Rupture of Reissner's membrane during acute endolymphatic hydrops in the guinea pig: a model for Ménière's disease?

Conclusion. The changes in cochlear function during a destructive acute endolymphatic hydrops were relatively small. This might be consistent with the hypothesis that an endolymphatic hydrops is a marker of disordered inner ear homeostasis rather than the cause of the clinical symptoms of Ménière's disease. Objective. Assessment of cochlear function during induction of a destructive acute endolymphatic hydrops. Materials and methods. During repetitive microinjections of 0.5 µl of artificial endolymph at a rate of 50 nl/s the 2f₁?f₂ and f₂?f₁ cochlear microphonics distortion products (CMDP) and 2f₁?f₂ distortion products otoacoustic emissions (DPOAE) were recorded in the guinea pig. Results. A ‘catastrophe’ occurred in the inner ear when 2.5–3.5 µl of artificial endolymph was injected. A rupture of Reissner's membrane was then found, most often in the apical turn of the cochlea. This rupture had only minor effects on the endocochlear potential, whereas it caused a marked decrease in 2f₁?f₂ DPOAE amplitude. The 2f₁?f₂ and f₂?f₁ CMDP amplitude increased during each injection prior to the rupture. After the rupture the f₂?f₁ CMDP amplitude decreased during each injection, possibly due to a shift of the cochlear transducer operating point position.     

Effect of acute inner ear pressure changes on low-level distortion product otoacoustic emissions in the guinea pig

Objective—To determine a relation between acute inner ear pressure changes and cochlear function as measured by low-level 2f₁–f₂ distortion product otoacoustic emissions (DPOAEs).

Material and Methods—During and after a change in inner ear pressure induced by injection or aspiration of perilymph, the 2f₁–f₂ DPOAE at 4.5 kHz generated by low-level primaries was recorded in the guinea pig.

Results—Large changes in overall inner ear pressure produced only small changes in the 2f₁–f₂ amplitude and phase. During injection of 0.5 μl of artificial perilymph into the scala tympani over a 10-s period, the mean inner ear pressure increased by ≈500 Pa, with an accompanying mean increase in the 2f₁–f₂ amplitude of 0.7 dB. During aspiration of 0.5 μl of perilymph over a 10-s period, the mean inner ear pressure decreased by ≈700 Pa, with an accompanying mean decrease in the 2f₁–f₂ amplitude of 0.9 dB. Changes in DPOAE amplitude followed inner ear pressure changes with a delay of 1–2 s. The magnitude and sign of the amplitude changes can (partly) be explained by a change in oval window stiffness. No explanation was found for the measured delay.

Conclusion—Clinically, these experiments can be of value in gaining insight into the pathophysiological mechanisms of pathological pressure changes as seen in Ménière's disease and perilymphatic fistulae.     

Complex level alterations of the 2<Emphasis Type="Italic">f</Emphasis><Subscript>1</Subscript>−<Emphasis Type="Italic">f</Emphasis><Subscript>2</Subscript> distortion product due to hypoxia in the guinea pig

