While audiometric quantification of hearing loss is useful in many contexts including medical, rehabilitation, and workplace health and safety settings, current research suggests that there are subclinical hearing impairments that are not adequately captured in pure tone audiometric results but that, despite this, still cause functional communication difficulties in day‐to‐day life. For instance, the prevalence rate of hearing difficulties in the absence of recordable audiometric loss has been reported as being around 10% (Tremblay et al., 2015). We have only a nascent understanding of the underlying pathophysiology and perceptual consequences involved in this type of hearing loss, but it is thought to be in some way linked to noise exposure.
3.2.2 Physiological Correlates of Noise‐Induced Hearing Loss
Our understanding of the physiological changes that contribute to noise‐induced hearing loss have recently undergone substantial revision. Previously, exposure to high‐intensity sounds were thought to lead to the mechanical damage of structures in the cochlea, including the sensory stereocilia of the inner hair cells and also to secondary effects that included the mixing of fluid from the normally separate cochlear compartments and alteration of the supporting cells (Slepecky, 1986). Noise‐induced damages to the cochlea have now been attributed not only to direct mechanical stress, but also to secondary metabolic disruption. Direct mechanical stress occurs during noise exposure when acoustic stimuli apply a physical force to the cochlea causing immediate trauma. Metabolic disruption is likewise initiated during noise exposure, but the effects continue to develop for a number of weeks after the cessation of noise exposure.
The damage to the cochlea can be either reversible, when there is only a slight structural insult resulting in a temporary threshold shift, or irreversible if the damage is severe, causing permanent hearing loss. The most important alteration in cochlear morphology after intense noise exposure is the degeneration of hair cells in the organ of Corti. The degeneration usually occurs in clusters and causes hair cell lesions, the site of which is directly related to the intensity and spectral content of the noise. In this tonotopic fashion, high‐frequency noise damages the basal end of the organ of Corti, while low‐frequency noise damages the apical portion. High‐intensity noises have a wider spread of damage, while low‐intensity noises cause more focal lesions. The severity of hair cell impairment is a function of the nature and the conditions of the noise. More severe damage is associated with higher intensity levels, high‐frequency noise, and continuous exposure to noise (Hu, 2012).
One of the most consequential revisions to our understanding of the causes of noise‐induced hearing loss is that the connection between afferent nerve terminals and sensory hair cells is likely to be compromised at a stage that pre‐dates morphological damage to the hair cell (Kujawa & Liberman, 2009). This disconnection between sensory cell and neural relay system selectively affects auditory nerve fibers that transmit supra‐threshold stimuli, that is, those with a low spontaneous firing rate and a high activation threshold. The perceptual consequence of this disconnection is that challenging tasks, like listening in noise, become harder, while auditory thresholds remain unchanged. This, in turn, has prompted a fundamental re‐evaluation of the previously widely held view that only noise exposure resulting in permanent threshold shifts is damaging to hearing (Liberman, 2017).
3.2.3 Hearing Loss and the Individual
In considering hearing loss and the individual, let us turn to one of the greatest individuals, who is arguably also the greatest Romantic composer of all time. Ludwig van Beethoven (1770–1827) was such an individualist that he broke with the tradition of indenture, which was servitude to the aristocracy. In doing so he became the first composer of Western music who was able to make a living essentially as a freelance artist. He was also plagued by hearing loss, with onset at the age of approximately 26, a perilous condition for one whose livelihood revolved around creating music. His 1802 unsent letter to his brother, what has come to be called the Heiligenstadt Testament, offers a unique view into the inner world of one who suffered due to their hearing loss:
Oh I cannot do it; therefore forgive me when you see me draw back when I would have gladly mingled with you. My misfortune is doubly painful to me because I am bound to be misunderstood; for me there can be no relaxation with my fellow men, no refined conversations, no mutual exchange of ideas.
It is evident that at this stage Beethoven has given up on coping strategies and withdrawn into himself. He also admits that his hearing loss encroaches on his ability to participate in community and also to articulate and respond to abstract thought. Or in the terminology of the International Classification of Functioning, Disability and Health Core Sets (World Health Organization [WHO], 2019), Beethoven articulates a disability which is both an activity limitation and a participation restriction. He goes on:
I must live almost alone, like one who has been banished; I can mix with society only as much as true necessity demands. If I approach near to people a hot terror seizes upon me, and I fear being exposed to the danger that my condition might be noticed.
This fear of exposure is the stigma of hearing loss; that more than wrinkles and gray hair (or lack of hair), hearing loss, when disclosed, is an outer signal that the body is aging. This attests to our individual vanity, but also indicates that the stigma of hearing loss penetrates our collective conscious. An example of this can be found in the Nepalese cultural belief that to accept food from a deaf person is to accept bad karma and thus open oneself to spiritual pollution (Hoffmann‐Dilloway, 2016). While of course unfounded, this folklore demonstrates that the stigma of hearing loss encompasses a broader sense than the merely personal. The stigma of hearing loss is the stigma of being identified as a member of the hearing‐impaired other, an association that implies at least a deficiency in communicative ability, and possibly an associated cognitive impairment.
Had Beethoven been alive today, and, of course, depending on the diagnosis and type of his hearing loss, he may have been a candidate for cochlear implantation. CIs may have been helpful for his communication needs, but it is unlikely that he would have been wholly satisfied with his implants due to the poor cuing of pitch that many CI recipients experience.
3.2.4 Hearing Loss and Cochlear Implants
The CI, which as both a neural prosthesis and a device that facilitates communication, has transformed the treatment of hearing loss by offering an alternative to amplification for those with severe and profound hearing loss. A descriptive model of the aural acuity of a typical adult patient has been developed from the analysis of a large multicenter study (n = 2,251) of factors that influence CI candidature (Lazard, Vincent, et al., 2012) (see Figure 3.2). To perform this regression over different languages, speech materials and clinical protocols, postoperative speech scores in quiet were transformed into percentile rankings of patients within each center, and these are the basis for the “auditory performance” axis shown in Figure 3.2. The model shows, among other things, the effect of hearing aid use in the period prior to implantation where the typical candidate has a severe or profound hearing loss. If bilateral hearing aids (HA) are fitted and worn in this period, the expected rate of decline in auditory performance is approximately half that of the rate of decline if HA are not used. This adds important detail