Ear Reacts in Like a Broken Speaker to Certain Loud Noises / Pitches / Frequencies

[serendipity1996]

I agree with you and that inflammation lasts months to years in some cases.

This sentence from the 2016 ARO Hyperacusis conference stood out to me as it feel it may be applicable to my case.

"Important phenomenon: If inflammation is present, sympathetic activity can activate undamaged nociceptors."

Interestingly, I have found that my facial symptoms seem to be exacerbated when I consume caffeine or stimulant medications. I take it 'sympathetic activity' refers to stimulation of the nervous system? Could this possibly explain why I have had spikes then in the absence of noise exposure?

I was very perplexed by this as it wasn't brought on by noise but if I'm reading this correctly then that could make sense? I have found that these symptoms have calmed down significantly so that seems to indicate that the inflammation is going away but I'm still wary of consuming caffeine.

https://hyperacusisresearch.org/an-md-summary-of-the-2016-aro-hyperacusis-symposium/

 

[serendipity1996]

Yes it's that tingle or stab that I think indicates a setback and I'd love to know what that is. I still have my doubts but given it seems to be frequency specific and generally non-noxious (I can't get near noxious noise any more) I go with the ATP/Type II sensitization theory more that anything at the moment. I sort of know what you mean that it can be an indicator to stop right now if it's very mild, but generally for me I get a kind of pressure in my ear that tells me to stop but once I get that stab it's too late and the pain will follow. It happened just last week with someone coughing next to me. Straight away I knew it was too much and I went into a small setback for about a week. What I've learned to do now though is just head straight for a silent environment. There seems to be a definite healing pattern to a setback, at first it's too painful for any noise and more worryingly a risk of more damage very easily that quickly turns healing time from weeks to months. Then it turns into a not too painful but still very vulnerable state, and then finally to the point where it gradually starts to build tolerance again. Until next time.

I've noticed the upward trend twice now, unfortunately the first 10 to 12 months were brutal both times, I'd say the distortions and fluctuating tinnitus lasted around 3 - 4 months. The only reason I had the second acoustic shock was because I thought I'd recovered and went back to music and loud stuff (when I say loud, I mean loud in a way that wouldn't affect the vast majority of people). This time I will be very cautious though until I can ever get healed in a measurable way.

I read about your visual snow, I don't know anything about it though because I don't have that symptom. I can't imagine how this can be worse but I hope that if these drugs can fix noxacusis that your visual snow is linked to it as well.

I don't think noxacusis turns into hearing loss in the long run. I think it causes a degree of it at the outset of the acoustic shock or could even be the cause of the acoustic shock but I'd say you were now very unlikely to get near the sort of noise levels needed for further NIHL as setbacks seem to happen at non-noxious levels. Although if setbacks are cochlea ATP release, what damage ATP does to healthy OHCs in the cochlea who knows. I've read that it stimulates nociceptors and also possibly damages OHCs.

I feel you - I experience the exact same phenomenon where my ears feel sort of 'raw' and tingly but this only occurs when exposed to certain specific frequencies e.g. phone speaker or my laptop speaker. If I take that warning and stop it usually doesn't escalate into anything although saying that when my setback was at its worst 6 months ago I would then experience a sort of delayed reaction. I don't really get a delayed reaction anymore which could indicate that the inflammation is decreasing. Or I would get facial/trigeminal tension.

At the end of July I remember going into the grocery store and even just the radio playing overhead and the noise of the scanners caused my facial symptoms to flare up. This seems to have pretty much gone away as I went into a grocery store recently and didn't experience any symptoms but it still feels sort of like skating on thin ice - like I've realised I would be unable to work in retail because my ears would get triggered by the radio constantly playing lmao. I'm about 10 months in now and definitely feel I've regained some sense of normality but it's still a bit of a gamble.

I also agree that noxacusis wouldn't necessarily turn into hearing loss in the long run. It's sort of ironic because having hyperacusis forces you to be extra vigilant about your ears - we probably take more care of them than the vast majority of the population.

 

[FGG]

This sentence from the 2016 ARO Hyperacusis conference stood out to me as it feel it may be applicable to my case.

"Important phenomenon: If inflammation is present, sympathetic activity can activate undamaged nociceptors."

Interestingly, I have found that my facial symptoms seem to be exacerbated when I consume caffeine or stimulant medications. I take it 'sympathetic activity' refers to stimulation of the nervous system? Could this possibly explain why I have had spikes then in the absence of noise exposure?

I was very perplexed by this as it wasn't brought on by noise but if I'm reading this correctly then that could make sense? I have found that these symptoms have calmed down significantly so that seems to indicate that the inflammation is going away but I'm still wary of consuming caffeine.

https://hyperacusisresearch.org/an-md-summary-of-the-2016-aro-hyperacusis-symposium/

Sympathetic activity refers to sympathetic activation in the nervous system, yes.

That's an interesting find in regards to noxacusis.

Makes me wonder... Since anxiety also activates that arm of the nervous system, maybe the reason desensitization therapy helps some people (even though it potentially adds to inflammation to have chronic auditory stimulation) is that it makes them less hypervigilant about expecting noise since it's on all the time.

 

[100Hz]

I feel you - I experience the exact same phenomenon where my ears feel sort of 'raw' and tingly but this only occurs when exposed to certain specific frequencies e.g. phone speaker or my laptop speaker. If I take that warning and stop it usually doesn't escalate into anything although saying that when my setback was at its worst 6 months ago I would then experience a sort of delayed reaction. I don't really get a delayed reaction anymore which could indicate that the inflammation is decreasing. Or I would get facial/trigeminal tension.

At the end of July I remember going into the grocery store and even just the radio playing overhead and the noise of the scanners caused my facial symptoms to flare up. This seems to have pretty much gone away as I went into a grocery store recently and didn't experience any symptoms but it still feels sort of like skating on thin ice - like I've realised I would be unable to work in retail because my ears would get triggered by the radio constantly playing lmao. I'm about 10 months in now and definitely feel I've regained some sense of normality but it's still a bit of a gamble.

I also agree that noxacusis wouldn't necessarily turn into hearing loss in the long run. It's sort of ironic because having hyperacusis forces you to be extra vigilant about your ears - we probably take more care of them than the vast majority of the population.

@serendipity1996 It is ironic how we do probably have better protected cochleas now than most. Maybe due to a certain amount of damaged OHC and sensitized type II's, our systems are now providing what appears to be such a strong defense mechanism to protect the rest of the cochlea that we'd be unlikely to even be near potentially noxious sound. It made me think about something I read recently though, I'm just mulling the idea that our warning threshold for noxious noise (the normal healthy threshold that warns healthy people that noise is getting too loud) could in fact remain constant and intact at the same level it always has or at least is still much higher than our new noxacusis breaking points for setbacks, which are independently governed now by our current levels of cochlea damage. It's like when we hear noise that gets progressively louder (or sometimes not, duration seems to have the same effect sometimes) particularly at specific frequencies and we think we're OK it might go something like, 'I'm OK, I'm OK, I'm OK, Pressure building in ear-something not quite right, Setback'. I don't think this pressure in ear is a warning threshold. I think it's actual damage happening. It can happen quite slowly or instantaneously depending on the nature of the noise and if we're very lucky we withdraw from noise just before it reaches 'critical mass' and causes the setback (that's the way I think of it). I mean what if our tolerance to noise has never actually changed, but a physical pathology that's not even concerned with noise level in the typically sense, is getting triggered way beforehand giving the illusion of a lower tolerance to noise. I'm trying to think of a good analogy for this, I'm sure there's one somewhere.

