Subject: Re: Tinnitus and a dip in the audiogram From: Mark Fletcher <markfletcher22@xxxxxxxx> Date: Wed, 12 Sep 2012 11:31:36 +0100 List-Archive:<http://lists.mcgill.ca/scripts/wa.exe?LIST=AUDITORY>--_0c22b1a8-3156-4fa1-a993-bf32bb326165_ Content-Type: text/plain; charset="Windows-1252" Content-Transfer-Encoding: quoted-printable If I understand you correctly then a problem with this idea is that the med= ial efferents don't stimulate the outer hair cells and drive more amplifica= tion=2C but reduce it - the MOC efferents make up a negative feedback loop. Mark Date: Tue=2C 11 Sep 2012 10:30:38 -0500 From: flatmax@xxxxxxxx To: markfletcher22@xxxxxxxx Subject: Re: [AUDITORY] Tinnitus and a dip in the audiogram =20 =20 =20 =20 Yes I think you are on the right track ... =20 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 @xxxxxxxx tinnitus frequencies. =20 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2170278/pdf/v065p00523.pdf =20 Matt =20 On 09/11/2012 10:13 AM=2C Mark Fletcher wrote: =20 =20 =20 =20 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)? =20 =20 Mark =20 > Date: Mon=2C 10 Sep 2012 10:03:24 -0500 > From: flatmax@xxxxxxxx > Subject: Re: [AUDITORY] Tinnitus and a dip in the audiogram > To: AUDITORY@xxxxxxxx >=20 > Your second point here is one I like. However it may also be the same as=20 > your first point :) >=20 > Our mixed-mode Cochlear amplifier supports your hypothesis. > http://adsabs.harvard.edu/abs/2011AIPC.1403..611F >=20 > The general idea is that certain types of Cochlea damage enhance the=20 > peripheral hearing circuit. >=20 > For example=2C consider this thought experiment based on our mixed-mode=20 > Cochlear amplifier model : >=20 > Imagine that your stereocillia are lopped off in a small region of inner=20 > hair cells - the same can be said for outer hair cells. This may happen=20 > due to ageing or damage. > In this case assume that the stereocillia resistance is reduced - due to=20 > gaping open ion channels - and ionic currents into the cell (potassium)=20 > and our from the cell (sodium) are enhanced ... the hair cell now=20 > experience a depolarisation. This depolarisation generates more=20 > spontaneous neurotransmitter release. > The neurotransmitters generate more synaptic transmission in the=20 > cochlear nerve. > The cochlear nerve excites the superior olive and this not only=20 > generates perception of the tone=2C but sends signals back to the Cochlear=20 > over the lateral and medial efferents. > The medial efferents stimulate the motors in the outer hair cells and=20 > they in turn generate movement at the inner hair cells which start the=20 > process again ... over and over again ... the end result is a=20 > mecho-neural standing wave ... or 'tinnitus'. > This type of tinnitus masks low level sound heard through the ear ...=20 > however if the external sound gets loud enough=2C then it masks the tinnitus ! >=20 > What do you think ? >=20 > Matt >=20 > On 09/10/2012 08:22 AM=2C Matt Winn wrote: > > > > Mark and everyone=2C > > > > Although I am not a tinnitus researcher=2C I have had lots of experience=20 > > with patients with tinnitus in the audiology clinic. Generally=2C we try=20 > > to avoid the confusion of tinnitus with testing tones by using pulsed=20 > > and/or warbled tones. As you point out=2C this doesn=92t always work out=20 > > perfectly. > > > > It has been my experience that dips in the audiogram are indeed=20 > > frequently accompanied by tinnitus. having measuring hearing at the=20 > > VA=2C this connection might be limited to hearing loss that is=20 > > noise-induced. The two most common explanations I have heard for this=20 > > are 