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The responses of cochlear hair cells to sound stimuli depend on the resting position of their stereocilia bundles, which is sensitive to the chemical and mechanical environment. Cochlear hydrops, a hallmark of Menière's disease (MD), which is likely to come with disruption of this environment, results in hearing symptoms and electrophysiological signs, such as excessive changes in the cochlear summating potential (SP) and in the postural shifts of distortion-product otoacoustic emissions (DPOAEs). Here, SP from the basal part of the cochlea and DPOAEs from the apical part of the cochlea were recorded concomitantly in 73 patients with a definite MD, near an attack (n = 40) or between attacks with no clinical symptoms (n = 33), to compare their sensitivities to posture and evaluate their stability. The phase of the 2f1-f2 DPOAEs was monitored during body tilt, with stimuli f1 = 1 kHz and f2 = 1.2 kHz at 72 dB SPL. Extratympanic electrocochleography was performed in response to 95-dBnHL clicks. The normal limits of the DPOAE phase shift with body tilt, [-18°, +38°], and of the SP to action-potential (AP) ratio, <0.40, were exceeded in 75% and 60% of patients, respectively, near an attack. In these patients, but not in the asymptomatic ones, both tests reveal fluctuating cochlear responses from one data sample to the next. They emphasize how hydrops hinders normal hair-cell operation and may generate fast fluctuations in inner-ear functioning. If these fluctuations also occur on shorter time scales, it might explain the imperfect diagnostic sensitivity of SP and DPOAE tests, as averaging procedures would tend to level out transient fluctuations characteristic of hydrops., (Copyright © 2015 Elsevier B.V. All rights reserved.)

In cerebellopontine angle (CPA) surgery, postoperative deafness can be due to alteration of cochlear blood flow that is supplied by the labyrinthine artery (LA). In particular, vasospasm is likely to occur and, if so, can be reversed. This work attempted to track down vascular events occurring during CPA surgery. Twenty consecutive patients with vestibular schwannoma were tested with useful preoperative hearing and presence of otoacoustic emissions (OAEs). Distortion-product otoacoustic emissions (DPOAEs), well-known to react within seconds to cochlear ischemia, were used intraoperatively to indirectly monitor cochlear blood flow. Continuous intraoperative monitoring of DPOAEs revealed three different time patterns associated with distinct auditory outcomes. Pattern P1-acute (n = 4) happened when the LA was severed: DPOAEs immediately and irreversibly foundered and led to postoperative deafness. Pattern P2-protracted (n = 7) revealed a progressive deterioration of DPOAEs from the beginning of tumor debulking, likely due to a steady decrease of cochlear blood flow, with postoperative deafness. Pattern P3-unstable (n = 5) corresponded to large DPOAE oscillations between their normal level and noise floor. It was due to acute LA vasospasm that could be reversed in three cases by topical nimodipin. Last, four patients had uneventful cochlear monitoring. In conclusion, cochlear ischemia can occur in vestibular schwannoma surgery, giving three different patterns among which vasospasm can be reversed if detected early.

The presence of endolymphatic hydrops as a marker of Menière's disease (MD) suggests abnormal pressure in the intralabyrinthine compartments of patients and excessive stiffness of sound-sensitive structures. Otoacoustic emissions (OAEs) have been reported to respond to changes in the ear's stiffness, including those produced by intracranial pressure steps, by a characteristic phase shift around 1 kHz, thereby suggesting a noninvasive means of monitoring MD. Here, body tilt was used for modulating intracranial pressure in forty-one patients with definite MD who were tentatively measured at two stages, with and without active symptoms. Their distortion-product OAEs (DPOAEs) were dynamically monitored around 1 kHz every few seconds in response to body tilt. In a control sample of thirty normal ears, the maximum phase rotation of DPOAEs produced by body tilt was between -18° and +37°. In MD ears with the complete set of symptoms, the posture-induced phase shifts in 32 out of 35 tests fell outside the normative interval, and in 10 tests, although DPOAEs were well above noise floor, their phase was always so abnormally erratic that body tilt produced hardly any additional effect. When MD ears were asymptomatic, nine out of 32 posture tests were abnormal. The excessive DPOAE phase shift is consistent with either a too stiff cochlear partition or a displacement of the operating point of outer hair cells by endolymphatic hydrops., (Copyright © 2011 Elsevier B.V. All rights reserved.)

