Latency of auditory brain-stem responses and otoacoustic emissions using tone-burst stimuli

A comparison of the latency of auditory brain-stem responses (ABR) and evoked otoacoustic emissions (EOAE) has led to an interpretation for the travel of transients in the peripheral auditory system that is consistent with both sets of data. The "cochlear echo" theory for the origin of the EOAE indicates that the latency of a particular frequency component back to the ear canal should be twice the forward latency of its characteristic place in the cochlea. The latency of wave V of the ABR to tone-burst stimuli can be described as the sum of two components: (1) a component that varies with intensity and frequency in an orderly and predictable manner and (2) a component that is independent of both intensity and frequency. Because the EOAE data can be predicted by taking twice the value of component (1) of the ABR latency, this component is interpreted to be due to mechanical travel through the cochlea. A consequence of this interpretation is that the remaining neural component of the ABR latency must be relatively independent of frequency and intensity.     

Evidence of upward spread of suppression in DPOAE measurements

Measurements of DPOAE level in the presence of a suppressor were used to describe a pattern that is qualitatively similar to population studies in the auditory nerve and to behavioral studies of upward spread of masking. DPOAEs were measured in the presence of a suppressor (f3) fixed at either 2.1 or 4.2 kHz, and set to each of seven levels (L3) from 20 to 80 dB SPL. In the presence of a fixed f3 and L3 combination, f2 was varied from about 1 oct below to at least 1/2 oct above f3, while L2 was set to each of 6 values (20-70 dB SPL). L1 was set according to the equation L1 = 0.4L2 + 39 [Janssen et al., J. Acoust. Soc. Am. 103, 3418-3430 (1998)]. At each L2, L1 combination, DPOAE level was measured in a control condition in which no suppressor was presented. Data were converted into decrements (the amount of suppression, in dB) by subtracting the DPOAE level in the presence of each suppressor from the DPOAE level in the corresponding control condition. Plots of DPOAE decrements as a function of f2 showed maximum suppression when f2 approximately = f3. As L3 increased, the suppressive effect spread more towards higher f2 frequencies, with less spread towards lower frequencies relative to f3. DPOAE decrement versus L3 functions had steeper slopes when f2 > f3, compared to the slopes when f2 < f3. These data are consistent with other findings that have shown that response growth for a characteristic place (CP) or frequency (CF) depends on the relation between CP or CF and driver frequency, with steeper slopes when driver frequency is less than CF and shallower slopes when driver frequency is greater than CF. For a fixed amount of suppression (3 dB), L3 and L2 varied nearly linearly for conditions in which f3 approximately = f2, but grew more rapidly for conditions in which f3 < f2, reflecting the basal spread of excitation to the suppressor. The present data are similar in form to the results observed in population studies from the auditory nerve of lower animals and in behavioral masking studies in humans.     

Cochlear compression estimates from measurements of distortion-product otoacoustic emissions

Evidence of the compressive growth of basilar-membrane displacement can be seen in distortion-product otoacoustic emission (DPOAE) levels measured as a function of stimulus level. When the levels of the two stimulus tones (f1 and f2) are related by the formula L1 = 39 dB + 0.4 x L2 [Kummer et al., J. Acoust. Soc. Am. 103, 3431-3444 (1998)] the shape of the function relating DPOAE level to L2 is similar (up to an L2 of 70 dB SPL) to the classic Fletcher and Munson [J. Acoust. Soc. Am. 9, 1-10 (1933)] loudness function when plotted on a logarithmic scale. Explicit estimates of compression have been derived based on recent DPOAE measurements from the laboratory. If DPOAE growth rate is defined as the slope of the DPOAE I/O function (in dB/dB), then a cogent definition of compression is the reciprocal of the growth rate. In humans with normal hearing, compression varies from about 1 at threshold to about 4 at 70 dB SPL. With hearing loss, compression is still about 1 at threshold, but grows more slowly above threshold. Median DPOAE I/O data from ears with normal hearing, mild loss, and moderate loss are each well fit by log functions. When the I/O function is logarithmic, then the corresponding compression is a linear function of stimulus level. Evidence of cochlear compression also exists in DPOAE suppression tuning curves, which indicate the level of a third stimulus tone (f3) that reduces DPOAE level by 3 dB. All three stimulus tones generate compressive growth within the cochlea; however, only the relative compression (RC) of the primary and suppressor responses is observable in DPOAE suppression data. An RC value of 1 indicates that the cochlear responses to the primary and suppressor components grow at the same rate. In normal ears, RC rises to 4, when f3 is an octave below f2. The similarities between DPOAE and loudness compression estimates suggest the possibility of predicting loudness growth from DPOAEs; however, intersubject variability makes such predictions difficult at this time.     

Growth of suppression in humans based on distortion-product otoacoustic emission measurements

Distortion-product otoacoustic emissions (DPOAEs) were used to describe suppression growth in normal-hearing humans. Data were collected at eight f(2) frequencies ranging from 0.5 to 8 kHz for L(2) levels ranging from 10 to 60 dB sensation level. For each f(2) and L(2) combination, suppression was measured for nine or eleven suppressor frequencies (f(3)) whose levels varied from -20 to 85 dB sound pressure level (SPL). Suppression grew nearly linearly when f(3) ≈ f(2), grew more rapidly for f(3)?< f(2), and grew more slowly for f(3)?> f(2). These results are consistent with physiological and mechanical data from lower animals, as well as previous DPOAE data from humans, although no previous DPOAE study has described suppression growth for as wide a range of frequencies and levels. These trends were evident for all f(2) and L(2) combinations; however, some exceptions were noted. Specifically, suppression growth rate was less steep as a function of f(3) for f(2) frequencies ≤ 1 kHz. Thus, despite the qualitative similarities across frequency, there were quantitative differences related to f(2), suggesting that there may be subtle differences in suppression for frequencies above 1 kHz compared to frequencies below 1 kHz.     

Reducing reflected contributions to ear-canal distortion product otoacoustic emissions in humans

Distortion product otoacoustic emission (DPOAE) fine structure has been attributed to the interaction of two cochlear-source mechanisms (distortion and reflection sources). A suppressor presented near the 2f1-f2 frequency reduces the reflection-source contribution and, therefore, DPOAE fine structure. Optimal relationships between stimulus and suppressor conditions, however, have not been described. In this study, the relationship between suppressor level (L3) and stimulus level (L2) was evaluated to determine the L3 that was most effective at reducing fine structure. Subjects were initially screened to find individuals who produced DPOAE fine structure. A difference in the prevalence of fine structure in two frequency intervals was observed. At 2 kHz, 11 of 12 subjects exhibited fine structure, as compared to 5 of 22 subjects at 4 kHz. Only subjects demonstrating fine structure participated in subsequent measurements. DPOAE responses were evaluated in 1/3-octave intervals centered at 2 or 4 kHz, with 4 subjects contributing data at each interval. Multiple L3's were evaluated for each L2, which ranged from 20 to 80 dB SPL. The results indicated that one or more L3's at each L2 were roughly equally effective at reducing DPOAE fine structure. However, no single L3 was effective at all L2's in every subject.