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1 d by normal auditory brainstem responses and distortion product otoacoustic emissions.
4 as assessed by auditory brainstem response, distortion product otoacoustic emission and cochlear mic
6 onth, by 4 months, mutants show only minimal distortion product otoacoustic emissions and 70-80 dB th
7 cell and neuronal function was assessed via distortion product otoacoustic emissions and auditory br
10 y the absence of middle ear muscle reflexes, distortion product otoacoustic emissions and cochlear mi
11 cell numbers and efferent function measures (distortion product otoacoustic emissions and contralater
12 ve I/Wave V ratios in the presence of normal distortion product otoacoustic emissions and normal audi
13 urements of cochlear microphonic potentials, distortion product otoacoustic emissions, and basilar me
14 Although brain-stem evoked responses and distortion product otoacoustic emissions are, for most f
15 reening included otoscopy, tympanometry, and distortion product otoacoustic emissions as near the tim
16 eflex metric was the amount of change in the distortion product otoacoustic emission (at 2f(1)-f(2))
17 es: (a) electrophysiological tests including distortion product otoacoustic emissions, auditory brain
18 icantly greater noise-induced suppression of distortion product otoacoustic emissions derived from ou
19 stimuli that can be functionally assessed by distortion product otoacoustic emission (DPOAE) analysis
21 a similar tonotopically tuned effect on the distortion product otoacoustic emission (DPOAE) and the
25 ction was measured with the cubic 2f(1)-f(2) distortion product otoacoustic emissions (DPOAE) at the
27 ing the auditory brainstem response (ABR) or distortion product otoacoustic emissions (DPOAE) or is b
28 nts of auditory brainstem response (ABR) and distortion product otoacoustic emissions (DPOAE) to asse
29 ry brainstem response -- ABR thresholds, and distortion-product otoacoustic emission -- DPOAE magnitu
30 easured by contralateral suppression (CS) of distortion product otoacoustic emissions (DPOAEs) in hum
31 re-tone audiometry (0.5 to 8 kHz) and evoked distortion product otoacoustic emissions (DPOAEs) were c
33 in relation to cochlear status, assessed by distortion product otoacoustic emissions (DPOAEs), and t
36 included pure-tone audiometry, tympanometry, distortion-product otoacoustic emissions (DPOAEs), trans
37 r-current-driving-voltage, low-mid-frequency distortion-product-otoacoustic-emissions (DPOAEs), and p
38 hlear responses (compound action potentials, distortion product otoacoustic emissions) during efferen
39 ty of extended high-frequency audiometry and distortion product otoacoustic emissions for ototoxicity
40 through P19, but deafness by P25 and reduced distortion product otoacoustic emissions from P15 onward
41 urements of auditory brainstem responses and distortion product otoacoustic emissions from these mice
42 y-brain stem response thresholds and reduced distortion-product otoacoustic emissions, in the presenc
43 a 10-15 dB shift in auditory threshold, and distortion product otoacoustic emission measurements ind
44 r hair cell (OHC) properties, as measured by distortion product otoacoustic emissions, neither before
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