I'm not saying there couldn't be some heightened neural response somewhere especially while initial injuries are very raw, probably more so if acoustic shock was involved as well, but if this is the case, the fact that tolerance to noise does generally increase over time suggests that like inflammation, this is not permanent either and could well be fully recoverable, (we obviously can't know for sure though until the cochlea can be fixed). The permanent damage in the cochlea however remains the same or only gets worse and I would say that the only variable it could have is the amount of inflammation present. If there's zero or low inflammation it could be thought of that it has a 'budget' to play with. Once the inflammation was high and as long as you could know when to rest and recover from it, a setback would be avoided. But if the inflammation was already quite high and then you got a relatively small shock noise it could easily push it over the edge.

I've got a bit of a lazy question, maybe you might know @FGG. We keep talking about cochlea inflammation, and we also have read that OHC support cells release ATP that stimulate nociceptors. Is there a difference between cochlea inflammation and ATP? We're suggesting that our cochleas remain inflamed for some time, but that residual inflammation is obviously not stimulating the nociceptors constantly is it (not to be confused with possibly the TGN cochlea nerve branches or anything else which may be getting stimulated by the inflammation)? I just think we'd be in a permanent state of setback if that were the case (the actual point of setback being triggered, constantly). But it doesn't really happen like that so I wonder if ATP release is actually quite a rare event that causes a spark of inflammation when it stimulates a nociceptor. I've got a couple of theories why we could get the pin prick pain even in silence which I'll hold off from for now, but in the above example if a rogue bit of ATP was floating around in the cochlea could it stimulate a nociceptor long after the noise exposure even in silence? This is obviously where my actual science skills start to fall short of my thinking on this subject, hence would be useful to know if ATP is actually different from inflammation. I hope I'm articulating that well enough.

Also, as we know drugs can diffused from the middle ear to the cochlea, and apparently ATP can also do this. Something else I've started to wonder is can this happen the other way from the cochlea to the middle ear?

 

[FGG]

@serendipity1996 It is ironic how we do probably have better protected cochleas now than most. Maybe due to a certain amount of damaged OHC and sensitized type II's, our systems are now providing what appears to be such a strong defense mechanism to protect the rest of the cochlea that we'd be unlikely to even be near potentially noxious sound. It made me think about something I read recently though, I'm just mulling the idea that our warning threshold for noxious noise (the normal healthy threshold that warns healthy people that noise is getting too loud) could in fact remain constant and intact at the same level it always has or at least is still much higher than our new noxacusis breaking points for setbacks, which are independently governed now by our current levels of cochlea damage. It's like when we hear noise that gets progressively louder (or sometimes not, duration seems to have the same effect sometimes) particularly at specific frequencies and we think we're OK it might go something like, 'I'm OK, I'm OK, I'm OK, Pressure building in ear-something not quite right, Setback'. I don't think this pressure in ear is a warning threshold. I think it's actual damage happening. It can happen quite slowly or instantaneously depending on the nature of the noise and if we're very lucky we withdraw from noise just before it reaches 'critical mass' and causes the setback (that's the way I think of it). I mean what if our tolerance to noise has never actually changed, but a physical pathology that's not even concerned with noise level in the typically sense, is getting triggered way beforehand giving the illusion of a lower tolerance to noise. I'm trying to think of a good analogy for this, I'm sure there's one somewhere.

I'm not saying there couldn't be some heightened neural response somewhere especially while initial injuries are very raw, probably more so if acoustic shock was involved as well, but if this is the case, the fact that tolerance to noise does generally increase over time suggests that like inflammation, this is not permanent either and could well be fully recoverable, (we obviously can't know for sure though until the cochlea can be fixed). The permanent damage in the cochlea however remains the same or only gets worse and I would say that the only variable it could have is the amount of inflammation present. If there's zero or low inflammation it could be thought of that it has a 'budget' to play with. Once the inflammation was high and as long as you could know when to rest and recover from it, a setback would be avoided. But if the inflammation was already quite high and then you got a relatively small shock noise it could easily push it over the edge.

I've got a bit of a lazy question, maybe you might know @FGG. We keep talking about cochlea inflammation, and we also have read that OHC support cells release ATP that stimulate nociceptors. Is there a difference between cochlea inflammation and ATP? We're suggesting that our cochleas remain inflamed for some time, but that residual inflammation is obviously not stimulating the nociceptors constantly is it (not to be confused with possibly the TGN cochlea nerve branches or anything else which may be getting stimulated by the inflammation)? I just think we'd be in a permanent state of setback if that were the case (the actual point of setback being triggered, constantly). But it doesn't really happen like that so I wonder if ATP release is actually quite a rare event that causes a spark of inflammation when it stimulates a nociceptor. I've got a couple of theories why we could get the pin prick pain even in silence which I'll hold off from for now, but in the above example if a rogue bit of ATP was floating around in the cochlea could it stimulate a nociceptor long after the noise exposure even in silence? This is obviously where my actual science skills start to fall short of my thinking on this subject, hence would be useful to know if ATP is actually different from inflammation. I hope I'm articulating that well enough.

Also, as we know drugs can diffused from the middle ear to the cochlea, and apparently ATP can also do this. Something else I've started to wonder is can this happen the other way from the cochlea to the middle ear?

ATP isn't at all part of classic inflammation, it just leaks out of the cell in this case when the cochlea is damaged and acts as an irritant to the nerves. This sets up noxacusis when the nerve then gets sensitized to sound stimuli from the irritation.

So the question is, is there ongoing inflammation preventing the nerve from healing (or perpetuating cell leakage somehow) or is the nerve primarily sensitized from the initial damage (if it's the latter, certain ion channel drugs will be needed for noxacusis).

It's also possible it's a combination of the two and the nerve could get less sensitized over time without irritation.

What's frustrating for noxacusis sufferers is I don't think anyone knows.

What else have you come across @serendipity1996?

 

[100Hz]

ATP isn't at all part of classic inflammation, it just leaks out of the cell in this case when the cochlea is damaged and acts as an irritant to the nerves. This sets up noxacusis when the nerve then gets sensitized to sound stimuli from the irritation.

So the question is, is there ongoing inflammation preventing the nerve from healing (or perpetuating cell leakage somehow) or is the nerve primarily sensitized from the initial damage (if it's the latter, certain ion channel drugs will be needed for noxacusis).

It's also possible it's a combination of the two and the nerve could get less sensitized over time without irritation.

What's frustrating for noxacusis sufferers is I don't think anyone knows.

What else have you come across @serendipity1996?

Thanks so much for all your answers.

Those are good counter questions, and if ATP is a totally different thing as a direct result of OHC damage then I think it could be a really good thing if it turns out that FX-322 does what we all hope it will do and fix OHCs that in turn results in no further ATP release.