1) damage to the auditory system at the site of the hearing loss=20 > > underlies both the threshold elevation and improper firing by damaged=20 > > nerves=2C and 2) tinnitus that exists in the region of the dip is not=20 > > masked out by external stimulation because the external sounds are=20 > > less audible=3B thus rendering tinnitus more noticeable. This latter=20 > > explanation accounts for the relief from tinnitus experienced by many=20 > > people who use hearing aids. Specifically=2C tinnitus isn=92t =93cured=2C=94 but=20 > > it is masked out by the amplified input=2C and then the tinnitus returns=20 > > after the hearing aid is removed. > > > > Returning to the point of tinnitus without apparent hearing loss=2C I=20 > > have found that salt intake and stress level are two (among many)=20 > > contributing factors to and my own tinnitus=2C and I don=92t have hearing=20 > > loss. The dependence of OHCs on metabolic factors underscores this=20 > > connection=2C which seems anecdotally to be exacerbated in patients with=20 > > M=E9ni=E8re=92s. > > > > Matt > > > > =20 =20 =20 =20 =20 = --_0c22b1a8-3156-4fa1-a993-bf32bb326165_ Content-Type: text/html; charset="Windows-1252" Content-Transfer-Encoding: quoted-printable <html> <head> <style><!-- .hmmessage P { margin:0px=3B padding:0px } body.hmmessage { font-size: 10pt=3B font-family:Tahoma } --></style></head> <body class=3D'hmmessage'><div dir=3D'ltr'> If I understand you correctly then a problem with this idea is that the&nbs= p=3Bmedial efferents don't stimulate the outer hair cells and drive more am= plification=2C but reduce it - the MOC efferents make up a <i>negative</i> = feedback loop.<br><br>Mark<br><br><div><div id=3D"SkyDrivePlaceholder"></di= v><hr id=3D"stopSpelling">Date: Tue=2C 11 Sep 2012 10:30:38 -0500<br>From: = flatmax@xxxxxxxx<br>To: markfletcher22@xxxxxxxx<br>Subject: Re: [AUDITORY= ] Tinnitus and a dip in the audiogram<br><br> =20 =20 =20 =20 <div class=3D"ecxmoz-cite-prefix">Yes I think you are on the right trac= k ...<br> <br> 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 @xxxxxxxx tinnitus frequencies.<br= > <br> <a class=3D"ecxmoz-txt-link-freetext" href=3D"http://www.ncbi.nlm.nih.gov/p= mc/articles/PMC2170278/pdf/v065p00523.pdf" target=3D"_blank">http://www.ncb= i.nlm.nih.gov/pmc/articles/PMC2170278/pdf/v065p00523.pdf</a><br> <br> Matt<br> <br> On 09/11/2012 10:13 AM=2C Mark Fletcher wrote:<br> </div> <blockquote cite=3D"mid:BLU162-W20D29ED3BAFEBDAE849621D7930@xxxxxxxx"> <style><!-- .ExternalClass .ecxhmmessage P {padding:0px=3B} .ExternalClass body.ecxhmmessage {font-size:10pt=3Bfont-family:Tahoma=3B} --></style> <div dir=3D"ltr"> 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)? <div><br> </div> <div>Mark<br> <br> <div>>=3B Date: Mon=2C 10 Sep 2012 10:03:24 -0500<br> >=3B From: <a class=3D"ecxmoz-txt-link-abbreviated" href=3D"m= ailto:flatmax@xxxxxxxx">flatmax@xxxxxxxx</a><br> >=3B Subject: Re: [AUDITORY] Tinnitus and a dip in the audiogram<br> >=3B To: <a class=3D"ecxmoz-txt-link-abbreviated" href=3D"mai= lto:AUDITORY@xxxxxxxx">AUDITORY@xxxxxxxx</a><br> >=3B <br> >=3B Your second point here is one I like. However it may also be the same as <br> >=3B your first point :)<br> >=3B <br> >=3B Our mixed-mode Cochlear amplifier supports your hypothesis.<br> >=3B <a class=3D"ecxmoz-txt-link-freetext" href=3D"http://ads= abs.harvard.edu/abs/2011AIPC.1403..611F" target=3D"_blank">http://adsabs.ha= rvard.edu/abs/2011AIPC.1403..611F</a><br> >=3B <br> >=3B The general idea is that certain types of Cochlea damage enhance the <br> >=3B peripheral hearing circuit.