Pain Hyperacusis in Relation to Acoustic Shock & Synapse Disconnection

Hi,

I've been reading the research and support categories here for around 18 months and have been considering whether a synapse regeneration drug vs. a hair cell regeneration drug would benefit me more for my own condition as well as quite a few other people I've seen in here who also have similar symptoms (fluctuating moderate to severe tinnitus & hyperacusis, mild hearing loss, through acoustic shock / noise exposure), particularly because there always seems to be quite a flat response whenever anyone raises regenerative medicine in respect of hyperacusis. Based on what I've read and researched I am becoming more hopeful that a synapse regeneration drug could be the most beneficial treatment in one case, but maybe not in another and I'm finding the information quite confusing. I'm building up a 3D web of theories and questions in my head and would like to share it all as some of it I have not yet seen discussed, I'll try and explain best I can.

My audiogram is quite normal although it does start dropping off at 6 kHz down 20 dB to 8 kHz and I have generally good hearing and no obvious deafness (I am planning to get an extended audiogram done). When I had my acoustic shock years ago, it felt like a jolting shocking sensation in my ear, it made me physically flinch and was from what I remember, a different sensation to the pin prick feeling that was to follow in the years to come that I now associate with being a precursor to hyperacusis setbacks. I wonder sometimes could it be possible that it is the actual event of the acoustic shock itself that causes the initial disconnection of the synapses from the hair cells. Something is responsible for initiating H, and based on the timing of events alone (never had H in my life, suffered acoustic shock, now have H), it just makes sense that the initiating factor of an acoustic shock could be the trigger of a process that disconnects synapses and then effectively turns them into raw nerve endings. Consequently the subsequent tell tale pin prick sensations following a noise exposure equate to an overstimulation / assault on these nerve endings, which then causes the inflammation that ultimately leads to the radiating aching pain of the ear, jaw, cheek and neck followed by weeks and months of rest, and then repeat. I am no doctor or researcher, and all this is only what perceive it could possibly be.

I think that the above is possibly also what others loosely theorize either in terms of tinnitus or hyperacusis, but it is in particular the acoustic shocks possible relationship to the initial detachment of the synapses that I am so focused on because if this is the case, then synapse reconnection could in theory reverse the process by effectively and correctly re-terminating the exposed nerve endings / synapses.

When I consider someone who has good hearing but suffers tinnitus / hyperacusis, I imagine a row of microphones arranged in order of the frequency they can pick up, and that several of the cable/jacks in the ultra high freqs are unplugged from the mics even though the mics are all switched on still (ie no hair cell damage but disconnected synapses left with who knows what kind of interference flapping around in the inner ear). In contrast, when I consider someone who is profoundly deaf through old age, ie, no tinnitus / hyperacusis, or known acoustic shock, just pain free deafness and presumably no synapse disconnection, I imagine the same row of microphones but this time they all have the cable/jacks plugged into them but the mics are mostly switched off (dead hair cells but synapses are attached still). I've also wondered if a person who is deaf in the latter way could still suffer an acoustic shock later in life (that presumably they wouldn't be able to hear based on the dead hair cells but could still be violent enough to disconnect the synapses), and all of a sudden begin to experience tinnitus / hyperacusis in addition to the deafness. I know lots of older people who are simply deaf, which is obviously bad enough, but at least with no other horrible problems like tinnitus or hyperacusis. And we presume / know that they are deaf due to dead hair cells, and so obviously something else affects the hearing of other groups of people in a very different way, military personnel, musicians, concert goers etc. that are unlucky enough, don't go deaf necessarily but have all kinds of other problems and by deduction, I can in my limited knowledge assume this is down to the synapses rather than the hair cells (unless there's yet something else to be discovered that it could possibly be).

I'm sure I probably have some combination of both dead hair cells and disconnected / damaged synapses, but based on my good hearing yet debilitating hyperacusis, the more I read and try to work out which type of treatment would be more beneficial, the more I'm starting to think that particularly in the above theory, a synapse reconnection drug will have the most important effect (taking away hyperacusis pain), because no matter what state the hair cells are in, a synapse drug will at the very least have the effect of properly terminating the exposed synapse / nerve ending once again. And whether or not the hair cells were alive, dying, or dead, with a reconnected synapse I would assume I'm suffering similar hearing problems to someone suffering from old age deafness.