I think until FX-322 is here, this is now nearing impossible to try and work out if ATP would still be released once OHCs were regenerated. I have a degree of optimism that it wouldn't be based on the above logic.

It would hopefully allow inflammation to disperse altogether if there was no more threat of ATP. I believe firmly that because tolerance to noise builds and pain subsides over time (when careful), that something is recovering due to inflammation slowly reducing, and regardless of the fact that something is fundamentally damaged somewhere, and is still lurking and waiting to trigger a setback, a massive degree of recovery can be achieved within this pain and tolerance area of noxacusis, seemingly over and over again.

The one part of your reply that worries me, if it's what you're suggesting, is the prospect that the sensitized Type II afferents could now be stimulated directly by noise even if their OHCs have been regenerated. I guess that's only going to be found out once FX-322 is finally here. However I also view setbacks and the tell tale pin prick stabby sensations that go along with them as a specifically separate and unique part of noxacusis to typical inflammation and pain, and I am really hoping that this is due to ATP release upon hearing the offending noise and not the noise directly stimulating the nerve if that makes sense.

 

[serendipity1996]

ATP isn't at all part of classic inflammation, it just leaks out of the cell in this case when the cochlea is damaged and acts as an irritant to the nerves. This sets up noxacusis when the nerve then gets sensitized to sound stimuli from the irritation.

So the question is, is there ongoing inflammation preventing the nerve from healing (or perpetuating cell leakage somehow) or is the nerve primarily sensitized from the initial damage (if it's the latter, certain ion channel drugs will be needed for noxacusis).

It's also possible it's a combination of the two and the nerve could get less sensitized over time without irritation.

What's frustrating for noxacusis sufferers is I don't think anyone knows.

What else have you come across @serendipity1996?

Ah, that's interesting to know about ATP - hadn't realised that! I basically just regurgitate the opinions of the researchers (lol). The good thing is that these questions are being actively worked on - at the Hopkins lab (run by Paul Fuchs) one of the researchers is exploring whether the Type 2 neurons and/or the surrounding tissue become hyperexcitable after peripheral trauma - this is the basis of a doctoral thesis currently. There is also a postdoctoral fellow who is exploring the impact of cochlear inflammation and Type 2 activity as additional factors in the prolonged pain response to sound. So I assume that this will eventually emerge as published research in the next few years. So we WILL get answers to these very questions (or at least have more pieces of the puzzle to fit together!).

There's an interesting excerpt from the 2015 paper on noxacusis - "More commonly, however, acoustic stress progressively damages OHCs, leading to their eventual death, and is known to increase ATP concentration in cochlear fluids in vivo." The thing I don't quite get about ATP leakage - is it generally considered a temporary phenomenon following damage? Or could cochlea damage lead to permanently elevated levels of ATP within the cochlea?

I'm also going to add a bit about my own personal experience with noxacusis. My first 'bout' of painful hyperacusis was in 2016 - it was a gradual onset but then reached a point where I had painful symptoms for about 3 months. After that, the pain and soreness went away and my ears felt pretty much 'normal'. However, I knew I was still at risk of a relapse if I went anywhere very noisy - concerts, clubs etc were out of the question of course. So, even though the majority of my symptoms were in remission in everyday life, there was still a much lower threshold for triggering further damage/symptoms than there would be in a healthy ear. On the whole, most noises weren't problematic for me.

My setback last year came as a result of attending a party where there was live music - although it wasn't insanely loud and actually felt 'okay' in the moment although I did worry slightly. Then the next day I was exposed to a loud car stereo for a few hours - my family were in the car and none of them were affected or complained that it was loud. In fact, I was wearing earplugs! I am noting this to highlight the fact that my ears clearly had a much lower threshold of re-initiating damage/noxacusis than a healthy ear would. My symptoms didn't come on immediately - it was only a few days later that I began experiencing the classic burning pain.

I do believe that there must be an inflammatory component at play. I experienced trigeminal nerve pain for months and months and it's only been very recently that it's pretty much fully gone away. For example, even just 2 months ago a trip to the grocery store would trigger facial/trigeminal symptoms from the scanners and radio playing overhead. I don't get that any longer. But I still have a damaged cochlea clearly. Even prior to this setback when I could do most things, my ears were clearly far more susceptible to further damage than a healthy ear. Even though my ears felt 'normal', I still had a damaged inner ear clearly.

It is indeed frustrating how little we know and what treatments would be most helpful for us. I've come across some literature on pain that suggests when the underlying primary pathology is resolved, secondary issues such as central sensitisation and pain would resolve. But I'm not sure how applicable all this is to the cochlea and Type 2s - are there any other pathologies we can look to where the nerves get sensitised from the initial damage?

Tagging @100Hz.

 

[FGG]

There's an interesting excerpt from the 2015 paper on noxacusis - "More commonly, however, acoustic stress progressively damages OHCs, leading to their eventual death, and is known to increase ATP concentration in cochlear fluids in vivo." The thing I don't quite get about ATP leakage - is it generally considered a temporary phenomenon following damage? Or could cochlea damage lead to permanently elevated levels of ATP within the cochlea?

The excessive ATP leakage from hair cell loss should be temporary and disappear once the cell is subject to apoptosis because if there is no cell, there is no leakage, right?

If there is a form of damaged hair cells that still leak ATP but are not subject to apoptosis, I would wonder why a cell damaged enough to leak ATP wouldn't be reabsorbed by the body so I sort of doubt that this is a common problem or even really occurs as the primary problem with noxacusis.

But, I just read though that another source of ATP may be from the gap junctions. These function to deliver ATP normally (which is required for the energy involved in hearing):

https://www.pnas.org/content/105/48/18770

It seems that inflammation can change their properties, potentially adding more ATP than normal during the process of inflammatory recruitment:

https://www.sciencedirect.com/science/article/pii/S0005273604002652

And in thinking about this further, a small amount (quiet) of noise requires a small amount of ATP release but does not cause noxacusis. So the amount of ATP released from the connexin gap junctions could be part of this picture and not just the sensitization of the nerve fibers.

It makes me wonder if hair cell regeneration is not going to be a big player for noxacusis and maybe controlling the inflammation is. Again, all my thinking out loud/speculation but this seems logical to me.

 

[serendipity1996]

The excessive ATP leakage from hair cell loss should be temporary and disappear once the cell is subject to apoptosis because if there is no cell, there is no leakage, right?

If there is a form of damaged hair cells that still leak ATP but are not subject to apoptosis, I would wonder why a cell damaged enough to leak ATP wouldn't be reabsorbed by the body so I sort of doubt that this is a common problem or even really occurs as the primary problem with noxacusis.

But, I just read though that another source of ATP may be from the gap junctions. These function to deliver ATP normally (which is required for the energy involved in hearing):

https://www.pnas.org/content/105/48/18770

It seems that inflammation can change their properties, potentially adding more ATP than normal during the process of inflammatory recruitment:

https://www.sciencedirect.com/science/article/pii/S0005273604002652

And in thinking about this further, a small amount (quiet) of noise requires a small amount of ATP release but does not cause noxacusis. So the amount of ATP released from the connexin gap junctions could be part of this picture and not just the sensitization of the nerve fibers.