It is controversially discussed inasmuch acute hearing disorders might originate from impaired cochlear circulation. Hypoxia-specific alterations of inner ear parameters measurable in patients with acute sensorineural hearing loss would therefore be of great interest. Aim of this study was to characterize hypoxia-related alterations of the 2f ₁−f ₂ distortion product. Nine guinea pigs were anaesthetized by i.m. administration of Midazolam, Medetomidin and Fentanyl. For introduction of hypoxia, the spontaneously breathing animals were offered a gas mixture of N₂O and O₂ containing either 21 or 12–13% O₂. Distortion product otoacoustic emissions (DPOAEs) were continuously monitored at f ₂ = 16 kHz; f ₂/f ₁ = 1, 2; DP-definition = 2f ₁−f ₂; L ₁ = 65 dB and L ₂ = 55 dB, while inhaled oxygen was switched from 21 to 12–13% and back. Oxygen saturation (SaO₂) was continuously monitored. Data from an hypoxic interval were only used for further data processing if DPOAE levels were stable before and after hypoxia. Six hypoxic intervals in five animals fulfilled the stability criterion. During the hypoxic interval with the highest measured SaO₂ (75%), no alterations of DPOAE levels were observed. During the remaining five hypoxic intervals, when SaO₂ ranged between 57 and 70%, DPOAE levels were on average lower with an increased standard deviation compared to mean pre-hypoxic levels. Mean decrease correlated with the decrease of SaO₂ (r = 0.90, P = 0.014). Alterations followed a characteristic time course—when hypoxia was started, DPOAE levels exhibited a short increase before they decreased and remarkably destabilized. After re-oxygenation DPOAE levels showed a pronounced level decrease, while SaO₂ already had recovered to pre-hypoxic values. After reaching a minimum, DPOAE levels slowly recovered to pre-hypoxic values. The decrease of DPOAE levels during hypoxia and the post-hypoxic level alterations have similarly been described by other authors before, while the distinct destabilization and transiently increased DPOAE levels have not been explicitly mentioned. A micromechanical mechanism that might explain a transient level increase and the post-hypoxic DPOAE level changes is discussed.     

Otoacoustic Emission Theories and Behavioral Estimates of Human Basilar Membrane Motion Are Mutually Consistent

When two pure tones (or primaries) of slightly different frequencies (f ₁ and f ₂) are presented to the ear, new frequency components are generated by nonlinear interaction of the primaries within the cochlea. These new components can be recorded in the ear canal as otoacoustic emissions (OAE). The level of the 2f ₁−f ₂ OAE component is known as the distortion product otoacoustic emission (DPOAE) and is regarded as an indicator of the physiological state of the cochlea. The current view is that maximal level DPOAEs occur for primaries that produce equal excitation at the f ₂ cochlear region, but this notion cannot be directly tested in living humans because it is impossible to record their cochlear responses while monitoring their ear canal DPOAE levels. On the other hand, it has been claimed that the temporal masking curve (TMC) method of inferring human basilar membrane responses allows measurement of the levels of equally effective pure tones at any given cochlear site. The assumptions of this behavioral method, however, lack firm physiological support in humans. Here, the TMC method was applied to test the current notion on the conditions that maximize DPOAE levels in humans. DPOAE and TMC results were mutually consistent for frequencies of 1 and 4 kHz and for levels below around 65 dB sound pressure level. This match supports the current view on the generation of maximal level DPOAEs as well as the assumptions of the behavioral TMC method.     

Changes in distortion of two-tone cochlear microphonic and otoacoustic emission signals during an acute endolymphatic hydrops in the guinea pig

An acute endolymphatic hydrops was induced by the injection of 1.1 l of artificial endolymph into the scala media of guinea pig cochleas. This volume corresponds with an acute endolymphatic hydrops of 23%. During and after the injection, cochlear function was assessed by measuring the 2f₁-f₂ and f₂-f₁ distortion products in cochlear microphonics (CMDP) and the 2f₁-f₂ distortion product otoacoustic emission (DPOAE). A reversible pressure increase of 23 Pa and a relatively stable endocochlear potential (EP) were accompanied by a mean decrease in 2f₁-f₂ DPOAE of only 3.4 dB. Similarly, the 2f₁-f₂ CMDP amplitude change was minimal during and after the injection. The only substantial change was measured in the f₂-f₁ CMDP amplitude. The measured range of distortion amplitudes during an acute endolymphatic hydrops can be related to small changes in the cochlear transducer operating point.     

A comparison of the effect of cochlear perfusion with ouabain on summating potentials and distortion product otoacoustic emissions in the guinea pig

In order to investigate whether or not the summating potential (SP) and the 2f ₁–f ₂ distortion product otoacoustic emission (DPOAE) are due to related cochlear non-linearities, their behavior was studied in the guinea pig after intracochlear perfusion with ouabain and subsequent rinsing. The SP was evoked with either 4 or 8 kHz tone bursts, and the 2f ₁–f₂DPOAE was evoked with simultaneous presentations of 6.6 and 8 kHz continuous tones. After ouabain perfusion, DPOAE was dramatically reduced while the SP underwent only a small reduction. After rinsing out the ouabain with artificial perilymph, the DPOAE showed partial recovery while the SP displayed a large and long-lasting increase when compared to its a initial value. These results suggest that the non-linear processes giving rise to the SP and DPOAE are not identical.     

