How Hearing Loss Can Change the Way Nerve Cells Are Wired

[Vinnitus]

Not sure if this has been posted yet, but I found it to be an interesting read.

It touches on the question if nerve cells return to their former wiring after hearing loss is restored; which they seem to do to some extend, although it is not sure if this happens fully. It also poses that even a few days of (conductive) hearing loss as a result of i.e. a cold, results in changes in this nerve wiring as well, potentially leaving Tinnitus.

Here's to hoping this research might one day help answering the question; will Tinnitus (or other hearing anomalies) go away once peripheral hearing is restored?

https://www.sciencedaily.com/releases/2016/12/161212095735.htm

 

[Reinier]

This I don't understand.
What is the difference between a blocked middle ear and lacking input because there is no sound entering the middle ear? (quit surroundings or using earplugs).
In both instances the inner ear does not receive sound.
Does this mean too little sound is not good?
Also in not damaged inner ears?

 

[Samir]

Here's to hoping this research might one day help answering the question; will Tinnitus (or other hearing anomalies) go away once peripheral hearing is restored?

I agree! This kind of research may lead to better understanding of neo-neurogenesis.

But this may not be what you think it is. The synaptic and neural connections between SGNs and IHC/OHCs have not been lost here, as in neural hearing loss. What they did in this study is they looked at behavioral and structural changes of nerve cells following imposed conductive hearing loss. When this happens, they observed that the cells change behavior and structure, which ultimately changes the signaling to the brain. So it's not that here is loss of signaling, as in neural hearing loss, but the existing signaling changes in some respect.

They also observed that when they restore the normal sound conduction by removing the obstacle, such as ear infection or middle ear fluid, the nerve cells started to change back to their original structure and behavior.

"When you undo the treatment, the cells start to go back to what they were like before," Xu-Friedman says.

But they said they need to do more research to see if this is in fact what happens.

"However, it's not clear that they completely recover, so we need to do more research to see if that's the case."

So this is not about regenerating nerve cells, as we often refer to when talking about sensorineural hearing loss. This is about understanding the basic science behind existing and functional nerve cells in normal cochleas. This is an important part of the puzzle nevertheless, and we will need this basic understanding in our attempts at regenerating new nerve cells in cochleas that have been damaged.

 

[Samir]

What is the difference between a blocked middle ear and lacking input because there is no sound entering the middle ear? (quit surroundings or using earplugs).

This I don't understand!

I will try to dissect this. First of all, I don't understand what you mean by "quit surroundings or using earplugs". The way I see it, there is no difference between a blocked middle ear and lacking input. They mean the same thing. Do they not? If the middle ear is blocked there will be no input, or any external sound source entering the ear will be muffled. The lack of input may or may not mean a complete loss of input. It's all relative. Ultimately, it depends on what you mean by "input".

Can you please rephrase the question or post two separate questions? I'm not exactly sure how to answer this since I am not sure what you mean.

In both instances the inner ear does not receive sound.

Again, I'm not sure what you mean by this. But generally speaking, the ear can receive sounds, even when your brain can't hear or interpret the sound! One such example is supersonic and infrasonic sounds! Sounds travel as mechanical waves and they hit your ears, regardless if you can hear them or not! The sense of hearing sits in the brain, not in the ears. Just like you perceive light with your brain, not with your eyes. Sound waves don't need to knock on the door and ask for your permission to enter your ear. They do this regardless, regardless of if you can hear them or not.

The inner ear, with the cochlea, the hair cells, and nerve cells, they are the most important components for hearing. Loose all of these and you won't be able to hear a thing. You become deaf! But hearing loss is a relative term. It's relative to what part of the ear is damaged, and also how severe the damage is. The easiest way to fix a bad ear is if the damage is in the outer ear or the middle ear and it's not too severe. The hardest part to fix is if the damage is in the inner ear, and especially if the damage is severe, which means you will have loss of sensory and neural cells. You are either deaf or nearly deaf. This is what biomedical researchers are up against, this is what they are trying to reverse. It's not an easy task.

Does this mean too little sound is not good?