It makes me wonder if hair cell regeneration is not going to be a big player for noxacusis and maybe controlling the inflammation is. Again, all my thinking out loud/speculation but this seems logical to me.

This is really informative. One question though - it seems from what I've read that is the damaged hair cells in addition to the supporting cells that release ATP. I take it the support cells remain and do not undergo apoptosis (otherwise treatments like FX-322 wouldn't work)? So could the supporting cells still be releasing ATP even once the hair cells themselves have been disposed of by the body? From the 2015 Hopkins paper: "Here, we show that type II afferents are excited by ATP released from supporting cells around damaged OHCs..."

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4664349/

I'm hoping very much that we will have more answers to these burning questions in the next few years!

Edit: another interesting excerpt from that paper that seems to support what you're saying:
"Of interest in this context is the previous report that sensitivity to ATP is reduced in type II afferents after the onset of hearing, consistent with the fact that loud sound is not usually painful to normal ears. However, purinergic signaling in the cochlea is up-regulated after noise exposure, raising the possibility that type II afferents become more sensitive after damage, in part by increased sensitivity to ATP."

 

[FGG]

This is really informative. One question though - it seems from what I've read that is the damaged hair cells in addition to the supporting cells that release ATP. I take it the support cells remain and do not undergo apoptosis (otherwise treatments like FX-322 wouldn't work)? So could the supporting cells still be releasing ATP even once the hair cells themselves have been disposed of by the body? From the 2015 Hopkins paper: "Here, we show that type II afferents are excited by ATP released from supporting cells around damaged OHCs..."

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4664349/

I'm hoping very much that we will have more answers to these burning questions in the next few years!

Edit: another interesting excerpt from that paper that seems to support what you're saying:
"Of interest in this context is the previous report that sensitivity to ATP is reduced in type II afferents after the onset of hearing, consistent with the fact that loud sound is not usually painful to normal ears. However, purinergic signaling in the cochlea is up-regulated after noise exposure, raising the possibility that type II afferents become more sensitive after damage, in part by increased sensitivity to ATP."

The gap junctions I was referring to are in the supporting cells.

 

[100Hz]

The good thing is that these questions are being actively worked on - at the Hopkins lab (run by Paul Fuchs) one of the researchers is exploring whether the Type 2 neurons and/or the surrounding tissue become hyperexcitable after peripheral trauma - this is the basis of a doctoral thesis currently. There is also a postdoctoral fellow who is exploring the impact of cochlear inflammation and Type 2 activity as additional factors in the prolonged pain response to sound. So I assume that this will eventually emerge as published research in the next few years. So we WILL get answers to these very questions (or at least have more pieces of the puzzle to fit together!).

Thanks for this info. It's good to know that these areas in particular are being worked on because they seem to be getting into the real detail now of why this happens. Your relationship with noise and pain seems to mirror exactly how mine was before I got a lot more careful. Its just a repeating cycle of recovering, thinking I'm OK and able to handle more than I thought, then (crucially) thinking you can do it again the next day, and then back to square 1. It really does seems to point to a ramping up of inflammation.

It is indeed frustrating how little we know and what treatments would be most helpful for us. I've come across some literature on pain that suggests when the underlying primary pathology is resolved, secondary issues such as central sensitisation and pain would resolve. But I'm not sure how applicable all this is to the cochlea and Type 2s - are there any other pathologies we can look to where the nerves get sensitised from the initial damage?

This is the trouble isn't it. I don't pay much attention to anything that says this or similar, 'when the underlying primary pathology is resolved, secondary issues such as central sensitisation and pain would resolve', because we don't know what the underlying pathology is, or whether it does cause any secondary independent pathology. It's been a really interesting discussion over the last few months and I suppose by accident it is what we are trying to do (work out the most plausible theory on the pathology) and then apply the proposed therapeutic elements of current drugs in trial to estimate our best chance of treatment.

With regards to any other pathology being responsible (unless there something completely unknown going on), I think a good thing is that there's really only several things that could be at play. Middle ear which I think plays its own secondary part in inflammation and facial pain but am skeptical about it being a primary cause of noxacusis or setbacks. Heightened neural response which again I think could play a part to an extent, more related to the middle ear, but am also skeptical about being an underlying cause because this element does recover. And back to the cochlea which I think now has too much actual evidence if I'm honest that it is responsible (the research on type IIs, cochlea damage is permanent, and significantly the frequency specific element of noxacusis). I think the sort of research like you highlight above is key to this now and it's going to boil down to, does regenerating the hair cells, and / or synapses do enough to also fix whats causing noxacusis, or will it uncover the need for a whole different area of research and treatment. I think we're in the right area though.

It makes me wonder if hair cell regeneration is not going to be a big player for noxacusis and maybe controlling the inflammation is. Again, all my thinking out loud/speculation but this seems logical to me.

Thanks for the links, I'll try and read and understand them if I can.

I agree with you that controlling the inflammation is probably the more realistic part of this to focus on right now. It will hopefully be here first anyway and who knows maybe for some sufferers may even be enough. Then as FX-322 trundles forwards plus research like @serendipity1996 posted it will help to fill in the gaps of the bigger picture of regeneration.

 

[serendipity1996]

Thanks for this info. It's good to know that these areas in particular are being worked on because they seem to be getting into the real detail now of why this happens. Your relationship with noise and pain seems to mirror exactly how mine was before I got a lot more careful. Its just a repeating cycle of recovering, thinking I'm OK and able to handle more than I thought, then (crucially) thinking you can do it again the next day, and then back to square 1. It really does seems to point to a ramping up of inflammation.

This is the trouble isn't it. I don't pay much attention to anything that says this or similar, 'when the underlying primary pathology is resolved, secondary issues such as central sensitisation and pain would resolve', because we don't know what the underlying pathology is, or whether it does cause any secondary independent pathology. It's been a really interesting discussion over the last few months and I suppose by accident it is what we are trying to do (work out the most plausible theory on the pathology) and then apply the proposed therapeutic elements of current drugs in trial to estimate our best chance of treatment.

With regards to any other pathology being responsible (unless there something completely unknown going on), I think a good thing is that there's really only several things that could be at play. Middle ear which I think plays its own secondary part in inflammation and facial pain but am skeptical about it being a primary cause of noxacusis or setbacks. Heightened neural response which again I think could play a part to an extent, more related to the middle ear, but am also skeptical about being an underlying cause because this element does recover. And back to the cochlea which I think now has too much actual evidence if I'm honest that it is responsible (the research on type IIs, cochlea damage is permanent, and significantly the frequency specific element of noxacusis). I think the sort of research like you highlight above is key to this now and it's going to boil down to, does regenerating the hair cells, and / or synapses do enough to also fix whats causing noxacusis, or will it uncover the need for a whole different area of research and treatment. I think we're in the right area though.

Thanks for the links, I'll try and read and understand them if I can.

