How Confident Are You That Treatments for Tinnitus May Help with Hyperacusis/Noxacusis?

It’s clear that both can be caused by noise. What also seems to be the case is that for a majority of people hyperacusis tends to “clear up” on it’s own over time, especially if it’s loudness hyperacusis.

The type that tends to stick around longer seems to be noxacusis, and the symptoms of trigeminal nerve irritation where people feel delayed burning pain either on their face or deep in the ear (geniculate nerve irritation?)

What do you guys think hyperacusis really is? Actual damage? Inflammation of some sort? There’s also the fact that some experience middle ear issues as well - Tensor Tympani syndrome. Some experience aural fullness and some don’t. Will restoring hair cells/synapses potentially help us? Are we more likely to be helped by hearing restoration drugs if we also have tinnitus (vs those who have hyperacusis from something like a neck injury and no tinnitus) ?

I personally don’t think that it’s psychosomatic at all. I also think that TRT tends to work for some because typically sufferers go through a period of “overprotection” before starting TRT or white noise therapy. (Not really overprotection in my opinion but much needed rest for the ears). So they do most of their healing on their own, and after that point the TRT is mostly placebo. I haven’t read a single story of someone with a fresh noise injury immediately starting TRT/noise therapy and improving that way.

 

I think it's actual damage that gets repeatedly inflamed with repeat noise exposure. I'm more confident now than I was before about that and also that the current regeneration drugs in trial will do something for noxacusis. I think there's a lot of evidence pointing to cochlea damage being responsible for causing noxacusis so I'm being patient and waiting for the drugs now.

There's one or two outside possibilities that the current drugs in trials might not work, but I think there's more in favor of them working than not.

 

Out of curiosity, what are you basing this on? I am only 1 month into my hyperacusis journey and would love to believe this

 

Stories I’ve seen on here and people I’ve talked to over the last year.

 

Thanks. Any sense of how long of a time frame this tends to happen over? E.g. does most recovery tend to happen within a year?

 

From what I've gathered on this forum, noxacusis seems to be caused by inflamed type II pain fibers caused by cochlear inflammation. The inflammation arises from damaged hair cells and synapses. All 3 elements are currently being worked on in the pipeline.

It becomes a vicious cycle of an inflamed cochlea being more sensitive to sounds, which causes pain and then more inflammation. This can go on for weeks. This is also why people tend to get better over time, since inflammation slowly subsides. But the underlying damage remains, leaving a recoveree susceptible to reinjury. Scroll down to @100Hz's model here.

I think we have a great shot at returning back to normalcy within the next few years assuming these are truly what cause pain hyperacusis. Most notably FX-322 for hair cells, OTO-413 for synapses, and SPI-1005 for inflammation.

It would also smash the current limbic theory out of the park.

 

Mild cases (my definition of mild is loudness hyperacusis) seem to improve within 6-8 months. I’ve seen people who experience pain also say they’ve gotten better within that time frame. I’ve also seen stories of people having pain for a few weeks and it going away in a pretty short time too.

Closer to 2-3 years for more moderate cases. Recovery isn’t linear and it’s a very slow and gradual improvement. Setbacks are almost guaranteed but just know it doesn’t mean more permanent damage. Hope you feel better soon

 

I don’t completely dismiss the limbic theory because it does seem to be a part for at least some people! There are stories of people who say they just stop thinking about their hyperacusis and it magically *improves* lol but agreed that for those of us on the more moderate - severe side it’s definitely not a limbic thing!!

 

Agreed that the limbic system probably does play some sort of role. For example, I get much more startled by surprise noises since developing hyperacusis. Probably because my brain is always on edge hyperanalyzing sounds around me, even if I don't realize it.

However, many audiologists that subscribe to Jastebroff's theories will tell you that the physical pain is actually just a form of emotional processing that can be overcome by exposing yourself to loud noises, which is outright dangerous to suggest to someone with noxacusis.

 

I think hyperacusis, both pain and loudness, is linked to actual damage. I believe what causes this is either loss of OHCs, IHCs or synapses. With both FX-322 and OTO-413 being released in a couple of years there is a good chance that it may help with both pain and loudness hyperacusis.

I do hope the theory of loss of OHCs causing pain is true since FX-322 will be the first drug to restore OHCs. If it turns out it is a loss of synapses that causes pain hyperacusis then we will be waiting a while for OTO-413 to come out, unless you have a lot of hair cell loss, in which case FX-322 will regrow synapses where there is hair cell loss.

 

@100Hz

Thank you for the great article.

Just want to clarify the portion below.