So in that theory above I can find some hope in a synapse drug. However when I read about the Hidden Hearing Loss / Type II Nerve Endings / ATP stuff it really muddies the water because this particular research points to the possibility that the pain comes from something that has nothing to do with a detached or damaged synapse. I've tried to understand it as much as I can but in this case these synapses connected to the type II nerves are being stimulated by ATP that is being released via support cells of a damaged (predominantly outer) hair cell, and these Type II nerves are then sending pain signals to the brain. Importantly again, these don't appear to be disconnected synapses (from the hair cell) from what I've read.

What really throws me by this particular research is that if hair cell damage is so common why is hyperacusis pain so uncommon. Surely any degree of deafness as a result of a damaged hair cell would lead to this release of ATP? And in the case of a profoundly deaf person with mostly dead hair cells, why is someone who is deaf in this way typically not susceptible to pain? Although I understand that a certain predisposition or genetics could apparently be a factor.

I've seen variations of this image several times of the disconnected synapses and to me it begs the question, what type of symptoms does this type of damage cause? If it is common knowledge then apologies I've either forgot since I read it, or I've just not found it yet, but the way synapse damage / disconnection gets banded around I would think there must be a theory on the particular type of hearing symptoms that arises from this type of damage.



What I take away from the 2 different synapse scenarios in the end, is that if it is down to disconnected synapses that causes tinnitus, hyperacusis or both tinnitus and hyperacusis, then I have real hope for The Hough Pill and the OTO medication.

If it is down to support cells releasing ATP and the type II nerves sending pain signals to the brain then, then I guess something like FX-322 would be more suited as long as FX-322 also fixes damaged cells and not just dead ones.

As for tinnitus as far as hyperacusis goes, in my case I believe they are very much linked. My tinnitus is reactive to noise and gets louder on exposure. It is either the case that when the hyperacusis starts it is usually at a point where the tinnitus is screaming, and vice versa, if my tinnitus is quite stable but I have a sudden loud prolonged enough exposure that it trigger my hyperacusis rapidly, the tinnitus will usually catch up. So I believe that if the hyperacusis can be fixed the tinnitus will be dealt with as well.

If any of this sounds easily debunkable please go ahead and debunk and fill in any gaps / facts, I'm just trying to understand more about it all as it raises so many questions.

 

Maybe there could be a drug to modulate the firing of neural areas that process sound, the gain or the way they process sound.

As for pain, some ENTs said that the ear has no pain receptors. I don't really know if this is true or not, because actually on dB graphics there is sometimes a reference to the "threshold of pain" for very loud sounds.

 

This is really interesting - I don't necessarily believe that the hair cell damage and synapse disconnection theories are mutually exclusive though. I don't know if you've heard of Paul Fuchs from Johns Hopkins - his research is devoted to pain hyperacusis and this interview with him is very illuminating on the subject.

Spoiler: Interview with Paul Fuchs

We are delighted to announce our interview with
PhD. Paul Fuchs, Co-director, the Center for Sensory Biology at Johns Hopkins University. He is one of the most knowledgeable Hyperacusis Researcher in the world, with his research he could prove that there are nerve fibers in the auditory nerve which cause the hyperacusis pain.

He talks about what is hyperacusis, how it affects peoples lifes, the causes and why is hyperacusis research is a big challenge.

Don't miss it!!!

Here is the interview with Dr. Paul Fuchs, a professor at the Johns Hopkins University School of Medicine, whose laboratory has investigated trauma to the cochlear hair cells. The transcript has been lightly edited and condensed.

Q. I’ll start with a with a basic question. What is hyperacusis?

A. This word is unfortunate because it’s not as specific as it should be for describing the disease state or the pathology. What it means, literally, is very sensitive hearing. That, as you know, is kind of inaccurate. Rather, one would like to have words which describe the set of conditions that people experience. Hyperacusis now more commonly means that people are disturbed or pained by loud sounds that previously were not painful. Hyperacusis as a clinical condition simply means that there is now an aversive or a painful experience when one hears sound.

Q. So do you think hyperacusis should have separate terms for people who perceive sound louder and for people that actually have pain from sound?