Complex level alterations of the 2f1–f2 distortion product due to hypoxia

Objective

For diagnostic purposes and a better understanding of the pathophysiology of inner ear hearing disorders it would be of great interest to have parameters available that indicate inner ear hypoxia. In animal studies typical hypoxia-related alterations of the 2f₁–f₂ distortion product otoacoustic emissions (DPOAE) such as a reversible level decrease and destabilization could be demonstrated. The goal of this study was to investigate whether these hypoxia-associated alterations can also be observed in humans because this might help develop a new diagnostic tool for patients with inner ear disorders.

Methods

In 16 volunteers DPOAE levels were continuously measured at first under normal room air conditions, during and after 8.5 h of oxygen deprivation (13% O₂) and during re-oxygenation. Saturation of oxygen of arterial blood (SaO₂) was monitored.

Results

The mean SaO₂ during the hypoxic interval was 78%. A significant decrease in DPOAE level under hypoxia occurred in five different test persons at one or more frequencies (f₂ = 1, 1.5, 2, 3, and 4 kHz). A destabilization of the DPOAE level with considerable fluctuations during hypoxia was observed in nine subjects at one or more frequencies. Furthermore, the so called ‘post hypoxia effect’ could be observed in five participants.

Conclusion

The observations made here have been described similarly in animal studies and seem to be characteristic of metabolic disorders of the cochlea caused by hypoxia. To our knowledge, this is the first study to examine DPOAE level alterations over time in humans under conditions of normobaric hypoxia. If DPOAE destabilization is observed in a clinical setting in patients with certain inner ear hearing disorders hypoxia can be suspected as one underlying pathophysiological cause which might influence treatment decisions.     

Changes in distortion product otoacoustic emissions during prolonged noise exposure

The aim of this study was to evaluate the reduction in 2f₁−f₂ distortion product otoacoustic emission (DPOAE) amplitude resulting from prolonged noise exposures. A group of five chinchillas was exposed continuously to an octave-band noise centered at 4.0 kHz for a total of 42 days, 6 days at each of seven exposure levels. Exposure level increased in 8-dB steps from 48 to 96 dB SPL. DPOAE input-output (I/O) functions were measured at octave intervals over a range of primary tone f₂ frequencies between 1.2 and 9.6 kHz. Measurements were obtained (1) pre-exposure, (2) during days 3–6 of each 6-day exposure, and (3) 4 weeks after the final exposure. Continuous noise exposure caused a reduction in DPOAE amplitude that was greatest at f₂ frequencies within and above (3.4–6.8 kHz) the octave-band noise exposure. For these f₂ frequencies, DPOAE amplitudes decreased as exposure level increased up to approximately 72–80 dB SPL; higher exposure levels failed to cause any further reduction in DPOAE amplitude. The noise level at which DPOAE amplitude began to decrease was approximately 50 dB SPL. Above this critical level, DPOAE amplitude decreased 1.3 dB for every dB increase in noise level up to approximately 75 dB SPL.     

Rupture of Reissner's membrane during acute endolymphatic hydrops in the guinea pig: a model for Ménière's disease?