Yes! This study showed that behavior and structure of nerve cells changed, following a conductive hearing loss in otherwise healthy ears. So yes, even a reversible conductive hearing loss can have a negative effect on otherwise healthy cochlea. That is what this study seems to suggest, yes.

Also in not damaged inner ears?

This study doesn't say anything about damaged inner ear, i.e. damaged cochlea. But judging by what they have concluded so far about nerve cell behavioral and structural changes following middle ear obstructions, I would say yes! Yes, I think it's best not to understimulate damaged inner ears.

Damaged or not, it seems to me that inner ear needs sound stimulation for long term nerve survival, which should prolong the window of opportunity for future biological treatments. How effective sound stimulation is would depend on the severity of the synaptic and hair cell damage, I presume. I am also under impression that damaged inner ears need sound stimuli to help the central processing in the brain to recover, which seems to help recover from hyperacusis. I would say that overprotecting the ears following inner ear damage is not good.

 

[Samir]

Here is the study report:
http://www.jneurosci.org/content/early/2016/12/01/JNEUROSCI.0523-16.2016

Normal hearing is important to everyday life, but abnormal auditory experience during development can lead to processing disorders.

In other words children growing up with frequent ear infections and other outer and middle ear obstructions may develop processing disorders, because unlike in an adult, their central auditory processing is not developed. Simply put, children need to hear sounds! Moreover, the sounds they hear need to be rich and unhindered! They need this more than adults! This is necessary for the young brains that are in the process of developing.

For example, otitis media reduces sound to the ear, which can cause long-lasting deficits in language skills and verbal production, but the location of the problem is unknown.

As I said, children don't just need to hear sounds, they need rich hearing! Otitis media and frequent ear infections are not helping to this end.

Now we go back on the lead researcher's comment on this topic:

"When she was young, my daughter had ear infections constantly. It seemed like she would get one every time she had a cold," Xu-Friedman says. "I have no idea what this did to her hearing, whether there are lasting effects from this repeated plugging of the ears, or whether any impacts are temporary. If the nerve cells don't go back completely to the way they were, it could have a permanent influence on the way you perceive sound."

Now we go back to the study report:

Here, we show that occluding the ear causes synapses at the very first stage of the auditory pathway to modify their properties, by decreasing in size and increasing the likelihood of releasing neurotransmitter.

Occluding means closing or obstructing an opening, i.e. closing the ears. This leads to decrease of size in synapses, and increased likelihood of signaling rate. Likelihood! Which seems to suggest their method is based on statistics. So they haven't proven it yet. But they have found an interesting lead.

This causes synapses to deplete faster, which reduces fidelity at central targets of the auditory nerve, which could affect perception. Temporary hearing loss could cause similar changes at later stages of the auditory pathway, which could contribute to disorders in behavior.

Reduced fidelity, reduced sound enrichment. Brain is understimulated during development, which is not good, etc, etc. So in conclusion, understiumlating the brain in children leads to hearing disorders, and in adults with damaged hearing it may lead to faster loss of nerve cells and a more narrow window of opportunity for future treatments.

 

[Vinnitus]

I agree! This kind of research may lead to better understanding of neo-neurogenesis.

But this may not be what you think it is. The synaptic and neural connections between SGNs and IHC/OHCs have not been lost here, as in neural hearing loss. What they did in this study is they looked at behavioral and structural changes of nerve cells following imposed conductive hearing loss. When this happens, they observed that the cells change behavior and structure, which ultimately changes the signaling to the brain. So it's not that here is loss of signaling, as in neural hearing loss, but the existing signaling changes in some respect.

They also observed that when they restore the normal sound conduction by removing the obstacle, such as ear infection or middle ear fluid, the nerve cells started to change back to their original structure and behavior.

"When you undo the treatment, the cells start to go back to what they were like before," Xu-Friedman says.

But they said they need to do more research to see if this is in fact what happens.

"However, it's not clear that they completely recover, so we need to do more research to see if that's the case."

So this is not about regenerating nerve cells, as we often refer to when talking about sensorineural hearing loss. This is about understanding the basic science behind existing and functional nerve cells in normal cochleas. This is an important part of the puzzle nevertheless, and we will need this basic understanding in our attempts at regenerating new nerve cells in cochleas that have been damaged.

