Inner Ear Hair Cell Regeneration — Maybe We Can Know More

[Reinier]

I read interview with some researcher and she said auditory nerve unlike other nervers dont degenerate after not use. She told she had patient succesfully fitted with CI after 60yrs of deafness in that ear.

That is a definite "like".
That post lifted my spirits up a little bit.
The door is not closed

 

[Nick Pyzik]

What I do not understand than is why cochlear implants are still able to work, even after decades? (Jeff had hearing loss for a long time and I understand he is detecting high frequencies again).
Also in this article (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4842978/) I read that that the reason that cochlear implants can still work after many years must be because of the long time surviving neurons. In order to make use of a cochlear implant you need it to get the signals from this implant to your brain.
Quote: Given that cochlear implants can continue to provide useful hearing for years after hair cell loss, these long-surviving neurons must remain electrically excitable and appropriately connected to their central targets10. Thus, in many types of sensorineural hearing loss, there is a long therapeutic window wherein a treatment to elicit neurite outgrowth could reconnect silenced cochlear ganglion cells with hair cells, and thereby potentially improve speech in noise performance and reduce tinnitus. End quote.

I hope it is like that, because by the time there is some sort of regeneration available, my hearing loss will be years "old".

I'm not too sure about neuronal/cellular death and how much time influences it. I do know that with acoustic trauma, excitoxicity is involved. Especially with one of the the spiral ganglion neurons. Once I starting reading up on them, I have a much better understanding of their background. My statement about nerve fiber/spiral ganglion neuronal death is because of what Charles Liberman stated in his article about nerve fiber loss/loud noise.

The focus on sensory hair cells is just very fishy to me. No pun intended.

Outer hair cells do amplify sound, but not in the way I'm sure it's pictured. I can only state this in a simplified manner because I don't know the technological terms, but it's the in-going nerve fibers that actually amplify frequencies into our brain. Amplification meaning better processing of the environment. If I understand correctly, Neurotransmitters like dopamine actually help the brain pick up sound in an amplified manner.

 

[Nick Pyzik]

So the only way to regrow these connections is by Stemcells or am I missing something?Is it possible to sprout new connections at all or is it an impossibility?I have T and H for a number of years now making any supplements pretty much useless at this stage I guess,but is it possible to sprout new connections from the CNS to the inner ear?

I'm only going off of the information I've gathered up as a whole. @Mentos was able to actually contact Charles Liberman himself. He even stated himself in one of a few articles talking about noise, hidden hearing loss, and nerve fiber damage.

Here is an excerpt from The Hearing Review article posted online on May 13th, 2014, "Each missing synapse represents a cochlear nerve fiber that has been disconnected due to retraction of the terminal segment—it will never reconnect," Liberman noted. "It no longer responds to sound, and, within a few months or years, the rest of the neuron will disappear."

So Liberman is explaining that there is a time period in which a therapeutic treatment is possible. He states this below.

Another excerpt, "Since the ultimate death of neural cell bodies and axonal projections to the brain is so slow, there is an extended therapeutic window where delivery of chemicals to elicit sprouting of the nerve terminals might be able to reestablish synaptic connections between neuron and hair cell," Liberman noted.

So really we don't know the actual length of time is takes for spiral ganglion neurons to retract back into the brain back into what presumably would be brain cells.

The ganglions themselves would have to be residing in the area where the bundle of auditory nerves lay in between the cochlea(s) and the brain for what I believe would allow them to therapeutically be grown back.

The studies put on where cochlear implants were used to regrow a rats auditory nerve was accomplished because neurotrophics factors were fed through the implants while the electrical currents of the implant basically encouraged the disconnected auditory nerves to grow back. You could see that the image shown in the articles displayed the rats spiral ganglion neurons residing in the area (I don't know what the actual name is for the region because I'm sure there is one) where the bundle of auditory nerve gather together.

Logically thinking, it would be very difficult to therapeutically regrow these neurons if they've already retracted back to the areas of the brain they took place in. Kyoto's study using the glial scars method with specifically differentiated stem cells would be a wonderful test to try and re-establish auditory connections which most likely would stop ones ringing. My understanding is that if you've had constant ringing, they are still alive. The louder your ringing is, the closer these nerve fibers/spiral ganglion neurons are to your inner ear. The quieter, the higher chance that they've already retracted back deep into the brain. That's why when you first develop ringing/tinnitus after let's say a loud concert, it's extremely loud.