CONCLUSION: The changes in cochlear function during a destructive acute endolymphatic hydrops were relatively small. This might be consistent with the hypothesis that an endolymphatic hydrops is a marker of disordered inner ear homeostasis rather than the cause of the clinical symptoms of Ménière's disease. OBJECTIVE: Assessment of cochlear function during induction of a destructive acute endolymphatic hydrops. MATERIALS AND METHODS: During repetitive microinjections of 0.5 microl of artificial endolymph at a rate of 50 nl/s the 2f1-f2 and f2-f1 cochlear microphonics distortion products (CMDP) and 2f1-f2 distortion products otoacoustic emissions (DPOAE) were recorded in the guinea pig. RESULTS: A 'catastrophe' occurred in the inner ear when 2.5-3.5 microl of artificial endolymph was injected. A rupture of Reissner's membrane was then found, most often in the apical turn of the cochlea. This rupture had only minor effects on the endocochlear potential, whereas it caused a marked decrease in 2f1-f2 DPOAE amplitude. The 2f1-f2 and f2-f1 CMDP amplitude increased during each injection prior to the rupture. After the rupture the f2-f1 CMDP amplitude decreased during each injection, possibly due to a shift of the cochlear transducer operating point position.     

Middle ear and cochlear disorders result in different DPOAE growth behaviour: implications for the differentiation of sound conductive and cochlear hearing loss

Input/output functions of distortion product otoacoustic emissions (DPOAE I/O-functions) give an insight into the compressive, non-linear sound processing of the cochlea. With an inner ear dysfunction a steeper I/O-function is observed. Due to the linear sound processing of the middle ear, one can assume that the DPOAE growth behaviour remains unaltered with a sound conduction dysfunction. If that is true, a differentiation between middle and inner ear dysfunction will be possible by using the slope of DPOAE I/O-functions as a means for assessing cochlear compression. In order to test that hypothesis, DPOAE I/O-functions were recorded in a wide primary tone level range at up to 8 f2 frequencies between 2.0 and 8.0 kHz (15 dB SPL < L2< 60 dB SPL; L1=0.46 L2 + 41 dB SPL; f2/f1=1.2) in guinea pigs in which middle (saline solution in the bulla) and inner ear (exposure to loud broadband noise) disorders were induced. Middle ear dysfunction resulted in a reduction of the DPOAE amplitude independent of the primary tone level. Consequently, DPOAE growth behaviour was not affected. In contrast to that, during cochlear impairment, steepened DPOAE I/O-functions were observed reflecting loss of compression of the cochlear amplifier. Accordingly, DPOAE I/O-functions allow a differentiation between middle and inner ear dysfunction. Further studies will have to show the usability of this method for clinical diagnostics, e.g. for detecting sound conduction disturbances in newborn hearing screening due to amniotic fluid or Eustachian tube dysfunctions during the early postnatal period.     

Effect of acute inner ear pressure changes on low-level distortion product otoacoustic emissions in the guinea pig

OBJECTIVE: To determine a relation between acute inner ear pressure changes and cochlear function as measured by low-level 2f(1)-f(2) distortion product otoacoustic emissions (DPOAEs). MATERIAL AND METHODS: During and after a change in inner ear pressure induced by injection or aspiration of perilymph, the 2f(1)-f(2) DPOAE at 4.5 kHz generated by low-level primaries was recorded in the guinea pig. RESULTS: Large changes in overall inner ear pressure produced only small changes in the 2f(1)-f(2) amplitude and phase. During injection of 0.5 microl of artificial perilymph into the scala tympani over a 10-s period, the mean inner ear pressure increased by approximately 500 Pa, with an accompanying mean increase in the 2f(1)-f(2) amplitude of 0.7 dB. During aspiration of 0.5 microl of perilymph over a 10-s period, the mean inner ear pressure decreased by approximately 700 Pa, with an accompanying mean decrease in the 2f(1)-f(2) amplitude of 0.9 dB. Changes in DPOAE amplitude followed inner ear pressure changes with a delay of 1-2 s. The magnitude and sign of the amplitude changes can (partly) be explained by a change in oval window stiffness. No explanation was found for the measured delay. CONCLUSION: Clinically, these experiments can be of value in gaining insight into the pathophysiological mechanisms of pathological pressure changes as seen in Meniere's disease and perilymphatic fistulae.     

