This third lecture focused on the vulnerability of the auditory system to noise, including the mechanisms involved in this vulnerability, and the therapeutic avenues envisaged for the treatment of associated hearing loss. At present, there is no curative therapy for these conditions: only hearing aids, conventional or cochlear implants, can be proposed. It is on the basis of an in-depth understanding of the mechanisms underlying the auditory system's vulnerability to noise that new and promising therapeutic avenues are opening up. The convergence of a number of factors has propelled research in this field to the forefront in recent years:
- awareness of the growing threat posed to the auditory system by overexposure to noise ;
- the discovery that some of the corresponding hearing damage in humans goes unnoticed: it escapes the standard audiological examination, the audiogram;
- the ability to decipher and treat the mechanisms involved.
Added to these factors is the fact that presbycusis, age-related sensorineural hearing loss, has both a hereditary and an environmental component. The latter, for the most part, is linked to overexposure to noise. Around 30% of the population over the age of 55 suffers from presbycusis, which impedes conversational exchanges. The impact of noise on hearing health is therefore a major problem, the consequences of which are becoming increasingly clear.
We began with a brief overview of the evolution of the world of noise. We then reviewed the cellular targets of damage associated with noise overexposure. These targets are located in the peripheral auditory system, both in the cochlea and in its innervation by the auditory neurons that form the spiral ganglion. Damage varies with the acoustic energy of exposure, i.e. sound intensity multiplied by exposure time. Damage occurring at the peripheral level induces disturbances in the central auditory system, at both cortical and subcortical levels.
We then turned our attention to damage to the peripheral auditory system and its mechanisms. This point had already been considered in a previous lecture, which dealt with all the agents that attack the auditory system. At that time, we presented a set of classic data, highlighting the essential role played by mechanisms linked to the production of reactive oxygen species and their deleterious effects. We have now turned our attention to a specific form of damage, cochlear synaptopathy, which is currently attracting attention because it is not subject to pure tone audiometry (the standard audiometric test) and could benefit from therapeutic advances in the future. We mentioned, but only briefly, the involvement of inflammatory mediators in the pathogenesis of cochlear damage. We then discussed in greater detail the proliferation of peroxisomes, as agents of defense against the oxidative stress caused by noise overexposure. We then illustrated, through a recent study by Charles Liberman's group, how the recovery of certain parameters such as auditory thresholds develops, following severe damage to cochlear neurons, thanks to the plasticity of the auditory system. This plasticity, which acts mainly at cortical and subcortical levels, operates on certain acoustic features of sounds, but not on others. In particular, it has little or no effect on the temporal parameters of sound detection, which are essential for understanding spoken language. Finally, we discuss the transfer of these advances to the clinic, both diagnostically and therapeutically.