 

[Christian78]

we will get implants, i am sure that is real solution as soon as tech advances, in every scifi movie they dont heal but they integrate implats inside human, so i am sure implant will be made to function as copleate ear that would be even better than real ear

 

[Kane Moffat]

So if our tinnitus gets quieter over the years that acctually means our nerves are degenerating, well thats fucking disturbing.

Theres also a time limit to save these nerve fibers? The closest we are to getting treatment for nerve fiber damage is years!

Is the conclusion then that we are all fucked and there is no way of fixing it within the time we have left?

 

[Nick Pyzik]

So if our tinnitus gets quieter over the years that acctually means our nerves are degenerating, well thats fucking disturbing.

Theres also a time limit to save these nerve fibers? The closest we are to getting treatment for nerve fiber damage is years!

Is the conclusion then that we are all fucked and there is no way of fixing it within the time we have left?

Kane,

Unfortunately the combination of information provided by recent research on tinnitus/hidden hearing loss and the not so distant research provided by Charles Liberman makes me have to say yes.

The best thing to keep your brain healthy and keep these brain cells/neurons alive is to keep your health intact. You can provide it neurotrophic factors just like Liberman and the crew have stated as a therapeutic method. Herbs and supplementation is a perfect way. I've been taking Turmeric, Lion's Mane, Ashwagandha, Astaxanthin, and Cordyceps for numerous months. They all include NF. Even exercise could help out which influences BDNF (Brain-Derived Neurotrophic Factor).

Liberman stated that this degeneration is very slow, which could mean the spiral ganglion neurons themselves die and retract back into the brain. But then the brain cells themselves could still be alive, thus causing a constant audible ringing for many many years. There are users on here who've had ringing for decades. There's no way they just die off like that.

 

[Kane Moffat]

I think over reacted abit just then lol. Yeah i suppose we need to just keep good health in general. Thanks.

 

[RB2014]

I think over reacted abit just then lol. Yeah i suppose we need to just keep good health in general. Thanks.

You T will get softer over time in general because you brain no longer sees it as a threat. I wouldnt use that reason alone to jump to any conclusions.
Agreed with Nick, it is a slow process. I read somewhere about CI and a gene therapy where connections become re-established or better established and the CI's work better with a gene therapy that was applied.
They are coming out with new ideas every day now and I think this is going to be a bell curve facing upward in the information we know. Things are looking better every day now.
Most of the research is on cells lost to old age. These people lost their hair cells slowly over time and they are working on getting them back. If they think there is hope there, then they must somehow believe that these connections can be re-established. I look at a newborn baby being formed and something has to give rise to these connections, so it must be possible, we just don't how to get there yet.

Agreed also on the exercise. Get your heart rate down and you age slower. This could buy you some time as well.

 

[Filip]

Does this mean we should give up on finding a cure for hearing loss and tinnitus?

 

[Mario martz]

Does this mean we should give up on finding a cure for hearing loss and tinnitus?

Nop!
there are many, many studies out there trying to restore hearing, that could totally help.
this is the worst time to gave up.
since there are exciting things coming up within the next 5 years.
there might be many studies, theories, but we dont know yet.
predicting the future is not an option, but for the first time in the last decade.
things seems to be moving.

 

[Filip]

Nop!
there are many, many studies out there trying to restore hearing, that could totally help.
this is the worst time to gave up.
since there are exciting things coming up within the next 5 years.
there might be many studies, theories, but we dont know yet.
predicting the future is not an option, but for the first time in the last decade.
things seems to be moving.

Ahh, good, good was worried about some of these posts on this thread that led me to doubt

 

[tomytl]

Hi,
the ironic thing of hearing regemeration research is, that there are so many approaches to achieve hair cell regeneration.

-Atoh 1 Gene Delivery
-Stem Cells
-Protein Delivery
-CRISPR Gene Editing
-siRNA Gene Silenceing
-Neurinal Grow Factors

I don't know excactly how realistic or advanced one of these approaches are,
and I don't really understand the mechanism behind.

I just have regularly email exchange with a top notch researcher and he is very excited about all the advances in the hearing research.
For the Atoh1 trial, all experts I asked didn't see a big potential for hearing regeneration because Atoh 1 alone won't do the job.