A. Yes. I think this is becoming clearer and clearer. There is probably a progression in hyperacusis from an initial condition when louder sounds become more irritating or annoying, to then becoming increasingly painful. But what will be helpful in the end is that we can define what the actual pathogenic mechanisms are and in so doing we can be clearer about what kinds of insults give rise to hyperacusis — what sorts of actual damage or other sorts of mechanistic changes underlie the symptoms that people experience. I think we’re stuck with “hyperacusis.” It is going to be a word that everybody will use, but at the end of the day, as we explore the biomedical mechanisms, we’ll realize that one has to be more precise in the language.

Q. What is the main mechanism known to date of hyperacusis? Is it a psychological disorder? Is it an injury to the auditory pathway? What are your studies revealing?

A. The studies of a variety of laboratories are beginning to make progress on the notion that there is an underlying biological mechanism that begins in the periphery. I think it’s a certainty that hyperacusis follows upon some kind of inner ear damage, and so this to me is a very firm indicator that hyperacusis is not simply psychological — which is complicated in itself — but rather is a consequence of peripheral inner ear damage. Whether there is one main mechanism, I don’t think that we can yet draw that conclusion. But what we can say is that, as we move forward, we are beginning to explore the kinds of changes that occur in the inner ear that may give rise to the conditions that then become hyperacusis.

Q. And is hyperacusis more a problem in the peripheral nervous system or is it something that happens in the internal structure of the ear — in the cochlea or the hair cells? Where does the problem reside?

A. I like to draw the comparison between hyperacusis and tinnitus. They are consequences of peripheral damage in some way. But when one looks at tinnitus, it is pretty clear that there are a lot of central plasticity and central changes that conspire to provide tinnitus to people. Hyperacusis seems more strongly associated with a change in the peripheral sense organ itself, so hyperacusis is more likely to be something where we can localize the actual mechanism to the inner ear as opposed to the brain.

This is not to say that there aren’t also changes in central connectivity that help to explain hyperacusis. That almost certainly will be true, but I think in comparison to tinnitus, hyperacusis is something which I’m pretty confident reflects a change in the properties of the inner ear itself.

Q. We’ll start talking now about tinnitus. Many patients report that sound gives them pain or they perceive hyperacusis, but there is also a link with tinnitus. Many patients report more sound exposure gives them louder tinnitus, hyperacusis and pain. Can you comment?

A. So this is where you start to see the interplay between peripheral changes —- the way the sense organ itself changes — and the way the central nervous system follows that up with some forms of plasticity and more complicated kinds of changes. By comparison to pain in the skin or in the body generally, we know that there are changes in the sensitivity and excitability of the nerve fibers that innervate skin — when you have a kind of painful nerve condition in the skin — but there are also central changes where connections between neurons become stronger or weaker. And so tinnitus is probably more like phantom pain, which I’m sure you may have heard of — that people who have lost a digit or a limb can report painful feelings in the missing limb.

So in conditions where the auditory periphery is no longer providing normal input, where you have some degree of hearing loss, then the brain begins to kind of self-generate activity as a replacement for the lost activity. This probably results from an imbalance in the input provided by what one would call the cognitive nerve fibers. In the somatic nervous system, for example, that means the fibers that tell us about touch and limb position, the cognitive inputs about our body — vs pain fibers. We don’t really want to think about that pain. We just want to get away from it. So pain fibers initiate withdrawal symptoms.

And in the normal nervous system, there is a balance between input coming on pain fibers and input coming on the cognitive, touch, motion or other fibers. And there’s even a pretty well established principle that those cognitive nerve fibers inhibit the pain pathways.

So when we come to tinnitus, as we begin to lose inputs that are delivered by the cognitive nerve fibers that tell us about sound, then conceivably the Type II neurons which we have been studying, which we think may be analogous to pain fibers, begin to gain more or stronger access to parts of the nervous system which are going to mediate sensations of pain and the kinds of behaviors that mean withdrawal or aversion.

Q. So the hypothesis is that nerve cells are not signaling the sound in the normal wau and that is one of the causes of hyperacusis?

A. Almost certainly. Everything that we’ve seen so far about these nerve fibers that look like pain fibers in the inner ear, is that they could become the basis for sensations that we now find as hyperacusis rather than normal hearing.

