Challenging the Current Terminology of Hyperacusis

I would love the opinion of everyone in this thread: is reactive tinnitus - esp. the fast-reacting tinnitus that overlays sounds in realtime - a subset of hyperacusis? I've argued that it's a very different symptom, but might it share a pathology?

 

This really depends on who you ask. I have come to think of it as three possibilities:

1) Yes a form of central gain/compensatory hyperacusis where you are hearing part of a complex sound (a single tone even) as much louder than the rest.

2) Local cochlear inflammation stimulating the NMDA receptor selectively at some IHC/SGN junctions so that there is too much excitability propagated by sound in some locations.

3) Middle ear muscle related. The ear drum is especially discordant at higher frequencies.

That probably didn't help since I just gave 3 different theories with very different pathologies.

 

I do get some of this and it's scary but tolerable... less now than a few months ago. In particular at 100 Hz and 1600 Hz. Both A flat, a hum and a whistle four octaves apart, now only noticeable in noisy things like fans and motors. Could be easily simulated with an equalizer just by making narrow boosts at those frequencies.

What I don't get, and don't know how to categorize, is when reactivity happens nowhere near the actual pitch of the sound. Any low humming in the real world agitates my ultra-high hissing/squealing. I don't think it's mechanical (eardrum/middle ear) because the hissing is all over the left-right panorama. And unlike most personal accounts of hyperacusis I've read, it doesn't react to short, louder sounds like clanking dishes, but mostly to sustained sounds at almost any volume.

 

This happens in particular with low frequencies specifically? I wonder if extra stimulation is happening at the "formants" of the low frequency sounds.

Is it both ears? Do the low frequency sounds sound otherwise normal?

 

From what Ive read I think a good theory is cochlear inflammation that stimulates the trigeminal nerve endings that are actually in the cochlea. The trigeminal nerve apparently links back to the dorsal cochlea nucleus and this fluctuating level of inflammation is what could be causing the excess modulation of dorsal cochlea nucleus neuron activity.

I like this theory because I think reactive tinnitus is like a dimmer switch. The worse the noise exposure, the more damaged hair cell activity, the more ATP / cytokine leakage there is, the more the trigeminal nerve gets stimulated (and the longer it gets stimulated for). And finally the louder and longer the tinnitus lasts for.

I'm the same though, there are certain high frequency noises I have to avoid because they'll give me instant setbacks but then there is sustained noise at more broad frequency that wouldn't necessarily give me an instant setback but would activate my tinnitus and give me ear fatigue. My guess it that even at broader lower frequencies but for a sustained time, the whole cochlea is to some degree still being stimulated including anything that is damaged and responsible for inflammation. I wonder if the damaged parts leak ATP no matter what, slowly and that's what steadily increases the tinnitus. And the difference between that and a setback is a full on assault on the actual damaged frequency hair cells (by that specific frequency noise) that not just releases ATP but also fires the type II action potential which then gets the middle ear involved as well and stimulates the trigeminal nerve from both ends.

 

Wouldn't this pathology apply more to noxacusis, specifically? Yes, the TN affects cochlear blood flow but I would think there would be at least some pain in TN irritation.

 

Both ears, but sometimes more noticeable in one or the other; lately more in the right.

It might be more noticeable on lower sounds because it so obviously doesn't belong there (say 12 kHz ringing over a 200 Hz sound); if it's a closer match (12 kHz over 8 kHz), it's easier to just believe it's part of the sound.

 

That's probably a big part of it. The contrast.

 

I've noticed this too. Isn't this part of "recruitment"?

 

I don't know but my symptoms range from ear fatigue/reactive tinnitus through to setback pain which is on a different level completely. Although it's kind of a scale, it isn't gradual, there's a trigger point along the scale where a switch gets tripped and the symptoms become infinitely worse, almost instantly. Say constant moderate broadband sound in general causes minute, size-wise in comparison to the middle ear, levels of cochlea inflammation that stimulate the TGN from within the cochlea (enough to lead to reactive tinnitus for example), but then if also Type II's reach action potential level and the much larger middle ear gets involved as well, the amount of inflammation generated there is massively increased compared to the tiny cochleas inflammation alone and is now also hitting the TGN innervated components within the middle ear. The reactive tinnitus then becomes screaming tinnitus (that I can feel), plus the facial pain to go with it. All just a theory but there's a snapping point somewhere (for me) that something else happens, I can feel it.

Or it could be down to whether or not a TGN is sensitized or not whether it causes tinnitus alone or both pain and tinnitus?

 

I consider reactive tinnitus to be (at the least) a pre-hyperacusis symptom. I have severe loudness hyperacusis and horrible reactive tinnitus. No question, high pitched noises are worse (and that's also my worst tinnitus frequencies). In my case, even though they are different symptoms, they correlate so strongly. Like if I'm around sound, my central gain from hyperacusis will get worse and my tinnitus will react, temporarily. They then go back down together during rest. I feel extremely confident that if I "cured" my hyperacusis, I would have very manageable tinnitus.