Genvec itself has very low expectations when it comes to hearing levels, I guess they talked about 5-10 dB of recovery.
I guess, this is really a proof of principle test, maybe more to proof that gene delivery works.

But yes, I'm just specuating..m.

 

[Mario martz]

Ahh, good, good was worried about some of these posts on this thread that led me to doubt

hehehe i mean i dont have the truth in my heads
but things are happening, its a terrible time to give up right now when there are things coming!
lets just wait and hope for the best

 

[Mario martz]

The louder your ringing is, the closer these nerve fibers/spiral ganglion neurons are to your inner ear. The quieter, the higher chance that they've already retracted back deep into the brain. That's why when you first develop ringing/tinnitus after let's say a loud concert, it's extremely loud.

This is fascinating....
But it also bring more question to my mind...
like why for some people it gets worse through the years? (from mild to severe tinnitus)
what happens with the cases of spontaneous remission? (people who had tinnitus for months and then it disappears? there are a few cases here)

 

[Nick Pyzik]

This is fascinating....
But it also bring more question to my mind...
like why for some people it gets worse through the years? (from mild to severe tinnitus)
what happens with the cases of spontaneous remission? (people who had tinnitus for months and then it disappears? there are a few cases here)

I'll answer your questions in a very simple manner. I was typing out a huge response, but there's really no point.

Neurons are electrically excitable. As I'm sure you know, they're involved all throughout the brain. Billions of them. As long as you have a synapse in relation to a neuron, then it'll have a response to chemicals called neurotransmitters.
Since recently, tinnitus and hidden hearing loss are being closely looked at as damage involving the spiral ganglion neurons of our auditory system. Charles Liberman of the University of Harvard/ Mass. Eye and Ear Infirmary stated that nerve fibers (part of the two different spiral ganglion neurons) can become disconnected from their associated sensory hair cell after an acoustic trauma event. They'll never reconnect and will eventually retract back into the brain and die (if not kept alive by neurotrophic factors). If this really is what happens when one's inner ear encounters extremely loud noise, then here is what I believe is happening to cause one's ringing/tinnitus to become louder over time.

The damaged spiral ganglion neurons/nerve fibers (ones part of the central nervous system) that had disconnected from one or several occurring events over ones lifetime are still trying to be used by the brains complex system. Feed the brain any sort of neurotransmitters, something especially like dopamine in any sort of pleasurable activity you can name and you will have a brain that's trying to do whatever is possible to hear again with those damaged auditory pathways. I'll say it time after time, but our hearing is our brains most informational sensory feature. Especially if it's containing emotional components.

So if you give the brain certain neurotransmitters, it will try to fix the damage that's taken place. It depends on how much "pleasure" you give your brain. The more chemicals your brain receives, the more it will try to use these damage circuits as they become excited. I also truly believe this is where the brain sends out "out-going" nerve fibers to try and repair the damaged "in-going" nerve fibers that it lost. Our brain is a very sly organ. The more "out-going" nerve fibers you have, the less your brain will be trying to use those damaged circuits as it now has a different way to receive information from the sensory hair cells. This is where you hear those cricket noises, your hearing goes out for a few seconds, etc.

In summary:

1) Neurotransmissions given to the brain = louder tinnitus/ringing because the auditory pathways that were damaged are trying to be used again.

2) The brain will try to repair the nerve fiber/spiral ganglion neuronal damage that's taken place by sending out "out-going" nerve fibers to take the place of the disconnected in-going nerve fibers. (This part was discovered by Johns Hopkins Medicine.

3) When the brain has new connections between the inner ear and itself (I'm assuming these "out-going" nerve fibers are coming from somewhere in the frontal lobe) then it doesn't have to push as hard to hear again with it's damaged spiral ganglion neurons/"in-going" nerve fibers. Therefore, ones ringing will not be as noticeable because of the change in it's hearing threshold from these new "out-going" nerve fibers as they pick up the frequencies mechanically sensed by the hair cells.



Just an extra bit: When you think about it, isn't it funny how people who are addicts to drugs, never actually become truly happy? It's almost like they're trying to fix something that's not there or what was once there. With the high amounts of feel good chemicals they're brains are receiving, you'd think they'd be ecstatic every second of the day.