Q. Now maybe a tricky question but there are a lot of people that get hearing damage and hearing loss especially after rock concerts, and they don’t experience hyperacusis even with worse hearing loss than many hyperacusis patients. There must be problems of some other kind.

A. I agree, and that is a difficult question, so without knowing what the real biological mechanisms are, we can’t really say why one person may be different than another. But I think we can look at other examples of how people respond to varieties of insults and have different kinds of responses. We know that some people are very allergic to particular things and other people are not, so that’s a genetic difference in their immune systems that confer different sensitivities. We know that some people have very sensitive skin. Other people do not.

In the case of acoustic trauma and why there may be differences in the way that people respond to that — with some developing the kind of pathologies and others not — then we can at least talk about the fact that there may be differences in the patterns of damage in the cochlea.

The way that we measure hearing loss typically is a fairly crude instrument. We just ask “Can you hear this, can you hear that?” But there may be much more subtle kinds of differences among people in the patterns of hearing loss. So we don’t know that the peripheral damage is the same in every case. There may also be differences in the genetics between people, so if it is the case that type II fibers are the pain fibers of the inner ear, they are not necessarily going to have the same pattern of gene expression in every person. They may be more or less subject to the kinds of changes that might give rise to hyperacusis and tinnitus.

And then we have to think about the fact that part of what happens in the ear are inflammatory responses — the same kinds of tissue damage responses that are produced by histamine or other sorts of immune mediators — and those are going to be different in different people. So one can imagine there to be a variety of ways in which the response differs, but until we know what the actual underlying biomedical process is, we can’t really address those differences.

Q. What is the state of hyperacusis research at the moment? What is the important focus and what studies should be done to study the mechanisms and to provide future hopes for treatment in the long term?

A. We’ve had a constant theme in our conversation, which is that until we understand the underlying mechanism, we can’t really begin to address ways of treating it. So from my view, I think we’ve had a genuine breakthrough in the basic research in that we’ve been able to confirm some elements of the idea that there really might be pain fibers in the cochlea, and that opens up a whole host of possibilities for exploring analogies between the way that people study pain in the rest of the body and what we might to do study pain in the ear.

I’ve been talking about these analogies as we’ve gone along and the Type II afferents that our laboratory and others have studied, and we have now begun to gain real momentum for those as being potential pain fibers. We know something about the mechanisms by which they operate, we know how they are excited by chemicals, we know what their likely non-response to sound is and we know that they can be activated by tissue damage.

So now we can begin to look at: What are the molecules that mediate that response to tissue damage? Are they similar to the molecules that serve for skin pain? If so, can we use the same kinds of anesthetics to quiet down Type II afferents?

We don’t know that yet, but these are the sorts of leading hypotheses that one gains from this very important finding that there is a population of neurons in the cochlea which are almost certainly not there to respond to sound and they do respond to tissue damage. So I think we’re on the right track. The most important thing for us to do now is to determine how these potential pain fibers respond to tissue damage. Do they become hyperexcitable as pain fibers in skin do when you have a sunburn, for example? And where do they project in the brain? Where does that information go? Does it get to pain pathways?

To do these things and to begin to test them in the hyperacusis condition, we need to have an animal model so that we can ask: Does this animal have hyperacusis, does that hyperacusis depend upon Type II afferents, can we treat that animal’s hyperacusis with drug XYZ, etc. We are on the way to doing that now. We are beginning to learn about the genetic specifications of the Type II afferent neurons, and that means we can manipulate those neurons genetically and so design experiments which are going to be much more informative about these questions.

Q. And this is exciting news and good news for people with hyperacusis — that in the medium term or long term, might some kind of treatment appear?

A. Yes. Can I add another word about this? In the last year or so, we’ve seen a significant increase in the interest of biomedical and pharmacology companies in these questions. So I’ve been very encouraged by the fact that, at the moment, for example, there’s three or four different contacts that I’ve received from the research and development people at big pharma and little pharma and biotech startups who are beginning to think about the commercial benefit of tackling these things. So I think that’s really encouraging and that will move things a lot faster.

Q. The main cause of hyperacusis?

A. The main cause is hearing loss, so that’s what we can say with any confidence — beyond that, that’s as far as it goes.

Dr. Paul Fuchs, thanks so much for this interview.

