Mechanically-Induced Morphological Changes in the Organ of Corti

Acute exposures to high-level noise impulses damage the cochlea via mechanical mechanisms that are associated with excessive displacements and stresses developed in the delicate epithelial tissues of the organ of Corti. Such damage has been discussed in the literaure a number of times, and an especially clear description was provided by Davis [1]. Davis and his colleagues used continuous noise at levels of nearly 150 dB SPL at the eardrum. They noted that the Hensen cell attachments represent a mechanically weak link in the structural organization of the organ of Corti. This result was confirmed by Beagley [2], who illustrated the separation of cell junctions between the Deiter and Hensen cells following overstimulation. Since then, others (notably Spoendlin [3] and Voldrich [4]), also using high levels of continuous noise, have demonstrated lesions on the basilar membrane of an equivocal mechanical origin, including rupture of the basilar membrane and Reissners membrane. Spoendlin suggested intensities of around 125 dB SPL as the threshold for mechanically-induced lesions as opposed to metabolically-induced damage. However, the dependance of this rms sound pressure on the exposure duration is not clear. Spoendlin is in agreement with Davis and Beagley concerning the susceptibility to acoustic trauma of the Hensen cell attachments, but he further implicates the pillar cells and the medial attachments of the inner hair cell cuticular area as, “weak spots.” This paper attempts to provide a clear documentation of the morphological sequence of events which is eventually responsible for producing massive structural damage to the organ of Corti. Using blast waves as a vehicle, we will further attempt to qualitatively illustrate a fundamental difference in the way in which continuous and impulse noise may need to be evaluated when assessing the potential for producing trauma.