 

[Foncky]

So Nick,

I love riding mountain bikes, for instance. If I do that a lot, dopamine will be produced and new outgoing nerve fibers will be created, therefore reducing the noise over time ? What if most of my outer hair cells are dead ? (I have huge hearing loss in the 4000-8000Hz range)

Since my last trauma, I stopped all physical activities and a lot of things I loved because of H (and T is louder when I run or ride because of blood pressure). So I didn't produce a lot of dopamine I think... Is that the biggest mistake I can change ?

 

[Reinier]

I wonder if a Eureka moment produces BDNF in the brain. I always get a feeling of euphoria when "the penny drops". This is how I feed my brain.
But I read it is till poorly understood if and why Brain Derived Neurotrophic Factor contribute to SGN survival.
I read this in an article from 2006. Perhaps a lot more is known?

And I keep coming back to the question how people can benefit from cochlear implants. When a cochlear implant is used apparently a lot of hair cells die when the implant is placed.
SGN need NT-3 from hair cells to function and survive. Why than do SGN survive if hair cells have died because of cochlear implant? I understand that NT-3 delivered to the inner ear can prevent degeneration of SGN after hair cell damage (because of cochlear implant, ototoxicity or NIHL?).

Or is it not the SGN that receive the signal from the implant?
Anyway, nerve fibres are needed, for sure, to get the signal from the implant to eventually brain. So they must still be there, even after many years of hearing loss.

 

[Nick Pyzik]

So Nick,

I love riding mountain bikes, for instance. If I do that a lot, dopamine will be produced and new outgoing nerve fibers will be created, therefore reducing the noise over time ? What if most of my outer hair cells are dead ? (I have huge hearing loss in the 4000-8000Hz range)

Since my last trauma, I stopped all physical activities and a lot of things I loved because of H (and T is louder when I run or ride because of blood pressure). So I didn't produce a lot of dopamine I think... Is that the biggest mistake I can change ?

What caused your hearing troubles?

 

[Reinier]

Since my last trauma, I stopped all physical activities and a lot of things I loved because of H (and T is louder when I run or ride because of blood pressure). So I didn't produce a lot of dopamine I think... Is that the biggest mistake I can change ?

Same with me. I slowly want to start fitness again and see if it benefits my tinnitus.

 

[Nick Pyzik]

I wonder if a Eureka moment produces BDNF in the brain. I always get a feeling of euphoria when "the penny drops". This is how I feed my brain.
But I read it is till poorly understood if and why Brain Derived Neurotrophic Factor contribute to SGN survival.
I read this in an article from 2006. Perhaps a lot more is known?

And I keep coming back to the question how people can benefit from cochlear implants. When a cochlear implant is used apparently a lot of hair cells die when the implant is placed.
SGN need NT-3 from hair cells to function and survive. Why than do SGN survive if hair cells have died because of cochlear implant? I understand that NT-3 delivered to the inner ear can prevent degeneration of SGN after hair cell damage (because of cochlear implant, ototoxicity or NIHL?).

Or is it not the SGN that receive the signal from the implant?
Anyway, nerve fibres are needed, for sure, to get the signal from the implant to eventually brain. So they must still be there, even after many years of hearing loss.

BDNF is a protein that allows neurons in the brain to survive. Loud noise first causes disconnection of nerve fibers from the sensory hair cells, then the fibers retract back to the spiral ganglion neurons they were associated with (I or II), and from their the neurons aren't receiving any sort of information/basic survival needs so they eventually retract and die. Liberman stated that they will die within a few months to a year. Unless you continuously feed your brain neurotrophic factors within that time frame. I've actually been doing the opposite of what most people want with their ringing/tinnitus. I want to hear more audible ringing because then I know that those spiral ganglion neurons that were damaged are still alive and looking to reconnect in the future when a treatment is available.

Where did you read that sensory hair cells are needed to keep SGN thriving? Could you link me to the document? There are two different spiral ganglion neurons that both play a different role in how our brain processes sound. It's what creates their bi-polar physique. Afferent and Efferent. In-going and Out-going nerve fibers that branch off from them. The connections between all of them are pretty complex.