I agree with you that controlling the inflammation is probably the more realistic part of this to focus on right now. It will hopefully be here first anyway and who knows maybe for some sufferers may even be enough. Then as FX-322 trundles forwards plus research like @serendipity1996 posted it will help to fill in the gaps of the bigger picture of regeneration.

I agree with you - treatments for inflammation could tide us over and even help mitigate setbacks. I think many of us with noxacusis would settle for a treatment that may not be a 100% panacea anyway e.g. if I were still unable to attend a concert or club it wouldn't bother me too much. It's the everyday noises and frequency-specific irritation that really gets me down.

 

[weab00]

With regards to any other pathology being responsible (unless there something completely unknown going on), I think a good thing is that there's really only several things that could be at play. Middle ear which I think plays its own secondary part in inflammation and facial pain but am skeptical about it being a primary cause of noxacusis or setbacks. Heightened neural response which again I think could play a part to an extent, more related to the middle ear, but am also skeptical about being an underlying cause because this element does recover. And back to the cochlea which I think now has too much actual evidence if I'm honest that it is responsible (the research on type IIs, cochlea damage is permanent, and significantly the frequency specific element of noxacusis). I think the sort of research like you highlight above is key to this now and it's going to boil down to, does regenerating the hair cells, and / or synapses do enough to also fix whats causing noxacusis, or will it uncover the need for a whole different area of research and treatment. I think we're in the right area though.

As you say, we will only have the answers to some of these burning questions once someone with noxacusis tries FX-322 and SPI-1005, hopefully coming out around the same time. Personally, I'm remaining cautiously optimistic.

 

[Aaron91]

Can anyone provide some insight into what is actually going on at a molecular/biological level when we say "ATP is leaking from the cell"? Does this mean the cell wall/membrane is compromised/has some kind of hole in it? Is the cell at some kind of 'maximum capacity' and the cell 'gates' are not able to keep the ATP "in"?

I apologise for asking these questions in such a crude fashion, but I'm not well versed in molecular biology lol.

 

[Juan]

Can anyone provide some insight into what is actually going on at a molecular/biological level when we say "ATP is leaking from the cell"? Does this mean the cell wall/membrane is compromised/has some kind of hole in it? Is the cell at some kind of 'maximum capacity' and the cell 'gates' are not able to keep the ATP "in"?

I apologise for asking these questions in such a crude fashion, but I'm not well versed in molecular biology lol.

I recently read that the Mass Eye and Ear researcher David Jung is working on developing a molecule that they can deliver to the middle ear to see if it can help with or reverse hearing loss.

It sounds a bit like science fiction, but I am happy there are research projects like this.

 

[100Hz]

Can anyone provide some insight into what is actually going on at a molecular/biological level when we say "ATP is leaking from the cell"? Does this mean the cell wall/membrane is compromised/has some kind of hole in it? Is the cell at some kind of 'maximum capacity' and the cell 'gates' are not able to keep the ATP "in"?

I apologise for asking these questions in such a crude fashion, but I'm not well versed in molecular biology lol.

I've read this several times. I understand it bit better every time so I'll see I I can break it down a bit.

Unmyelinated type II afferent neurons report cochlear damage

An experiment was performed where cells were ruptured and from I can get from the research, the supporting cells were deemed to be a major source of ATP acting on type II afferents.

Such immediate rupture of individual hair cells might occur in vivo. More commonly, however, acoustic stress progressively damages OHCs, leading to their eventual death, and is known to increase ATP concentration in cochlear fluids in vivo.

This work provides direct evidence that type II afferents, in addition to sensing glutamate release from OHCs, are activated by cochlear damage in the young rat's cochlea. This observation may help to resolve the decades-long conundrum that type II afferents in vivo are very insensitive to sound and yet presumably carry some information to the auditory brainstem. Likewise, measured ex vivo, synaptic excitation is weak and could activate type II afferents only if all of the presynaptic OHCs were maximally stimulated. Alternatively, ATP potently activates type II afferents and serves as a major contributor to the damage-induced response. ATP can be released into cochlear fluid after tissue stress (even without OHC ablation) in vitro, or noise exposure in vivo.​

I'm a bit confused by the above, I've tried to make some sense of it. It seems to suggest that in vivo or vitro, there is relatively low chance of Type II sensitization, but however if all of the associated hair cells become maximally stimulated then it will become sensitized. But also it alternatively seems to suggest that upon noise exposure, importantly not necessarily leading to hair cell death, ATP could still be released and cause Type II sensitization. I could well be reading this wrong though but it's what it seems to say.

Experimental ablation of OHCs was shown to initiate ATP-dependent calcium waves in nearby Hensen's (support) cells that further triggers release of ATP through their connexin hemichannels. P2X2 receptors have been located to the postsynaptic junction in the OHC region in adult guinea pig, and P2Y2 receptors have been identified in a small population of spiral ganglion neurons in both adult and neonatal rats, suggesting the expression of purinergic receptors in type II neurons.​

I understand that expression of purinergic receptors in type II neurons means the receptors respond to ATP.

Of interest in this context is the previous report that sensitivity to ATP is reduced in type II afferents after the onset of hearing, consistent with the fact that loud sound is not usually painful to normal ears. However, purinergic signaling in the cochlea is up-regulated after noise exposure, raising the possibility that type II afferents become more sensitive after damage, in part by increased sensitivity to ATP.​

This suggests to me that as we know, loud sound for the majority of people isn't painful and that the more the Type II afferents are exposed to ATP, which is more and more frequently after repeat noise exposure, the more they are stimulated by ATP, and then they become more and more sensitive to ATP until they finally become sensitized, at which point they do begin to transmit pain signal upon noise exposure. It seems to not be suggesting that its a one time switch where ATP automatically sensitizes a Type II afferent but cumulative damage.

What I seem to be getting from reading this again, is that it might be suggesting that Type II afferent can become sensitized without OHC death necessarily occurring. If I'm missing something obvious please let me know.

Type I afferents are strongly activated by glutamate release from IHCs, but not by ATP. Type II afferents are strongly activated by ATP, but only weakly by glutamate release from OHCs. These distinctions reinforce the hypothesis that type I and type II afferents serve different functional roles: as acoustic (type I) versus trauma (type II) detectors.

Finally, the KCNQ activator retigabine can silence both type II afferents and somatic pain fibers.​

That experiment you posted last week about the deaf mice still haunts me though because I wish they'd tested what repeat noise exposure would do after the hair cell death, because this question seems to be becoming more prominent now, its obvious that upon hair cell death ATP is released, and according to the above maybe even not necessarily upon hair cell death. What I'd love to know is what kind of activity occurs after the hair cell death. I don't believe Ive ever seen a study showing ATP being released over and over from support cells upon repeat noise exposure, ideally also measuring the specific frequencies used and the support cell response to each individual frequency.

 

[weab00]

I've read this several times. I understand it bit better every time so I'll see I I can break it down a bit.

Unmyelinated type II afferent neurons report cochlear damage

An experiment was performed where cells were ruptured and from I can get from the research, the supporting cells were deemed to be a major source of ATP acting on type II afferents.

Such immediate rupture of individual hair cells might occur in vivo. More commonly, however, acoustic stress progressively damages OHCs, leading to their eventual death, and is known to increase ATP concentration in cochlear fluids in vivo.

