The Neurophysiological Model of Tinnitus and Decreased Sound Tolerance

This chapter presents an outline of the neurophysiological model of tinnitus and decreased sound tolerance (hyperacusis and misophonia). The main postulates of the model are as follows: (1) Tinnitus is a phantom auditory perception, i.e., perception of tinnitus is not linked to any vibratory activity within the cochlea; (2) the model distinguishes tinnitus as an experience from bothersome (clinically significant) tinnitus because separate mechanisms are involved in the perception of tinnitus and in evoked by it negative reactions; (3) the auditory system is secondary for clinically significant tinnitus and for misophonia; (4) the spreading of tinnitus signal to other systems in the brain (particularly to the limbic and autonomic nervous systems) is responsible for negative reactions evoked by tinnitus; and (5) the subconscious connections, governed by the principles of conditioned reflexes, play a dominant role. It is postulated that hyperacusis results from an increased gain within the subconscious part of the auditory pathways and is determined solely by physical characteristics of sound. Misophonia results from enhanced subconscious functional connections between the auditory and limbic and autonomic nervous systems, with reactions occurring to a particular, for a given patient, patterns of sound—the sound energy being secondary or irrelevant. The neurophysiological model of tinnitus is a basis for habituation-based treatment (tinnitus retraining therapy).