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Re: mechanical cochlear model

Daniel, and others,

My lab has recently published a paper (Lupo et al., 2009; see below) and an abstract (Koka, Tringali, and Tollin, 2010) at the recent ARO meeting that also supports the idea of 'third windows'.

Your findings are much more compatible with a concept of hair cell excitation without fluid bulk shift, but via fluid borne sound waves. The candidates for "third windows" have been discussed at length for decades. The common understanding was that these "windows" are too small for an effective fluid bulk shift.

Your data, as well as plenty of other data (including a wealth of data on bone conduction) can much better be explained when the traveling wave hypothesis is abandoned. The slight threshold effect that you observed can be explained by assuming that stapes fixation slightly reduces the compliance of the round window even for the picometer displacements that are sufficient to trigger a sound wave in the cochlear fluids.


Martin Braun
Neuroscience of Music
S-671 95 Klässbol
email: nombraun@xxxxxxxxx
web site: http://www.neuroscience-of-music.se/index.htm

----- Original Message ----- From: "Tollin, Daniel" <Daniel.Tollin@xxxxxxxxxxxx>
To: <AUDITORY@xxxxxxxxxxxxxxx>
Sent: Monday, March 08, 2010 11:23 PM
Subject: Re: mechanical cochlear model


My lab has recently published a paper (Lupo et al., 2009; see below) and an abstract (Koka, Tringali, and Tollin, 2010) at the recent ARO meeting that also supports the idea of 'third windows'. In the Lupo et al paper we investigated the effect of experimentally-induced stapes fixation (super glue) on the cochlear microphonic (CM), compound action potential, and ABR thresholds obtained by mechanically stimulating the round window (RW) with a middle ear implantable hearing aid. RW-stimulated thresholds were moderately elevated after stapes fixation, but not abolished. Laser Doppler vibrometry confirmed that the stapes was not moving in these conditions.

Second, at ARO we reported that under conditions were mechanical stimulation of the RW produced the same amplitude CM as acoustic stimulation (thus, presumably, the same effective input to the inner ear), the measured stapes velocities for RW stimulation underestimated the acoustic by up to 20 dB. Thus, when the cochlea is driven in 'reverse' via the RW some mechanism reduces the stapes velocity. A third window is a potential explanation.

Note that these experiments were in chinchilla, and there is the real possibility of a species difference (humans vs animals) regarding third windows.

Lupo JE, Koka K, Holland NJ, Jenkins HA, and Tollin DJ (2009) Prospective Electrophysiologic Findings of Round Window Stimulation in a Model of Experimentally-induced Stapes Fixation, Otology & Neurotology, 30:1215-1224.

HYPOTHESIS: Mechanical stimulation of the round window (RW) with an active middle ear implant (AMEI) with and without experimentally induced stapes fixation (SF) results in equivalent electrophysiologic measures of cochlear microphonic (CM), compound action potential (CAP), and auditory brainstem response (ABR). BACKGROUND: Where normal oval window functionality is mitigated, the RW provides a pathway to mechanically stimulate the inner ear. METHODS: Measurements of the CM, CAP, and ABR were made in 5 ears of 4 chinchillas with acoustic stimulation and with application of the AMEI to the RW with and without experimentally induced SF using pure-tone stimuli (0.25-20 kHz) presented at differing intensities (-20 to 80 dB SPL vs. 0.01 mV to 3.16 V). RESULTS: Morphologies of the CM, CAP, and ABR were similar between acoustic and RW stimulation with and without SF. Stapes fixation increased CM thresholds relative to RW stimulation without fixation by a frequency-dependent 4- to 13-dB mV (mean, 7.9 +/- 3.2 dB mV). Although the thresholds changed with SF, CM sensitivities and amplitude dynamic range were identical to normal. The CAP in all conditions demonstrated equivalent decreasing amplitudes and increasing latency with decreasing intensity (decibel sound pressure level versus decibel millivolt). Stapes fixation increased the CAP thresholds at all frequencies, ranging from 9 to 24 dB mV (mean, 17.7 +/- 4.9 dB mV). Auditory brainstem response waveforms were preserved across experimental conditions. CONCLUSION: Mechanical stimulation of the RW in an animal model of SF generates functionally similar inputs to the cochlea as normal acoustic and RW mechanical inputs but with increased thresholds. With further study, AMEIs may provide a surgical option for correction of otosclerosis and ossicular chain disruption.

