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Re: Technique can pinpoint tinnitus



Hi all,

That's not my expertise area, but I know tinnitus reports around and pay attention to it.

What about tinnitus correlated with mandibular activity, such as tinnitus volume modulated when teeth are pressed, or when the mouth is widely opened? Is this peripheral or central? Notice that, in some cases, the only successful "treatment" (though temporary) has been "seen" with teeth anesthesia (exactly the one when you go to the dentist), showing that somehow a neural "leak" happens between nerves controlling jaw and the auditory neural area.

Regards,
Regis



Matt Flax escreveu:
I would like to support Arnaud's comments and expand a little...

I believe it is useful to define tinnitus as either of peripheral cause
or central cause - refs below. The peripheral cause is something to do
with a dysfunctional cochlear amplifier (nonlinear mechancis). The
central cause is to do with purely neural processes which are ill
understood. When looking at brain scans of any type, it is most likely
difficult to determine whether the tinnitus is of peripheral cause or
central cause - unless, the scans can also see peripheral activity
(activity in the inner ear and along the afferent/efferent nerves to and
from the inner ear).

It is clear that there are two types of tinnitus, peripheral [1] and
central. The argument for a central is found when looking at the
literature which discusses the success (or lack of success) when trying
to treat tinnitus using surgery [2, 3, 4, 5]. Only in around 50 to 60%
of cases does neurectomy solve the problem ... in these cases, one would
assume that the tinnitus is peripheral - i.e. caused by peripheral
cochlear amplifier dysfunction. The severing of the auditory nerve
(afferents) has obvious problems - the lack of transmission to the
brain, however there are also issues caused in severing the efferents.
In cases when severing the efferents solves the tinnitus problem, it is
most likely that the gain of the cochlear amplifier is reduced and it is
taken from an unstable state to a stable state again. You can get an
idea of how this would happen by referencing my compression wave
cochlear amplifier model [7].

Further, tinnitus can also be induced by head injury [6]. In this case,
it is possible that the inner ear is damaged and this causes a
peripheral type of tinnitus, which again is a cochlear amplifier
dysfunction. Until we can successfully trace this cause and develop
methods such as cellular regeneration possibly using stem cells - we can
tinker and experiment using all sorts of procedures to quash the
problem, but they will never be as sophisticated as actually repairing
the biology.

[1] @ARTICLE{Wilson:1980a,
  author = {Wilson, J.P.},
  title = {{Evidence for a cochlear origin for acoustic re-emissions,
threshold fine-structure and tonal tinnitus}},
  journal = {Hearing Research},
  year = 1980,
  volume = 2,
  pages = {233--252},
  number = {3-4},
  month = {June}
}

[2] @ARTICLE{silverstein:1986,
  author = {Silverstein, H. and Haberkamp, T. and Smouha, E.},
  title = {{The state of tinnitus after inner ear surgery.}},
  journal = {Otolaryngol Head Neck Surg},
  year = {1986},
  volume = {95},
  pages = {438--41},
  number = {4}
}

[3] @ARTICLE{jones:1989,
  author = {Jones, R. and Silverstein, H. and Smouha, E.},
  title = {{Long-term results of transmeatal cochleovestibular
neurectomy: an
	analysis of 100 cases.}},
  journal = {Otolaryngol Head Neck Surg},
  year = {1989},
  volume = {100},
  pages = {22--9},
  number = {1}
}

[4]@ARTICLE{wazen:1997,
  author = {Wazen, J.J. and Foyt, D. and Sisti, M.},
  title = {{Selective cochlear neurectomy for debilitating tinnitus}},
  journal = {The Annals of otology, rhinology \& laryngology},
  year = {1997},
  volume = {106},
  pages = {568--570},
  number = {7},
  publisher = {Annals Publishing Compagny}
}

[5] @ARTICLE{baguley:2002,
  author = {Baguley, DM and Axon, P. and Winter, IM and Moffat, DA},
  title = {{The effect of vestibular nerve section upon tinnitus}},
  journal = {Clinical Otolaryngology and Allied Sciences},
  year = {2002},
  volume = {27},
  pages = {219--226},
  number = {4},
  publisher = {Blackwell Synergy}
}


[6] @ARTICLE{ceranic:1998,
  author = {Ceranic, B.J. and Prasher, D.K. and Raglan, E. and Luxon,
L.M.},
  title = {{Tinnitus after head injury: evidence from otoacoustic
emissions}},
  journal = {Journal of Neurology, Neurosurgery \& Psychiatry},
  year = {1998},
  volume = {65},
  pages = {523--529},
  number = {4},
  publisher = {BMJ}
}

[7] Introducing the Compression Wave Cochlear Amplifier

M Flax, W Holmes - Conference proceedings: Interspeech 2008, 2008


On Tue, 2009-10-06 at 16:40 +0200, arnaud norena wrote:
Dear John,

we are far from knowing the fine mechanisms of tinnitus but there is a
consensus in the field (I think) stating that tinnitus is caused by
some central mechanisms (i.e. release from central inhibition) after a
decrease in sensory inputs (caused by hearing loss). Noise trauma,
which is known to decrease spontaneous activity at cochlear nerve
level, and which is a strong and common "tinnitus inducer",
corroborate the view of a central tinnitus (a decrease in neural
activity is likely not related to a perception). Interestingly, the
percept of tinnitus corresponds strictly to the frequency range of
hearing loss (Norena et al., 2002). Moreover, it is worth mentioning
that cochlear implant subjects often present a tinnitus and that a
section of the cochlear nerve does not always abolish tinnitus.
Finally, some papers have shown neural changes (both in term of firing
rate and synchrony) after noise trauma in AI of (anesthetized) cats
circumscribed to neurons with characteristic frequency corresponding
to the frequency range of hearing loss (for instance: Norena and
Eggermont, 2003 - sorry for the self-promotion :-) ).

This model suggests that the decrease in afferent inputs should be
compensated to prevent/reverse the central changes causing tinnitus.
Hearing aids could be a way for stimulating/reeducating the auditory
system (as long as the cochlea transmits sensory inputs, i.e. absence
of "dead regions"). However, the immediate release from tinnitus
caused by hearing aids is likely caused by the partial masking of
tinnitus by the amplified background.
regards,
arnaud norena

2009/10/6 Beerends, J.G. (John) <john.beerends@xxxxxx>
        Dear All,
In this paper there is no mentioning of any relation between
        tinnitus and hearing loss.
        The spontaneous neural activity may just be the result of
        unused neural capacity that was stimulated before getting
        damaged. Are there any experts that know if this relation
        exists? And if so, is this relation is linked to damage of
        both the outer and inner hair cells, or to either one of them?
I know experts who say that tinnitus often gets less when a
        subject with hearing loss (and tinnitus) starts wearing a
        correctly fitted hearing aid. This would support the idea of
        hearing loss induced spontaneous neural activity.
John Beerends
        TNO
        Delft
        The Netherlands
-----Original Message-----
        From: AUDITORY - Research in Auditory Perception
        [mailto:AUDITORY@xxxxxxxxxxxxxxx] On Behalf Of Kevin Austin
        Sent: dinsdag 6 oktober 2009 1:15
        To: AUDITORY@xxxxxxxxxxxxxxx
        Subject: Technique can pinpoint tinnitus
From the BBC: http://news.bbc.co.uk/1/hi/health/8287791.stm Best Kevin This e-mail and its contents are subject to the DISCLAIMER at
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