Your question about nerve fiber/spiral ganglion neuronal survival over time. The thing is with someone who was born pretty much deaf or has been hard of hearing their whole life, there wasn't Excitotoxicity involved which is basically known to cause the death of cells/neurons. I believe this is exactly what causes the spiral ganglion neurons that were damaged in the acoustic trauma to eventually retract back into the brain and turn back into a brain cell. Those who have had hearing issues most of their lives seemed to never notice a change in their hearing from time to time like various users who developed tinnitus/ringing after loud events do.

There definitely is something to do with the peripheral and central nervous system with these spiral ganglion neurons and ringing too. I just don't know enough about them to state anything about it.

 

[Mentos]

BDNF is a protein that allows neurons in the brain to survive. Loud noise first causes disconnection of nerve fibers from the sensory hair cells, then the fibers retract back to the spiral ganglion neurons they were associated with (I or II), and from their the neurons aren't receiving any sort of information/basic survival needs so they eventually retract and die. Liberman stated that they will die within a few months to a year. Unless you continuously feed your brain neurotrophic factors within that time frame.

Nick for all of us once the treatment to reconnect the neurons is available it will be too late if the window is one year. Based on Liberman research and treatments he is working on do you see any hope for chronic sufferers to be cured or the chances are only for future acute cases?

 

[Foncky]

What caused your hearing troubles?

A first acoustic trauma 12 years ago, which left me with a chronic mild T and H, and a second acoustic trauma 7 months ago, which left me with an unbearable T (always changing and loud) and severe H.

My ears were already quite bad before the first acoustic trauma (occasional distortion but no T and no H when I was a kid/teenager).

 

[Aaron123]

Nick for all of us once the treatment to reconnect the neurons is available it will be too late if the window is one year.

Liberman does not say months to one year. Year is plural in the paper. In the abstract of the paper being referenced, the abstract says "Because the cell bodies and central projections of these cochlear neurons survive for months to years, there is a long therapeutic window in which to re-establish functional connections and improve hearing ability." (emphasis added) He also responded to an email and said the timing is unknown - posted earlier in this thread.

The paper goes on to say "Given that cochlear implants can continue to provide useful hearing for years after hair cell loss, these long-surviving neurons must remain electrically excitable and appropriately connected to their central targets10. Thus, in many types of sensorineural hearing loss, there is a long therapeutic window wherein a treatment to elicit neurite outgrowth could reconnect silenced cochlear ganglion cells with hair cells, and thereby potentially improve speech in noise performance and reduce tinnitus."

Unfortunately, no one knows the window: "Although the success of local NT-3 delivery in regenerating cochlear synapses when administered 24 hrs post exposure is an important proof of concept, many key questions remain, most importantly how long after the insult can neurite extension and synaptogenesis still be elicited."

Regarding the idea that loud tinnitus somehow indicates that the SG are alive and "looking to reconnect", the paper does address tinnitus: "The idea that a significant, but ultimately reversible, noise-induced threshold shift can be associated with a 50% loss of cochlear nerve synapses has also provided a new hypothesis for the origins of tinnitus, the phantom perception of sound that is often the permanent result of a noise exposure even if the threshold elevation is transient55. It has been argued that the permanent loss of spontaneous and sound-driven activity in a subgroup of cochlear nerve fibers leads to a central gain readjustment that drives hyperactivity in central auditory pathways and thereby causes tinnitus5."

I'm not sure it is a new hypothesis, but Corfas and Liberman suggest that their findings are consistent with an adjustment in central gain, not neurons looking to reconnect.

You can read the original paper here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4842978/

 

[Mentos]

Liberman does not say months to one year. Year is plural in the paper. In the abstract of the paper being referenced, the abstract says "Because the cell bodies and central projections of these cochlear neurons survive for months to years, there is a long therapeutic window in which to re-establish functional connections and improve hearing ability." (emphasis added) He also responded to an email and said the timing is unknown - posted earlier in this thread.

The paper goes on to say "Given that cochlear implants can continue to provide useful hearing for years after hair cell loss, these long-surviving neurons must remain electrically excitable and appropriately connected to their central targets10. Thus, in many types of sensorineural hearing loss, there is a long therapeutic window wherein a treatment to elicit neurite outgrowth could reconnect silenced cochlear ganglion cells with hair cells, and thereby potentially improve speech in noise performance and reduce tinnitus."

Unfortunately, no one knows the window: "Although the success of local NT-3 delivery in regenerating cochlear synapses when administered 24 hrs post exposure is an important proof of concept, many key questions remain, most importantly how long after the insult can neurite extension and synaptogenesis still be elicited."

