INTENSITY CODING IN ACOUSTIC AND ELECTRIC HEARING

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The long-term objectives of the proposed study are to (1) develop a unified theory of the encoding of sound intensity in normal-hearing, hearing-impaired, and implant listeners, (2) differentiate the functional deficits that hearing-impaired and implant listeners may have due to the delivery of altered peripheral excitation patterns the brain, and (3) design rehabilitative devices that can maximally compensate for the functional deficits in these listeners with hearing impairment. This proposal addresses the dynamic range problem for the encoding of intensity in both acoustic and electric hearing. On one hand, the acoustic dynamic range problem refers to the discrepancy between the large psychophysical loudness range and the limited physiological range demonstrated by the majority of individual auditory neurons. On the other hand, the electric dynamic range problem is a practical and harsh reality facing clinicians in fitting speech processors: implant listeners who have typically 6-20 dB range must accommodate normal speech and environmental sounds containing important information over a 40-60 dB range. The specific aims are to (1) understand the underlying neural mechanisms of encoding the enormous dynamic range in acoustic hearing, (2) quantify loudness growth and discrimination functions in electric hearing, and (3) determine which normal mechanisms are missing in electric hearing and whether it is possible to increase the electric dynamic range by compensating for these missing normal mechanisms. Our hypothesis is that loudness growth and discrimination functions are primarily determined by the peripheral excitation pattern and the central system responds in a similar fashion regardless of the changes in the peripheral inputs. Our experimental design is to measure loudness growth and discrimination functions in conditions that alter the peripheral inputs to the central system. Methods used to alter the peripheral inputs include acoustic high-pass noise, low- and band-pass noise, forward masking, amplitude or phase- modulated stimuli, vestibular-nerve-section, electric stimulation of the auditory nerve and cochlear nucleus. Corresponding physiological mechanisms to be examined are: spread of excitation along the basilar membrane, suppressive and excitatory masking, adaptation and low- spontaneous rate auditory neurons, synchronization of neural firing, contributions of efferent neurons, nonlinear vibration of the basilar membrane and its associated phenomena (e.g. lateral suppression). A unique feature of this proposal is that it uses cochlear implant, auditory brainstem implant, and vestibular neurectomy patients to better understand the neural mechanisms of encoding the large dynamic range of sound intensity. The results obtained from this proposal could lead to better designs of auditory prostheses and hearing aids that will compensate for the reduced dynamic range that occurs with both electric stimulation of the auditory system and hearing loss.