Koka, K, Tringali S and Tollin DJ (2010). Can stapes velocity be used to estimate the efficacy of mechanical stimulation of the round window of the cochlea with an active middle ear implant? Assoc. Res. Otol. Vol. 33.

Mechanical stimulation of the round window membrane (RW) with active middle ear prostheses (AMEP) has shown some functional benefit in clinical reports in patients with mixed hearing loss. There are published standards for objective measurement of AMEP performance based on stapes velocity in human cadaver temporal bones for AMEPs when coupled to the ossicular chain. Here, stapes velocity is a reasonable measure of the input to the cochlea via the AMEP because the system is driven in the forward direction. However, these standards may not be applicable when estimating the efficiency of the RW drive with an AMEP because the stapes velocities in this case are expected to be more complex due to driving the cochlea in the reverse direction and the potential effects of "third windows". Here we test this hypothesis by measuring the cochlear microphonics (CM) and the stapes velocities in response to both acoustic stimulation (forward direction) and RW stimulation with an AMEP (reverse direction). Seven ears in five chinchillas were studied. For each stimulus frequency, the amplitude of the CM was measured separately as a function of intensity (dB SPL or dB mV). Equivalent vibrational input to the cochlea was estimated by equating the acoustic and AMEP CM amplitudes at a constant value. For the same CM amplitude output we assume that the same vibrational input to the cochlea was present regardless of the route of stimulation. The stapes velocities for these equivalent outputs were not significantly different for low and medium frequencies (0.25-4 kHz) but the velocities for AMEP-RW drive were significantly lower for higher frequencies (4-14 kHz). The results suggest that the measured stapes velocities when driving the RW underestimate the actual mechanical input to the cochlea. At frequencies above 4 kHz, stapes velocity underestimated the RW input by ~20 dB. The possible influences of cochlear third windows are discussed as well as alternative methods to assess AMEP performance when driving the RW.

Daniel J. Tollin, PhD
Assistant Professor

University of Colorado Denver Health Sciences Center
Department of Physiology and Biophysics/Mail Stop 8307
Research Complex 1-N, Rm 7106
12800 East 19th Ave
PO Box 6511
Aurora, CO 80045

Tel:  303-724-0625
Fax: 303-724-4501

-----Original Message-----
From: AUDITORY - Research in Auditory Perception [mailto:AUDITORY@xxxxxxxxxxxxxxx] On Behalf Of Richard F. Lyon
Sent: Monday, March 08, 2010 2:08 PM
To: AUDITORY@xxxxxxxxxxxxxxx
Subject: Re: mechanical cochlear model


Maybe I misinterpreted what was behind your statements, and I agree
it was impolitic (but maybe short of slander) to say what I thought.

Just one example. In the 1950s it was well established and widely
discussed that temporary threshold shift (TTS) due to high-level
sound exposure does not occur at the place of the characteristic
frequency (CF) of the stimulus (say, 2 kHz) but about half an octave
towards the base of the cochlea (i.e., at the CF place of 3 kHz).
These often repeated observations were, and still are, evidence for
the view that the basilar membrane traveling wave peaks about half
an octave basalwards of the neural CF. Yet, Bekesy and his followers
succeeded in treating this evidence as if it did not exist.

The half-octave shift was hard to interpret back when the view was
that the cochlea was pretty much linear, but has since been
incorporated as an inevitable side effect of variable-peak-gain
nonlinear models that match the observed BM mechanics.  It's easily
incorporated in nonlinear traveling wave models.

Nonlinear models, like the real cochlea, have a maximum response that
occurs at places basalward of the place that has the corresponding
CF.  You are correct in saying that there is good "evidence for the
view that the basilar membrane traveling wave peaks about half an
octave basalwards of the neural CF", for high enough levels.  Only at
very low levels does the wave, or the neural response, peak near the
CF place.  This is well known and accepted, like the traveling wave
concept itself, and is true independent of whether the model is based
on the traveling wave being the main mechanism of energy transport.
The half-octave basalward shift therefore doesn't provide much
support one way or the other for what I think this argument might be
about.  Or maybe I'm wrong on what it's about, since I seem to be
unable to fathom the motivations...

The half-octave shift of the response maximum with level (or at least
part of it) can also be induced by stimulating the efferents, or by a
loud contralateral sound that stimulates the efferents.  Anything
that "turns down the gain" of the "cochlear amplifier" will make the
wave peak earlier (more basally) and damp out sooner.  Noise-induced
TTS is just one extreme example, and it certainly hasn't been
ignored.  Other such effects are widely investigated.  Here's a
recent paper available online that talks about some:
(I don't know what this site in China is about, but they seem to have
a lot of JASA papers freely available -- is that legit?).

