Evidence of Cochlear Neural Degeneration in Normal-Hearing Subjects with Tinnitus

Nick47

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Jun 16, 2022
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Evidence of cochlear neural degeneration in normal-hearing subjects with tinnitus

A new study out of MIT.

Gives credence to Professor Peter McNaughton's work?

Summary:

A new study reveals that tinnitus, a common auditory issue characterized by ringing in the ears, is associated with undetected auditory nerve loss. This finding challenges the traditional understanding that tinnitus is solely a result of brain maladaptation to hearing loss.

The study shows that individuals with normal hearing tests but experiencing tinnitus actually suffer from cochlear synaptopathy, a type of "hidden hearing loss." This discovery paves the way for potential treatments, including nerve regeneration through neurotrophins, bringing hope for millions affected worldwide.

Key Facts:
  1. Tinnitus in individuals with normal hearing tests is linked to undetected auditory nerve loss.
  2. The study identifies cochlear synaptopathy, or hidden hearing loss, as a key factor in tinnitus genesis.
  3. Future treatment possibilities include auditory nerve regeneration, offering hope for a potential cure for tinnitus.
 
So is the only treatment path forward nerve regeneration? I feel like we're pretty far from that unfortunately.
 
A new study reveals that tinnitus, a common auditory issue characterized by ringing in the ears, is associated with undetected auditory nerve loss.
The auditory nerve is comprised of the axons of spiral ganglion neurons that project to the DCN, right?

Doesn't the term 'cochlear neural degeneration' also apply to the synaptic connection between the hair cells and the spiral ganglion neurons?

I don't understand why they would use that term if the issue is solely with auditory nerve.

Please someone help me understand.
 
Nice one. Of course don't rule out "undetected auditory nerve loss" plus something else... hair cell damage etc.

In my particular case I had what I would call very sensitive hearing as a teenager. When I ended up with tinnitus years later, the word "tinnitus" was pretty new... and of course I had never heard of it.
 
According to Dr- Shore, any type of tinnitus signal hits the DCN before being interpreted by the brain so I don't understand either. Say the fusiform cells are dampened in the DCN as proposed, isn't it irrelevant where the tinnitus signal therefore comes from?
 
Something I've expected for a long time - nerve damage/signal. The loss of hearing and the causal over activity of neurons in the brain only went so far in explanation. How could this alone account for variable and unstable tinnitus? How could this account for people with reactive tinnitus that instantly and dramatically increases with external sound? It had to be a pain signal from the auditory nerves.

So where does this fit in? Well, it shows promise for auditory nerve regeneration (Rinri Therapeutics) and also leads credence to Professor Peter McNaughton's work on HCN2 channels in the Spiral Ganglion.

It also explains how a cochlear implant that bypasses some of the auditory nerves often reduces tinnitus, even in a soundproof chamber as the signals from damaged synapses have been bypassed.

It fits into the treatment by Dr. Shore, where that signal is received by the cochlear nucleus.
 
Something I've expected for a long time - nerve damage/signal. The loss of hearing and the causal over activity of neurons in the brain only went so far in explanation. How could this alone account for variable and unstable tinnitus? How could this account for people with reactive tinnitus that instantly and dramatically increases with external sound? It had to be a pain signal from the auditory nerves.

So where does this fit in? Well, it shows promise for auditory nerve regeneration (Rinri Therapeutics) and also leads credence to Professor Peter McNaughton's work on HCN2 channels in the Spiral Ganglion.

It also explains how a cochlear implant that bypasses some of the auditory nerves often reduces tinnitus, even in a soundproof chamber as the signals from damaged synapses have been bypassed.

It fits into the treatment by Dr. Shore, where that signal is received by the cochlear nucleus.
I think reactivity is caused by hair cells that are damaged/vulnerable but not yet broken. These hair cells are much more susceptible to noise trauma. Over time they either break down (worsening early on) or stabilize (less reactive/strengthened) but are still easy to break. They are essentially connecting/disconnecting continuously from the auditory nerve, or not catching the sound signals well causing fluctuations in tinnitus - like a bad phone charger plug in a phone.

Damaged hair cells could break easily from loud sounds or cause long spikes - one loud sound causes the same effect as going to a festival for 16 hours with normal ears.

