Tinnitus may be defined as a clinical correlation of spontaneous neural activity of the auditory pathway in conditions responsible for absent stimuli in the cases of affected tonotopy. The contribution suggests a disinhibition hypothesis for the pathogenesis of tinnitus based on a feed-back regulation of neural transfer of auditory pathway, where de-afferentation results in hyperex-citation in the region of presynaptic nerve endings, and thereby to alternativě activation of ascendant NMDA synapses. In the pathogenesis of tinnitus we presume a combined action of inhibiting facilitation connections for the presynaptic membráně; moreover, we suppose the stress to be a decisive factor in the origin of chronic tinnitus. The authors also discuss efficiency in the treatment of tinnitus related to disinhibition hypothesis and possibilities of closer specification of the systém responsible for pathogenesis of tinnitus

        Key words: tinnitus, pathogenesis, descendent connections, auditory pathway