Managing Emotions at Work: A TCCM Systematic Literature Review of Empirical Emotional Labour Research.

While remarkably robust, cochlear physiology is susceptible to a spectrum of degradation from natural phenomena like aging and noise exposure. Both presbycusis and hearing loss secondary to noise exposure are classically attributed to the loss of or damage to outer hair cells (OHC) in the Organ of Corti. However, relatively recent work in human temporal bones () and in mice () suggests that aging can also lead to cochlear synaptopathy (CS) - a decoupling of Type I auditory nerve fibers from their conjoining inner hair cell (IHC) synapses - which is accelerated by the addition of acoustic overexposure (; ). CS has been highlighted as a significant, or even dominant, effect of moderate noise exposures that does not cause permanent elevations in auditory threshold—perhaps explaining the numerous cases of auditory perceptual deficits that remain idiopathic despite standard clinical workup (). It is unlikely that CS always occurs purely in isolation, however. Indeed, several animal models indicate CS can occur with concomitant outer hair cell (OHC) damage after noise exposure (; ; ). Therefore, isolating the effects of synaptopathy from OHC dysfunction, with the goal of a sensitive and specific diagnostic test, has recently become the focus of laboratory research studies (; ). However, IHC stereocilia damage has also been observed in animal studies of noise-induced hearing loss with at least equal degree and cochlear extent of stereocilia damage to OHCs (see for summary analysis of Liberman and Dodds’ 1984 stereocilia damage data); however, IHC dysfunction has not been considered as a potential additional confound to CS assays. Without a specific assay of CS, the perceptual consequences of CS remain unclear. Leading hypotheses suggest that a primary sequela of CS is a disruption in the ability to understand speech in noise (). This is partially supported by studies demonstrating correlations between speech in noise scores and measures thought to be indicative of CS; for example, ABR Wave I amplitude (; ) or subcortical envelope coding (; ). Some studies report a lack of association between speech in noise scores and amplitudes of electrophysiological responses (; ; ; ). Without a means of assessing cochlear micropathology , it remains quite unclear how specific and sensitive current assays of synaptopathy are in humans, and it is possible that these paradigms are not optimal (; ). The impediment to measuring the consequences of synaptopathy in humans has been primarily due to using assays that do not contain specific measures of synapse function alone. Rather, the interpretations of these assays are susceptible to confounding effects from IHC, OHC, and spiral ganglion damage, which are difficult to assess without histology. This lack of specificity limits their clinical and research utility. Importantly, damage to the IHC body and stereocilia could present independent physiological deficits that manifest similarly (and in some ways differently) to the phenotypic presentation of isolated synaptic damage.