Mechanisms of hearing loss resulting from middle-ear fluid

Ravicz, Michael E.; Rosowski, John J.; Merchant, Saumil N.

doi:10.1016/j.heares.2004.05.010

Cited by 94 publications

(179 citation statements)

References 35 publications

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“…5A, B). Previous results have also shown that V U is attenuated by MEE more at higher stimulus frequencies than lower (Ravicz et al 2004). We also found that V U was influenced by the amount of TM that was covered by fluid.…”

Section: Tympanometry Measurements With Fluid In the Middle-ear Spacementioning

confidence: 65%

“…This method of MEE simulation was adapted, in part, from the methods used by Goodhill and Holcomb (1958) and Hartley and Moore (2003). One viscosity of silicone oil was used (as opposed to a variety of viscosities) based on previous research that suggests that attenuation of sound as a result of middle-ear fluid depends mostly on fluid volume and not viscosity (Brown et al 1983;Wiederhold et al 1980;Marsh et al 1985;Ravicz et al 2004;Jeselsohn et al 2005;Thornton et al 2012). As a confirmation that the bullae were completely filled with fluid via this method, in some animals the silicone oil was mixed with food coloring.…”

Section: Umbo Velocity Measurementsmentioning

confidence: 99%

“…In some cases, MEEs can attenuate sound by more than 30 dB (Kokko 1974;Bluestone et al 1973). Previous studies have shown that the amount of fluid in the middle ear can significantly impact the magnitude of CHL, regardless of the viscosity of the fluid (Brown et al 1983;Wiederhold et al 1980;Jeselsohn et al 2005;Ravicz et al 2004;Thornton et al 2012). Furthermore, CHLs caused by MEEs have been shown to alter the binaural cues to sound location as represented by the inputs to the inner ear, the interaural time and level differences Thornton et al 2012).…”

Section: Introductionmentioning

confidence: 99%

“…Recently, Ravicz et al (2004) quantified in human cadaveric temporal bones the change in the umbo velocity transfer function as a result of an increasing volume of middle-ear fluid, but they did not test the more proximal aspects of the middle-ear system such as the resultant inputs to the inner ear. If the CHL is partially caused or modified by a mechanism proximal to the umbo, these experiments would not be able to accurately assess that change, as TM and umbo velocity measurements do not provide data on the transmission of sound through the middle ear.…”

Section: Introductionmentioning

confidence: 99%

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Conductive Hearing Loss Induced by Experimental Middle-Ear Effusion in a Chinchilla Model Reveals Impaired Tympanic Membrane-Coupled Ossicular Chain Movement

Thornton

Chevallier²,

Koka³

et al. 2013

JARO

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Otitis media with effusion (OME) occurs when fluid collects in the middle-ear space behind the tympanic membrane (TM). As a result of this effusion, sounds can become attenuated by as much as 30-40 dB, causing a conductive hearing loss (CHL). However, the exact mechanical cause of the hearing loss remains unclear. Possible causes can include altered compliance of the TM, inefficient movement of the ossicular chain, decreased compliance of the oval window-stapes footplate complex, or altered input to the oval and round window due to conduction of sound energy through middle-ear fluid. Here, we studied the contribution of TM motion and umbo velocity to a CHL caused by middle-ear effusion. Using the chinchilla as an animal model, umbo velocity (V U ) and cochlear microphonic (CM) responses were measured simultaneously using sinusoidal tone pip stimuli (125 Hz-12 kHz) before and after filling the middle ear with different volumes (0.5-2.0 mL) of silicone oil (viscosity, 3.5 Poise). Concurrent increases in CM thresholds and decreases in umbo velocity were noted after the middle ear was filled with 1.0 mL or more of fluid. Across animals, completely filling the middle ear with fluid caused 20-40-dB increases in CM thresholds and 15-35-dB attenuations in umbo velocity. Clinic-standard 226-Hz tympanometry was insensitive to fluid-associated changes in CM thresholds until virtually the entire middle-ear cavity had been filled (approximately 91.5 mL). The changes in umbo velocity, CM thresholds, and tympanometry due to experimentally induced OME suggest CHL arises primarily as a result of impaired TM mobility and TM-coupled umbo motion plus additional mechanisms within the middle ear.

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Section: Tympanometry Measurements With Fluid In the Middle-ear Spacementioning

confidence: 65%

Section: Umbo Velocity Measurementsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Conductive Hearing Loss Induced by Experimental Middle-Ear Effusion in a Chinchilla Model Reveals Impaired Tympanic Membrane-Coupled Ossicular Chain Movement

Thornton

Chevallier²,

Koka³

et al. 2013

JARO

View full text Add to dashboard Cite

show abstract

“…4A vs. B) is consistent with presence of a conductive hearing loss, since the OAE response amplitude is attenuated twice, by an acoustic round trip through the middle ear (Qin et al 2010). The frequency trend of the hearing loss is also consistent, since the replacement of middle-ear air by fluid and/ or the slightly negative middle-ear pressures often associated with a non-patent Eustachian tube, will affect transmission of low frequencies more than high frequencies (Ravicz et al 2004;Gan et al 2006). A possible role of sympathetic innervation in the control of bone remodeling in the bulla (Sherman and Chole 2001) must also be considered in the etiology of the conductive hearing loss in the Dbh −/− mice.…”

Section: Resistance To Acoustic Injury In Dbh −/− Micesupporting

confidence: 57%

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

Maison

Larsen

et al. 2010

JARO

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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.

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Detection of otoacoustic emissions in chinchilla when the middle ear contains amniotic fluid

2014

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Mechanisms of hearing loss resulting from middle-ear fluid

Cited by 94 publications

References 35 publications

Conductive Hearing Loss Induced by Experimental Middle-Ear Effusion in a Chinchilla Model Reveals Impaired Tympanic Membrane-Coupled Ossicular Chain Movement

Conductive Hearing Loss Induced by Experimental Middle-Ear Effusion in a Chinchilla Model Reveals Impaired Tympanic Membrane-Coupled Ossicular Chain Movement

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

Detection of otoacoustic emissions in chinchilla when the middle ear contains amniotic fluid

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