It's my theory and not backed by science.
 
According to Dr- Shore, any type of tinnitus signal hits the DCN before being interpreted by the brain so I don't understand either. Say the fusiform cells are dampened in the DCN as proposed, isn't it irrelevant where the tinnitus signal therefore comes from?
There had to be an explanation for our unstable sound reactive condition and the brain amping up after hearing loss did not cut it with me. This explains things better and fits with what Professor Bance told you about 'retrocochlear' disease. This doesn't discount Dr. Shore's work, if anything it links into it as the auditory nerves link directly into the cochlear nucleus, stimulating or not the cells in that first part of the brain.
 
Something I've expected for a long time - nerve damage/signal. The loss of hearing and the causal over activity of neurons in the brain only went so far in explanation. How could this alone account for variable and unstable tinnitus? How could this account for people with reactive tinnitus that instantly and dramatically increases with external sound? It had to be a pain signal from the auditory nerves.

So where does this fit in? Well, it shows promise for auditory nerve regeneration (Rinri Therapeutics) and also leads credence to Professor Peter McNaughton's work on HCN2 channels in the Spiral Ganglion.

It also explains how a cochlear implant that bypasses some of the auditory nerves often reduces tinnitus, even in a soundproof chamber as the signals from damaged synapses have been bypassed.

It fits into the treatment by Dr. Shore, where that signal is received by the cochlear nucleus.
So, do you think we absolutely have to fix this, or would HCN2 + Kv7 meds do the job?
 
There had to be an explanation for our unstable sound reactive condition and the brain amping up after hearing loss did not cut it with me. This explains things better and fits with what Professor Bance told you about 'retrocochlear' disease. This doesn't discount Dr. Shore's work, if anything it links into it as the auditory nerves link directly into the cochlear nucleus, stimulating or not the cells in that first part of the brain.
I understand the theory of it, in relation to the unstable nature of reactive tinnitus.

Do you agree with the theory that if you dampen the DCN stimulation, you dampen the sensation of the reactive tinnitus, regardless of what the auditory nerve is doing?

I think you've got a better handle of the science than I do.
 
I still can't understand how many people with hearing loss don't have tinnitus. Surely they'd have hidden hearing loss too?

I'd assume most people as they age would have hidden hearing loss and, if that's the case, tinnitus should be much more prevalent.

What a strange beast this is...
 
I still can't understand how many people with hearing loss don't have tinnitus. Surely they'd have hidden hearing loss too?

I'd assume most people as they age would have hidden hearing loss and, if that's the case, tinnitus should be much more prevalent.

What a strange beast this is...
Exactly the point I was trying to make.

My father has profound hearing loss, with no tinnitus.

Most people have hearing loss with no tinnitus.

I have NO detectable hearing loss. Yet I got tinnitus.

I have read lots of papers about age-related hearing loss and turns out, both synapses and hair cells deteriorate. I haven't found any information regarding the auditory nerve.

My point is, there is some mechanism there that got activated in us that did not get activated with people with hearing loss or people who are completely deaf.

And then, I know of a person who has lost half of his hearing after a bomb went off near him. He had ringing in the ears for 3 years. After which it went away. But the hearing loss remained. He is pretty much deaf as he has trouble understanding speech unless you talk to him loud. Oh and the guy checked the loudness of his tinnitus multiple times every day and on some days he said he put a gun to his head, contemplating suicide, so he saw his tinnitus as a threat, yet it went away. But according to the scam artist Pawel Jastreboff, him checking it should have made it stay and spread to other systems in the brain, right?

In my case, if serotonin damaged me, it did so via HCN2 channels, activating the fusiform cells, based on the papers I have read. So, these Kv7 & HCN2 drugs are my last hope, since Professor Thanos Tzounopoulos said the increase in Kv7 activitiy reduces HCN2 activity. If these drugs aren't it, we have to wait a long time for Neuralink, if they ever develop it for tinnitus...

I don't really think they'll be able to regenerate the auditory nerve that easily. But who knows.
 
Okay, so here is my problem with it: what does "nerve loss" mean? Like you have totally fine outer hair cell & inner hair cell situation in cochlea, and all of a sudden the nerve bundle between the cochlea and the brain gets damaged? Is this what they mean? I find this extremely unlikely to be a common thing, I would equal this to basically something like having tumor growth on the nerve. And why is tinnitus the only symptom? Why not balance issues?

