The physics of hearing: fluid mechanics and the active process of the inner ear.

Most sounds of interest consist of complex, time-dependent admixtures of tones of diverse frequencies and variable amplitudes. To detect and process these signals, the ear employs a highly nonlinear, adaptive, real-time spectral analyzer: the cochlea. Sound excites vibration of the eardrum and the three miniscule bones of the middle ear, the last of which acts as a piston to initiate oscillatory pressure changes within the liquid-filled chambers of the cochlea. The basilar membrane, an elastic band spiraling along the cochlea between two of these chambers, responds to these pressures by conducting a largely independent traveling wave for each frequency component of the input. Because the basilar membrane is graded in mass and stiffness along its length, however, each traveling wave grows in magnitude and decreases in wavelength until it peaks at a specific, frequency-dependent position: low frequencies propagate to the cochlear apex, whereas high frequencies culminate at the base. The oscillations of the basilar membrane deflect hair bundles, the mechanically sensitive organelles of the ear's sensory receptors, the hair cells. As mechanically sensitive ion channels open and close, each hair cell responds with an electrical signal that is chemically transmitted to an afferent nerve fiber and thence into the brain. In addition to transducing mechanical inputs, hair cells amplify them by two means. Channel gating endows a hair bundle with negative stiffness, an instability that interacts with the motor protein myosin-1c to produce a mechanical amplifier and oscillator. Acting through the piezoelectric membrane protein prestin, electrical responses also cause outer hair cells to elongate and shorten, thus pumping energy into the basilar membrane's movements. The two forms of motility constitute an active process that amplifies mechanical inputs, sharpens frequency discrimination, and confers a compressive nonlinearity on responsiveness. These features arise because the active process operates near a Hopf bifurcation, the generic properties of which explain several key features of hearing. Moreover, when the gain of the active process rises sufficiently in ultraquiet circumstances, the system traverses the bifurcation and even a normal ear actually emits sound. The remarkable properties of hearing thus stem from the propagation of traveling waves on a nonlinear and excitable medium.

Differential Volume Increase of Endolymphatic Compartments in Ménière's Disease Is Inversely Associated With Membrane Thickness.

OBJECTIVES: Our aim in this study was to characterize the morphology of the endolymphatic compartment on histopathology in individuals with Ménière's disease (MD) and to determine why hydrops of the saccule is more pronounced than that of other compartments of the inner ear in MD. METHODS: Temporal bones from 9 patients with idiopathic MD and from 10 individuals without MD/endolymphatic hydrops were examined. The inner ear fluid compartments in normal ears, and ears with MD were three-dimensionally reconstructed and their volume was calculated. The thickness of the membranes of the labyrinth was measured, and both ruptures of the membranes and patency of the utriculoendolymphatic (UEV; Bast's) valve were assessed. RESULTS: In ears with MD, the saccule and the cochlear duct were most frequently hydropic; the utricle was involved approximately half as frequently. In ears without MD, the Reissner's membrane and the membranous wall of the saccule were thinner than that of the utricle and of the lateral semicircular canal ( p < 0.01). The lateral semicircular canal did not show signs of hydrops. In all ears with MD in which the utricle exceeded the average volume of normals (6 of 12), the UEV was open or there was a rupture in the utricle. CONCLUSION: Increases in endolymphatic pressure may cause a primary swelling of the apical cochlear duct and saccule, both of which have relatively thin membranes. Hydrops in the utricle may occur less frequently because of a thicker wall, because of a functioning UEV, and when the saccule has already occupied most of the vestibular perilymphatic space.

Labyrinthine Fluid Signal Intensity on T2-Weighted MR Imaging in Patients With Vestibular Schwannomas Undergoing Proton Radiotherapy: A Longitudinal Assessment.

