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The fine structures of 2f1-f2 acoustic distortion products (ADP) were measured in four groups of human subjects: (1) young with normal hearing, (2) aged with normal or near-normal hearing, (3) aged subjects with more severe hearing loss above 2000 Hz, and (4) young with hearing similar to those of the normal- or near-normal-hearing aged group. The purpose of this study was to investigate how ADP fine structure changes with age and hearing loss. Results show that the fine structure is observable whenever the ADP is measurable, and its sharpness, defined as the peak-to-peak frequency distance, is independent of age hearing loss, and longitudinal amplitude change. There is a large variance in ADP peak amplitudes in aged subjects with or without hearing loss as compared to young normal hearing subjects, the aged group generally having lower peak amplitudes than those of the young group. According to an ANOVA analysis with absolute threshold as covariate, the null hypothesis stating that there is no aging effect on the ADP peak responses cannot be ruled out, a conclusion similar to that made by Stover and Norton [J. Acoust. Soc. Am. 94, 2670-2681 (1993)]. On the other hand, threshold changes cannot explain all the differences in ADP amplitude. It is clear that the relationship between ADP amplitudes and behavioral thresholds can differ between young and aged populations. At primary levels of 50 dB SPL, almost normal ADP magnitudes are often found in aged subjects even when associated with a 35-dB hearing loss, whereas for young subjects ADPs typically were not measurable when associated with the pure-tone thresholds of 20 dB HL or higher. This dichotomy may be explained by the different etiologies of cochlear pathologies predominant in the two groups.

The fine structure of the 2f1-f2 acoustic distortion product (ADP) as a function of frequency has been measured in human subjects and shows a series of sharp peaks and valleys (rippling) with peak-to-valley level differences of up to 15-20 dB. In order to delineate the cause of the ADP rippling pattern, a computer model was developed to simulate the behavior of the ADP, specifically the ADP fine structure. The ADP model includes the middle ear and cochlea. The middle ear was treated as a simple signal delivery system in both the forward and reverse directions. The ADP was assumed to be generated within the cochlea by nonlinear elements taken to be the outer hair cells (OHCs), and an array of ADP generators was used to simulate the OHCs along the basilar membrane (BM). The magnitude and phase of the output of each of the ADP generators were functions of the local responses of the two primary traveling waves. The traveling waves were calculated from a passive transmission line model of the BM using the WKB approximation, coupled to a second-order resonance to mimic the contribution from active OHC feedback. The system output of ADP in dB was proportional to the weighted vectorial sum of all the components, arriving at the stapes. Parameters such as lateral coupling and feedback gain were examined.