Andrew Stuart1 & Alyson Butler Lake2
1Department of Communication Sciences & Disorders, East Carolina University, Greenville, NC
2Blue Ridge Ear, Nose, Throat & Plastic Surgery, Lynchburg, VA
Electrocochleography (ECochG) has been employed to assess stimulus-related cochlear potentials and the compound action potential (AP) of the auditory nerve. The cochlear potentials include the cochlear microphonic (CM) and summating potential (SP). ECochG is a clinically useful tool in the diagnosis, assessment, and monitoring of inner ear disease, as well as in diagnosis of eighth nerve disorders. The most common applications for ECochG include diagnosing, assessment, and monitoring of inner ear disorders (e.g., Ménière’s Disease), enhancement of wave I of the auditory brainstem response, and monitoring of auditory nerve function during surgery (Ferraro, 2010). ECochG is also an invaluable diagnostic tool for auditory neuropathy/dys-synchrony with its ability to identify a presynaptic or postsynaptic site of lesion. More recently, there has been an increased interest in the role of ECochG as a means to assess auditory function following noise exposure.
Excessive noise exposure can result in either noise induced temporary threshold shift, noise induced permanent threshold shift, or acoustic trauma. A noise induced temporary threshold shift is characterized by reduced hearing sensitivity, aural fullness, and/or tinnitus. Within a few hours to days, hearing sensitivity typically returns to normal – that is, the ear recovers. The pathophysiology of permanent noise induced hearing loss has been presumed to be damage of outer hair cells and an associated loss of hearing sensitivity (Schmiedt, 1984). Further, auditory neurons subsequently die due to the outer hair cell deterioration (Liberman & Dodds, 1984). However, research over the past decade has challenged such notions (Kujawa & Liberman, 2009). It has been found that cochlear neuronal degeneration may occur during temporary threshold shift. That is, loss of synapses between inner hair cells and auditory neurons is occurring without the loss of outer hair cells. Further, while this cochlear synaptopathy does not affect audiometric thresholds, it may contribute to difficulties in understanding speech in noise.
How does one assess auditory function following noise exposure? Research and clinical protocols have historically relied on behavioral measures of auditory function to evaluate changes in audition. Audiometric threshold measures have been considered the gold standard for assessing hearing loss. However, as noted above, the pure tone audiogram may be insensitive to cochlear insult at noise doses below those inducing permanently elevated thresholds. A complete test battery is necessary, if one is interested in assessing the functional status of different structures in the cochlea and auditory nerve following noise exposure. We recommend the test battery include audiometric threshold measures, otoacoustic emissions (OAEs), and ECochG.
OAEs provide a means of assessing the functional integrity of the cochlea – specifically robust outer hair cell somatic electromotility (Brownell, 1990). The auditory brainstem response can evaluate the AP. However, the ECochG has an added advantage due to its ability to identify “hidden” insult to inner hair cells, outer hair cells, inner hair cell/type I auditory nerve synapse, and spiral ganglion neurons through SP and AP measures. The generators of the CM are attributed to both outer and inner hair cells. However, outer hair cells are believed to contribute the most (Dallos, 1983). The SP generator is recognized to be predominately the inner hair cells and to a lesser degree the outer hair cells (Zheng et al., 1997). The AP is the synchronized type I auditory nerve fiber onset response (Eggermont, 1976).
There is ample evidence that OAEs are useful for assessing cochlear damage due to noise overexposure (e.g., Engdahl & Kemp, 1996; Hooks-Horton et al., 2001; Lapsley Miller et al., 2006; Marshall & Heller, 1998; Shupak et al., 2007; Vinck et al., 1999). There is also emerging evidence of changes in ECochG measures following noise exposure (e.g., Kim et al., 2005; Liberman et al., 2016; Nam & Won, 2004; Prendergast et al., 2017, 2018). We recently examined the effect of short-term noise exposure in young adults (Lake & Stuart, in press) using a test battery including audiometric threshold measures, OAEs, and ECochG.
Specifically, we examined audiometric thresholds, distortion product otoacoustic emissions (DPOAEs), and ECochG indices in 32 adult females and males. The participants were exposed to a 2000 Hz narrowband noise presented at 105 dBA for ten minutes. We examined pre-exposure and post-exposure measures for noise-induced changes. Audiometric thresholds were tested at 2000, 3000, 4000, and 6000 Hz. DPOAEs were obtained at five L1, L2 levels (i.e., 65, 65 dB SPL; 60, 52.5 dB SPL; 55, 40 dB SPL; 50, 27.5 dB SPL; and 45, 15 dB SPL). Recordings were obtained at four f2 frequencies (i.e., 2051 Hz, 2783 Hz, 3760 Hz, and 4980 Hz). ECochG responses were evoked with 90 dB nHL 100 μs click stimuli. We examined five ECochG indices: SP amplitude, AP latency, AP amplitude, SP/AP amplitude ratio, and SP/AP area ratio.
Following noise exposure, we observed significant changes in auditory thresholds (i.e., thresholds were poorer) and the changes were more pronounced in left ears. Larger auditory threshold differences were also observed in the mid-frequencies (i.e., greater changes at 3000 and 4000 Hz vs. 2000 and 6000 Hz). DPOAE absolute amplitudes decreased following noise exposure. The DPOAE absolute amplitude differences were more pronounced with decreasing L1, L2 level. DPOAE absolute amplitude differences also significantly increased with increasing f2 frequencies. The female group generally had larger DPOAE absolute amplitude decreases when compared to the male group. We also found changes in ECochG indices following noise exposure. Summating potential amplitudes were significantly larger following noise exposure and the effect was more pronounced for female left ears. In addition, left ear SP/AP amplitude ratios and SP/AP area ratios were increased following noise exposure. Approximately 70% of our study participants returned for post-auditory threshold measures 48 hours following noise exposure. We confirmed that there were no significant differences between the original audiometric thresholds and the 48-hour retest thresholds.
We found that utilizing a test battery to examine the effects of short-term noise exposure can reveal the functional status of different structures in the cochlea. Considering the generators of the recorded responses, we inferred that the changes in audiometric thresholds reflect cochlear insult following short-term noise exposure in our study participants. With a decrease in DPOAE amplitude, we also inferred outer hair cell dysfunction. Changes in SP amplitudes, SP/AP amplitude ratios, and SP/AP area ratios would imply insult to inner hair cells due to the absence of significant changes in AP latency, as well as amplitude following the short-term noise exposure. Since audiometric thresholds return to pre-exposure levels, we presumed that outer hair cell function returned. Cochlear synaptopathy, however, may persist.
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