OBJECTIVE: In vestibular schwannoma patients, a loss of signal intensity (SI) on T2-weighted magnetic resonance imaging (MRI) has been reported within the ipsilateral labyrinth. The purpose of this study was to quantitatively evaluate the occurrence and course of this intensity loss in relation to proton radiotherapy and its possible association with hearing loss. STUDY DESIGN: Retrospective chart review. SETTING: Tertiary referral center. PATIENTS: Patients who received proton therapy for a vestibular schwannoma and underwent at least two high-resolution T2-weighted cisternographic sequence (constructive interference in steady state/fast imaging employing steady-state acquisition/DRIVE) MRIs and audiometry assessments. MAIN OUTCOME MEASURES: Relative T2 SIs from the vestibules and basal/apical cochlear turns of the labyrinth, bilaterally. RESULTS: Ninety-five MRI scans from 34 patients were included. The apical turn of the ipsilateral cochlea showed a lower mean cochlear SI than on the contralateral side (±3.5 versus 5.0). The mean relative cochlear SI did not significantly change after proton radiotherapy. The ipsilateral vestibule showed a higher SI than the cochlea. The relative mean cochlear SI was not directly correlated to (the degree of) hearing loss before or after proton radiotherapy, nor did it predict future hearing loss. CONCLUSION: The relative mean cochlear SI on cisternographic T2-MRI in vestibular schwannoma patients is diminished on the treated side, when compared with the ipsilateral vestibule and the contralateral cochlea/vestibule. The SI of the ipsilateral cochlea does not further decrease after proton radiotherapy and seems to be related to the tumor rather than the therapy. The diminished cochlear SI does not correlate with subsequent loss of hearing.

Hydrostatic fluid pressure in the vestibular organ of the guinea pig.

Since inner ear hair cells are mechano-electric transducers the control of hydrostatic pressure in the inner ear is crucial. Most studies analyzing dynamics and regulation of inner ear hydrostatic pressure performed pressure measurements in the cochlea. The present study is the first one reporting about absolute hydrostatic pressure values in the labyrinth. Hydrostatic pressure of the endolymphatic system was recorded in all three semicircular canals. Mean pressure values were 4.06 cmH(2)O ± 0.61 in the posterior, 3.36 cmH(2)O ± 0.94 in the anterior and 3.85 cmH(2)O ± 1.38 in the lateral semicircular canal. Overall hydrostatic pressure in the vestibular organ was 3.76 cmH(2)O ± 0.36. Endolymphatic hydrostatic pressure in all three semicircular canals is the same (p = 0.310). With regard to known endolymphatic pressure values in the cochlea from past studies vestibular pressure values are comparable to cochlear values. Until now it is not known whether the reuniens duct and the Bast's valve which are the narrowest passages in the endolymphatic system are open or closed. Present data show that most likely the endolymphatic system is a functionally open entity.

[Clinical and anatomical features of the middle ear in the premature infants at different gestational time].

The objective of the present study was to analyse anatomical features of the middle ear in the premature infants of different gestational age. Materials from 100 still-born and live-born babies (200 temporal bones) were available for the investigation. The study has revealed a number of distinctive clinical and morphological peculiarities in the structure of tympanic membranes in both the prematurely born infants depending on the gestational age and in the full-term babies. The fluid from the tympanic cavity was found to contain human beta-chorionic gonadotropin.

Fluid coupling in a discrete model of cochlear mechanics.

A discrete model of cochlear mechanics is introduced that includes a full, three-dimensional, description of fluid coupling. This formulation allows the fluid coupling and basilar membrane dynamics to be analyzed separately and then coupled together with a simple piece of linear algebra. The fluid coupling is initially analyzed using a wavenumber formulation and is separated into one component due to one-dimensional fluid coupling and one comprising all the other contributions. Using the theory of acoustic waves in a duct, however, these two components of the pressure can also be associated with a far field, due to the plane wave, and a near field, due to the evanescent, higher order, modes. The near field components are then seen as one of a number of sources of additional longitudinal coupling in the cochlea. The effects of non-uniformity and asymmetry in the fluid chamber areas can also be taken into account, to predict both the pressure difference between the chambers and the mean pressure. This allows the calculation, for example, of the effect of a short cochlear implant on the coupled response of the cochlea.

Correlation Between Adenoid Hypertrophy, Tympanometry Findings, and Viscosity of Middle Ear Fluid in Chronic Otitis Media With Effusion, Southern Oman.

