Daniel B. Polley1,2 
Eaton-Peabody Laboratories, Mass. Eye and Ear, Boston, USA
2Department of Otolaryngology, Harvard Medical School, Boston, USA

Hearing disorders are typically studied and treated from the perspective of wanting to make inaudible sounds audible. Yet three of the most common and debilitating adult hearing complaints reflect just the opposite problem: not what persons cannot hear, but what they cannot stop hearing. Older adults or persons with a history of noise exposure often struggle to suppress the awareness of background noise sources when listening to a target speaker, they are often assaulted by the irrepressible perception of phantom sounds (tinnitus), and they can experience moderate intensity sounds as loud, distressing, or even painful (hyperacusis). Although age, noise exposure, and hearing status are risk factors for these perceptual disorders, their connection is indirect at best, prompting much speculation about the intervening neural processes that may be more closely related. Work from our lab and others shows that an underlying root cause for each of these disorders may be found in a dialog gone wrong between cochlear primary afferent neurons and neurons in sound processing centers of the brain. Our work in animal models has shown that cochlear neural degeneration (CND) triggers a compensatory plasticity at higher stages of the central auditory pathway that often over-shoots the mark, rendering neurons hyperactive, hypersensitive, hyper-synchronized, and internally ‘noisy’. Using in situ mRNA profiling, optogenetics, single unit electrophysiology, and calcium imaging in behaving animals, I will show how CND triggers excess central gain in the auditory cortex and how this central pathophysiology directly underlies poor hearing in noise. I will also describe our ongoing efforts to develop physiological biomarkers for these maladaptive central plasticity processes in human subjects and well as interventions that improve multi-talker speech intelligibility in older adults with sensorineural hearing loss by targeting noisy processing in the brain rather than focusing on the signal transmitted from the ear.  

Acknowledgements: The National Institute on Deafness and Other Communication Disorders grants R01-DC009836 and P50-DC015857