 

I too believe that if my tinnitus were completely stable - with the exception of one tone - it would be 100% manageable. What's strange is that I have no hyperacusis symptoms except for really oddly presenting reactive tinnitus.

It's can react to any sound/frequency but seems to mostly react to constant noise of any volume. Except it doesn't always react to the same noises. Sometimes it reacts to taking a shower and sometimes it doesn't. I can't make sense of it at all.

Personally, I think that inflammation is the most likely origin of my reactivity issues, but who knows.

 

I think inflammation and sensitization at the IHC/SGN NMDA receptor seems like a logical source for a lot of people's reactive tinnitus (though some people presumably could have a middle ear component instead or also).

Makes logical sense to me because glutamate release at the IHC terminal is a normal part of hearing but when you have sensitization at the NMDA receptor, it's going to produce hyperexcitability that can be propagated up the auditory system (vs say a constant baseline tinnitus that's mediated through central excitement when the brain tries to push a signal-- through ion channels? Increased glutamate signaling? centrally when it's not getting a signal. Aka "phantom cochlea").

 

I have similar experiences. The static noise I’ve been having since February can get pretty reactive—but only to certain sounds. Running water, a vacuum, the fan of a computer or console turn the static really high-pitched. Other noises like clattering dishes don’t bother me at all.

Once the sounds I’ve listed above stop, the static calms down again and returns to base line after a while.

Question is, could this permanently worsen my tinnitus? Technically those noises clearly aren’t loud enough to do any actual damage in general, but obviously there are other things that factor into the whole issue, so I’m wondering what anyone more knowledgeable than me thinks.

 

Same here - the shower, computer fans, and road noise all raise the volume of my tinnitus and give it a scratchy buzzy quality.

 

Could inflammation possibly be the reason behind tinnitus that fluctuates wildly? My tinnitus fluctuates a lot from day to day and is sometimes extremely reactive, while other days it's more akin to how it was when it was "normal" (before I developed severe hyperacusis and worsened tinnitus).

 

Sorry to jump in. I would just like to throw in my 2 cents regarding my experience with reactive tinnitus. I think my case is really weird.

Since onset, my tinnitus would spike from consistent sounds like driving/fans etc. This could be mitigated by hearing protection. If I weren't exposed to such noise, my tinnitus would be very very stable.

In February, during the course of roughly 1.5 weeks where I 1. Took an anticholinergic drug, Hydroxyzine for sleep, and 2. Severely over-protected (almost complete sound deprivation) due to anxiety. I was left with way worse loudness hyperacusis and severely reactive tinnitus. Now, ANY sound causes the tinnitus to react and get louder. Whatever went down during those weeks in February, I assume it can't be a result of further cochlear damage. My only guess is that the Hydroxyzine messed a bit with the nervous system, but I don't see how it would do permanent damage to my hearing.

I would conclude that this severely reactive tinnitus is in direct connection with the loudness hyperacusis, and I doubt that it would be as a result from inflammation since my tinnitus were actually really stable before February. Sadly, I have yet to see any improvements.

With respect that every case is different, just thought I would share it.

 

I do think so. My tinnitus in contrast is always the same no matter what and it corresponds only to my hearing loss.

 

Hydroxyzine is kind of a unique drug. It has dopamine effects (linked with tinnitus) and anti-cholinergic effects. Even occasionally has brain stem effects:

https://link.springer.com/content/pdf/10.1007/s13312-018-1451-9.pdf

May take some time to get better.

It's a good reminder that there are outliers and pathology is pretty diverse for this kind of stuff.

 

I also fear my reactivity is a result of some nervous system dysfunction, meaning restorative therapies for the ear will be of limited benefit. I just have no way to tell. Most of my hyperacusis like symptoms are gone, but I still can't listen to sustained noise.

Last night I was struggling to sleep so I played rain sounds at a low level on my echo - I woke up with a large spike I've been dealing with all day. This was probably 30 decibels on a speaker 10 ft away, approximating normal rain noises. If I could eliminate reactivity, I'd be much closer to finally achieving some peace.

 

I'm sorry to hear that. It's an extremely distressing tinnitus component to have. I know this thread maybe wasn't intended to be a reactivity Q&A, but I'm curious; have you seen any improvement whatsoever in your reactivity tolerance? Would you say the trend is headed in the right direction, albeit slowly?

 

Have you had any improvements in the reactivity part?

 

Thanks for reaching out.

Unfortunately, not yet, but hopefully it will turn the corner soon.

All the best,
Stacken

 

Rationale and Efficacy of Sound Therapies for Tinnitus and Hyperacusis

Does anyone have a full version of this article?

 

Yes