One really interesting thing he mentions is that as a consequence of damage to the Type 1 regular nerve fibers that transmit sound, the Type 2 neurons, which are usually inactive, begin to step in and become more active thus resulting in pain provoked by sound.

"So when we come to tinnitus, as we begin to lose inputs that are delivered by the cognitive nerve fibers that tell us about sound, then conceivably the Type II neurons which we have been studying, which we think may be analogous to pain fibers, begin to gain more or stronger access to parts of the nervous system which are going to mediate sensations of pain and the kinds of behaviors that mean withdrawal or aversion."

"Q. So the hypothesis is that nerve cells are not signaling the sound in the normal wau and that is one of the causes of hyperacusis?

A. Almost certainly. Everything that we’ve seen so far about these nerve fibers that look like pain fibers in the inner ear, is that they could become the basis for sensations that we now find as hyperacusis rather than normal hearing."

Q. Now maybe a tricky question but there are a lot of people that get hearing damage and hearing loss especially after rock concerts, and they don’t experience hyperacusis even with worse hearing loss than many hyperacusis patients. There must be problems of some other kind.

A. I agree, and that is a difficult question, so without knowing what the real biological mechanisms are, we can’t really say why one person may be different than another. But I think we can look at other examples of how people respond to varieties of insults and have different kinds of responses. We know that some people are very allergic to particular things and other people are not, so that’s a genetic difference in their immune systems that confer different sensitivities. We know that some people have very sensitive skin. Other people do not.

Regarding the hair cell damage theory, there was somebody who actually contacted one of the researchers (who worked on the study from 2016 that showed that OHC rupture activates the Type 2 neurons. Interestingly, someone from this forum, @Soren got in touch with him a while ago and his response indicated that the issue with pain hyperacusis is that it is not triggered by damage to the OHCs.

https://www.tinnitustalk.com/threads/frequency-therapeutics-—-hearing-loss-regeneration.18889/page-54#post-356547

I have also emailed Paul Fuchs myself and his team are continuing to work on research into the Type 2 neurons. I honestly think that we could very well see some benefit from the regenerative drugs whether it be hair cell or synapse drugs - who knows perhaps we will have to try out both. We know that hyperacusis fundamentally stems from hearing loss, so it seems logical that restoring input would mend the dysfunctional auditory system. I think either that or drugs that target the dysfunctional Type 2 neurons themselves to dampen the pain such as Retigabine - there are anecdotal reports on this forum of people who have experienced significant relief and even cessation of pain hyperacusis symptoms e.g. burning and tingling. Nav 1.7 blockers could also help us too.

I think the upshot is that nobody really knows for certain at this point - Hyperacusis Research, run by Bryan Pollard is very research-oriented and they always post updates about Frequency on their Facebook when they hit a new milestone so it's probably a good idea to keep tabs on regenerative medicine as it could possibly help us.

 

That used to be the dogma for 50 years or so that the ear has no pain receptors but the discovery of the Type 2 neurons acting as pain receptors was significant as it turned that on its head according to Bryan Pollard. That discovery was only made like 4 years ago so I guess it's not surprising that ENTs aren't generally up to date on this stuff.

 

Interesting. For me it seemed just baffling and conflicting to talk about no pain receptors and use the concept of "threshold of pain". Also, my personal experience with noise induced hearing loss is that ears can hurt like hell and trigger massive headaches through irradiation of pressure and pain.

 

lol

https://hyperacusisfocus.org/innerear/#painreceptors

 

This is all very interesting. However, unless I missed something, why do none of these hypothesis have a secondary hypothesis on why some people see their hyperacusis (pain or not) go away?

I had pretty bad pain and loudness hyperacusis for about 5-months until it gradually started to clear up over the remainder of the 12-month period. Well, what got better to allow this to happen? Synapses reconnecting? Cells healing? Both?

One would think that the explanation for why it clears up might help understand why it happens to begin with.. no?

 

Yes this is a really good point and clearly deserves further exploration - why are people's experiences with hyperacusis highly variable. My hyperacusis is also almost gone but how come some pain hyperacusis gets entrenched and some doesn't. Pain is a really complex and individual phenomenon - perhaps there's some sort of central sensitisation that takes place for people whose condition doesn't improve.

