A new method for direct pure-tone threshold estimation from input/output functions of distortion product otoacoustic emissions (DPOAEs) in humans is presented. Previous methods use statistical models relating DPOAE level to hearing threshold including additional parameters e.g., age or slope of DPOAE I/O-function. Here we derive a DPOAE threshold from extrapolated DPOAE I/O-functions directly. Cubic 2 f1-f2 distortion products and pure-tone threshold at f2 were measured at 51 frequencies between f2=500 Hz and 8 kHz at up to ten primary tone levels between L2=65 and 20 dB SPL in 30 normally hearing and 119 sensorineural hearing loss ears. Using an optimized primary tone level setting (L1 = 0.4L2 + 39 dB) that accounts for the nonlinear interaction of the two primaries at the DPOAE generation site at f2, the pressure of the 2 f1-f2 distortion product pDP is a linear function of the primary tone level L2. Linear regression yields correlation coefficients higher than 0.8 in the majority of the DPOAE I/O-functions. The linear behavior is sufficiently fulfilled for all frequencies in normal and impaired hearing. This suggests that the observed linear functional dependency is quite general. Extrapolating towards pDP=0 yields the DPOAE threshold for L2. There is a significant correlation between DPOAE threshold and pure-tone threshold (r=0.65, p<0.001). Thus, the DPOAEs that reflect the functioning of an essential element of peripheral sound processing enable a reliable estimation of cochlear hearing threshold up to hearing losses of 50 dBHL without any statistical data.
Otoacoustic emission (OAE) tests of the medial-olivocochlear reflex (MOCR) in humans were assessed for viability as clinical assays. Two reflection-source OAEs [TEOAEs: transient-evoked otoacoustic emissions evoked by a 47 dB sound pressure level (SPL) chirp; and discrete-tone SFOAEs: stimulus-frequency otoacoustic emissions evoked by 40 dB SPL tones, and assessed with a 60 dB SPL suppressor] were compared in 27 normal-hearing adults. The MOCR elicitor was a 60 dB SPL contralateral broadband noise. An estimate of MOCR strength, MOCR%, was defined as the vector difference between OAEs measured with and without the elicitor, normalized by OAE magnitude (without elicitor). An MOCR was reliably detected in most ears. Within subjects, MOCR strength was correlated across frequency bands and across OAE type. The ratio of across-subject variability to within-subject variability ranged from 2 to 15, with wideband TEOAEs and averaged SFOAEs giving the highest ratios. MOCR strength in individual ears was reliably classified into low, normal, and high groups. SFOAEs using 1.5 to 2 kHz tones and TEOAEs in the 0.5 to 2.5 kHz band gave the best statistical results. TEOAEs had more clinical advantages. Both assays could be made faster for clinical applications, such as screening for individual susceptibility to acoustic trauma in a hearing-conservation program. [http://dx
A 22-year-old woman consumed approximately 10 g of salicylate with suicidal intent. She had a severe hearing loss and a strong tinnitus within 22 h of the overdose, and then 24 h later a subsequent hearing restoration and tinnitus abolishment. Transiently evoked otoacoustic emissions ͑TEOAEs͒ and 2 f 1Ϫ f 2 distortion product otoacoustic emissions ͑DPOAEs͒ were measured in both states. In the state of intoxication DPOAEs could be recorded well in the frequency range that corresponded to the appearance of the tinnitus despite the 50-dB hearing loss. The corresponding DPOAE I/O-functions were linearized, indicating loss of outer hair cell compression. After recovery, DPOAE level and DPOAE growth were within the normal range and showed normal physiological compression. The TEOAEs were missing in the acute state of intoxication. This case supports the hypothesis that aspirin-induced tinnitus is generated at the outer hair cell level. Whereas TEOAEs only give evidence that something might have changed in the cochlea, DPOAEs are a more useful and robust quantitative indicator of the underlying mechanism of some forms of cochlear tinnitus.A young female ͑22 years͒ who had just overdosed on salicylates was brought to our attention. She had a severe high-frequency hearing loss associated with a strong tinnitus in both ears. The patient reported that she swallowed all capsules in an aspirin box with suicidal intent. She was unable to give precise information on the dose or how many capsules she swallowed. On the assumption that she swallowed the content of a standard package of aspirin containing, 1000-mg capsules, a dose of 10 g can be estimated. Her approximate height was 165 cm, her weight 60 kg. The patient reported that she did not take additional drugs. Because aspirin-induced tinnitus is known to be reversible ͑Myers and Bernstein, 1965; McFadden and Pattsmier, 1984;Long and Tubis, 1988;Wier et al., 1988;Stypulkowski, 1990͒, the patient was not referred for any medical treatment.The clinical audiogram, measured 22 h after swallowing the aspirin capsules, revealed a sensorineural hearing loss with a 50-dB notch at 6 kHz in both ears, and the patient reported hearing a high-frequency hissing noise in both ears. She estimated the loudness of the tinnitus to be somewhat above the audiometric threshold in the high-frequency region. Forty-six hours after swallowing the aspirin capsules hearing sensitivity had been completely restored and the tinnitus had disappeared ͑see audiograms for the right ear in Fig. 1͒.Distortion product otoacoustic emissions ͑DPOAEs͒ and transiently evoked otoacoustic emissions ͑TEOAEs͒ were measured in the state of aspirin intoxication and after recovery in both ears immediately after audiogram recording.The DPOAEs were measured between f 2 ϭ488 and 8008 Hz ͑Cubedis/ER10-C instrumentation, Mimosa Acoustics/Ethymotic Research, USA͒ using a special primary tone level setting ͑L 1 ϭ0.4L 2 ϩ38 with 20ϽL 2 Ͻ65 dB SPL and f 2 / f 1 ϭ1.2, see Kummer et al., 1998͒ that accounts for the nonlinear basilar...
Outer hair cells (OHC) are thought to act like piezoelectric transducers that amplify low sounds and hence enable the ear's exquisite sensitivity. Distortion product otoacoustic emissions (DPOAE) reflect OHC function. The present study investigated potential effects of electromagnetic fields (EMF) of GSM (Global System for Mobile Communication) cellular phones on OHCs by means of DPOAEs. DPOAE measurements were performed during exposure, i.e., between consecutive GSM signal pulses, and during sham exposure (no EMF) in 28 normally hearing subjects at tone frequencies around 4 kHz. For a reliable DPOAE measurement, a 900-MHz GSM-like signal was used where transmission pause was increased from 4.034 ms (GSM standard) to 24.204 ms. Peak transmitter power was set to 20 W, corresponding to a specific absorption rate (SAR) of 0.1 W/kg. No significant change in the DPOAE level in response to the EMF exposure was found. However, when undesired side effects on DPOAEs were compensated, in some subjects an extremely small EMF-exposure-correlated change in the DPOAE level (< 1 dB) was observed. In view of the very large dynamic range of hearing in humans (120 dB), it is suggested that this observation is physiologically irrelevant.
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