Basal Cochlear Lesions Result in Increased Amplitude of Otoacoustic Emissions

Abstract

We have measured the changes in transient otoacoustic emissions (TEOAEs) and distortion product otoacoustic emissions (DPOAEs) during and after ototoxic amikacin treatment in an animal (chinchilla) model. TEOAE and DPOAE were recorded from 6 adult chinchillas over a 6-week time course starting just before a 5-day or 7-day treatment period with amikacin sulphate (400 mg/kg/day, i.m.). After final recordings, cochlear morphology was assessed by scanning electron microscopy. Generally, both DPOAE and TEOAE amplitudes change during and after treatment in a systematic fashion. High-frequency components change first, followed by lower-frequency components. We note that there is often a long latency to the onset of changes in otoacoustic emissions (OAE), and that these changes can continue for weeks after treatment. Most importantly we report that when the basal region of the cochlea is damaged in the frequency region above the OAE recording bandwidth (0.6–6 kHz for TEOAE; 1–6.7 kHz for DPOAE), we often find an increase in OAE amplitudes. More specifically, we note that as a cochlear lesion progresses apically, there is often a transient increase in a frequency-specific OAE before it reduces or is lost. Our results suggest that the increase in OAE amplitudes precedes the expression of detectable cochlear pathology.

Meta-Analysis of Distortion Product Otoacoustic Emission Retest Variability for Serial Monitoring of Cochlear Function in Adults

“…In addition, Konrad-Martin et al (2012b) reported that DPOAE enhancements were most common at frequencies below the damaged region identified by pure-tone hearing changes among Veterans exposed to cisplatin. Enhancement below the "audiometric edge" of the presumed damage is consistent with animal models of noise (Harding and Bohne 2004) and ototoxic exposures (Kakigi et al 1998;Mei et al 2009). Researchers have hypothesized that reduced activity of the medial olivocochlear system and/or removal of contributions from additional "basal sources" may play a role in generating enhancements in this context (Kakigi et al;Martin et al 2011).…”

“…Enhancement below the "audiometric edge" of the presumed damage is consistent with animal models of noise (Harding and Bohne 2004) and ototoxic exposures (Kakigi et al 1998;Mei et al 2009). Researchers have hypothesized that reduced activity of the medial olivocochlear system and/or removal of contributions from additional "basal sources" may play a role in generating enhancements in this context (Kakigi et al;Martin et al 2011). In addition, DPOAEs are thought to arise from at least two generator mechanisms, nonlinear distortion and linear reflection, which interact constructively or destructively depending on their phase relationship (Shera & Guinan 1999).…”

Insights into elevated distortion product otoacoustic emissions in sickle cell disease: Comparisons of hydroxyurea-treated and non-treated young children

“…Their most interesting observation was increased OAE amplitudes at frequencies basal to the lesioned frequency areas. Kakigi et al (1998) measured hearing status in chinchillas with DPOAEs and TEOAEs before, during, and after amikacin treatment. Kakigi et al (1998) found that when the basal most hair cells of the cochlea were damaged, OAE amplitudes increased particularly for stimulus frequencies bordering the damaged tonotopic region.…”

“…It is possible that inflammatory process(es) somehow affect the mechanics of the basilar membrane and/or organ of Corti. Kakigi et al (1998) suggested that the site of lesion basal to the area being monitored might be responsible whereby the increased OAE amplitude is a "result of a more effective basal transmission signal across a less active, and therefore less interfering cochlear region" (p. 371). This speculation is not consistent with the significant interaction of frequency by group; namely that both groups of children with SCD showed similar increased DPOAE amplitudes in the lower frequencies (i.e., f 2 < 1546 Hz).…”

“…Their findings were consistent with the notion that increased DPOAE amplitudes could not be attributed to differences in outer/middle ear function as assessed with tympanometry. DPOAE amplitudes have been reported to increase before reduction or loss secondary to localized cochlear lesions in animal studies suggesting that increased DPOAE amplitudes may precede the manifestation of measurable behavioral changes in cochlear pathology (Huang et al, 2005;Kakigi et al, 1998;Raveh et al, 1998). It stands to reason that increased DPOAE amplitude may be related to the inflammatory process of SCD since markers of vascular inflammation have been observed in the cochlea following other cochlear lesions (e.g., Suzuki and Harris, 1995;Zhang et al, 2000) and inflammatory responses can lead to cochlear damage and hearing loss (Ryan et al, 2002).…”