It is known that by influencing stapes stiffness thus the ear's impedance, changes in intracranial and intralabyrinthine pressure induce a characteristic phase shift in otoacoustic emissions (OAE) around 1 kHz in human ears. Thus, if the regulation of pressure in intralabyrinthine compartments were abnormal in Menière patients, OAEs might help detect it. Body tilt, which acts on intracranial pressure, and administration of an osmotically active substance provide two simple ways of manipulating intralabyrinthine pressure. Here, 14 patients with typical signs of an attack of unilateral endolymphatic hydrops were submitted to postural changes and a glycerol test. Their OAEs initially collected in upright position served as references, then OAEs were measured in supine position, and back to the upright posture one and 3h after glycerol intake. Twenty control subjects were also tested for body tilt. The main effect of body tilt and glycerol was a phase rotation of OAEs peaking around 1 kHz. Its frequency dependence matched the one due to a pressure-related change in stapes or basilar membrane stiffness predicted by the ear model of Zwislocki (1962). The average glycerol-induced phase shifts were similar in size in Menière vs. asymptomatic ear and audiometric thresholds were stable after glycerol intake in line with the model predicting little change in the magnitude of the transfer function. These data support a simple conductive pressure-related mechanism explaining the action of glycerol on inner ear responses. The fact that the mean postural shift was three times larger in Menière than asymptomatic and control ears suggests an additional effect in allegedly hydropic ears.

Objectives: To report the known data on the functional consequences of cochlear ischemia and the tools available to detect them., Methods: Review of the main integrated in vivo models described in mammals., Results: The main integrated models of cochlear ischemia use laser doppler velocimetry to measure the degree of ischemia. Cochlear function can be effectively monitored during cochlear ischemia through the cochlear potentials and otoacoustic emissions, each of these signals giving specific information. The cochlea appears to be particularly resistant to several minutes of reversible ischemia. Indirect monitoring of cochlear ischemia can be achieved through distortion-product otoacoustic emissions during surgical procedures to the cerebellopontine angle. It is still impossible to directly and noninvasively detect cochlear ischemia in nonsurgical clinical practice., Conclusions: Integrated models of cochlear ischemia have contributed greatly to our knowledge of the functional behavior of the cochlea in this specific situation. Clinical practice now needs to be able to detect cochlear ischemia early and noninvasively, for example in cases of sudden hearing loss.

Objectives: Otoacoustic emissions (OAEs), discovered in 1978, have a well-established cochlear origin. They strongly depend on the outer hair cells and are widely used in experimental research as a means for testing cochlear function. However, outside screening, OAEs are only rarely used in clinical practice. The objective of this paper was to show their vast clinical utility., Material and Methods: First, a review of the biophysical and physiological knowledge on OAEs is provided, concerning transient OAEs as well as distortion-product OAEs, recalling the origin and the meanings of these acoustic signals. Several clinical situations are then presented, and the corresponding OAE alterations are explained, such as hearing screening in neonates, diagnosis of hearing impairment with particularities related to the age of the patient, situations critical to the cochlea such as ototoxic treatments, and surgical procedures to the cerebellopontine angle., Results: OAEs appear to be a powerful tool in clinical practice, particularly in hearing screening and diagnosis of deafness. They can also be used to monitor hearing function during cerebellopontine angle tumor resection., Conclusion: OAEs are still rarely used as a diagnostic tool by clinicians despite their clinical value, which should make them a primary choice.

Distortion product otoacoustic emissions (DPOAEs) are thought to stem from the outer hair cells (OHCs) around the normally narrow place tuned to the primary tone stimuli. They are thus said to be frequency-specific: their local absence should accurately pinpoint local OHC damage. Yet the influence of impaired tuning on DPOAE frequency specificity is poorly documented. Mice with local damage to OHCs were examined. Their DPOAEs were frequency-specific in that audiometric notches were accurately tracked. The same cochleae were further impaired by ischemia or furosemide injection inducing strial dysfunction with flat loss of sensitivity and tuning, while the preexisting pattern of damaged OHCs remained unaltered. Despite the loss of cochlear activity, DPOAEs produced by high-level (> or =70 dB SPL) primaries remained large in about the same interval where they had been initially normal, i.e., that with nondamaged OHCs, albeit with a slight frequency shift, of -1.1 kHz on average. Thus, the ability of DPOAEs to map structurally intact OHCs cannot be a mere consequence of cochlear tuning as it largely persists in its absence. The key element for this correct mapping is likely part of intact OHC structures (e.g., stereocilia bundles) and must have some tuning of its own.