This work provides direct evidence that type II afferents, in addition to sensing glutamate release from OHCs, are activated by cochlear damage in the young rat's cochlea. This observation may help to resolve the decades-long conundrum that type II afferents in vivo are very insensitive to sound and yet presumably carry some information to the auditory brainstem. Likewise, measured ex vivo, synaptic excitation is weak and could activate type II afferents only if all of the presynaptic OHCs were maximally stimulated. Alternatively, ATP potently activates type II afferents and serves as a major contributor to the damage-induced response. ATP can be released into cochlear fluid after tissue stress (even without OHC ablation) in vitro, or noise exposure in vivo.​

I'm a bit confused by the above, I've tried to make some sense of it. It seems to suggest that in vivo or vitro, there is relatively low chance of Type II sensitization, but however if all of the associated hair cells become maximally stimulated then it will become sensitized. But also it alternatively seems to suggest that upon noise exposure, importantly not necessarily leading to hair cell death, ATP could still be released and cause Type II sensitization. I could well be reading this wrong though but it's what it seems to say.

Experimental ablation of OHCs was shown to initiate ATP-dependent calcium waves in nearby Hensen's (support) cells that further triggers release of ATP through their connexin hemichannels. P2X2 receptors have been located to the postsynaptic junction in the OHC region in adult guinea pig, and P2Y2 receptors have been identified in a small population of spiral ganglion neurons in both adult and neonatal rats, suggesting the expression of purinergic receptors in type II neurons.​

I understand that expression of purinergic receptors in type II neurons means the receptors respond to ATP.

Of interest in this context is the previous report that sensitivity to ATP is reduced in type II afferents after the onset of hearing, consistent with the fact that loud sound is not usually painful to normal ears. However, purinergic signaling in the cochlea is up-regulated after noise exposure, raising the possibility that type II afferents become more sensitive after damage, in part by increased sensitivity to ATP.​

This suggests to me that as we know, loud sound for the majority of people isn't painful and that the more the Type II afferents are exposed to ATP, which is more and more frequently after repeat noise exposure, the more they are stimulated by ATP, and then they become more and more sensitive to ATP until they finally become sensitized, at which point they do begin to transmit pain signal upon noise exposure. It seems to not be suggesting that its a one time switch where ATP automatically sensitizes a Type II afferent but cumulative damage.

What I seem to be getting from reading this again, is that it might be suggesting that Type II afferent can become sensitized without OHC death necessarily occurring. If I'm missing something obvious please let me know.

Type I afferents are strongly activated by glutamate release from IHCs, but not by ATP. Type II afferents are strongly activated by ATP, but only weakly by glutamate release from OHCs. These distinctions reinforce the hypothesis that type I and type II afferents serve different functional roles: as acoustic (type I) versus trauma (type II) detectors.

Finally, the KCNQ activator retigabine can silence both type II afferents and somatic pain fibers.​

That experiment you posted last week about the deaf mice still haunts me though because I wish they'd tested what repeat noise exposure would do after the hair cell death, because this question seems to be becoming more prominent now, its obvious that upon hair cell death ATP is released, and according to the above maybe even not necessarily upon hair cell death. What I'd love to know is what kind of activity occurs after the hair cell death. I don't believe Ive ever seen a study showing ATP being released over and over from support cells upon repeat noise exposure, ideally also measuring the specific frequencies used and the support cell response to each individual frequency.

So why does too much noise exposure lead to a setback in hyperacusis sufferers?

 

[Aaron91]

I've read this several times. I understand it bit better every time so I'll see I I can break it down a bit.

Unmyelinated type II afferent neurons report cochlear damage

An experiment was performed where cells were ruptured and from I can get from the research, the supporting cells were deemed to be a major source of ATP acting on type II afferents.

Such immediate rupture of individual hair cells might occur in vivo. More commonly, however, acoustic stress progressively damages OHCs, leading to their eventual death, and is known to increase ATP concentration in cochlear fluids in vivo.

This work provides direct evidence that type II afferents, in addition to sensing glutamate release from OHCs, are activated by cochlear damage in the young rat's cochlea. This observation may help to resolve the decades-long conundrum that type II afferents in vivo are very insensitive to sound and yet presumably carry some information to the auditory brainstem. Likewise, measured ex vivo, synaptic excitation is weak and could activate type II afferents only if all of the presynaptic OHCs were maximally stimulated. Alternatively, ATP potently activates type II afferents and serves as a major contributor to the damage-induced response. ATP can be released into cochlear fluid after tissue stress (even without OHC ablation) in vitro, or noise exposure in vivo.​

I'm a bit confused by the above, I've tried to make some sense of it. It seems to suggest that in vivo or vitro, there is relatively low chance of Type II sensitization, but however if all of the associated hair cells become maximally stimulated then it will become sensitized. But also it alternatively seems to suggest that upon noise exposure, importantly not necessarily leading to hair cell death, ATP could still be released and cause Type II sensitization. I could well be reading this wrong though but it's what it seems to say.

Experimental ablation of OHCs was shown to initiate ATP-dependent calcium waves in nearby Hensen's (support) cells that further triggers release of ATP through their connexin hemichannels. P2X2 receptors have been located to the postsynaptic junction in the OHC region in adult guinea pig, and P2Y2 receptors have been identified in a small population of spiral ganglion neurons in both adult and neonatal rats, suggesting the expression of purinergic receptors in type II neurons.​

I understand that expression of purinergic receptors in type II neurons means the receptors respond to ATP.

Of interest in this context is the previous report that sensitivity to ATP is reduced in type II afferents after the onset of hearing, consistent with the fact that loud sound is not usually painful to normal ears. However, purinergic signaling in the cochlea is up-regulated after noise exposure, raising the possibility that type II afferents become more sensitive after damage, in part by increased sensitivity to ATP.​

This suggests to me that as we know, loud sound for the majority of people isn't painful and that the more the Type II afferents are exposed to ATP, which is more and more frequently after repeat noise exposure, the more they are stimulated by ATP, and then they become more and more sensitive to ATP until they finally become sensitized, at which point they do begin to transmit pain signal upon noise exposure. It seems to not be suggesting that its a one time switch where ATP automatically sensitizes a Type II afferent but cumulative damage.

What I seem to be getting from reading this again, is that it might be suggesting that Type II afferent can become sensitized without OHC death necessarily occurring. If I'm missing something obvious please let me know.

Type I afferents are strongly activated by glutamate release from IHCs, but not by ATP. Type II afferents are strongly activated by ATP, but only weakly by glutamate release from OHCs. These distinctions reinforce the hypothesis that type I and type II afferents serve different functional roles: as acoustic (type I) versus trauma (type II) detectors.

Finally, the KCNQ activator retigabine can silence both type II afferents and somatic pain fibers.​

That experiment you posted last week about the deaf mice still haunts me though because I wish they'd tested what repeat noise exposure would do after the hair cell death, because this question seems to be becoming more prominent now, its obvious that upon hair cell death ATP is released, and according to the above maybe even not necessarily upon hair cell death. What I'd love to know is what kind of activity occurs after the hair cell death. I don't believe Ive ever seen a study showing ATP being released over and over from support cells upon repeat noise exposure, ideally also measuring the specific frequencies used and the support cell response to each individual frequency.