In my opinion (and of course I am not an MIT researcher), most of us have tinnitus simply because our hair cells got damaged and lost synapses which resulted in loss of signaling between the hair cells and brain, hence we got tinnitus.

Synapses are very important and this is what connects our hair cells to the nerve bundle.

I think that in order to cure most cases with tinnitus, we would need to regenerate hair cells + synapses, which would restore communication between sensor (hair cells) and main board (brain) and that would get rid of the check engine light (tinnitus).
 
My point is, there is some mechanism there that got activated in us that did not get activated with people with hearing loss or people who are completely deaf.
Indeed. But maybe it is about gradual vs. sudden onset, i.e. the theory that gradual hearing loss allows the brain to adjust. It's the sudden (due to noise trauma) loss that makes the brain go haywire. And people's tolerances may vary here.

I had a fair amount of noise exposure in my youth - discharged a rifle indoors, went to some loud concerts, drove mopeds, always liked to listen to music pretty loud. But I always thought my hearing was "great"! I have now substantial hearing loss (40 dB at 6 kHz, 55 dB at 8 kHz) and I still do not think my hearing suffered much. In fact the damn hyperacusis makes it feel like too good. Basically I wonder if I had some hearing loss for long time, but only the recent noise trauma pushed me over the edge and triggered tinnitus.
And then, I know of a person who has lost half of his hearing after a bomb went off near him. He had ringing in the ears for 3 years. After which it went away. But the hearing loss remained. He is pretty much deaf as he has trouble understanding speech unless you talk to him loud. Oh and the guy checked the loudness of his tinnitus multiple times every day and on some days he said he put a gun to his head, contemplating suicide, so he saw his tinnitus as a threat, yet it went away. But according to the scam artist Pawel Jastreboff, him checking it should have made it stay and spread to other systems in the brain, right?
Absolutely fascinating. It belongs to the "Success Stories" section. I think many of us wouldn't mind hearing loss if that meant silence. Do you know more details of his story? Did his tinnitus go away gradually or suddenly?
 
I think reactivity is caused by hair cells that are damaged/vulnerable but not yet broken. These hair cells are much more susceptible to noise trauma. Over time they either break down (worsening early on) or stabilize (less reactive/strengthened) but are still easy to break. They are essentially connecting/disconnecting continuously from the auditory nerve, or not catching the sound signals well causing fluctuations in tinnitus - like a bad phone charger plug in a phone.

Damaged hair cells could break easily from loud sounds or cause long spikes - one loud sound causes the same effect as going to a festival for 16 hours with normal ears.

It's my theory and not backed by science.
OK, I had very reactive tinnitus with HORRIBLE sound distortions. And I mean horrible. This happened 18 days after I stopped Mirtazapine, after Fluoroquinolones damaged my brain. At the onset of this, I got back to using Mirtazapine for sleep (BIG MISTAKE). Over time it got worse and worse.

I was about to end it, before my father convinced me to go to a University Hospital to have my ears checked out.

Turned out, my hearing was perfect indeed with perfect DPOAEs. Can hear up to 20 kHz no problems... It wasn't ototoxicity that was the cause, it was neurological...

Immediately after I dropped Mirtazapine cold turkey (still have problems to this day by doing it but I had to), the distortions were COMPLETELY gone, and the reactivity only happens after I get home and lie down on the bed. My tinnitus goes up for 5 minutes or so before settling down. But even that does not happen all the time these days.

Meaning, reactivity might have more than one cause.
Absolutely fascinating. It belongs to the "Success Stories" section. I think many of us wouldn't mind hearing loss if that meant silence. Do you know more details of his story? Did his tinnitus go away gradually or suddenly?
I don't have any other details, sorry. Only that he shares the same sentiment, that he doesn't care about his hearing loss as long as his ears remain silent.
 
How in the heck is this news or a development?

"This just in, it's probably from nerve damage. This paves the way for future treatments with nerve regeneration"

Uhhhh no s***. They've been talking about that since I got it 5 years ago.
 
Here is an article from Live Science discussing this study and what Mass Eye and Ear are looking into.

"Not just a treatment, but a cure."

