FIGURE 6.

(A) Summary of the hypothesis. Noise exposure (most commonly music) causes dysfunction/damage in the high-frequency (>6.0 kHz) region of the cochlea) in >85% of patients. This leads to high-pitched tinnitus, most commonly at about 8.0 kHz. Bioelectrical impulse flow from the damaged cochlear region toward auditory cortex diminishes or ceases (”dead” region). This leads to reduced (inhibitory) regulation with subsequent neuronal hyperactivity in the central auditory pathway, first in the auditory nuclei of brainstem, later in the auditory cortex. The normal (spontaneous) alpha activity (in EEG) changes to gamma activity. The central auditory pathway is intimately connected to the limbic system (that controls emotions). Tinnitus is experienced as an emotionally negative sensation including uncertainties and fears (”what is this all about?”; “does it ever go away?”). Thereby, the perceptive (hearing) network is connected to the distress network (stress). The stressor leads to imbalance of the central autonomous network (CAN) with hyperactivity of the sympathetic nervous system (flight or fight or freeze response) and, correspondingly reduced activity of the parasympathetic nervous system (PNS) (relax, calm down). (B) Vagus nerve is the main player of the PNS. Therefore, activation of the vagal system increases PNS activity. For taVNS we have used a specially designed Salustim device that uses an ear-clip electrode inserted to the tragus and electrically stimulates ABVN. The taVNS reverses sympathetic hyperactivity in the limbic system and the CAN imbalance toward parasympathetic direction. Reduction of distress also facilitates the reversal of gamma-hyperactivity back to normal alpha-activity in the auditory central pathway.