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Physiology of the cochlea and auditory nerve can be assessed with electrocochleography (ECochG), a technique that involves measuring auditory evoked potentials from an electrode placed near or within the cochlea. Research, clinical, and operating room applications of ECochG have in part centered on measuring the auditory nerve compound action potential (AP) amplitude, the summating potential (SP) amplitude, and the ratio of the two (SP/AP). Despite the common use of ECochG, the variability of repeated amplitude measurements for individuals and groups is not well understood. We analyzed ECochG measurements made with a tympanic membrane electrode in a group of younger normal-hearing participants to characterize the within-participant and group-level variability for the AP amplitude, SP amplitude, and SP/AP amplitude ratio. Results show that the measurements have substantial variability and that, especially with smaller sample sizes, significant reduction in variability can be obtained by averaging measurements across repeated electrode placements within subjects. Using a Bayesian-based model of the data, we generated simulated data to predict minimum detectable differences in AP and SP amplitudes for experiments with a given number of participants and repeated measurements. Our findings provide evidence-based recommendations for the design and sample size determination of future experiments using ECochG amplitude measurements, and the evaluation of previous publications in terms of sensitivity to detecting experimental effects on ECochG amplitude measurements. Accounting for the variability of ECochG measurements should result in more consistent results in the clinical and basic assessments of hearing and hearing loss, either hidden or overt.

Electrocochleography (ECochG) has been used to assess Ménière's disease, a pathology associated with endolymphatic hydrops and low-frequency sensorineural hearing loss. However, the current ECochG techniques are limited for use at high-frequencies only (≥1 kHz) and cannot be used to assess and understand the low-frequency sensorineural hearing loss in ears with Ménière's disease. In the current study, we use a relatively new ECochG technique to make measurements that originate from afferent auditory nerve fibers in the apical half of the cochlear spiral to assess effects of endolymphatic hydrops in guinea pig ears. These measurements are made from the Auditory Nerve Overlapped Waveform (ANOW). Hydrops was induced with artificial endolymph injections, iontophoretically applied Ca to endolymph, and exposure to 200 Hz tones. The manipulations used in this study were far smaller than those used in previous investigations on hydrops. In response to all hydropic manipulations, ANOW amplitude to moderate level stimuli was markedly reduced but conventional ECochG measurements of compound action potential thresholds were unaffected (i.e., a less than 2 dB threshold shift). Given the origin of the ANOW, changes in ANOW amplitude likely reflect acute volume disturbances accumulate in the distensible cochlear apex. These results suggest that the ANOW could be used to advance our ability to identify initial stages of dysfunction in ears with Ménière's disease before the pathology progresses to an extent that can be detected with conventional measures.

Electrocochleography (ECochG) to high repetition rate tone bursts may have advantages over ECochG to clicks with standard slow rates. Tone burst stimuli presented at a high repetition rate may enhance summating potential (SP) measurements by reducing neural contributions resulting from neural adaptation to high stimulus repetition rates. To allow for the analysis of the complex ECochG responses to high rates, we deconvolved responses using the Continuous Loop Averaging Deconvolution (CLAD) technique. We examined the effect of high stimulus repetition rate and stimulus duration on SP amplitude measurements made with extratympanic ECochG to tone bursts in 20 adult females with normal hearing. We used 500 and 2,000 Hz tone bursts of various stimulus durations (12, 6, 3 ms) and repetition rates (five rates ranging from 7.1 to 234.38/s). A within-subject repeated measures (rate x duration) analysis of variance was conducted. We found that, for both 500 and 2,000 Hz stimuli, the mean deconvolved SP amplitudes were larger at faster repetition rates (58.59 and 97.66/s) compared to slower repetition rates (7.1 and 19.53/s), and larger at shorter stimulus duration compared longer stimulus duration. Our concluding hypothesis is that large SP amplitude to short duration stimuli may originate primarily from neural excitation, and large SP amplitudes to long duration, fast repetition rate stimuli may originate from hair cell responses. While the hair cell or neural origins of the SP to various stimulus parameters remains to be validated, our results nevertheless provide normative data as a step toward applying the CLAD technique to understanding diseased ears.

Purpose Tone-pip-evoked otoacoustic emissions (PEOAEs) are transient-evoked otoacoustic emissions (OAEs) that are hypothesized to originate from reflection of energy near the best-frequency (BF) cochlear place of the stimulus frequency. However, individual PEOAEs have energy with a wide range of delays. We sought to determine whether some PEOAE energy is consistent with having been generated far from BF. Methods PEOAEs from 35 and 47 dB SPL tone pips were obtained by removing pip-stimulus energy by subtracting the ear-canal sound pressure from scaled-down 59 dB SPL tone pips (which evoke relatively small OAEs). PEOAE delays were measured at each peak in the PEOAE absolute-value waveforms. While measuring PEOAEs and auditory-nerve compound action potentials (CAPs), amplification was blocked sequentially from apex to base by cochlear salicylate perfusion. The perfusion time when a CAP was reduced identified when the perfusion reached the tone-pip BF place. The perfusion times when each PEOAE peak was reduced identified where along the cochlea it received cochlear amplification. PEOAEs and CAPs were measured simultaneously using one pip frequency in each ear (1.4 to 4 kHz across 16 ears). Results Most PEOAE peaks received amplification primarily between the BF place and 1–2 octaves basal of the BF place. PEOAE peaks with short delays received amplification basal of BF place. PEOAE peaks with longer delays sometimes received amplification apical of BF place, consistent with previous stimulus-frequency-OAE results. Conclusion PEOAEs provide information about cochlear amplification primarily within ~ 1.5 octave of the tone-pip BF place, not about regions > 3 octaves basal of BF.

