What do tinnitus, the perception of sounds without an internal or external source of noise, hyperacusis, the pathological hypersensitivity to noise, or misophonia, an intolerance to certain everyday noises, have in common, and what differentiates them? A large number of excellent studies focused in the last few decades on identifying the neural correlates of tinnitus, hyperacusis, or misophonia on the basis of central triple-network changes. In this perspective review we explicitly examine, possible differential and causal involvement of peripheral components as a presumptive trigger that may drive observed triple-network changes. Based on our results, we venture to hypothesize that: (i) tinnitus, hyperacusis, and misophonia can occur despite clinically normal hearing thresholds, and are likely causally independent of sex and age, (ii) tinnitus and hyperacusis, but possibly also misophonia are related to altered auditory processing that through desynchronized (tinnitus) or hyperactive (hyperacusis, misophonia) bottom-up ascending processing potentially explains the activity changes in, e.g., default or salient brain networks, as suggested in various studies of these different diseases. (iii) In misophonia a stress-induced top-down influence, as deep as the auditory nerve fibers, may be discussed as a contributor to generating misophonia-trigger sounds, a hypothesis that can be tested in future studies. We hope that the selective consideration of a possible interaction between peripheral and central components will help to minimize the greatest handicap of these pathologies to date towards successful therapy: the lack of clarification of the underlying causative mechanism of the diseases.