On the detection of early cochlear damage by otoacoustic emission analysis

Abstract

Theoretical considerations and experimental evidence suggest that otoacoustic emission parameters may be used to reveal early cochlear damage, even before it can be diagnosed by standard audiometric techniques. In this work, the statistical distributions of a set of otoacoustic emission parameters chosen as candidates for the early detection of cochlear damage (global and band reproducibility, response level, signal-to-noise ratio, spectral latency, and long-lasting otoacoustic emission presence) were analyzed in a population of 138 ears. These ears have been divided, according to a standard audiometric test, in three classes: (1) ears of nonexposed bilaterally normal subjects, (2) normal ears of subjects with unilateral noise-induced high-frequency hearing loss, and (3) their hearing impaired ears. For all analyzed parameters, a statistically significant difference was found between classes 1 and 2. This difference largely exceeds the difference observed between classes 2 and 3. This fact suggests that the noise exposure, which was responsible for the unilateral hearing loss, also caused subclinical damage in the contralateral, audiometrically normal, ear. This is a clear indication that otoacoustic emission techniques may be able to early detect subclinical damages.

Metabolic Presbycusis: Differential Changes in Auditory Brainstem and Otoacoustic Emission Responses with Chronic Furosemide Application in the Gerbil

“…Such cases result in the points seen in the region labeled ''pre-clinical acoustic damage'' in Figure 5. As this label suggests, in humans there is a similar relative weakness in emissions observed in ears with apparently normal hearing when there is significant audiometric threshold elevation in the contralateral ear due to presumptive noise damage (Lucertini et al 2002). In contrast, note that the low-EP condition does not result in points in the same region (Figs.…”

“…Potential causes include noise damage (e.g., Rosenhall et al 1990;Lucertini et al 2002) as well as several types of hearing loss associated with aging, known collectively as presbycusis. Sensory presbycusis is ascribed to the primary loss of outer hair cells (OHCs; e.g., Schuknecht 1964), neural presbycusis to the primary loss of eighth nerve fibers (Schuknecht and Gacek 1993;Felder and SchrottFischer 1995), and metabolic or strial presbycusis to the decline of endocochlear potential (EP; Johnsson and Hawkins 1972;Pauler et al 1988;Gates et al 2002).…”

Comparison of cochlear delay estimates using otoacoustic emissions and auditory brainstem responses

“…If present, these may confound estimates of latency for the OAE recordings. Previous studies have investigated the latencies of TEOAEs in the time domain ͑Norton and Neely, 1987;Şerbetçioğlu and Parker, 1999;Kapadia and Lutman, 2000;Hoth and Weber, 2001;Goodman et al, 2004;Thornton et al, 2006͒ and in the time-frequency domain ͑Elberling et Probst et al, 1986;Tognola et al, 1997;Lucertini et al, 2002;Sisto and Moleti, 2002;Jedrzejczak et al, 2005͒. Unlike clicks which are broadband stimuli, TBs offer the advantage of being limited in frequency and can therefore be used to investigate limited regions of the cochlea.…”

Cochlear Function in Adults with Epilepsy and Treated with Carbamazepine

“…OAE analysis has proven to be more sensitive in detecting subclinical hearing impairment than PTA. OAE analysis is used to differentiate sensory neural types of hearing losses and permits the sensitive assessment of the dynamic function of the cochlea [Kemp, 1987;Probst and Harris, 1993;Lucertini et al, 2002]. The OAE amplitude indicates the summed potential activities of the OHCs of the organ of Corti.…”