Cochlear outer hair cells (OHC) receive direct efferent feedback from the caudal auditory brainstem via the medial olivocochlear (MOC) bundle. This circuit provides the neural substrate for the MOC reflex, which inhibits cochlear amplifier gain and is believed to play a role in listening in noise and protection from acoustic overexposure. The human MOC reflex has been studied extensively using otoacoustic emissions (OAE) paradigms; however, these measurements are insensitive to subsequent \"downstream\" efferent effects on the neural ensembles that mediate hearing. In this experiment, click- and chirp-evoked auditory nerve compound action potential (CAP) amplitudes were measured electrocochleographically from the human eardrum without and with MOC reflex activation elicited by contralateral broadband noise. We hypothesized that the chirp would be a more optimal stimulus for measuring neural MOC effects because it synchronizes excitation along the entire length of the basilar membrane and thus evokes a more robust CAP than a click at low to moderate stimulus levels. Chirps produced larger CAPs than clicks at all stimulus intensities (50-80 dB ppeSPL). MOC reflex inhibition of CAPs was larger for chirps than clicks at low stimulus levels when quantified both in terms of amplitude reduction and effective attenuation. Effective attenuation was larger for chirp- and click-evoked CAPs than for click-evoked OAEs measured from the same subjects. Our results suggest that the chirp is an optimal stimulus for evoking CAPs at low stimulus intensities and for assessing MOC reflex effects on the auditory nerve. Further, our work supports previous findings that MOC reflex effects at the level of the auditory nerve are underestimated by measures of OAE inhibition.

Stimulus-frequency otoacoustic emissions (SFOAEs) have been used to study a variety of topics in cochlear mechanics, although a current topic of debate is where in the cochlea these emissions are generated. One hypothesis is that SFOAE generation is predominately near the peak region of the traveling wave. An opposing hypothesis is that SFOAE generation near the peak region is deemphasized compared to generation in the tail region of the traveling wave. A comparison was made between the effect of low-frequency biasing on both SFOAEs and a physiologic measure that arises from the peak region of the traveling wave—the compound action potential (CAP). SFOAE biasing was measured as the amplitude of spectral sidebands from varying bias tone levels. CAP biasing was measured as the suppression of CAP amplitude from varying bias tone levels. Measures of biasing effects were made throughout the cochlea. Results from cats show that the level of bias tone needed for maximum SFOAE sidebands and for 50% CAP reduction increased as probe frequency increased. Results from guinea pigs show an irregular bias effect as a function of probe frequency. In both species, there was a strong and positive relationship between the bias level needed for maximum SFOAE sidebands and for 50% CAP suppression. This relationship is consistent with the hypothesis that the majority of SFOAE is generated near the peak region of the traveling wave.

An analytic compound action potential (CAP) designed by convolving functions representing the post-stimulus time histogram summed across auditory nerve fibers [P(t)] and a single fiber action potential [U(t)] was fit to human CAPs. Applying the analytic CAP to click-evoked CAPs before and after a noise-induced temporary hearing threshold shift (TTS) provided estimates of the number of neurons contributing to the CAPs (N), as well as in vivo P(t) and U(t), in normal and temporarily damaged cochleae. Click levels varied from 75 to 125 dBpSPL in 10 dB steps. Hierarchical Linear Modeling was used to characterize changes in the parameters governing the profile of N, P(t) and U(t) as a function of signal level. The width of P(t) decreased with increasing signal level. During TTS, P(t) width increased at the lowest signal level indicating less synchrony of neuronal discharge. The latency of P(t) decreased with increasing signal level. Following noise exposure, P(t) latency was shorter at all signal levels suggesting that neurons of more basal cochlear location dominated the response following noise exposure. Parameter N increased with signal level. During TTS, the lowest signal level N decreased indicating the number of responding neurons was reduced. U(t) rang less with increasing signal level. For subjects with large amounts of TTS, low signal level U(t) rang less. The frequency of U(t) oscillation increased with signal level. Following noise exposure, U(t) oscillated with a lower frequency at all signal intensities. Together, these results show that during TTS less neurons contribute to the CAP and these neurons have shorter latency and less response synchrony. Moreover, the oscillation of single fiber action potentials decay more rapidly and with a lower frequency during TTS.