Regarding the idea that loud tinnitus somehow indicates that the SG are alive and "looking to reconnect", the paper does address tinnitus: "The idea that a significant, but ultimately reversible, noise-induced threshold shift can be associated with a 50% loss of cochlear nerve synapses has also provided a new hypothesis for the origins of tinnitus, the phantom perception of sound that is often the permanent result of a noise exposure even if the threshold elevation is transient55. It has been argued that the permanent loss of spontaneous and sound-driven activity in a subgroup of cochlear nerve fibers leads to a central gain readjustment that drives hyperactivity in central auditory pathways and thereby causes tinnitus5."

I'm not sure it is a new hypothesis, but Corfas and Liberman suggest that their findings are consistent with an adjustment in central gain, not neurons looking to reconnect.

You can read the original paper here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4842978/

I read through the paper, what I could not understand is if cochlear synaptopathy can be diagnosed by DPOAE and ABR. I have normal audiogram, my DPOAE and ABR are fine according to my audiologist, still I have T noise induced after rock concert. Do you know any good audiologist I could consult my DPOAE and ABR online to help me understand which ear disfunction I may have?

 

[Aaron123]

I read through the paper, what I could not understand is if cochlear synaptopathy can be diagnosed by DPOAE and ABR. I have normal audiogram, my DPOAE and ABR are fine according to my audiologist, still I have T noise induced after rock concert. Do you know any good audiologist I could consult my DPOAE and ABR online to help me understand which ear disfunction I may have?

There's currently no test for what is being discussed here. It's an area of research (http://www.ncbi.nlm.nih.gov/pubmed/26323349, http://www.ncbi.nlm.nih.gov/pubmed/26657094, and http://www.ncbi.nlm.nih.gov/pubmed/27030760) ABR wave-I is what is used in animals but is apparently difficult to measure in humans. The third paper I listed seems to be the most promising to me though I don't know whether a normal audiologist would be able to perform it (as opposed to an audiologist in a research setting). In the discussion they say "Unlike absolute ABR peak amplitude and latency analyses, in which intersubject variability is large and dependent on numerous factors independent from coding fidelity, we show that the relative change in latency in noise is a robust measure of hidden hearing loss."

If you read back through this thread there is also discussion of research on imaging techniques to be able to look for hair cell and other damage in a non-invasive way.

 

[Nick Pyzik]

Liberman does not say months to one year. Year is plural in the paper. In the abstract of the paper being referenced, the abstract says "Because the cell bodies and central projections of these cochlear neurons survive for months to years, there is a long therapeutic window in which to re-establish functional connections and improve hearing ability." (emphasis added) He also responded to an email and said the timing is unknown - posted earlier in this thread.

The paper goes on to say "Given that cochlear implants can continue to provide useful hearing for years after hair cell loss, these long-surviving neurons must remain electrically excitable and appropriately connected to their central targets10. Thus, in many types of sensorineural hearing loss, there is a long therapeutic window wherein a treatment to elicit neurite outgrowth could reconnect silenced cochlear ganglion cells with hair cells, and thereby potentially improve speech in noise performance and reduce tinnitus."

Unfortunately, no one knows the window: "Although the success of local NT-3 delivery in regenerating cochlear synapses when administered 24 hrs post exposure is an important proof of concept, many key questions remain, most importantly how long after the insult can neurite extension and synaptogenesis still be elicited."

Regarding the idea that loud tinnitus somehow indicates that the SG are alive and "looking to reconnect", the paper does address tinnitus: "The idea that a significant, but ultimately reversible, noise-induced threshold shift can be associated with a 50% loss of cochlear nerve synapses has also provided a new hypothesis for the origins of tinnitus, the phantom perception of sound that is often the permanent result of a noise exposure even if the threshold elevation is transient55. It has been argued that the permanent loss of spontaneous and sound-driven activity in a subgroup of cochlear nerve fibers leads to a central gain readjustment that drives hyperactivity in central auditory pathways and thereby causes tinnitus5."

I'm not sure it is a new hypothesis, but Corfas and Liberman suggest that their findings are consistent with an adjustment in central gain, not neurons looking to reconnect.

You can read the original paper here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4842978/

I apologize for not including a s to "year" Aaron. But yes, I should of included his actual statement from "The Hearing Review" posted on May 13th, 2014.

