Cochlear Neural Loss in Noise and Aging

Noise exposure and aging are two common causes of hearing loss in humans. Historically, our focus has been on hair cell damage and the threshold elevations this causes. However, we now know that, for both noise and aging, inner hair cell synapses with cochlear neurons are primary targets. Well before threshold elevations and hair cell damage compromise function by reducing the audibility of sound signals, synapse loss compromises function by interrupting sensory-neural communication. In unexposed ears, this loss is gradual, reaching ~50% in advanced age. After noise, it is sudden; up to 50% of synapses can be lost within minutes, including many producing only temporary threshold shifts. Cochlear ganglion cell loss follows and parallels the synaptic loss in magnitude and cochlear location. Thresholds are quite insensitive to these losses, because only cochlear neurons with high thresholds are affected. Thus, the neuropathy has remained hidden. In humans, there is a steady age-related decline in cochlear ganglion cell counts, even when a full complement of hair cells remains. Further study will determine whether differences in synaptic and neural losses contribute to the variability in performance outcomes that have been documented for individuals with normal thresholds as well as those hearing with the aid of a cochlear implant.
Research supported by the NIH/NIDCD.