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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.)

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.

Cochlear ischemia induces a sensorineural hearing loss, in part through a fast functional impairment of outer hair cellls. Assuming that the cochlea is rendered fragile during ischemia and reperfusion and that stimulation itself can jeopardize its functional recovery, we used a model of reversible selective cochlear ischemia in Mongolian gerbils to establish what type of sound exposure can be deleterious during and immediately after reversible ischemia. Several groups of gerbils were used, with different ischemia durations and levels of sound exposure. Control groups were only exposed to tones at 80 and 90 dB SPL during 30 min, while other groups underwent complete and fully reversible blockage of the labyrinthine artery, during 5.5 or 8 min, and were exposed to 60 or 80 dB SPL tones during 30 min. The amount of ischemia and reperfusion was measured by means of laser Doppler velocimetry, whereas outer hair cells' function was continuously monitored through distortion-product otoacoustic emissions (DPOAEs). The losses of DPOAE levels after 8 min transient ischemia and 60 dB SPL exposure were as large as those induced by 80 dB SPL exposures combined with 5.5 min ischemia, or 90 dB SPL exposures without ischemia, with a maximum loss around 25-30 dB, half an octave above the stimulus frequency. These results give evidence for an extremely high cochlear vulnerability to low-level sound exposure when associated with reversible ischemia. This vulnerability may have important clinical consequences in patients with cochlear circulatory disturbances.

The levels of distortion product otoacoustic emissions (DPOAEs) were measured in a strain of hearing-impaired mutant mice (CD1) at various stages of outer hair cell impairment and compared to those of a control inbred strain (CBA/J). Parallel measurements of cochlear potentials and auditory brainstem evoked responses (ABRs) were performed and surface preparations of organs of Corti were observed using phalloidin staining of filamentous actin. Comparison of DPOAEs (elicited by stimulus levels of 60 and 70 dB SPL) with standard functional tests allowed the categorization of CD1 ears into two groups on the basis of the presence or absence of DPOAE, which corresponded to mean ABR thresholds greater or less than 40 dB nHL respectively. When adopting ABR threshold as the gold standard, this procedure yielded rates of false-positives and -negatives ranging from 5 to 16%. However, individual predictions of electrophysiological function from DPOAE levels were not accurate, owing to their large variance, and attempts to optimize stimulus levels did not reduce this variance. In contrast, the profiles of DPOAE level vs. f2 exhibited large correlations with ABR threshold profiles as a function of f2. It was also noteworthy that the mean levels of DPOAEs in CD1 mice recorded in frequency intervals with normal ABR thresholds were significantly smaller than those of CBA/J mice. Although hearing loss was revealed early both by DPOAEs and by other functional tests, surface preparations often remained normal until about 3-4 months of age.