TY - JOUR
T1 - Locus of generation for the 2 f1-f2 vs 2 f2-f1 distortion-product otoacoustic emissions in normal-hearing humans revealed by suppression tuning, onset latencies, and amplitude correlations
AU - Martin, Glen K.
AU - Jassir, David
AU - Stagner, Barden B.
AU - Whitehead, Martin L.
AU - Lonsbury-Martin, Brenda L.
N1 - J Acoust Soc Am. 1998 Apr;103(4):1957-71. Comparative Study; Research Support, U.S. Gov't, P.H.S.
PY - 1998/4
Y1 - 1998/4
N2 - The present study used distortion-product otoacoustic emission (DPOAE) suppression tuning curves (STCs), DPOAE onset latencies (OLs), and DPOAE amplitude correlations to investigate the locus of generation of the 2f1- f2 DPOAE versus the 2f2-f1 DPOAE in humans. The results of the tuning study revealed that, for the 2 f1-f2 DPOAE, the tips of the STCs tuned consistently below the geometric-mean (GM) frequency of the primary tones. In contrast, for the 2 f2-f1 DPOAE, STCs tuned above the GM of the primaries, with 50% of the tip frequencies at, or above, the 2 f2-f1 frequency place. When the average ratio of the 2 f2-f1 to the 2 f1 -f2 tip frequencies was computed, a factor of 1.44 provided an estimate of the frequency shift needed to align the two DPOAE generation sites. Other results showed that OLs for the 2 f2-f1 DPOAE were uniformly shorter than those for the 2 f1-f2, with differences at the low frequencies amounting to as much as 6-7 ms. Further, for both DPOAEs, curves describing latency decreases as a function of increasing GM frequencies were best fit by power functions. Shifting the GM frequency producing the 2f2-f1 DPOAE by a factor of 1.6 caused the latency distributions for both DPOAEs to overlap thus resulting in a single function that described cochlear delay as a function of GM frequency. Finally, for each GM frequency in the DP-gram, sliding correlations from 108 normal ears were performed on both DPOAEs by holding the primaries producing the 2f1- f2 DPOAE constant, while all 2f2-f1 DPOAE amplitudes were successively correlated with the 2 f1-f2 amplitudes. This procedure demonstrated that, for a given GM frequency producing the 2 f1-f2, the correlations between the two DPOAEs peaked when the primaries of the 2 f2-f1 were at a GM frequency that positioned the 2 f2-f1 frequency place near the GM of the primaries that produced the 2f1-f2 DPOAE. As a whole, the above findings strongly suggest that the 2 f2-f1 DPOAE in humans is generated basal to the primary-tone place on the basilar membrane.
AB - The present study used distortion-product otoacoustic emission (DPOAE) suppression tuning curves (STCs), DPOAE onset latencies (OLs), and DPOAE amplitude correlations to investigate the locus of generation of the 2f1- f2 DPOAE versus the 2f2-f1 DPOAE in humans. The results of the tuning study revealed that, for the 2 f1-f2 DPOAE, the tips of the STCs tuned consistently below the geometric-mean (GM) frequency of the primary tones. In contrast, for the 2 f2-f1 DPOAE, STCs tuned above the GM of the primaries, with 50% of the tip frequencies at, or above, the 2 f2-f1 frequency place. When the average ratio of the 2 f2-f1 to the 2 f1 -f2 tip frequencies was computed, a factor of 1.44 provided an estimate of the frequency shift needed to align the two DPOAE generation sites. Other results showed that OLs for the 2 f2-f1 DPOAE were uniformly shorter than those for the 2 f1-f2, with differences at the low frequencies amounting to as much as 6-7 ms. Further, for both DPOAEs, curves describing latency decreases as a function of increasing GM frequencies were best fit by power functions. Shifting the GM frequency producing the 2f2-f1 DPOAE by a factor of 1.6 caused the latency distributions for both DPOAEs to overlap thus resulting in a single function that described cochlear delay as a function of GM frequency. Finally, for each GM frequency in the DP-gram, sliding correlations from 108 normal ears were performed on both DPOAEs by holding the primaries producing the 2f1- f2 DPOAE constant, while all 2f2-f1 DPOAE amplitudes were successively correlated with the 2 f1-f2 amplitudes. This procedure demonstrated that, for a given GM frequency producing the 2 f1-f2, the correlations between the two DPOAEs peaked when the primaries of the 2 f2-f1 were at a GM frequency that positioned the 2 f2-f1 frequency place near the GM of the primaries that produced the 2f1-f2 DPOAE. As a whole, the above findings strongly suggest that the 2 f2-f1 DPOAE in humans is generated basal to the primary-tone place on the basilar membrane.
UR - https://www.scopus.com/pages/publications/0031596739
UR - https://www.scopus.com/pages/publications/0031596739#tab=citedBy
U2 - 10.1121/1.421347
DO - 10.1121/1.421347
M3 - Article
C2 - 9566319
SN - 0001-4966
VL - 103
SP - 1957
EP - 1971
JO - Journal of the Acoustical Society of America
JF - Journal of the Acoustical Society of America
IS - 4
ER -