Great post, @100Hz. I've read this several times now over the last few days and I'm still trying to gather my own thoughts, but thought I'd share a few of them while they're still fresh in my mind. I'm curious to further understand how the ATP "leak" theory fits in with this maximal stimulation you have referred to above. Does maximal stimulation mean that every single OHC needs to be exposed to some kind of threshold of sound, or do some OHCs need to be stimulated to their maximum "capacity"? The quote clearly says "only if all the presynpatic OHCs", so I presume it's the former. I wonder why then every single OHC would need to be maximally stimulated and not, say, some or most of them.

With that in mind and more critically: does the sensitisation of the type II fibres occur because there is an overload of ATP production due to the sheer number of OHCs producing it, or because some OHCs "break" and the ATP "spills out" onto the innervated type II fibres? I suppose what I'm trying to understand is whether the sensitisation occurs because too many OHCs are producing too much ATP for an extended period of time (an ATP "flood", if you will), or because type II afferents are not supposed to be exposed to ATP at all - hence the commonly used phrase "leak". There is a grey area here in that, if one were exposed to a sound where all OHCs were stimulated, one could argue that the probability of some of them becoming damaged would be much higher, and so that's why all OHCs would need to be stimulated - to maximise the chances of "breaking" some OHCs, causing them to leak.

Of interest in this context is the previous report that sensitivity to ATP is reduced in type II afferents after the onset of hearing, consistent with the fact that loud sound is not usually painful to normal ears. However, purinergic signaling in the cochlea is up-regulated after noise exposure, raising the possibility that type II afferents become more sensitive after damage, in part by increased sensitivity to ATP."

This is interesting as well. "Noise exposure", as opposed to "sound exposure", would suggest that they are referring to an unhealthy level of sound. In this same paragraph, it says that sensitivity to ATP is reduced in type II afferents after onset of hearing. In other words, purinergic signaling is downregulated upon exposure to healthy levels of sound. But what I'm also curious about is the wording here. It says that the type II afferents become more sensitive "in part by increased sensitivity to ATP". I don't mean to be pedantic here, but it's not clear to me whether this increased sensitivity to ATP is the result of the upregulated purinergic signalling, or whether the exposure to ATP is upregulating the purinergic receptors. If it's the former, then there must be some other kind of mechanism going on that is unrelated to the leaking of ATP (but presumably coinciding with it).

I hope this all makes sense and I'm curious to know @serendipity1996's thoughts on this as well.

 

[Aaron91]

Great post, @100Hz. I've read this several times now over the last few days and I'm still trying to gather my own thoughts, but thought I'd share a few of them while they're still fresh in my mind. I'm curious to further understand how the ATP "leak" theory fits in with this maximal stimulation you have referred to above. Does maximal stimulation mean that every single OHC needs to be exposed to some kind of threshold of sound, or do some OHCs need to be stimulated to their maximum "capacity"? The quote clearly says "only if all the presynpatic OHCs", so I presume it's the former. I wonder why then every single OHC would need to be maximally stimulated and not, say, some or most of them.

With that in mind and more critically: does the sensitisation of the type II fibres occur because there is an overload of ATP production due to the sheer number of OHCs producing it, or because some OHCs "break" and the ATP "spills out" onto the innervated type II fibres? I suppose what I'm trying to understand is whether the sensitisation occurs because too many OHCs are producing too much ATP for an extended period of time (an ATP "flood", if you will), or because type II afferents are not supposed to be exposed to ATP at all - hence the commonly used phrase "leak". There is a grey area here in that, if one were exposed to a sound where all OHCs were stimulated, one could argue that the probability of some of them becoming damaged would be much higher, and so that's why all OHCs would need to be stimulated - to maximise the chances of "breaking" some OHCs, causing them to leak.


This is interesting as well. "Noise exposure", as opposed to "sound exposure", would suggest that they are referring to an unhealthy level of sound. In this same paragraph, it says that sensitivity to ATP is reduced in type II afferents after onset of hearing. In other words, purinergic signaling is downregulated upon exposure to healthy levels of sound. But what I'm also curious about is the wording here. It says that the type II afferents become more sensitive "in part by increased sensitivity to ATP". I don't mean to be pedantic here, but it's not clear to me whether this increased sensitivity to ATP is the result of the upregulated purinergic signalling, or whether the exposure to ATP is upregulating the purinergic receptors. If it's the former, then there must be some other kind of mechanism going on that is unrelated to the leaking of ATP (but presumably coinciding with it).

I hope this all makes sense and I'm curious to know @serendipity1996's thoughts on this as well.

Ok, so since posting this I decided to do a bit more digging. I'm not well versed in molecular biology and hopefully someone who is can shed a bit more light on this, but my understanding from this is that ATP is required for a P2X purinoreceptor (the ones mentioned in @100Hz's post) to be activated. This would suggest then that it is indeed the increased production/leakage of ATP that upregulates these receptors. Wikipedia, for what it's worth as a source, also says that "the sensitivity of P2X receptors to ATP is strongly modulated by changes in extracellular pH and by the presence of heavy metals (e.g. zinc and cadmium). For example, the ATP sensitivity of P2X1, P2X3 and P2X4 receptors is attenuated when the extracellular pH<7, whereas the ATP sensitivity of P2X2 is significantly increased."

I wonder therefore, for us hyperacusis sufferers, if there's anything we can do through dietary means to take advantage of this.

 

[serendipity1996]

Great post, @100Hz. I've read this several times now over the last few days and I'm still trying to gather my own thoughts, but thought I'd share a few of them while they're still fresh in my mind. I'm curious to further understand how the ATP "leak" theory fits in with this maximal stimulation you have referred to above. Does maximal stimulation mean that every single OHC needs to be exposed to some kind of threshold of sound, or do some OHCs need to be stimulated to their maximum "capacity"? The quote clearly says "only if all the presynpatic OHCs", so I presume it's the former. I wonder why then every single OHC would need to be maximally stimulated and not, say, some or most of them.

With that in mind and more critically: does the sensitisation of the type II fibres occur because there is an overload of ATP production due to the sheer number of OHCs producing it, or because some OHCs "break" and the ATP "spills out" onto the innervated type II fibres? I suppose what I'm trying to understand is whether the sensitisation occurs because too many OHCs are producing too much ATP for an extended period of time (an ATP "flood", if you will), or because type II afferents are not supposed to be exposed to ATP at all - hence the commonly used phrase "leak". There is a grey area here in that, if one were exposed to a sound where all OHCs were stimulated, one could argue that the probability of some of them becoming damaged would be much higher, and so that's why all OHCs would need to be stimulated - to maximise the chances of "breaking" some OHCs, causing them to leak.


