Music-Induced Hearing Loss (MIHL) is a special case of noise-induced hearing loss (NIHL) insofar as the methodology of quantification is concerned, while it presents a particularly acute challenge in respect of music's conflicting demands. These include the desire, particularly in the young, to gain euphoria from music which may be loud enough to traumatize the cochlea. If going to a loud music event were to produce actual physical pain or giddiness we would not do it. Enigmatically, the cochlea does not possess pain receptors. Maybe this is because the evolution of our very wide dynamic range (120+dB) seems to have obviated the need, at least up until modern times. But now the music industry appears to be going through a phase of believing that amplification with compression is necessary to bring music alive and that modern music capabilities constitute an important new cultural modality. To hearing-industry professionals, although the contra-indications of exposure to loud sound are clear, the message is ignored. By now we have incredible macroscopic and microscopic detail about cochlear mechanisms, but perhaps we do not have a sufficiently good holistic model of how they all work together to make a convincing case? There is also the issue that our best measures of measuring audibility lack precision due to huge data variability, the source of which has never been explained. Our presentation draws together the key issues and reviews two of our early results to restate the problem. The first result concerns what we in 1998 termed "latent hearing loss" due to the rise in preclinical damage to the outer hair cell population measured using click-evoked otoacoustic emissions (OAE). We showed that this can be determined with a better overview than pure tone thresholds and thus can serve as the basis of personal dosimetry e.g. for those who frequently dose-up on loud music. The second result questions the traditional assumption that the frequency-place map is fixed in the manner depicted by the grid of a standard audiogram. We re-introduce our 1987 model which expresses the leading edge of the excitation pattern in spatial coordinates and show that many kinds of hearing data are actually consistent with the notion that mapping from frequency to place is dynamic. The potential mechanism responsible follows the suggestion by Henson that the type IV fibrocytes of the spiral ligament actively tension the radial fibres of the basilar membrane. There is substantial recent literature to support this view and the relevance to this presentation is these cells appear to be the direct targets of noise-fatigue. Taken together we have the key ingredients to explain the so-called "half-octave shift", a key indicator of fatigue. We will present new evidence that we can quantify this behaviour readily in humans during the usual click-evoked OAE test. Thus the model accounts for variability in pure tone thresholds, and may provide a direct measure of susceptibility to fatigue given directly by the OAE test. We outline several other consequences from this model such as a new distinction possible between place pitch and periodicity pitch. Since the music is strongly carried by the timing of neural responses, music-goers can be oblivious to the onslaught of cochlear damage which will eventually affect speech perception and ruin their thriving social lives. A clear message of this presentation is that it is not true that there is no human cost for unjustified or extreme amplification. The OAE technology gives us the capability, not just to track the growth of hidden cochlear damage, but also the mechanical operation of the fibrocytes through a process which is outlined. We should be using, in moderation, the OAE technology for personal dosimetry in respect of MIHL.
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