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David Mountain wrote:
>I don't understand your statement "it is possible to see a direct
>link between action of the stapedius muscle on the stapes and
>intracochlear pressure." A static displacement of the stapes would not be
>expected to cause a change in intracochlear pressure because the
>helicotrema and round window act as a pressure release system.
But the round window is a membrane with a compliance. It requires a pressure to distend it. Pushing the stapes in must raise intracochlear pressure because the cochlear fluids (water) are incompressible. The only escape clause is if there are other pressure relief points (so-called "third windows").
The most likely third window is the cochlear aqueduct, and much research into its patency has been made. It is narrow and apparently filled with tissue. Some researchers claim the time constant for pressure relief is many seconds, others that it is much shorter. When a subject is inverted, intracochlear pressure rises and hearing and SOAE frequencies are altered; on reverting to normal, SOAE frequencies (and impedance measures) take about 20 seconds to return to normal. I think 20 seconds is a reasonable time constant, in which case the cochlea is pretty well sealed.
At the same time, we have the clinical fact that people with fixated stapes (otosclerosis) have a negative Gellé test, whereas normal people do not. That is, if air pressure is applied to the ear canal and a tuning fork applied to the skull (bone conducted sound), the sound is reduced in loudness when air pressure is applied (for normals = positive Gellé), whereas the sound is unchanged in otosclerotics (negative Gellé). This makes sense if the intracochlear pressure is raised in the normal case, but not for otosclerotics.
On this basis we can interpret the action of the middle ear muscles as increasing intracochlear pressure and damping down the gain of the pressure-sensitive cochlear amplifier. This is the classic intralabyrinthine pressure theory of middle ear muscle action, which Gellé formulated in 1881. There is a wide literature devoted to proving or disproving it, and here is perhaps not the place to discuss it in detail (in keeping with past requests to keep cochlear theory out of the Auditory list). Let me just say that it is eminently credible and makes sense of a diverse literature, including that on Menieres disease, although it has not retained wide currency (probably because of a wish to retain the dominant paradigm, traveling wave theory, in which it is hard to see how hydrostatic pressure could have any effect on the motion of the basilar membrane).
One example only: Feldman et al. (1979) measured the hydrostatic pressures in the cochlear compartments of the guinea pig and concluded that "the tympanic membrane and ossicles exert a constant pressure on the oval window which is reflected in and partially responsible for the perilymphatic pressure." [Neurological Research 1, 11-18] A problem is that water is so incompressible and the stapes movements so small that it is difficult to measure intracochlear pressures accurately -- the smallest leak and the results are out.
Nevertheless the alternative conclusion -- that the middle ear muscles have no effect on pressure -- implies that nature has designed an elaborate gain control system (the m.e. muscles) which attenuate sound by ineffective amounts: Loth et al. (Acta Acustica 2, 1994, 149-155) found that m.e. muscles provided _no_ attenuation for at least a quarter of their subjects. So what (in those cases anyway) are the muscles doing? If one looks at the results of Avan et al. (Hear.Res.140, 2000, 189-201) on otoacoustic emissions there is a striking similarity between the effect of increased intracranial pressure and the effect of stapedius muscle contractions. The similarity comes, of course, from them both increasing intracochlear pressure.
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