[Central and peripheral aspects of noise-induced hearing loss]

Noise is an important socioeconomic problem in industrialized countries. Development of efficient treatment options for the audiological phenomena resulting from noise-induced hearing loss requires in-depth understanding of the underlying damage mechanisms causing peripheral and central nervous changes. Mechanical damage, ischemia and excitotoxicity are mainly responsible for noise-induced cell death and biophysical changes in the cochlea. Auditory synaptopathy is an additional consequence. Besides these cochlear pathologies, noise exposure leads to extensive changes within the central auditory pathway. Overstimulation causes early cell loss in the ventral cochlear nucleus just after noise exposure, which is in accordance with enhancement of apoptotic mechanisms within the corresponding timeframe. In contrast to the cell loss in lower auditory structures due to overstimulation, the later significant reduction of cell density in higher auditory structures is due to sensory deprivation. Changes in network homeostasis seem to partially compensate structural losses by modulation of spontaneous activity. However, central nervous processing of auditory information is permanently impaired by the neuroplastic changes. Unfortunately, the various noise-induced peripheral and central pathologies are difficult to treat. New therapeutic approaches are required, particularly for treatment of central nervous processing disorders and auditory synaptopathy, which contribute to audiological phenomena such as tinnitus, hyperacusis and poor speech perception in noise.