Histopathology of noise deafness.
The psychophysical effects of sound stimulation at increasing intensity include adaptation, temporary threshold shift, and permanent hearing loss. The mechanisms involved in permanent loss are direct mechanical destruction, following high intensity noise exposure, and metabolic decompensation with subsequent degeneration of sensory elements, following moderate intensity noise exposure. Both these cause their own pattern of cochlear histological abnormality, while the only morphological correlate to temporary threshold shift is an increase in the number and size of liposomes, mainly in the outer hair cells after longer periods of repeated temporary threshold shift. There are critical intensity levels which determine the type and extent of damage, and for any given exposure intensity a saturation of damage is reached over time. There is great variability in acoustic cochlear damage, especially that of the delayed metabolic type, the type which results from conditions which predominate in our actual noise environment.
D000818:Animals; D001305:Auditory Fatigue; D003056:Cochlear Nerve / Q000473:pathology; D006168:Guinea Pigs; D006198:Hair Cells, Auditory / Q000473:pathology; D006199:Hair Cells, Auditory, Inner / Q000473:pathology; D006317:Hearing Loss, Noise-Induced / Q000473:pathology*; D006801:Humans; D009925:Organ of Corti / Q000473:pathology*