 

Reading these different theories on why does hyperacusis cause pain is making me anxious. I just hope FX-322 is the answer since it restores outer hair cells, inner hair cells and synapses where there is hair cell loss. Will restoring the outer hair cells make pain hyperacusis go away?

My biggest worry is that if hyperacusis pain is cause by synapses, OTO-413 might not pass the clinical trials since they are mainly testing for hearing loss but for hyperacusis sufferers we may need both FX-322 and OTO-413.

I just hope the theory of outer hair cells causing pain hyperacusis is actually correct and that FX-322 should get rid of pain hyperacusis.

 

Ok, based on what is known, it sounds like there is some acceptance that hyperacusis is a result of peripheral damage in the cochlea. Which, based on further discussion is hypothesized as:

A - Dead/Missing Hair Cells
B - Damaged Hair Cells
C - Broken Synapses / Damaged Synapses on otherwise healthy cells

Let's now consider that it is probably likely that most of us likely have a mixture of all 3 types of damage causing hyperacusis. For this example let's assume it's split evenly 3-ways, so 1/3 A, 1/3 B, 1/3 C.

ASSUMING that reversing damage will treat the underlying cause of hyperacusis:

FX-322 would solve for A and B, but not C. Therefore solving 2/3 of this example.

OTO-413 would solve for C, or 1/3.


Although neither will lead to a complete reversal of the symptoms, ASSUMING that A,B, and C cause hyperacusis in this example; either one would likely reduce the severity of the symptom.

The bar is so low on hyperacusis, I think most would go for either one if it reduced their symptoms by say, 33%.

 

I think there are not only the two groups for which hyperacusis improves and not. There are also the ones for which it improves and some setback has thrown them at square one. And after multiple setbacks it is much harder to improve than when hyperacusis just started.

 

@serendipity1996 Thanks for all that info, very interesting. The material I read was similar and particularly mentions Type II afferents were being stimulated by ATP from damaged hair cells' supporting cells and sending pain signals to the brain. The part from @Soren is really interesting because I also can't see how OHC's have anything to do with H because of how common OHC damage appears to be compared to H. But if it is down to this (quote from Anoveros),

"The hypothesis is that the normal pain system of the type II afferents has been sensitized, so that they now become active in response to the vibrations caused by normal sounds."

then I wonder if this could be the damage that an acoustic shock causes to set everything in motion for H. And I equally agree that sometimes I think what H could actually need is probably more like some kind of blocker in the right location.

 

I still really hope that the reason why pain hyperacusis happens is because of the OHC’s getting damaged from noise exposure. If we can restore them it could cause the brain or whatever to reset due to OHC’s getting restored and basically have normal ears again and stop it from leaking ATP and making the type 2 neuron fibres sensitised.

If the cause is due to damaged synapses we will be waiting a bit longer for it come out. I’ll say 1-2 years after FX-322 is released unless somehow they open up compassionate use.

 

So do I, I'd love it if it was down to a predisposition or genetics or something like that being the reason some of us suffer OHC related nerve pain. It would be like getting an FX322 freebie thrown in. Would need to take care of the hair cells for life if it does go that way.

 

I think the reason why hyperacusis happened for us is when we got exposed to loud noises it was a sudden acoustic shock which caused the hair cells and brain to somehow react causing the pain we know as pain hyperacusis. If it’s true that once we restore the hair cells to get hearing restored I really hope the pain hyperacusis goes away.

 

@Diesel I'll expand the hypothesis to incorporate this as well, as its very relevant. Good point.

What I think covers this is inflammation level / healing time of whatever the acoustic shock damaged in the first place. Acoustic shock inflammation seems to have an incredibly long timeline, is very fragile and easily provoked.

I'll give a bit more detail on my own illness because it will help explain my view on it.

I got my first acoustic shock about 3 years ago, for the first 6 months I was in huge pain, every time I thought I was getting better I'd go back to doing slightly louder things and got the pain back all over again until finally I stopped doing anything remotely noisy at all, by the way I was doing pink noise TRT. After 12 months I started to feel much better and did start creeping back to more normal life again, nothing too much, only this time I was getting away with it. As long as I didn't push it for more than a couple of days it was OK. I got careless once or twice and had a couple of small setbacks but it was becoming how I can describe as manageable. At 18 months I was so good I was back to doing pretty everything once again as normal with the only caveat that I was still being careful not to go for too many days without some ear rest, and despite how good it was I still felt the need to be careful . I had about 4 months of normal life back. Then I pushed too far and had a massive setback which I believe may possibly also have been a second acoustic shock. I wasn't doing anything dangerously loud at all but I had been carrying on for about 4 days and it was too much.