Yes, but isn't the point here that the hearing loss, in this case conductive, gave rise to the neurons changing their signaling? And aren't neurons thought to be involved in Tinnitus generation (hyperactive neurons)? Both conductive and sensorineural hearing loss result in a reduction of input to the brain. Both conductive and sensorineural hearing loss can also lead to Tinnitus. There have been people who've acquired Tinnitus due to a prolonged period of conductive loss because of infection, a cold or one of many other reasons this can happen. Some of them got rid of their reason for the conductive loss, but not completely of their Tinnitus (or it took a long time). My thinking by reading this article is that neuron signaling can change regardless of the type of hearing loss. After all, in the brain's perspective it doesn't matter whether the loss is conductive or sensorineural; there is a loss and if this loss exists for a few days it can trigger the rewiring. Restoration of input by removing the conductive loss resulted in recovery, but it isn't clear to what extend. Couldn't that mean that a peripheral sensorineural recovery could result in the same outcome? Maybe not to the point that the Tinnitus disappears like some expect, but that is the question at hand here.

I think some hearing anomalies, like Tinnitus, some forms of Hyperacusis and distorted hearing could in certain cases be attributed to neuronal rewiring. Like the article said in the last sentence: 'it could have a permanent influence on the way you perceive sound'.

If what is said in that last sentence turns out to be true, this might be potential bad news for Tinnitus resolution due to restored sensorineural hearing as well. If it's the nerve rewiring causing the Tinnitus, and the rewiring isn't always completely undone upon restoring conductive loss, then what does this mean for restoring sensorineural loss? Perhaps the Tinnitus persists for some people, perhaps in reduced form. Quite like it did in some cases of restored conductive loss. We might need additional treatment for these cases. Regeneration of peripheral input might not cut it completely in all of the cases.

But I'm getting ahead here. Just thinking out loud. I'll be curious to see where this research goes.

 

[Vinnitus]

This I don't understand.
What is the difference between a blocked middle ear and lacking input because there is no sound entering the middle ear? (quit surroundings or using earplugs).
In both instances the inner ear does not receive sound.
Does this mean too little sound is not good?
Also in not damaged inner ears?

My thinking is there is not much difference. But the total silence you experience with good earplugs is kind of rare without them; these days there's almost always a faint sound going on somewhere. Totally quiet environments are rare and quite unnatural. In fact total silence usually means danger (a predator approaching) in natural terms.

I have to say my apartment is well insulated and at night quite close to perfect silence (apart from my Tinnitus of course). It would be interesting to know what this can do to the neurons when viewed over a longer period of time. During the daytime there's some ambient noise around breaking this silence.

The Heller & Bergman experiment during the early 50s was interesting, but people stayed in the anechoic chamber for a relative short time. They started hearing some kind of Tinnitus-like sound after a few minutes, but the duration is probably too short to trigger any neuronal rewiring. It would be interesting to know if people could acquire long-term hearing anomalies (i.e. Tinnitus) by staying in such chamber for too long (more than a few days like in this study).

I vaguely remember a user signing up here a while ago. She claimed to have acquired Tinnitus after visiting a ghost town (Ah yes, @Emz96 https://www.tinnitustalk.com/threads/im-about-to-start-college-soon-help.17008/). Those are interesting cases. Perhaps noise as such is not our greatest enemy in regard to Tinnitus, but silence. Or rather; sudden silence after significant noise (like when coming out of a loud city to a quiet place or coming out of a concert to a quiet bed, etc). This is when we usually notice we acquired an "acoustic trauma". But what is the real trauma here in regard to Tinnitus? The extreme noise potentially causing a hearing loss? The silence after? Or the sudden move from extreme noise to extreme silence (the sudden difference, which is also quite unnatural)? And what does this do to the neurons? Perhaps even after a little while?

There has been some discussion about musical therapy and white noise administered early after an "acoustic trauma" preventing Tinnitus chronification... That seems to fit into this idea.

https://www.tinnitustalk.com/thread...n-to-prevent-chronification-of-tinnitus.8830/

Interesting things to think about.