Effect of inner and outer hair cell lesions on electrically evoked otoacoustic emissions

When the cochlea is stimulated by a sinusoidal current, the inner ear emits an acoustic signal at the stimulus frequency, termed the electrically evoked otoacoustic emission (EEOAE). Recent studies have found EEOAEs in birds lacking outer hair cells (OHCs), raising the possibility that other types of hair cells, including inner hair cells (IHCs), may generate EEOAEs. To determine the relative contribution of IHCs and OHCs to the generation of the EEOAE, we measured the amplitude of EEOAEs, distortion product otoacoustic emissions (DPOAEs), the cochlear microphonic (CM) and the compound action potential (CAP) in normal chinchillas and chinchillas with IHC lesions or IHC plus OHC lesions induced by carboplatin. Selective IHC loss had little or no effect on CM amplitude and caused a slight reduction in mean DPOAE amplitude. However, IHC loss resulted in a massive reduction in CAP amplitude. Importantly, selective IHC lesions did not reduce EEOAE amplitude, but instead, EEOAE amplitude increased at high frequencies. When both IHCs and OHCs were destroyed, the amplitude of the CM, DPOAE and EEOAE all decreased. The increase in EEOAE amplitude seen with IHC loss may be due to (1) loss of tonic efferent activity to the OHCs, (2) change in the mechanical properties of the cochlea or (3) elimination of EEOAEs produced by IHCs in phase opposition to those from OHCs.     

Mice Lacking Adrenergic Signaling Have Normal Cochlear Responses and Normal Resistance to Acoustic Injury but Enhanced Susceptibility to Middle-Ear Infection

The vasculature and neurons of the inner ear receive adrenergic innervation from the cervical sympathetic chain, and adrenergic receptors may be expressed by cells of the organ of Corti and stria vascularis, despite a lack of direct sympathetic innervation. To assess the functional role of adrenergic signaling in the auditory periphery, we studied mice with targeted deletion of the gene for dopamine β-hydroxylase (DBH), which catalyzes the conversion of dopamine to noradrenaline; thus, these mutant mice have no measurable adrenaline or noradrenaline. Dbh ^−/− mice were more susceptible to spontaneous middle-ear infection than their control littermates, consistent with a role for sympathetics in systemic and/or local immune response. At 6–8 weeks of age, cochlear thresholds and suprathreshold responses assessed by auditory brainstem responses and distortion product otoacoustic emissions, as well as light-microscopic morphology, were indistinguishable from controls, if ears with conductive hearing loss were eliminated. Dbh ^−/− mice were no more susceptible to acoustic injury than controls, despite prior reports that sympathectomy reduces noise damage. Dbh ^−/− mice showed enhancement of shock-evoked olivocochlear suppression of cochlear responses, which may arise from the loss of adrenergic inputs to olivocochlear neurons in the brainstem. However, adrenergic modulation of olivocochlear efferents does not mediate the protective effect of contralateral cochlear destruction on ipsilateral response to acoustic overexposure.     

Role of thromboxane A2 in a microcirculation disorder of the rat inner ear

Summary Since thromboxane (TX) A₂ causes vasoconstriction and platelet aggregation, we evaluation the effect of a TXA₂ receptor antagonist (vapiprost) and a TXAZ synthetase inhibitor (Y-20811) on a microcirculation disorder in the rat inner ear that was induced by a photochemical reaction between an intravenous injection of rose bengal (RB) and green light. A gradual decrease of the cochlear action potential (CAP) to an 8 kHz sound stimulus was measured with an electrocochleogram and occurred after the RB injection. The CAP then disappeared 5 min after the injection of RB. Both vapiprost and Y-20811 significantly prolonged the time required to complete suppression of the CAP as compared with saline as control. These findings indicate that TXAZ may play an important role in microcirculation disorders in the rat inner ear.     