Distortion product otoacoustic emissions emitted by the cochlea at 2f1-f2 in response to pairs of pure tones at f1 and f2 (DPOAE) form a class of otoacoustic emissions and as such, are viewed as a reliable tool for screening outer hair cell (OHC) dysfunctions on a pass/fail basis. However, the persistence of residual DPOAEs from impaired cochleae at high stimulus levels has suggested that above 60-70 dB SPL, instead of reflecting "active" cochlear motion, DPOAEs might represent another "passive" modality: they would thus become unsuitable for analyzing cochlear function. The present work reports the consequences on high- vs low-level DPOAEs of three types of cochlear impairments involving OHCs: progressive OHC degeneration of genetic origin in CD1 mice, complete cochlear ischemia in gerbils, and furosemide injection vs ischemia-reperfusion in gerbils. An alternative to the "active-passive" model was used wherein regardless of stimulus level, cubic DPOAEs are produced by N (probably OHC-borne) nonlinear elements driven by input I and modulated by a function F3 of their operating point o; thus, DPOAE proportional to NI3F3(o). When OHCs degenerated, thereby implying a decrease of N, DPOAE levels also decreased regardless of the stimulus level up to 80 dB SPL, in line with the previous formula but at variance with the prediction of the active-passive concept. Instead of affecting N, the other two experiments impaired the efficiency of the cochlear feedback loop as a result of its electrical drive being decreased by strial dysfunction. As it is well accepted that the impaired basilar-membrane motion, although greatly reduced at low levels, tends to catch up with a normal one at higher levels, it was assumed the same was true with I so that DPOAE levels had to be, and indeed were little affected at high levels while plummeting at low levels, without any need for invoking two modalities for DPOAE generation. Finally, comparisons of furosemide vs ischemia effects revealed additional influences on DPOAEs, possibly accounted for by function F3(o). These results lead to the proposal that although high-level DPOAEs are expected to be poor audiometric indicators, they seem well adapted to assessing the functional integrity of nonlinear elements in OHCs, i.e., presumably their mechanoelectrical transduction channels.

Guinea pigs were exposed to a pure tone at 6 kHz and 80 dB SPL for 30 minutes in order to induce mild reversible auditory fatigue over the 4 hours following exposure. Cochlear monitoring aimed to compare the shifts in round-window compound action potentials (CAP) thresholds to those of 2f1-f2 distortion-product otoacoustic emissions (DPOAE, frequency of stimuli f1 and f2). Both responses were evaluated every 1/10th octave between 6 and 12 kHz for CAP thresholds, and from 4 to about 14 kHz for DPOAEs in response to 50- and 70-dB SPL stimuli. The auditory fatigue turned out to be sufficiently mild that DPOAEs remained present, so that their microstructure could be followed up while the stimulus frequency ratio f2/f1 was swept from 1.06 to 1.30 (fixed f2) so as to derive DPOAE level profiles against f2/f1 and group latencies. CAP thresholds decreased by about 10 dB above 7.2 kHz, whereas DPOAE amplitudes decreased at most f2 frequencies from 6.6 kHz to 15.2 kHz, with the range of decrease being slightly narrower at higher stimulus intensities. While the mean DPOAE shift after 1 hour was around 5 dB irrespective of stimulus intensity, it tended to increase slightly after 2 hours despite stable CAP thresholds. DPOAE profiles against f2/f1 were slightly modified by the auditory fatigue, so that the maximum tended to be reached at lower ratio. No significant variation of DPOAE latencies was found after acoustic overstimulation. These experiments show that complex DPOAE changes were induced by auditory fatigue and their relationship to CAP threshold changes does not seem to be straight-forward. Nonetheless, fine DPOAE recordings might be useful to detect early changes in cochlear mechanics.