<br> >=3B <br> >=3B For example=2C consider this thought experiment based on our mixed-mode <br> >=3B Cochlear amplifier model :<br> >=3B <br> >=3B Imagine that your stereocillia are lopped off in a small region of inner <br> >=3B hair cells - the same can be said for outer hair cells. This may happen <br> >=3B due to ageing or damage.<br> >=3B In this case assume that the stereocillia resistance is reduced - due to <br> >=3B gaping open ion channels - and ionic currents into the cell (potassium) <br> >=3B and our from the cell (sodium) are enhanced ... the hair cell now <br> >=3B experience a depolarisation. This depolarisation generates more <br> >=3B spontaneous neurotransmitter release.<br> >=3B The neurotransmitters generate more synaptic transmission in the <br> >=3B cochlear nerve.<br> >=3B The cochlear nerve excites the superior olive and this not only <br> >=3B generates perception of the tone=2C but sends signals back to the Cochlear <br> >=3B over the lateral and medial efferents.<br> >=3B The medial efferents stimulate the motors in the outer hair cells and <br> >=3B they in turn generate movement at the inner hair cells which start the <br> >=3B process again ... over and over again ... the end result is a <br> >=3B mecho-neural standing wave ... or 'tinnitus'.<br> >=3B This type of tinnitus masks low level sound heard through the ear ... <br> >=3B however if the external sound gets loud enough=2C then i= t masks the tinnitus !<br> >=3B <br> >=3B What do you think ?<br> >=3B <br> >=3B Matt<br> >=3B <br> >=3B On 09/10/2012 08:22 AM=2C Matt Winn wrote:<br> >=3B >=3B<br> >=3B >=3B Mark and everyone=2C<br> >=3B >=3B<br> >=3B >=3B Although I am not a tinnitus researcher=2C I have had lots of experience <br> >=3B >=3B with patients with tinnitus in the audiology clinic. Generally=2C we try <br> >=3B >=3B to avoid the confusion of tinnitus with testing tones by using pulsed <br> >=3B >=3B and/or warbled tones. As you point out=2C this doesn=92t always work out <br> >=3B >=3B perfectly.<br> >=3B >=3B<br> >=3B >=3B It has been my experience that dips in the audiogram are indeed <br> >=3B >=3B frequently accompanied by tinnitus. having measuring hearing at the <br> >=3B >=3B VA=2C this connection might be limited to hearing loss that is <br> >=3B >=3B noise-induced. The two most common explanations I have heard for this <br> >=3B >=3B are 1) damage to the auditory system at the site of the hearing loss <br> >=3B >=3B underlies both the threshold elevation and improper firing by damaged <br> >=3B >=3B nerves=2C and 2) tinnitus that exists in the regi= on of the dip is not <br> >=3B >=3B masked out by external stimulation because the external sounds are <br> >=3B >=3B less audible=3B thus rendering tinnitus more noticeable. This latter <br> >=3B >=3B explanation accounts for the relief from tinnitus experienced by many <br> >=3B >=3B people who use hearing aids. Specifically=2C tinnitus isn=92t =93cured=2C=94 but <br> >=3B >=3B it is masked out by the amplified input=2C and th= en the tinnitus returns <br> >=3B >=3B after the hearing aid is removed.<br> >=3B >=3B<br> >=3B >=3B Returning to the point of tinnitus without apparent hearing loss=2C I <br> >=3B >=3B have found that salt intake and stress level are two (among many) <br> >=3B >=3B contributing factors to and my own tinnitus=2C an= d I don=92t have hearing <br> >=3B >=3B loss. The dependence of OHCs on metabolic factors underscores this <br> >=3B >=3B connection=2C which seems anecdotally to be exacerbated in patients with <br> >=3B >=3B M=E9ni=E8re=92s.<br> >=3B >=3B<br> >=3B >=3B Matt<br> >=3B >=3B<br> >=3B >=3B<br> </div> </div> </div> </blockquote> <br></div> </div></body> </html>= --_0c22b1a8-3156-4fa1-a993-bf32bb326165_--