Otitis media with effusion is a common cause of diminished hearing in children younger than 12 years. Hypertrophy of adenoids is one of the commonest etiologies of this condition. It has been mentioned that with increased size of the adenoid tissue, the more likely the incidence of fluid in the middle ear. The aim of this study was to find whether there is a correlation between adenoid size, tympanometric findings, and type of fluid in the middle ear irrespective of disease duration. This is a prospective study done on 100 pediatric patients (12 years and less) presented with chronic otitis media with effusion (COME) and adenoid hypertrophy from July 2015 till July 2017. Cases with tympanometry evidence of COME (B, Cs) and adenoid hypertrophy seen by nasal endoscopy were included. Adenoid size was graded and correlated with the type of tympanometry and type of fluid in the middle ear. Sixty male children and 40 female children were involved. Age ranged from 3 to 12 years with a mean of 7.19 ± 2.489 years. Highly significant relation existed between grade 4 adenoid hypertrophy and mucoid nature of middle ear fluid (P value = .000). There is a highly significant relation between adenoid hypertrophy grade Ⅳ and type B tympanometry. There is a highly significant relation between adenoid size and nature of middle ear fluid irrespective of the duration of complaints, where grade Ⅳ adenoid hypertrophy showed more increase in middle ear effusion viscosity making adenoid size a very important predictor for the tympanometry type and the nature of the fluid in the middle ear.

A two-dimensional cochlear fluid model based on conformal mapping.

Using conformal mapping, fluid motion inside the cochlear duct is derived from fluid motion in an infinite half plane. The cochlear duct is represented by a two-dimensional half-open box. Motion of the cochlear fluid creates a force acting on the cochlear partition, modeled by damped oscillators. The resulting equation is one-dimensional, more realistic, and can be handled more easily than existing ones derived by the method of images, making it useful for fast computations of physically plausible cochlear responses. Solving the equation of motion numerically, its ability to reproduce the essential features of cochlear partition motion is demonstrated. Because fluid coupling can be changed independently of any other physical parameter in this model, it allows the significance of hydrodynamic coupling of the cochlear partition to itself to be quantitatively studied. For the model parameters chosen, as hydrodynamic coupling is increased, the simple resonant frequency response becomes increasingly asymmetric. The stronger the hydrodynamic coupling is, the slower the velocity of the resulting traveling wave at the low frequency side is. The model's simplicity and straightforward mathematics make it useful for evaluating more complicated models and for education in hydrodynamics and biophysics of hearing.

Bone-conduction hyperacusis induced by superior canal dehiscence in human: the underlying mechanism.

Our ability to hear through bone conduction (BC) has long been recognized, but the underlying mechanism is poorly understood. Why certain perturbations affect BC hearing is also unclear. An example is BC hyperacusis (hypersensitive BC hearing)-an unnerving symptom experienced by patients with superior canal dehiscence (SCD). We measured BC-evoked sound pressures in scala vestibuli (PSV) and scala tympani (PST) at the basal cochlea in cadaveric human ears, and estimated hearing by the cochlear input drive (PDIFF = PSV - PST) before and after creating an SCD. Consistent with clinical audiograms, SCD increased BC-driven PDIFF below 1 kHz. However, SCD affected the individual scalae pressures in unexpected ways: SCD increased PSV below 1 kHz, but had little effect on PST. These new findings are inconsistent with the inner-ear compression mechanism that some have used to explain BC hyperacusis. We developed a computational BC model based on the inner-ear fluid-inertia mechanism, and the simulated effects of SCD were similar to the experimental findings. This experimental-modeling study suggests that (1) inner-ear fluid inertia is an important mechanism for BC hearing, and (2) SCD facilitates the flow of sound volume velocity through the cochlear partition at low frequencies, resulting in BC hyperacusis.

Type II collagen-induced autoimmune endolymphatic hydrops in guinea pig.

Endolymphatic hydrops was induced in guinea pigs by immunizing them with native bovine type II collagen. Histopathologic changes consisted of moderate extension of the Reissner's membrane, spiral ganglion degeneration, atrophied organ of Corti, and mild atrophy of the surface epithelium in the endolymphatic duct. These findings suggest that an immune response directed against type II collagen--a type of collagen found in the membranous labyrinth, subepithelial layer of the endolymphatic duct, spiral ligament, and enchondral layer of the otic capsule--may induce endolymphatic hydrops.

