These include acoustic trauma, ototocity, idiopathic sudden SNHL, post-meningitis SNHL, autoimmune SNHL, Mnire's disease, and retrocochlear hearing loss from acoustic neuroma or demyelination. Though not the most common causes of SNHL, these conditions are disproportionately important because of the unique opportunities they provide to study basic physiologic mechanisms. The mechanisms and systems whose disruption might account for reversible pathology in SNHL include hair cell micromechanics, cochlear ion and fluid homeostasis, neurotransmitters and receptors, and auditory neuronal conduction. This first of five talks on various clinical and basic science issues related to reversible SNHL will describe illustrative clinical cases and introduce some of the interesting questions confronting otolaryngologists and basic scientists.
Hair cells are sensitive mechanical-stimulus detectors.
By consequence of their ability to respond to vanishingly small stimulus energies, hair cells are also vulnerable to much larger stimuli, which can induce reversible or irreversible hair-cell damage. This talk will review present biophysical, anatomical, and molecular understanding of the hair cell's transduction apparatus, focusing on those components that might be particularly vulnerable to reversible or irreversible damage. Particular focus will be placed on sensitive mechanical elements of the bundle, including its stereociliary actin filaments and the interstereociliary crosslinks like tip links. The apparent fragility of hair-cell transduction suggests that it may have developed unique methods for repair of damage to allow restoration of sensitive transduction. The molecular bases of immune mediated hearing loss and of recovery of hearing following steroid treatment are not well understood.