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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
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.