Objective: We describe an animal model of auditory neuropathy in which subjects have extensive, scatered inner haircell loss but with a relatively intact outer haircell population.
Design: Such a pattern of cochlear haircell damage can be produced in the chinchilla by treatment with the anticancer agent carboplatin.
Results: In these subjects, otoacoustic emissions (OAEs) and cochlear microphonics remain normal while auditory brain stem evoked potential (ABR) thresholds are significantly elevated. However, in the same subjects, central auditory neurons (in the inferior colliculus) have response thresholds that are considerably lower (by up to 50 dB) than ABR thresholds. These findings parallel the characteristics of auditory neuropathy in humans, in which absent or abnormal ABRs are recorded in patients with only mild to moderate audiometric thresholds and preserved OAEs.
Conclusions: We suggest that scattered inner haircell lesions also can result from long-term cochlear hypoxia, and we propose that this is a likely candidate for the etiology of many types of auditory neuropathy in human subjects.