Cochlear neurons: frequency selectivity altered by perilymph removal.

Removal of perilylmph from the scala tympani of the guinea pig cochlea reversibly broadened the tuning curves of single spiral ganglion cells emanating from the basilar membrane. Thus, fluid continuity along the membrane is essential for normal cochlear function, in particular for sharp neural tuning curves. These data reveal a possible source of error in some estimates of basilar membrane motion and suggest a reappraisal of current concepts of the mechanism of sharp tunig in primary auditory nerve fibers.

Changes in endolymphatic potential and crossed olivocochlear bundle stimulation alter cochlear mechanics.

Mechanical nonlinearity in the cochlea produces acuoustic distortion products that can be measured in the ear canal. These distortion products can be altered by changes in the endolymphatic potential as well as by stimulation of the crossed olivocochlear bundle, which provides efferent innervation to cochlear hair cells.

Detection of an auditory nerve--activating substance.

A substance or substances capable of increasing the firing rate of primary auditory fibers is detectable in the perilymph of frogs and guinea pigs subjected to sound stimulation. The increase in firing rate occurs in single units of the frog auditory nerve after perilymph obtained from frogs or guinea pigs during sound stimulation is infused into the frog perilymphatic sac. Perilymph collected from animals maintained in silence failed to cause an increase in firing rate of primary auditory fibers of the frog.

Ouabain and streptomycin: their different loci of action on saccular hair cells in goldfish.

Ouabain, when applied to the periotic spaces, that is, to the basal end of the saccular hair cells, suppressed microphonic potentials of the inner ear in goldfish. In contrast, streptomycin produced such an effect only when it was applied directly into the endolymph, that is, to the hair-bearing ends of the hair cells.

Lateral Semicircular Canal Pressures During Cochlear Implant Electrode Insertion: a Possible Mechanism for Postoperative Vestibular Loss.

HYPOTHESIS: Insertion of cochlear implant electrodes generates transient pressure spikes within the vestibular labyrinth equivalent to high-intensity acoustic stimuli. BACKGROUND: Though cochlear implant (CI) surgery is regarded as having low risk of impacting the vestibular system, several studies have documented changes in vestibular function after implantation. The mechanism of these changes is not understood. We have previously established that large, potentially damaging pressure transients can be generated in the cochlea during electrode insertion, but whether pressure transients occur within the vestibular labyrinth has yet to be determined. Here, we quantify the exposure of the vestibular system to potentially damaging pressure transients during CI surgery. METHODS: Five human cadaveric heads were prepared with an extended facial recess and implanted sequentially with eight different CI electrode styles via a round window approach. Fiber-optic sensors measured intralabyrinthine pressures in scala vestibuli, scala tympani, and the lateral semicircular canal during insertions. RESULTS: Electrode insertion produced a range of high-intensity pressure spikes simultaneously in the cochlea and lateral semicircular canal with all electrodes tested. Pressure transients recorded were found to be significantly higher in the vestibular labyrinth than the cochlea and occurred at peak levels known to cause acoustic trauma. CONCLUSION: Insertion of CI electrodes can produce transients in intralabyrinthine fluid pressure levels equivalent to high-intensity, impulsive acoustic stimuli. Results from this investigation affirm the importance of atraumatic surgical techniques and suggest that in addition to the cochlea, the vestibular system is potentially exposed to damaging fluid pressure waves during cochlear implantation.

Superior canal dehiscence with tegmen defect revealed by otoscopy: Video clip demonstration of pulsatile tympanic membrane.

Superior canal dehiscence is a pathologic condition of the otic capsule acting as aberrant window of the inner ear. It results in reduction of inner ear impedance and in abnormal exposure of the labyrinthine neuroepithelium to the action of the surrounding structures. The sum of these phenomena leads to the onset of typical cochleo-vestibular symptoms and signs. Among them, pulsatile tinnitus has been attributed to a direct transmission of intracranial vascular activities to labyrinthine fluids. We present the first video-otoscopic documentation of spontaneous pulse-synchronous movements of the tympanic membrane in two patients with superior canal dehiscence. Pulsating eardrum may represent an additional sign of third-mobile window lesion.