 

[Samir]

Restoration of input by removing the conductive loss resulted in recovery, but it isn't clear to what extend. Couldn't that mean that a peripheral sensorineural recovery could result in the same outcome? Maybe not to the point that the Tinnitus disappears like some expect, but that is the question at hand here.

Good question! Have you approached the researcher with this question? I think you should.

If what is said in that last sentence turns out to be true, this might be potential bad news for Tinnitus resolution due to restored sensorineural hearing as well.

I see your point. Yes, this might be something worth looking into. It may be hard to overcome, but at least we would know what it is that causes tinnitus. That's always something. We would have a target to work against. Right now we don't even have a good target because we are not sure where tinnitus starts.

But I'm getting ahead here. Just thinking out loud. I'll be curious to see where this research goes.

Indeed! It's still too early to make any definitive conclusion.

 

[Samir]

Totally quiet environments are rare and quite unnatural. In fact total silence usually means danger (a predator approaching) in natural terms.

(...)

The Heller & Bergman experiment during the early 50s was interesting, but people stayed in the anechoic chamber for a relative short time. They started hearing some kind of Tinnitus-like sound after a few minutes, but the duration is probably too short to trigger any neuronal rewiring.

Interesting hypothesis... So this would mean that tinnitus is like a natural response to the lack of sound? Like a way to sense danger? Maybe that's why we get anxious about it?

Perhaps noise as such is not our greatest enemy in regard to Tinnitus, but silence. Or rather; sudden silence after significant noise (like when coming out of a loud city to a quiet place or coming out of a concert to a quiet bed, etc).

I agree! There might be something to this. I know @MikeGreen talked about this idea where his tinnitus would go away for a moment just as he shut off his vacuum cleaner.

This is when we usually notice we acquired an "acoustic trauma". But what is the real trauma here in regard to Tinnitus? The extreme noise potentially causing a hearing loss? The silence after? Or the sudden move from extreme noise to extreme silence (the sudden difference, which is also quite unnatural)? And what does this do to the neurons? Perhaps even after a little while?

I must say I am impressed! Where are you getting all these fantastic ideas?

Is there anyone taking this seriously and researching these ideas to try to answer these question? Someone really should! The study you linked to is definitely on track of these ideas.

 

[Reinier]

Can you please rephrase the question or post two separate questions? I'm not exactly sure how to answer this since I am not sure what you mean.

@Vinnitus was able to better explain what I was trying to putt in words.

Both conductive and sensorineural hearing loss result in a reduction of input to the brain.

In my situation I think about two experiences with my hearing a lot. Experiences before tinnitus and experiences after tinnitus.
The tinnitus is in my mind without any doubt because of noise a incident. So, damage to the inner ear. Before the incident I was able to experience absolute silence (I used earplugs because plains woke me up in the middle of the night). I used the yellow foam earplugs and they blocked any sound in an already quit bedroom. (Apart from the occasional plain a few times in a night). The only sounds I heard was my heartbeat.
It never gave me tinnitus or hyperacusis.
I understand this is only 8 hours per day on average.
I understand it is relative like @Samir mentioned, but I can not understand that a blocked middle ear will allow even less sound entering the inner ear.
I hope research shows that the cells are capable of more adaptation than previously seen.

 

[Samir]

I can not understand that a blocked middle ear will allow even less sound entering the inner ear.

I'm not sure what it is you don't understand here. If you block the middle ear, by for example putting ear plugs in, less sound will enter the inner ear. No? The sounds need to be strong enough to get past the ear plugs. Just like you have to shout to someone who has bad hearing if you want to be heard.

The sound travels through the outer ear, via middle ear, and into the inner ear. Of course if you block sounds at the outer ear or middle ear, less sound will enter the inner ear. Another way sound enters the inner ear is also via bone conduction, so straight through your skull bone into the inner ear.

I hope research shows that the cells are capable of more adaptation than previously seen.

They are capable of adapting, and this is what this study shows. But they are working under the assumption that this is maladaption, that it's a bad kind of adaptation. One which may or may not be fully reversible, they don't know that yet.