I am cautiously optimistic that FX-322, OTO-413 and SPI-1005 will bring relief to us, but I have also read OLD posts that said cures was coming and they never came for one reason or another.

I have noxacusis and in pain most of the time. I don't think I can tolerate this for years until regenerative options were available to the public.

Is the information below based on just time for healing without regenerative, or if regenerative FX-322 for hair cells, OTO-413 for synapses, and SPI-1005 for inflammation are part of the equation?

6.01 - Post Recovery & Potential Triggers for Setbacks

This indicates that certain symptoms of an acoustic shock or setback do settle over time. Typically, although it can take weeks, months or even years, radiating facial pain as well the middle ear and the tolerance to noise can and do improve.

It assumes however that the TGN remains sensitized and also that the OHC damage and sensitized Type II afferents remain, suggesting that the threat of setbacks and repeat acoustic shocks remains in place. It also assumes that lingering TTN damage could also remain. The degree of likelihood and possibly severity of further setbacks could be relative to the level of damage that the cochlea, and mid ear currently have.

Finally the threat of setbacks being caused by heightened neural responsiveness to noise also possibly remains, however the fact that tolerance to noise does increase over time suggests this also is not permanent and decreases over time if indeed it is even a factor.​

 

I've had severe tinnitus for 30 years. Still waiting for a better treatment or cure. What I now read in the ATA Tinnitus Today magazine is the same I read 30 years ago.

 

Jastreboff doesn’t even seem to address that noxacusis and hyperacusis are different conditions. That’s the biggest issue of all.

 

Without. Tincture of time.

 

That's right.

Thanks @LindaS Those models aren't just my own work, I have to give huge credit to @serendipity1996, @Juan, @grate_biff, and @Diesel in particluar, plus the other amazing contributors on this site for the elements to put it together. And yes, that's based in theory on what happens currently without any drugs (i.e. where a lot of us seem to be). I hope that once the cochlea gets fixed that crucially, setbacks effectively stop (as far as I'm concerned, setbacks are 99% of noxacusis) and that even though a trigeminal nerve may remain sensitized that it at least no longer can become stimulated indirectly by noise.

 

And of course @FGG who seems to tirelessly and selflessly provide sterling info every time, regardless of whether or not it's her own particular ailment. Thank you.

 

The ease of setbacks is one of the worst parts. I don’t think I’ll ever feel at peace until there’s an actual cure or until we know what’s broken (or what caused “damage”)

 

Yes that's why I leave a degree of uncertainty for things that these drugs might not do anything for. Heightened neural response is one thing, but I believe that does recover over time and has more to do with an acoustic shock than with cochlea damage so I don't worry too much about it because someone getting repeat setbacks over and over might be re-heightening their neural response each time a setback happened. This would in theory stop if setbacks were stopped thanks to cochlea regeneration. Even if it finally recovered but plateaued at a lower, but importantly, non noxious level, although you could get another acoustic shock I doubt you'd get repeat cochlea damage which would still mean no more setbacks.

I was worried about auditory nerve damage higher up (outside of the cochlea), however, this recent thread puts my mind at ease about it:

https://www.tinnitustalk.com/threads/auditory-neuropathy-—-neural-and-synaptic-mechanisms.41402/.

Things that do worry me though are other types of ATP leak in the cochlea that may have been spawned by the original noise damage that won't be cured by fixing hair cells or possibly synapses (whether or not further leakage is in response to noise or not). This stuff starts to go over my head a bit now but @FGG posted some research on it possibly coming from something called Gap Junctions. I wonder about this but I can't find an answer to it - do the Type II afferents remain sensitized even if in theory all OHCs are now brand new again? If so ATP leakage coming from anywhere else (not just OHC support cells) could stimulate the afferents, however it could be suggested that if it was not a noise activated ATP leak but some other event (or just random), then noise would no longer be a trigger, and that you'd be getting setbacks spuriously for seemingly no reason at all. This angle makes me feel a bit better that it is unlikely because I believe setbacks are fundamentally caused by noise, BUT, if it was a noise activated ATP leak coming from somewhere other than OHC support cells then we could still be in trouble. Again though I'm trying to be optimistic that this is also unlikely based on the fact we assume/know that the noise-cochlea relationship is directly between noise itself and hair cell (damaged OHC support cell?) stimulation.

I've seen a couple of other theories on how ATP could be causing the pain and maybe even the perception of gain, but what seems really important is where the possible ATP is coming from. If its coming from OHC support cells, it could be fixable no matter what its mechanism that results in pain is, anywhere else would raise further questions.