Pneumolabyrinth, intracochlear and vestibular fluid loss after cochlear implantation.

The present case was a 38-year-old male who presented with progressive hearing loss, resulting in profound bilateral hearing loss. He had a past history of childhood medulloblastoma, which was treated with posterior fossa craniotomy and radiotherapy. A ventriculoperitoneal (VP) shunt was put in place to manage the hydrocephalus. Cochlear implantation (CI) was carried out on his right ear by a standard procedure. At CI activation, the electric impedance of the electrode was very high, and computed tomography revealed that there was no area of liquid density, suggesting depletion of the perilymph in the cochlea and vestibule. Eight months later, the impedance improved gradually, and the cochlea was filled with perilymph. Consequently, one of the causes of the pneumolabyrinth in the present case was that a scarred stenotic cochlear canaliculus secondary to surgery or radiation therapy might have prevented the CSF from filling the scala. In addition, it is also possible that the VP shunt might have altered the CSF pressure, leading to depletion of the perilymph.

The mutual independence of the endolymphatic potential and the concentrations of sodium and potassium in endolymph.

The relationship between the endolymphatic potential (EP) and the sodium and potassium concentration gradients between endolymph and interstitial fluid was studied both by measuring the EP at varying concentrations of sodium and potassium in endolymph and by measuring the effect of a depressed EP on the concentrations of these cations. Ethacrynic acid was used in dogs to change the concentration of sodium and potassium (meq/liter) in endolymph from 5.8 and 148 to 134 and 24.3, respectively. No change in the EP accompanied these alterations. In a second series of experiments the EP was reduced from + 72 mV to + 31 mV for a mean duration of 20 min. No change in the concentration of sodium and potassium in endolymph was found during the period of reduced EP. These data suggest that there is little relationship between the EP and the sodium and potassium concentrations in endolymph.

Transmission of infrasonic pressure waves from cerebrospinal to intralabyrinthine fluids through the human cochlear aqueduct: Non-invasive measurements with otoacoustic emissions.

The cochlear aqueduct connecting intralabyrinthine and cerebrospinal fluids (CSF) acts as a low-pass filter that should be able to transmit infrasonic pressure waves from CSF to cochlea. Recent experiments have shown that otoacoustic emissions generated at 1kHz respond to pressure-related stapes impedance changes with a change in phase relative to the generator tones, and provide a non-invasive means of assessing intracochlear pressure changes. In order to characterize the transmission to the cochlea of CSF pressure waves due to respiration, the distortion-product otoacoustic emissions (DPOAE) of 12 subjects were continuously monitored around 1kHz at a rate of 6.25epochs/s, and their phase relative to the stimulus tones was extracted. The subjects breathed normally, in different postures, while thoracic movements were recorded so as to monitor respiration. A correlate of respiration was found in the time variation of DPOAE phase, with an estimated mean amplitude of 10 degrees , i.e. 60mm water, suggesting little attenuation across the aqueduct. Its phase lag relative to thoracic movements varied between 0 degrees and -270 degrees . When fed into a two-compartment model of CSF and labyrinthine spaces, these results suggest that respiration rate at rest is just above the resonance frequency of the CSF compartment, and just below the corner frequency of the cochlear-aqueduct low-pass filter, in line with previous estimates from temporal bone and intracranial measurements. The fact that infrasonic CSF waves can be monitored through the cochlea opens diagnostic possibilities in neurology.

Aquaporins and Meniere's disease.

PURPOSE OF REVIEW: Review of the role of aquaporins in inner ear homeostasis and potential role in the pathogenesis of Meniere's disease. RECENT FINDINGS: Recent findings include the immunolocalization of aquaporins in the inner ear of mouse, rat, and human to cell types that are likely to undergo high ionic perturbances (e.g. potassium flux) and to putative areas of endolymph resorption or cycling. SUMMARY: The expression of aquaporins and related proteins in the human cochlea and vestibular periphery resembles the distribution found in animal models, suggesting a critical role of aquaporins in inner ear water homeostasis and their potential role in the pathogenesis of Meniere's disease.