Using growth factors called neurotrophins to the auditory nerve is mentioned.

They hope, if successful, that "the brain would no longer have to compensate for hearing loss, so the tinnitus may ultimately subside".

Of course, it is early stages of research, but glad to see someone big like Mass Eye and Ear on this.
 
I think reactivity is caused by hair cells that are damaged/vulnerable but not yet broken. These hair cells are much more susceptible to noise trauma. Over time they either break down (worsening early on) or stabilize (less reactive/strengthened) but are still easy to break. They are essentially connecting/disconnecting continuously from the auditory nerve, or not catching the sound signals well causing fluctuations in tinnitus - like a bad phone charger plug in a phone.

Damaged hair cells could break easily from loud sounds or cause long spikes - one loud sound causes the same effect as going to a festival for 16 hours with normal ears.

It's my theory and not backed by science.
I have kind of thought about this myself. It would be good for anyone else who has had reactivity and recovered from it to chime in; did the tinnitus sort of stabilize as well when the reactivity did?

I fully get what you mean about the phone charger description. Sometimes it feels like a loose connection and the buzzing sort of changes, like trying to find a good connection with a crappy AUX cord.
 
Evidence of cochlear neural degeneration in normal-hearing subjects with tinnitus

A new study out of MIT.

Gives credence to Professor Peter McNaughton's work?

Summary:

A new study reveals that tinnitus, a common auditory issue characterized by ringing in the ears, is associated with undetected auditory nerve loss. This finding challenges the traditional understanding that tinnitus is solely a result of brain maladaptation to hearing loss.

The study shows that individuals with normal hearing tests but experiencing tinnitus actually suffer from cochlear synaptopathy, a type of "hidden hearing loss." This discovery paves the way for potential treatments, including nerve regeneration through neurotrophins, bringing hope for millions affected worldwide.

Key Facts:
  1. Tinnitus in individuals with normal hearing tests is linked to undetected auditory nerve loss.
  2. The study identifies cochlear synaptopathy, or hidden hearing loss, as a key factor in tinnitus genesis.
  3. Future treatment possibilities include auditory nerve regeneration, offering hope for a potential cure for tinnitus.
How wasn't this known forever ago?
 
I have kind of thought about this myself. It would be good for anyone else who has had reactivity and recovered from it to chime in; did the tinnitus sort of stabilize as well when the reactivity did?
I recovered from my reactivity, for the most part. When my intrusive tinnitus began (20 months ago), the reactive component was rather bad. Noises would readily cause it to react, and if the noise was loud enough (say, hearing the ocean at the beach), it would spike the reactivity for the rest of the day. The reactivity settled down in about 6 months nonlinearly. Now it's just a sliver of its former self. It still reacts but it's like a whisper of a sound and settles down in a few minutes. My tinnitus has persisted in strength well past that, although at about a year in, I started to notice the average volume drop steadily (some days much more than others).

I do have hearing loss, but I haven't suffered from noise trauma. Here's the kicker: I don't have tinnitus every day, and I don't/haven't had reactivity every day. They each come and go by the day. Some days I have one, some days the other, some days both, and some days neither. This leads me to believe tinnitus can be neurological. Like, it can have a physical cause, like noise trauma, but it can then just persist on its own whether that original cause heals.
 
I don't understand how this is the answer when cutting the cochlear nerve doesn't help tinnitus in 55% of sufferers. Maybe it works for some, but tinnitus seems more like a brain thing to me.
 
I don't understand how this is the answer when cutting the cochlear nerve doesn't help tinnitus in 55% of sufferers. Maybe it works for some, but tinnitus seems more like a brain thing to me.
I think current evidence is showing it's both. Activity starts in the peripheral nerves and that changes firing in brain cells.
 
I think current evidence is showing it's both. Activity starts in the peripheral nerves and that changes firing in brain cells.
So we would need both, a treatment for the brain, and this treatment to prevent it from getting to the brain?
 
From my understanding, fixing the issue with the nerves will fix the issue with the brain misinterpreting the signals.
I agree. Nerve repair should be on higher on the list of things to investigate rather than hearing repair. Not saying hearing restoration wouldn't be nice but I've been noticing more and more articles on nerve repair discussion and brain trimming than anything else.
 

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