I had plotted the first recovery cycle timeline in a spreadsheet and did the same for second recovery. I'm 12 months into the second recovery now and it has been almost identical to the first. The only difference this time is that I'm not doing TRT. I am finding the same pattern of it becoming gradually more and more manageable as the months go by. I'm hoping that by next Feb I'll reach the same 18 month mile stone only this time Ill not be going back to my old life style at all. I'm going to live as quiet life as possible. I sold all my music instruments, music gear, power tools, speakers etc. The main thing I learnt from this is that I now think it very dangerous to ever think I am cured of H. Until a proven scientific model for the underlying cause of H is discovered and then a measurable cure is found I'll have no confidence that I'm ever cured of it. I'll consider myself somewhere within the H spectrum until then.

As for why I believe inflammation is so important in this, I made the graphs below of how I feel at various H stages compared to how I felt with normal hearing and I think the recovery time from any single noise event no matter how loud is lengthened in a H sufferer. I'm talking about the ears natural recovery to any sound I guess, this would not ever be noticeable in a healthy ear as its instantaneous but for a H ear that gets fatigued over hours and days there is that need for extra quiet time. A normal person (us before we got H) for example hears a sound and then goes instantly back to a hypothetical baseline but I think H sufferers return to baseline far slower and so noise has an accumulative effect that kind of bumps up and spends your hearing budget faster than normal.

Another important factor in these graphs is the acoustic shock inflammation baseline. I think there are 2 types of inflammation. There's the inflammation caused by actual damage as a result of the shock, that lets say takes 18 months to really improve, and then there is the subsequent irritations of whatever it is that is inflamed that causes the ups and downs of pain throughout the 18 month period, like a stock market graph on a downward trend. Could this be to do with the way that disconnected raw synapses or maybe altered type II afferents are dealing the signals they receive? If someone was recovering really well, and say they now have reasonably low inflammation and quite a high tolerance for noise again, that is a good thing but I don't think the bumping up effect goes away even though the inflammation does, and if pushed hard enough another huge setback can occur even if it takes a lot more effort. None of this is fact, it just my interpretation of what's happening to me as a sufferer, trying to build up some kind of picture based on the little that is known.

Do synapses reconnect? Do Type II afferents fixed themselves? Possible, because I like so many others did recover very well and get basically back to normal but if in my case the main issue did resolve after the first recovery, it either very soon broke again, or left me susceptible to more of the same while I was only exposed to relatively normal noise, nothing that would generally harm the average person. Maybe 18 months just wasn't long enough first time round for myself.

I think there's a danger that the recovery can eventually appear to be going so well that it takes on the illusion that you are cured but all that's actually happened is that the inflammation has significantly subsided enough to build that LDL threshold back up, that now naturally doesn't get breached nearly so easily as it did when the threshold was far lower. You are easily fooled into thinking you can carry on as normal now, but the underlying broken X factor whatever it is remains broken and very susceptible to subsequent over stimulation from you gaining confidence living an ever noisier life once again. So my best guess is that it is down to inflammation levels of something that is physically broken in the ear. I won't be putting it to the test this time round which is what it really equates to in order to know if I'm cured or not though.

Just a final thing regarding the question of can you consider yourself cured from H? Take 3 people who all suffer an acoustic shock and develop H. 2 of them are regular music loving concert goers and the third is someone who lives alone and has a very quiet life but got unlucky with say an airbag deployment. Assume at 18 months they all feel as good as recovered as they have avoided noise. One music loving concert goer goes back to his old life and has a setback very quickly, he clearly isn't cured and is back at square 1. The second music lover doesn't return to his old life because he's too cautious. His H never returned, is he cured though? How would he know without going back and testing it, he could be cured but maybe not? And finally the one who lives the quiet life goes back to their peaceful life, The H never returned, is he cured? I guess you could say so according to his lifestyle but I doubt he'd want to test it with another airbag deployment. I don't think I could consider myself cured until I could go back to doing all the noisy things that I love doing to test it out but I wouldn't take a chance again until I could be quite sure. I'm sure there are people believe they're cured and Its great for them though.