I didn't know von Bekesy, but probably some of "his followers" are
among the people I know who have incorporated nonlinearity into our
understanding of hearing over the last four decades.  Why do you say
they treat the evidence as if it does not exist?  Evidence that's
hard to explain is always good to examine; that's where new ideas and
findings come from.  So bring on some more.

As an example of evidence that's hard to explain, we have the
blocked-round-window experiment of Perez 2009.  It needs to be
investigated further, so we can see if it can be replicated, and if
so what it means.  If occlusion by super-glue is really stiff enough
to prevent the stapes initiating a traveling wave, we should be able
to see that by greatly reduced stapes motion, or reflected energy in
the ear canal, or impedance change at the eardrum or some such
measurement.  If the threshold of hearing is really unchanged when
the stapes isn't moving, that's one thing.  If the stapes is moving
in spite of super-glue on the round window, that's something else.

The comment on Martin's site says
"Immobilization of the round window reduces, or even abolishes, a
local motion of the basilar membrane (BM) toward the scala timpani
upon sound exposure. The reason is that a volume shift in the scala
timpani is impeded, or even made impossible, if the round window
membrane can no longer bulge outwards. Therefore, a sound induced BM
traveling wave along the cochlea must necessarily be greatly reduced
under this condition.
The findings that a reduction of the BM traveling wave leaves hearing
thresholds unchanged, but increases vulnerability against acoustic
overload, constitute a direct experimental confirmation of a
completely new theory of cochlear functions that was first published
16 years ago. (Comment Martin Braun)"

This seems to be way beyond what the authors of the paper could dare
to conclude.  If it turns out to be true, then we would all have to
admit that the traveling wave isn't the effective stimulus for
hearing; but we're not there yet.

I'm not convinced that Reinhart's explanation solves the problem.  If
the stapes moves and initiates a traveling wave, the fluid has to
have some place to go; that is, the basal region is in the long-wave
region, not just a wave confined to the around the membrane.

If it's not the round window, then maybe there's another possible
path, as Dave mentioned, "There is some very good evidence that there
is a third window in the cochlea from H. Nakajima et al that was
presented at this year's ARO meeting."  They considered various
possibilities.  For those who were not there, here's their abstract:

Is There a Physiological Third Window? Measurements of Human
Cadaveric Intracochlear
Differential Pressures for Round Window Stimulation with Fixed Stapes
Hideko Nakajima, Saumil N. Merchant, John Rosowski
It has been hypothesized that the inner ear is a rigid structure
filled with incompressible fluid, with only two flexible windows to
produce differential pressure across the partition for transduction
of sound. This hypothesis has been supported with experiments in the
past for the case of a normal inner ear with forward stimulation
through the oval window. However, this evidence does not rule out the
existence of a normal physiological third window that is small in
conductance compared to the oval and round windows, such that the
small third window influence is insignificant under normal
conditions. In the case of reverse round window (RW) cochlear
stimulation, fixation of the stapes should prevent cochlear
transduction if the hypothesis held true. However, it has been
reported that RW stimulation has improved hearing in patients with
fixed stapes (Beltrame et al 2009). RW stimulation has potential as a
treatment for stapes fixation when stapedectomy is contraindicated.
Our experimental results in cadaveric temporal bone preparations show
that reverse RW stimulation after fixation of the stapes resulted in
higher pressures in both scalae, which were similar (within 1 dB) in
magnitude. However, the calculation of the complex differential
pressure revealed significant pressure difference, indicating
achievable hearing. These results suggest that a clinically-relevant
physiological third window likely exists in the scala vestibuli
compartment. Possible fluid release mechanisms include the
endolymphatic duct, neural and vascular channels, as well as the
possibility that the bone surrounding the inner ear is not infinitely
rigid throughout, and/or that the combination of having unequal
volumes in scala vestibuli and scala tympani with slight fluid
compressibility results in a physiological third window.

I think this is pretty good evidence that people are working on
understanding the data, not ignoring it.

Martin, since I don't have the Perez paper handy, can you tell us
what the statistical support was for their observation that "In the
four control ears, there was no change in ABR threshold 24 hours
after the round window was occluded."?  Would a hypothesis of a few
dB of threshold rise be equally compatible with their data?  That's
what the "third physiological window" idea would suggest.