"Each missing synapse represents a cochlear nerve fiber that has been disconnected due to retraction of the terminal segment—it will never reconnect," Liberman noted. "It no longer responds to sound, and, within a few months or years, the rest of the neuron will disappear."

So yes, adding an s to year adds a much larger therapeutic window to spiral ganglion neuronal damage causing tinnitus. I'm trying to keep my memory working correctly with all the troubles I have, but I definitely jumbled my words there. I'm really sorry about that.


What do you mean by "not neurons looking to reconnect"?

 

[Nick Pyzik]

There's currently no test for what is being discussed here. It's an area of research (http://www.ncbi.nlm.nih.gov/pubmed/26323349, http://www.ncbi.nlm.nih.gov/pubmed/26657094, and http://www.ncbi.nlm.nih.gov/pubmed/27030760) ABR wave-I is what is used in animals but is apparently difficult to measure in humans. The third paper I listed seems to be the most promising to me though I don't know whether a normal audiologist would be able to perform it (as opposed to an audiologist in a research setting). In the discussion they say "Unlike absolute ABR peak amplitude and latency analyses, in which intersubject variability is large and dependent on numerous factors independent from coding fidelity, we show that the relative change in latency in noise is a robust measure of hidden hearing loss."

If you read back through this thread there is also discussion of research on imaging techniques to be able to look for hair cell and other damage in a non-invasive way.

Have you seen these Aaron? Both recently posted in the same month by different researchers:

Tinnitus is associated with reduced sound level tolerance in adolescents with normal audiograms and otoacoustic emissions

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4893619/


Decreased Speech-In-Noise Understanding in Young Adults with Tinnitus

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4923253/

 

[Kane Moffat]

So there is solid evidence to suggest that if we all have take supplements that increase nutrophic factors in the brain then we give our cells the best chance of survival.

Dopamine + supplements = keeping cells alive.

Should everyone not be informed of this? Seems critical.

Im also still shocked by the fact that your tinnitus being louder is acctually a good sign, looks like the success story section of this forum could now just be poeople who have had cells die off?

 

[Nick Pyzik]

So there is solid evidence to suggest that if we all have take supplements that increase nutrophic factors in the brain then we give our cells the best chance of survival.

Dopamine + supplements = keeping cells alive.

Should everyone not be informed of this? Seems critical.

Im also still shocked by the fact that your tinnitus being louder is acctually a good sign, looks like the success story section of this forum could now just be poeople who have had cells die off?

There's a lot to still be understood about what can be titled as Hidden Hearing Loss / Tinnitus. The damage that occurs is much more hidden than we think.

@Aaron123 was able to spot and correct my false information about how long these neurons/cells can survive without connection the inner ear. Charles Liberman stated that they can last a few months to years.

There are two reasons I believe "louder tinnitus" could actually mean less damage.

1) The nerve fibers that were disconnected are still lingering close to the associated sensory hair cell(s) in the area between the inner ear and brain. As they retract back more into the spiral ganglion neuron(s) they sprouted from and eventually farther back into the brain, the subject doesn't notice their ringing as much. Plus, new "out-going" nerve fibers taking the place of the damaged and lost "in-going" nerve fibers causes the brain to process sound differently. Therefore, the brain is "hearing" sound actively higher and you don't audibly hear the damaged areas of your auditory system as much.

2) There's something with excitable neurons that makes me wonder if giving the brain or having certain neurotransmitter chemicals in it will cause those damaged auditory pathways to try and be used again. I've noticed myself with experimentation on how neurotransmitters that affect our mood, also affect the loudness of tinnitus and how dynamically well one can hear sound. What happens to ones ringing/hearing as they become depleted of a good portion of their mood lifting chemicals?

 

[Reinier]

Where did you read that sensory hair cells are needed to keep SGN thriving?

I read this in an article I purchased on the internet.
This is a quote from this article which you can find here: https://books.google.nl/books/about...Ganglion_Neu.html?id=M-riaA2waBYC&redir_esc=y
Quote:
"Recent studies indicate that the survival of SGN can be profoundly altered by neurotrophic factor 3 (NT-3) and brain derived neurotrophic factor (BDNF) released by hair cells of the inner ear."
End quote.
I was looking for insight into the functioning of the inner ear and found this.