoughts evoke emotions. In CBT emphasis is placed on cognitive functions, selective attention, and the distorted perception of tinnitus. The Cognitive Behavioral model of tinnitus proposed by McKenna (2014) postulates that patients' interpretation of tinnitus and the behavioral changes caused by it play a central role in creating and maintaining tinnitus-evoked distress. In the neurophysiological model of tinnitus, and consequently in TRT, all factors listed in Cognitive Behavioral model are taken into account; however, the role of the subconscious centers of the brain and the consequences of created conditioned reflexes that connect the auditory system with other systems in the brain are also included. In the initial stage cognitive processes (upper loop on the diagram of the neurophysiological model of tinnitus) play dominant role, but in the chronic stage of tinnitus the subconscious levels (lower loop) become dominant. Connections within the neural networks involved in the adverse effects of tinnitus are governed by the principles of conditioned reflexes. The primary goal of TRT is to disable the functional connections between the auditory and other systems of the brain and consequently to achieve habituation of tinnitus-evoked reactions. Habituation is initiated and further facilitated by the method of modified passive extinction of these conditioned reflexes. This process involves: 1) teaching/counseling aimed at reclassification of the tinnitus signal to the category of neutral stimuli and 2) using sound therapy to decrease 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. Note, that habituation of perception occurs automatically once a sufficient level of habituation of reaction is achieved. It is proposed that because TRT targets both the conscious and subconscious levels of the brain and furthermore takes decreased sound tolerance and hearing loss into account, TRT seems to be more effective than CBT with regard to tinnitus management. This view is supported by the published results of clinical studies. The differences between the neurophysiological model of tinnitus and assumptions of CBT have a significant impact on how counseling is performed in these two approaches. Clinical observations indicate that tinnitus treatment is impaired or blocked if decreased sound tolerance is not treated concurrently with tinnitus. Further systematic clinical studies are needed to clarify specific postulates of CBT and TRT and through this to optimize the treatment of tinnitus patients. [ABSTRACT FROM AUTHOR]