In vitro regulation of neutrophil migration by β2 integrins (LFA-1 and Mac-1) in patients with otitis media

β₂ integrins are located on the surface of neutrophils and have important roles in cell migration to an inflammatory site. We investigated the inhibitory effect of antibodies to the β₂ integrin family for neutrophil migration into middle ear effusion (MEE) during acute otitis media in children and chronic otitis media with effusion in both children and adults. Neutrophil migration to MEE samples was assessed in vitro in a 48-well Boyden chamber. The migration index value and the activity of chemo-attractants in MEE was found to be proportional to the number of infiltrated cells. Migration of activated neutrophils into MEE was significantly inhibited by blocking surface-expressed cell adhesion molecules (CAM) with anti-CD11b (Mac-1α) and anti-CD18 (common β₂ subunit) antibodies (P < 0.001) but not with anti-CD11a (LFA-1α) antibody. These inhibitory effects of anti-CAM antibodies were found in all types of MEE in all age groups studied. A new therapeutic approach to inflammation has been considered recently that utilizes inhibition of neutrophil migration with a blocking antibody to CAM. Our in vitro data support a possible therapeutic effect of anti-CAM antibody, indicating that administration of anti-CD11b and CD18 antibodies may be useful for treating human otitis media.     

High-Resolution Measurements of Middle Ear Gas Volume Changes in the Rabbit Enables Estimation of its Mucosal CO2 Conductance

Transmucosal CO₂ exchange in the middle ear (ME) of the New Zealand White rabbit (Oryctolagus cuniculus) was studied using an accurate novel detecting and recording system for measuring gas volume changes at constant pressure, based on a principle that was previously used by Kania et al. (Acta Otolaryngol 124:408–410, 2004). After the ME cavity was washed with ambient air, the initial diffusion rate of CO₂ () from the blood perfusing the ME mucosa was calculated from gas volume change measurements. In nine cases, the calculated after normalization due to shifts in baseline was 314 ± 112 μL·h⁻¹ (mean ± SD). In two cases where normalization was not needed, was 409 μL·h⁻¹ (276 and 543 μL·h⁻¹). Normalization of data was also made in five additional cases where secretion of fluids from the lining of the ear canal was observed. In these cases was 245 ± 142 μL·h⁻¹. No differences were found between results obtained in the three groups. Thus, an overall mean value of of 305 ± 131 μL·h⁻¹ (n = 16) was calculated. An effective coefficient of conductance of CO₂ (G ₂) between the mucosal circulation and the ME gas cavity of the New Zealand White rabbit was estimated to be ≈0.05 μL (h·Pa)⁻¹ and compared to the G ₂ estimated for humans in a different study.     

Detailed f 1, f 2 Area Study of Distortion Product Otoacoustic Emissions in the Frog

Distortion product otoacoustic emissions (DPOAEs) are weak sounds emitted from the ear when it is stimulated with two tones. They are a manifestation of the nonlinear mechanics of the inner ear. As such, they provide a noninvasive tool for the study of the inner ear mechanics involved in the transduction of sound into nerve fiber activity. Based on the DPOAE phase behavior as a function of frequency, it is currently believed that mammalian DPOAEs are the combination of two components, each generated by a different mechanism located at a different location in the cochlea. In frogs, instead of a cochlea, two separate hearing papillae are present. Of these, the basilar papilla (BP) is a relatively simple structure that essentially functions as a single auditory filter. A two-mechanism model of DPOAE generation is not expected to apply to the BP. In contrast, the other hearing organ, the amphibian papilla (AP), exhibits a tonotopic organization. In the past it has been suggested that this papilla supports a traveling wave in its tectorial membrane. Therefore, a two-mechanism model of DPOAE generation may be applicable for DPOAEs from the AP. In the present study we report on the amplitude and phase of DPOAEs in the frog ear in a detailed f₁, f₂ area study. The result is markedly different from that in the mammalian cochlea. It indicates that DPOAEs generated by neither papilla agree with the two-mechanism traveling wave model. This confirms our expectation for the BP and does not support the hypothesized presence of a mechanical traveling wave in the AP.     

