THE NEUROPHYSIOLOGICAL MODEL FOR HYPERACUSIS AND MISOPHONIA

Tinnitus patients frequently complain about Decreased Sound Tolerance (DST) as well. 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. It is possible to have tinnitus, hyperacusis, and misophonia in combination or as isolated conditions. On the basis of analysis of characteristic features of patients with DST, and general neuroscience, the neurophysiological model for both misophonia and hyperacusis has been proposed. The key characteristic of misophonia is the formation of inappropriate, pattern-specific, subconscious connections, between the auditory system and other systems of the brain, 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. 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 a 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 development of incorrect pattern-specific connections yield abnormally strong activations of various systems in the brain. In hyperacusis and misophonia reactions evoked by bothersome sound are very similar, even identical and cannot be used to differentiate these two disorders. Importantly, both clinical observations and predictions of the model point out that misophonia requires a different approach for diagnosis and treatment than hyperacusis.