ABSTRACT: Distortion product otoacoustic emissions emitted by the cochlea at 2f1-f2 in response to pairs of pure tones at f1 and f2 (DPOAE) form a class of otoacoustic emissions and as such, are viewed as a reliable tool for screening outer hair cell (OHC) dysfunctions on a pass/fail basis. However, the persistence of residual DPOAEs from impaired cochleae at high stimulus levels has suggested that above 60-70 dB SPL, instead of reflecting "active" cochlear motion, DPOAEs might represent another "passive" modality: they would thus become unsuitable for analyzing cochlear function. The present work reports the consequences on high- vs low-level DPOAEs of three types of cochlear impairments involving OHCs: progressive OHC degeneration of genetic origin in CD1 mice, complete cochlear ischemia in gerbils, and furosemide injection vs ischemia-reperfusion in gerbils. An alternative to the "active-passive" model was used wherein regardless of stimulus level, cubic DPOAEs are produced by N (probably OHC-borne) nonlinear elements driven by input I and modulated by a function F3 of their operating point o; thus, DPOAE proportional to N I³ F₃(o). When OHCs degenerated, thereby implying a decrease of N, DPOAE levels also decreased regardless of the stimulus level up to 80 dB SPL, in line with the previous formula but at variance with the prediction of the active-passive concept. Instead of affecting N, the other two experiments impaired the efficiency of the cochlear feedback loop as a result of its electrical drive being decreased by strial dysfunction. As it is well accepted that the impaired basilar-membrane motion, although greatly reduced at low levels, tends to catch up with a normal one at higher levels, it was assumed the same was true with I so that DPOAE levels had to be, and indeed were little affected at high levels while plummeting at low levels, without any need for invoking two modalities for DPOAE generation. Finally, comparisons of furosemide vs ischemia effects revealed additional influences on DPOAEs, possibly accounted for by function F3(o). These results lead to the proposal that although high-level DPOAEs are expected to be poor audiometric indicators, they seem well adapted to assessing the functional integrity of nonlinear elements in OHCs, i.e., presumably their mechanoelectrical transduction channels.

ABSTRACT: Nobili and colleagues (2003, J. Assoc. Res. Otolaryngol., 4:478­494) propose that transient evoked otoacoustic emissions (TEOAEs) result from spatially complex “residual oscillations” of the basilar membrane that trace their origin to spectral irregularities in the forward middle-ear transfer function. In this paper we comment on Nobili et al.’s model and conclusions while trying to clarify some of the broader issues they raise. Although Nobili et al.’s published OAE simulations are of uncertain reliability, simple arguments that do not depend on solving the model equations establish that their proposed middle-ear filtering mechanism conflicts with basic experimental findings about TEOAEs. Furthermore, the proposed mechanism cannot produce spontaneous (SOAEs) or stimulus-frequency emissions (SFOAEs) at any level of stimulation. Models of TEOAEs, SFOAEs, and SOAEs based on wave reflection due to scattering by impedance perturbations in the mechanics of the cochlear partition suffer none of these deficiencies.

 

ABSTRACT: Distortion product otoacoustic emissions (DPOAE), permanent threshold shifts (PTS) and outer hair cell (OHC) losses were analyzed in a population of 187 noise-exposed chinchillas to determine the predictive accuracy (sensitivity and specificity) of the DPOAE for PTS and OHC loss. Auditory evoked potentials (AEP) recorded from the inferior colliculus of the brainstem were used to estimate hearing thresholds and surface preparation histology was used to determine sensory cell loss. The overlapping cumulative distributions and high variability in emission responses for both PTS and OHC loss made it difficult to predict AEP threshold and OHC loss from DPOAE level measurements alone. Using a strict criterion (i.e. emissions better than the 5th percentile of the preexposure DPOAE level, and PTS< or = 5 dB or OHC loss< or = 5%), it was found that the postexposure DPOAE level could be used with reasonable confidence to determine if the status of peripheral auditory system was either normal (i.e. PTS< or = 5 dB) or abnormal (PTS>30 dB or OHC loss>40%). However, the high variability of individual DPOAE responses resulted in a broad region of 'uncertainty' (i.e. 5<PTS< or = 30 dB and 5%<OHC loss< or = 40%) making it difficult in the chinchilla model to use the postexposure DPOAE level with confidence to predict in individual subjects the amount of PTS or OHC loss. Our results also indicate that significant reductions in the amplitude of the DPOAE are related primarily to a systematic loss of OHCs, and that a postexposure DPOAE level< or = 10 dB SPL, obtained with a low frequency primary level of 65 dB SPL, represents a criterion value which can serve as an indication of significant OHC loss (> or = 50%) or PTS (> or = 35 dB) in noise-exposed chinchillas. Based on an exponential regression analysis of individual subjects, correlations were higher for PTS/DPOAE than for OHC loss/DPOAE.