This is interesting as well. "Noise exposure", as opposed to "sound exposure", would suggest that they are referring to an unhealthy level of sound. In this same paragraph, it says that sensitivity to ATP is reduced in type II afferents after onset of hearing. In other words, purinergic signaling is downregulated upon exposure to healthy levels of sound. But what I'm also curious about is the wording here. It says that the type II afferents become more sensitive "in part by increased sensitivity to ATP". I don't mean to be pedantic here, but it's not clear to me whether this increased sensitivity to ATP is the result of the upregulated purinergic signalling, or whether the exposure to ATP is upregulating the purinergic receptors. If it's the former, then there must be some other kind of mechanism going on that is unrelated to the leaking of ATP (but presumably coinciding with it).

I hope this all makes sense and I'm curious to know @serendipity1996's thoughts on this as well.

So sorry, only just seeing now that you tagged me in this! One thing that nags at me is - what are the underlying mechanisms of chronic, prolonged noxacusis? Like, it makes sense that there would be hair-cell death and perhaps a "flood" of ATP following an acoustic trauma and in the short-term. But presumably the damaged/dead hair cells must undergo apoptosis and be naturally discarded by the body at some point? How does chronic noxacusis become maintained? I'm doing better now, personally speaking but my symptoms seem to be triggered randomly and even caffeine exacerbates them - this makes me think there must be a huge amount of inflammation that can persist for a long time afterwards.

Thankfully the Hopkins lab are studying the long-term prognosis of the Type 2s and cochlea after damage but I feel like I keep on endlessly poring over the same handful of research papers desperately seeking answers. I will be so relieved when we have further research to guide us. In the meantime, I appreciate the high-quality analysis of these posts.

 

[Angela Bedford]

Hello, I am new to the forum. This is my first post. I hope that everyone is doing well, considering the circumstances.

I have had tinnitus since 20th of August 2020. And the whistling sound and the broken speaker distortion started on that day. All this was because of a head injury on 15th of August, when I fell asleep standing up straight, and then I fell into a concrete floor with the left side of my head.

I had improvements, especially on the broken speaker issue, until 18th of October, when I had a setback, because of using my voice too loud at work for about 15 minutes, and in loud restaurant the same evening.

Today I went to see a clinic that treats people with issues related to ears. The audiologist, tested my hearing. I could hear up to 15 kHz on the right ear, and 13 kHz on my left ear, which is the one with issues.
She also tested for hyperacusis, where she ran several types of frequencies into my ear, up to about 100 decibels.
I had no significant issues with that, only thing was that on one frequency I could hear it distort a little bit, but only close to 100 dB. Because of no bad reaction, she did not think I needed any treatment for hyperacusis. The entire issue is very strange, because it is only certain sounds that sounds distorted. If I shout, or speak loud, it sounds very distorted through my own voice. Running faucets sounds distorted, banging cutlery and plates sounds "hard". So it is only particular sounds that makes this impact on my left ear.

I tried reading through these posts to find clues, but it is a bit cryptic for me, since I do not know much about this stuff.

Does anyone know specifically what issue I have with this broken speaker phenomenon? Does it have a name?

I have started TRT for tinntus, so I will be careful with distorting sounds, and try to talk softly. See if it improves again as it did two months ago after the first time.


Thanks to anyone replying to this post

 

[koohai]

Hello, I am new to the forum. This is my first post. I hope that everyone is doing well, considering the circumstances.

I have had tinnitus since 20th of August 2020. And the whistling sound and the broken speaker distortion started on that day. All this was because of a head injury on 15th of August, when I fell asleep standing up straight, and then I fell into a concrete floor with the left side of my head.

I had improvements, especially on the broken speaker issue, until 18th of October, when I had a setback, because of using my voice too loud at work for about 15 minutes, and in loud restaurant the same evening.

Today I went to see a clinic that treats people with issues related to ears. The audiologist, tested my hearing. I could hear up to 15 kHz on the right ear, and 13 kHz on my left ear, which is the one with issues.
She also tested for hyperacusis, where she ran several types of frequencies into my ear, up to about 100 decibels.
I had no significant issues with that, only thing was that on one frequency I could hear it distort a little bit, but only close to 100 dB. Because of no bad reaction, she did not think I needed any treatment for hyperacusis. The entire issue is very strange, because it is only certain sounds that sounds distorted. If I shout, or speak loud, it sounds very distorted through my own voice. Running faucets sounds distorted, banging cutlery and plates sounds "hard". So it is only particular sounds that makes this impact on my left ear.

I tried reading through these posts to find clues, but it is a bit cryptic for me, since I do not know much about this stuff.

Does anyone know specifically what issue I have with this broken speaker phenomenon? Does it have a name?

I have started TRT for tinntus, so I will be careful with distorting sounds, and try to talk softly. See if it improves again as it did two months ago after the first time.


Thanks to anyone replying to this post

I have exactly the same issues but only in my left ear since my tinnitus started about 6 weeks ago, tinnitus is not the problem but this broken speaker effect and the whistling over some sounds drives me crazy.

Over which sounds do you notice the whistling? I notice it especially over female voices -- those sound distorted.

 

[Angela Bedford]

I have exactly the same issues but only in my left ear since my tinnitus started about 6 weeks ago, tinnitus is not the problem but this broken speaker effect and the whistling over some sounds drives me crazy.

Over which sounds do you notice the whistling? I notice it especially over female voices -- those sound distorted.

Hi,

What I meant by whistling was actually the tinnitus. I didn't mean whistling related to the broken speaker issue.

The broken speaker feeling, especially comes through when I hear my own voice when I speak out loud. And I am sure it goes through the sound-waves of my voice, because if I have ear protection then it does not have the same effect.

I guess it means that certain frequencies sounds distorted to my ear. It might be the same for you, and loud female voices often have a lighter frequency than, for instace, men, so men's voices will not give you the same result.

What I find strange is that despite this being something people experience, I cannot find any medical expression for it, and I cannot find any advice on how to resolve it.

If I am outside on a rainy day, and I listen to cars, the sound of the tires running on wet asphalt also gives me the same feeling. My left ear is very sensitive to that high frequency fizzing sound.

 

[__nico__]

My ear crackles too with certain loud sounds. For example, a hair trimmer too close to my ear sets it off, and I need to wear earplugs for haircut, and using the electric shaver which prevents it.

Do your ears still do this?

 

[Digital Doc]

Do your ears still do this?

Yes, but not nearly as easily or badly.

 

[Jayden]

Yes, I have this exact problem. I have had tinnitus all my life and it's gotten worse since COVID-19 and having twins. My hearing caps out these days and sounds like a broken speaker or sort of a robotic sound which kind of hurts, even my own voice can set it off.

I'm on Effexor antidepressants and thought it may have something to do with it but I'm not sure. I just can't believe how bad it's getting and I can only assume that having kids screaming all day everyday might have something to do with it.

 

[SD7]

When your guys ear crackle, does it also vibrate? To be clear, the crackle sounds like someone too close to the microphone?

 

[Tau]

When your guys ear crackle, does it also vibrate? To be clear, the crackle sounds like someone too close to the microphone?

Kind of, yes, a bit like an idiot too close to a mic.

My ears do not vibrate.

 

[SD7]

Yes, but not nearly as easily or badly.

Was your crackle sensation accompanied by a vibration?

 

[Digital Doc]

Was your crackle sensation accompanied by a vibration?

No.