Many of the sophisticated characteristics of human auditory system are attributed to cochlea. Also, most of patients with a hearing loss suffer from impairments that originate from cochlea (sensorineural). Despite this, today's clinical diagnostic methods do not probe the specific origins of such cochlear lesions. The aim of this research is to introduce a physiological signal transmission model to be clinically used as a tool for diagnosis of cochlear losses. This model enables simulation of different bio‐mechano‐electrical processes which occur in the auditory organ of Corti inside the cochlea. What makes this model different from many available computational models is its loyalty to physiology since the ultimate goal is to model each single physiological phenomenon. This includes passive BM vibration, outer hair cells' performances such as nonlinear mechanoelectrical transduction (MET), active amplifications by somatic motor, as well as vibration to neural conversion at the inner hair cells.

The electrical, acoustical, and mechanical elements of the cochlea are explicitly integrated into a transmission-line model to develop a physiological interpretation of the human cochlea insofar. The model enables fundamental simulation of specific cochlear lesions such as metabolic presbyacusis. A sound pressure field in the air is transmitted via the outer and middle ear to the inner ear. It causes the stapes to vibrate resulting in a traveling wave along the organ of Corti propagating from base towards apex. As the endocochlear potential (EP) decreases, the MET produces less receptor current which, eventually leading to a decline in the force/displacement generated by the somatic motor. The CFs of the curves tend to move backwards in a presbyacusis cochlea, this result is consistent with Robles and Ruggem where in a passive cochlea, the CFs are shifted backwards.

In the presented model, electrical, acoustical, and mechanical elements of the cochlea are explicitly integrated into a signal transmission line where these elements convey physiological interpretations of the human cochlear structures. As a result, this physiologically-motivated model enables simulation of specific cochlear lesions such as presbyacusis. The hypothesis is that high-frequency hearing loss in older adults may be due to metabolic presbyacusis whereby age-related cellular/chemical degenerations in the lateral wall of the cochlea cause a reduction in the endocochlear potential. The simulations quantitatively confirm this hypothesis and emphasize that even if the outer and inner hair cells are totally active and intact, metabolic presbyacusis alone can significantly deteriorate the cochlear functionality. Specifically, in the model, as the endocochlear potential decreases, the transduction mechanism produces less receptor current such that there is a reduction in the battery of the somatic motor. This leads to a drastic decrease in cochlear amplification and frequency sensitivity, as well as changes in position-frequency map (tuning pattern) of the cochlea. In addition, the simulations show that the age-related reduction of the endocochlear potential significantly inhibits the firing rate of the auditory nerve which might contribute to the decline of temporal resolution in the aging auditory system.

A physiologically-based electromechanical model of the human cochlea is used in this study to explicitly simulate the effects of acoustical overstimulation, and the associated cellular deficiencies, on the gain of the cochlear amplifier. The simulations demonstrate that as the micromechanics of the stereocillia transduction channels is altered due to the traumatic acoustical overstimulation, the compressive/nonlinear behavior of the cochlear amplifier is significantly modified. When the loudness growth is estimated by the integral of the cochlear amplification with respect to the sound intensity, these modifications lead to an impaired loudness function reminiscent of the recruitment phenomenon. Furthermore, when a severe noise-induced loss of outer hair cells is assumed at basal regions of the cochlea, the model predicts a mild loss at lower frequencies followed by a steeply sloping notch-like amplification loss of approximately 80 dB around 4.5 kHz. This prediction is reasonably in line with the threshold elevations observed clinically from the noise-damaged human ears. Moreover, the results quantitatively demonstrate that the center frequency, the width and the depth of the amplification loss are directly determined by the severity and the location of the outer hair cell loss along the cochlear duct.

Objective: This study includes a battery of psychoacoustical and electrophysiological tests to quantitatively investigate the changes in the frequency and the temporal features of the human auditory periphery caused by aging (presbyacusis) and noise-induced lesions, two common types of sensorineural hearing impairments. The scores are comparatively analyzed.

Design: These clinical experiments have been implemented in MATLAB software.

Study sample: 20 normal hearing adults (aged 30-54), 20 older hearing-impaired subjects (aged 65-70) with no history of Ototoxic medication or noise exposure and 7 adult men with a traceable noise-induced hearing impairment.

Results: The observed temporal and spectral declines are generally consistent with the high-frequency audiometric loss depicted by the audiogram, for each group. Moreover, the test battery provides valuable information on the frequency sensitivity, temporal resolution, loudness growth, compression and otoacoustic emissions.

Conclusion: These scores are compared with the predictions of a physiologicallybased cochlear model to provide evidence about specific inner-ear pathologies, beyond what the audiogram can indicate. Among these 7 clinical experiments, the results from the forward temporal masking test, the categorical loudness discrimination test and the distortion product otoacoustic emission test provide the most differential information about the underlying cellular lesions. The results indicate that the reduction in the temporal resolution is substantially age-relate since the presbyacusis listeners, unlike the other groups, obtained almost no benefit from the temporal cues provided by the gap duration at any of the experiments. Moreover, the results suggest that the DPOAEs reflect the cellular lesions associated with the acoustic overstimulation rather than the age-related strial degenerations.