 

Yes, I completely agree - I don't really think hyperacusis ever truly goes away. Perhaps extremely mild cases of slightly sensitive hearing for a week after a concert maybe. I've had hyperacusis for 4 years now and after the initial hyperacusis episode in 2016 I went back to 'normal' although still couldn't tolerate excessively noisy environments e.g. clubs etc although this didn't bother me much as is to be expected but could pretty much lead a 'normal' life. So my hyperacusis honestly wasn't something I thought about all that much and every now and then I had very mild setbacks that lasted for like a week or so until the end of last year when a party + car stereo pushed me over the edge and resulted in my worst and lengthiest setback yet. I honestly think I got too relaxed and lulled myself into a false sense of security prior to this setback.

6 months later and thank goodness I am 90% back to normal although I am still oddly sensitive to certain sounds (artificial/processed sound from my laptop speakers seems to trigger pain hyperacusis/reactive tinnitus) but even that seems to be improving albeit slowly. I think there must be an initial injury to the ear and then inflammation and even if it 'goes' away your auditory system is still weakened and you have to tread carefully. I'm at the point where I don't have to worry about my ears shattering at every sudden noise but I think it was a wake-up call for me. I'm much more invested in regen med etc and keeping tabs on the research than I was before because until then (or retigabine etc) I don't think it will 100% go away.

 

I hope with regenerative hearing medicine it could make pain hyperacusis and tinnitus go away and we can resume our lives properly but with earplugs when we are in loud situations.

 

Yes your story is very similar to mine, I'm also focused on regenerative meds and research now, or some kind of nerve termination / blocker if hyperacusis turns out to be really a more stand alone condition and something less related to typical hearing damage, I don't think its out of the question seeing how many people have hyperacusis but also good hearing. And since you pointed me towards it, I think that the possibility of type IIs becoming sensitized and subsequently a self sustaining problem on their own is a really interesting theory.

I read several stories about mainly musicians and producers recovering after their first acoustic shock, not always to full capacity but to at least allow them to allow to return to what they love to some degree. I hope some do / did recovery fully. I've never read about anyone recovering from their second acoustic shock / major setback, I think because by that time it becomes obvious that you don't recover, you calm the symptoms down and then protect yourself. Would I love to hear an update on that 2nd hand anecdote from the guy with hyperacusis who went back to touring after the Regain trial though, saying he was still fine and back to full on concert noise exposure.

 

Let's just hope FX-322 can do it’s job at getting rid of pain hyperacusis. If you want to find out more about 2nd hand anecdote from the musician who was able to go back on tour due to his hyperacusis improving contact @síocháin and she may be able to contact him again to get more information on the type of hyperacusis he had.

 

Wait, was this after someone took FX-322?

 

No, this was an anecdote from the Regain (Audion) trial. But FX-322 is perceived as far better than what Audion has. So if Audion's drug can cure hyperacusis, FX-322 should do so even better.

 

No this was the Audion trial.

 

Shit man, that’s inspiring. To think that we’ll get our lives back is so beautiful. These reports keep me from jumping off a bridge man.

 

Me too man. I’m trying to find out more about which type of hyperacusis did the musician had but waiting for a reply.

 

It doesn't MATTER. One anecdotal case of someone's hyperacusis improving means SHIT. It could have improved WITHOUT the trial too.

 

No, it does MATTER. One anecdotal case of someone’s hyperacusis improving means A LOT to most of us. Their hyperacusis could have improved WITH the trial too.

Why the FUCK are you so negative? You were talking SHIT about Timo Werner having hyperacusis now you are talking SHIT about the musician able to rejoin his band due to his hyperacusis improving.

 

I'm realistic. There were people who "improved" in the Autifony AUT-00063 trial too and the drug failed in the trials at the end.

If your band guy had had serious hyperacusis, he would never have re-joined his band after being cured from his hyperacusis. Unless he was a moron. Hyperacusis and tinnitus can come back with a vengeance at any time even if you've been cured once.

 

There are cases which recovered from serious hyperacusis and now go to parties again.

Maybe he now wears earplugs when playing with the band.

 

That’s what I’m thinking too.