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Re: Tinnitus and a dip in the audiogram

Yes, I think OAEs are an increase in system gain.

I think MOC efferent stimulation increase system gain at mid and apex cochlea locations. I think MOC efferent stimulation is more classical at higher frequencies (base Cochlea locations) ... this is the fundamental concept in our mixed-mode Cochlear amplifier model I have mentioned.

You should read Guinan's more recent publications in which he starts to discuss the non-classical results of his experiments. These results are discussed with respect to the apex and possibly may occur in the middle of the Cochela. If this is the case, then this is where SOAEs are common place.

Guinan 2012 : " presents a new view of how the cochlea works at frequencies below 3 kHz."


On 09/12/2012 10:43 AM, Mark Fletcher wrote:
OK, this sounds quite interesting. I'm aware of a lot of evidence of the MOC system causing a reduction in amplification (OAEs, all sort of physiology (e.g. Cooper and Guinan, 2006)). Do you know of evidence of MOC activation causing an increase in cochlear gain?


Date: Wed, 12 Sep 2012 09:24:26 -0500
From: flatmax@xxxxxxxxxxx
Subject: Re: [AUDITORY] Tinnitus and a dip in the audiogram
To: AUDITORY@xxxxxxxxxxxxxxx

Nope ...

The concept of the MOC efferents as a 'negative feedback loop' is classical and under rates the value of the MOCs in the system. The main argument for this point is that they are too slow to be significant otherwise ... which is a very weak argument.

The problem causing Tinnitus is that the stereocilia (in the case I described) are less resistive to ion currents. Consequently the operating point of the ear is taken out of stability. According to our model, the ear has infinite states, the first few of which are significant. Tinnitus, SOAEs and other phenomena are examples of the ear operating in a different state to what we normally consider.

p.s. This email discussion was off-list, now it is back on list ... I prefer one or the other ... otherwise we have context loss.

On 09/12/2012 05:31 AM, Mark Fletcher wrote:
If I understand you correctly then a problem with this idea is that the medial efferents don't stimulate the outer hair cells and drive more amplification, but reduce it - the MOC efferents make up a negative feedback loop.


Date: Tue, 11 Sep 2012 10:30:38 -0500
From: flatmax@xxxxxxxxxxx
To: markfletcher22@xxxxxxx
Subject: Re: [AUDITORY] Tinnitus and a dip in the audiogram

Yes I think you are on the right track ...

The link below is an article which discusses emissions in Tinnitus patients ... I have another link somewhere (can't find it now) which actually shows spontaneous emissions @ tinnitus frequencies.



On 09/11/2012 10:13 AM, Mark Fletcher wrote:
It's an interesting idea. Would you not expect to see evidence for this in otoacousitc emission work in tinnitus patients (I don't know if you do or not)?


> Date: Mon, 10 Sep 2012 10:03:24 -0500
> From: flatmax@xxxxxxxxxxx
> Subject: Re: [AUDITORY] Tinnitus and a dip in the audiogram
> To: AUDITORY@xxxxxxxxxxxxxxx
> Your second point here is one I like. However it may also be the same as
> your first point :)
> Our mixed-mode Cochlear amplifier supports your hypothesis.
> http://adsabs.harvard.edu/abs/2011AIPC.1403..611F
> The general idea is that certain types of Cochlea damage enhance the
> peripheral hearing circuit.
> For example, consider this thought experiment based on our mixed-mode
> Cochlear amplifier model :
> Imagine that your stereocillia are lopped off in a small region of inner
> hair cells - the same can be said for outer hair cells. This may happen
> due to ageing or damage.
> In this case assume that the stereocillia resistance is reduced - due to
> gaping open ion channels - and ionic currents into the cell (potassium)
> and our from the cell (sodium) are enhanced ... the hair cell now
> experience a depolarisation. This depolarisation generates more
> spontaneous neurotransmitter release.
> The neurotransmitters generate more synaptic transmission in the
> cochlear nerve.
> The cochlear nerve excites the superior olive and this not only
> generates perception of the tone, but sends signals back to the Cochlear
> over the lateral and medial efferents.
> The medial efferents stimulate the motors in the outer hair cells and
> they in turn generate movement at the inner hair cells which start the
> process again ... over and over again ... the end result is a
> mecho-neural standing wave ... or 'tinnitus'.
> This type of tinnitus masks low level sound heard through the ear ...
> however if the external sound gets loud enough, then it masks the tinnitus !
> What do you think ?
> Matt
> On 09/10/2012 08:22 AM, Matt Winn wrote:
> >
> > Mark and everyone,
> >
> > Although I am not a tinnitus researcher, I have had lots of experience
> > with patients with tinnitus in the audiology clinic. Generally, we try
> > to avoid the confusion of tinnitus with testing tones by using pulsed
> > and/or warbled tones. As you point out, this doesn’t always work out
> > perfectly.
> >
> > It has been my experience that dips in the audiogram are indeed
> > frequently accompanied by tinnitus. having measuring hearing at the
> > VA, this connection might be limited to hearing loss that is
> > noise-induced. The two most common explanations I have heard for this
> > are 1) damage to the auditory system at the site of the hearing loss
> > underlies both the threshold elevation and improper firing by damaged
> > nerves, and 2) tinnitus that exists in the region of the dip is not
> > masked out by external stimulation because the external sounds are
> > less audible; thus rendering tinnitus more noticeable. This latter
> > explanation accounts for the relief from tinnitus experienced by many
> > people who use hearing aids. Specifically, tinnitus isn’t “cured,” but
> > it is masked out by the amplified input, and then the tinnitus returns
> > after the hearing aid is removed.
> >
> > Returning to the point of tinnitus without apparent hearing loss, I
> > have found that salt intake and stress level are two (among many)
> > contributing factors to and my own tinnitus, and I don’t have hearing
> > loss. The dependence of OHCs on metabolic factors underscores this
> > connection, which seems anecdotally to be exacerbated in patients with
> > Ménière’s.
> >
> > Matt
> >
> >