The use of distortion product otoacoustic emissions in the estimation of hearing and sensory cell loss in noise-damaged cochleas

A synopsis from the article published in Hearing Research 2004 Jan;187 (1-2):12-24

Bob Davis
Auditory Research Laboratory
Plattsburgh State University of New York
107 Beaumont Hall
101 Broad St.
Plattsburgh, New York 12901
TELEPHONE: (518) 564-7700
E-MAIL: Robert.Davis@plattsburgh.edu

I. Introduction

    The distortion product otoacoustic emission (DPOAE), which is a consequence of normal nonlinear processes in the cochlea, has gained popularity as a clinical test for hearing screening and diagnostic purposes. Several studies have evaluated the clinical utility of DPOAE test performance to determine how well DPOAEs identify hearing loss in humans (Gorga et. al 1993; Kimberley et al., 1994; Gorga et al., 1996; Gorga et al., 1997; Attais et al., 2001; Boege and Janssen, 2002; Gorga et al., 2003) and in animal models (Canlon et al., 1993; Hamernik et al., 1996; Hofstetter et al., 1997; Le Calvez et al., 1998; Hamernik et al., 1998; Hamernik et al., 2000; Avan et al., 2001; Mills, 2003). In general, results have shown considerable variability in the distribution of response properties from normal ears as well as in those with damaged cochleas.

Attempts to refine the predictive power of the DPOAE in order to estimate behavioral thresholds in humans have been met with varying degrees of success (Kimberley et al., 1994; Gorga et al., 1996, 1997, 2003; Boege and Janssen, 2002). Overall, these studies utilized the DPOAE (e.g., level, SNR, threshold) to make a dichotomous decision as to whether hearing was normal or impaired. The large variance of DPOAE levels found in human studies, however, did not seem to allow for an accurate prediction of the amount of hearing loss despite good statistical correlations (Gorga et al., 1993; Gorga et al., 1996, 1997; Le Calvez et al., 1998).

Evidence from experiments in animal models on the potential value of DPOAEs as a sensitive indicator of hearing threshold or OHC loss have also been inconclusive. The few studies that have attempted to correlate DPOAEs with histopathology in animals have been conflicting (Brown et al., 1989; Canlon et al., 1993; Subramaniam et al., 1995; Hamernik et al.,1996; Le Calvez et al., 1998; Hamernik and Qiu, 2000; Harding et al., 2002). Several studies for instance have reported generally weak correlations between DPOAE’s and either pure tone thresholds or OHC loss (Canlon et al., 1993; Subramaniam et al., 1994; Emmerich et al., 2000), while good correspondence between DPOAE change and OHC loss has been reported by e.g. Hofstetter et al. (1997) and Hamernik and Qiu (2000). The inconsistent relations between the DPOAE and OHC loss may be attributed, in part, to the inability to easily quantify other morphological changes (e.g. stereocilia defects, altered tip links) over the entire extent of the basilar membrane in large numbers of animals, or to changes in the endocochlear potential which may affect the function of cells that are present. This report presents the results of a population study on the relations among OHC loss, PTS and the DPOAE in an effort to resolve some of the ambiguity that exists in the literature on the use of the DPOAE in: 1) predicting the amount of PTS or OHC loss, 2) defining the specific PTS and OHC loss values which represent clear boundaries for predictive accuracy, and 3) determining the extent of overlap between normal and abnormal response distributions of the DPOAE as a function of the magnitude of PTS and OHC loss. This information may provide insight into the use of the DPOAE as a reliable metric in the assessment of auditory functioning in animals both before and following noise exposure, especially in cases where auditory thresholds or histological information cannot be easily obtained.

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