Low-frequency modulation of the 2f1−f2 distortion product otoacoustic emissions in the human ear

Low-frequency masking is a recent clinical procedure for the differential diagnosis of sensory hearing loss. Currently this requires the recording of the phase-dependent masked subjective threshold, which is time consuming and not always accurate. As an objective method, the recording of modulated distortion product otoacoustic emissions (DPOAEs) can be performed continuously, and with better frequency specificity. Results of measurements of the low-frequency modulated two-tone DPOAE 2f₁−f₂ in the human ear, and its dependence on various acoustic parameters, are presented here for the first time. Similar to the masked hearing threshold, the pattern of the phase-dependent modulated DPOAEs displayed two minima, at the phases of maximal rarefaction and condensation, respectively, with a latency of about 4 ms (suppressor frequency 32.8 Hz). The smaller dip, at maximal condensation, appeared only for a high suppressor level, and for a low level of the primary tone f₂. The modulating effect measured for the primary frequencies f₁=2.5 kHz and f₂=3 kHz, decreased for 4 and 4.8 kHz, and vanished for 5 and 6 kHz. The results are discussed using a cubic distortion model based on the Boltzmann function for mechano-electrical transduction of the hair cells. The saturation behavior of the increase of the DPOAE level at different phases is compared with the growth rates of the DPOAE level in normal hearing and in sensory hearing loss.     

Differential Intracochlear Sound Pressure Measurements in Normal Human Temporal Bones

We present the first simultaneous sound pressure measurements in scala vestibuli and scala tympani of the cochlea in human cadaveric temporal bones. The technique we employ, which exploits microscale fiberoptic pressure sensors, enables the study of differential sound pressure at the cochlear base. This differential pressure is the input to the cochlear partition, driving cochlear waves and auditory transduction. In our results, the sound pressure in scala vestibuli (P _SV) was much greater than scala tympani pressure (P _ST), except for very low and high frequencies where P _ST significantly affected the input to the cochlea. The differential pressure (P _SV − P _ST) is a superior measure of ossicular transduction of sound compared to P _SV alone: (P _SV−P _ST) was reduced by 30 to 50 dB when the ossicular chain was disarticulated, whereas P _SV was not reduced as much. The middle ear gain P _SV/P _EC and the differential pressure normalized to ear canal pressure (P _SV − P _ST)/P _EC were generally bandpass in frequency dependence. At frequencies above 1 kHz, the group delay in the middle ear gain is about 83 μs, over twice that of the gerbil. Concurrent measurements of stapes velocity produced estimates of cochlear input impedance, the differential impedance across the partition, and round window impedance. The differential impedance was generally resistive, while the round window impedance was consistent with compliance in conjunction with distributed inertia and damping. Our technique of measuring differential pressure can be used to study inner ear conductive pathologies (e.g., semicircular dehiscence), as well as non-ossicular cochlear stimulation (e.g., round window stimulation and bone conduction)—situations that cannot be completely quantified by measurements of stapes velocity or scala vestibuli pressure by themselves.     

Effects of experimental cochlear thrombosis on oxygenation and auditory function of the inner ear

To elucidate the etiology and pathogenesis of sudden hearing loss, the effect of experimental cochlear thrombosis on oxygenation and the auditory function of the inner ear was investigated in anesthetized guinea pigs. Impairment of cochlear blood flow (CBF) was induced by ferromagnetic obstruction of cochlear blood vessels at lowered body temperature. Perilymphatic oxygen partial pressure (PO₂) in the basal scala tympani (about 200 m below the round window membrane) was measured polarographically using micro-coaxial needle electrodes. Auditory function was examined by recording cochlear microphonic (CM) frequency responses, compound action potentials (CAP) and auditory evoked brainstem responses (ABR). Findings demonstrated a considerable decrease in the mean perilymphaticPO₂ of 40%, 2 h after the start of the experiment. Mean CM and N₁ CAP amplitudes were reduced by about 25% each and ABR by 18%. No significant changes were observed in the latencies of either CAP or ABR. Mean basal CBF was found to decrease by 35%, as measured by laser Doppler flowmetry in a parallel study. The present findings demonstrate that vascular impairment in the inner ear results in a considerable drop in intracochlear oxygenation, causing a significant loss in the auditory response.