The spectral quasi-periodicity of transient-evoked otoacoustic emissions (TEOAE) is well acknowledged since Zwicker described a preferred spacing of 0.4 bark between consecutive peaks in the spectrum of otoacoustic emissions from normal ears. While there is scarce evidence of any anatomical reason for this regularity, several functional models of the cochlea have predicted that the structure of emission spectra reflects important characteristics of cochlear filters. In an attempt to check such predictions, the average regularity of TEOAE spectra was studied in three groups of human subjects, normally hearing adults, healthy neonates, and adults suffering from noise-induced hearing loss. Significant differences in emission periodicities were found. Around 1 kHz, the preferred spacing was close to 130 Hz in normally hearing adult ears and neonates. In contrast, no clear periodicity was found in the group of damaged ears, even though they had clinically normal pure-tone audiometry below 2 kHz. Around 4 kHz, the preferred spacing was close to 240 Hz in normal adults and neonates, whereas TEOAEs were absent in many impaired ears. A phenomenological model assuming that TEOAEs stem from the responses of a slightly disarrayed bank of highly tuned filters predicts that the filter width would be the same in healthy young adults and neonates. In contrast, ears suffering from high-frequency hearing loss could exhibit early damaged filters. The proposed method might provide an objective assessment of parameters otherwise difficult to evaluate, especially in neonatal cochleas.

Impairment to the cochlear blood flow likely induces many types of sensorineural hearing loss. Models using several small laboratory animals have been described in the literature that permit the simultaneous monitoring of the cochlear blood flow with laser-Doppler flowmetry and cochlear function using evoked responses. However, these models have not permitted a direct application of the resulting knowledge to the human condition, primarily due to differences in the translucence of the otic capsule between species. In the present study, to approximate conditions relevant to the human patient, the rabbit was utilized to develop a procedure in which laser-Doppler flowmetry could be used to measure the cochlear blood flow in an animal with an opaque otic capsule. At the same time, the cochlear function was monitored non-invasively using distortion-product otoacoustic emissions. In this manner, a laser-Doppler probe was positioned in the round window niche and the cochlear function measured using distortion-product otoacoustic emissions during a systematic series of ischemic episodes. Cochlear ischemia was produced by deliberately compressing the eighth nerve complex at the porus of the internal acoustic meatus, for periods lasting from 1-3 min, while cochlear blood flow and distortion-product otoacoustic emission measures were obtained simultaneously before, during and following the occlusion. Results demonstrated that the cochlear blood flow sharply decreased within 1 s after compression onset, whereas distortion-product otoacoustic emissions showed obstruction-induced changes after a delay of several seconds, provided that the blood flow decreased, at least 40%. Similarly, upon release of the compression, the cochlear blood flow began to recover within 1 s, whereas the recovery of the corresponding distortion-product otoacoustic emissions was slightly delayed. Although not apparent in the distortion-product otoacoustic emission recovery time course, the cochlear blood flow consistently overshot its initial baseline value during the recovery process. Thus, although cochlear ischemia produced changes in the distortion-product otoacoustic emission activity that generally followed the resulting alterations in the cochlear blood flow, the detailed relationship between the two measures was complex.

Objective/hypothesis: Examine and compare in detail the time courses of the auditory brainstem response (ABR) wave I amplitude and latency to the distortion-product otoacoustic emission (DPOAE) amplitude and phase measured in the rabbit model following deliberate obstruction of cochlear blood flow (CBF)., Methods: Using a posterior fossa craniotomy in five rabbits, the internal auditory artery (IAA) was compressed with a probe. ABR and otoacoustic emission were continuously monitored before, during, and after the compressions., Results: ABR wave I amplitudes demonstrated measurable decreases at a mean of 28.3 s after IAA compression, whereas DPOAE amplitudes decreased after a mean of 14.8 s. Wave I latencies began to increase at a mean of 18.3 s after occlusion, while DPOAE phase measures changed after a mean of only 4.8 s following IAA compression. The time-course patterns were similar for the amplitudes of both ABR wave I and DPOAE., Conclusions: ABR wave I amplitude follows a similar, though delayed (by approximately 10 s) time-course pattern to that of the DPOAE following IAA compression. The implication of these findings for intraoperative auditory monitoring is that changes in many currently employed measures will lag actual surgically induced alterations in CBF by at least 20 to 30 s.