New York Post Article on Hyperacusis

People can get T/H from braces. People can get T from messing around with their jaw. That tinnitus researcher Will Sedley (sorry if misremembering name) said he gave himself T by doing some jaw exercizes while on the train...and it hasn't gone away. In cases like this I doubt they are damaging the cochlea, so...

 

The auditory nerve go though the neck and I think the jaw so that's what they can damage by messing around with your jaw and having bad posture

 

I agree, but I am sure the auditory nerve also is related to, or can sense stuff from the middle ear... In particular "hyperacusis" may be conflated with TTTS/stapedial spasms.

 

I doubt that the auditory nerve also pass through the eustachian tube and those patients with both hyperacusis and autophonia from issues in the tube. What about that patient with hyperacusis over at the facebook Tonic tensor tympani support group who was diagnosed by germany's PET specialist as having patulous tube despite having no autophonia? What about those patients that get T and H from only from syringing or those that get it only from a broken eardrum? Or how my tinnitus and probably most tinnitus changes just from earwax on the membrane, ''changing the way the membrane vibrates'', according to one synopsis? Or that patient at FB H sufferers that got a very similar type of H to mine but instead of from ''acoustic trauma to the cochlea'' fantastic conjecture, got it from an operation to fill out his eustachian tubes to treat his patulous condition at the tube, and mind you got the H on the unoperated ear, almost as if all H was was a problematic tube. What about when Astrid over at chat-h had her stapedial cut on one ear and became sensitive in the other, back then she thought it was the stapedial reflex but it could have just been the tube again. What about the papers that link aural fullness to eustachian tube disorders and known middle ear disorders, and the ''coincidence'' that people with TTTS and or hyperacusis also have aural fullness? I could come up with a lot of these examples. There are also other strange coincidences when you look at it from the otalgia angle, and other ones.

 

Harold Kim reportedly told someone on the forum that the middle ear was capable of imitating external sounds (dysacusis?), but apparently everyone in the West USA prefers to read the NY Post and tinnitustalk instead of verifying how deep these claims go.

 

Isn't recruitment like a feature of ''meniere's'' that thing ENTs don't agree what it actually is? Well an austrian guy named Franz claims to deal with menieres through tenotomy of the middle ear muscles, just saying... he says something along the lines ''enlarged cochlear aqueduct--- middle ear muscle tension'' or something. As for forums, the guys at tinnitustalk are talking about user generated knowledge over at Tinnet, it's about time the Hyperacusis section should be less deferential to the crappy official ''peer-reviewed'' literature, like when Jastreboff would quote himself as proof, or how on earth did the official hyperacusis questionnaire used in clinics worldwide get to be more superficial and useless than a Kardashian crossbred with a Snooki.

 

Actor Burt Reynolds had long-lasting hyperacusis after being struck on the jaw during a movie fight scene.

 

No, it's supposed to be hearing loss related.

I'm interested in the middle ear issues, it's "easier" to fix than the inner ear for now. But tell me what's going on with my ears after I got H, T and hearing loss after an acoustic trauma.

 

Well, you know me, I'm equally focused on hidden hearing loss/synaptopathy/glial scarring or whatever. I also have a few TTTS symptoms which is why the middle ear is of interest to me. But I'm sure lots of us probably have inner and middle ear problems. I don't think Japongus is suggesting that your hearing loss is middle ear related instead of inner.

 

My Hyperacusis went away almost completely after my stapedotomy. It is mostly a middle ear surgery, with a small component affecting the inner ear (cochlea) since a hole has to be drilled in it for the prosthesis (piston) to actuate and propagate the sound waves.
I don't think anyone understands the workings of H in otosclerosis, but in my case at least the surgery made a tremendous difference: I used to have horrible T and horrible H, and now I only have horrible T. One down, one to go!

 

Well I have enough on my table and don't know what recruitment is. I read Bungler's ,
Bauman's
and then @AnxiousJon said his understanding of what Harold Kim told him was that the tensor tympani was the one involved in making certain frequencies seem amplified, that if the dysacusia were only thumps there was a great possibility the veli palatini was involved. The first says it's when your deaf up to a very loud point and then bam you're getting shouted at, while the second said it was only specific keys on a frequency, same decibels.

There are a few references to recruitment in menieres disease, or maybe just hearing loss. The austrian guy, Peter Franz, doing tenotomies for menieres I phoned him he corrected me when I asked whether he was also curing H, he said no that sometimes what the menieres patients also had was recruitment. Hain says enlarged cochlear aqueducts cause hearing loss, the austrian guy said enlarged cochlear aqueducts cause menieres attacks in the middle ear through the middle ear muscles, but Hain says the austrian guy is only placebo and his logic difficult to understand. Also Hain says his hearing loss cases are idiopathic not acoustic trauma.

Starting at the other end, acoustic trauma and cochlear damage or pseudo-damage has been linked (in a shitty way but has been) to patulous tube and treated with diathermy of the eustachian tube, while a belgian guy has linked patulous dysfunction to TTTS symptoms, unaware that TTTS could just be a myth and the only real problem could be the patulous dysfunction. Apparently if the tube is open tests has shown that the stapes vibrates at a lower frequency, and that autophony doesn't always have to happen. The argument is the loss of a middle ear cushion due to a hole in the eustachian tube. That could be behind the dysacusia, perhaps even me and my thumps, not the middle ear muscles, and yet maybe the middle ear muscles could be what holds open or shut the eustachian tube. Failures and successes in tenotomy in retrospect seem linked more closely to eustachian tube function than they do to lofty notions of the acoustic reflex, as over at chat-h trashboat was complaining postop of pressure fluctuations riding a car up and down a mountain and iirc astrid was complaining of air from belches going up the other ear postop, as well as pressure issues when doors were shut. This also makes sense in the guy at H sufferers in fb who got my type of H in one ear from bioplastic inserted in his other ear to treat patulous dysfunction. There's someone at benzobuddies who claims to have treated his H with botox up the nose and into the eustachian tube, and aural fullness while claimed to be a TTTS symptom, appears in other aural fullness articles from decades ago where the eustachian tube is mentioned as a companion to H.

So the middle ear could certainly be involved in some way or another

 

Most doctors believe in central gain and that the middle ear has nothing to do with H, and will say that was only because you recovered the hearing that you'd temporarily lost before the op. I think you answered me this the other time we spoke, but was your H improvement a lot larger than your hearing gain?

 

What else could it be if I'm seeing people say things like ''the middle ear can lose it's air cushion effect and make the tympanic membrane vibrate more than it should''. That makes so much more sense than synaptopathy hidden hearing loss and glial thingies.

 

They were both good in terms of outcomes. The H went away almost completely, so that's 90% success there. And the hearing went back to within 5 dB of the bone conduction thresholds so that's also quite good. A stapedotomy is not expected to recover the sensorineural part of the loss, so that was my upper limit.
What remains is sensorineural losses, in particular from 1 kHz and above, which is a ski slope down to 55 dB @ 8 kHz and worse as we keep going higher in frequencies (I did an extended test once and the trend before 8 kHz does extend to higher frequencies).

But clearly, at least for me, one of the biggest upside of the surgery (if not the biggest) is the obliteration of H, as it was really debilitating for me. I couldn't type on the keyboard, I couldn't talk, etc.

 

So conductive HL goes, sensorineural HL remains, and yet we're supposed to believe the circus of hyperacusis conference muppets claiming the fault lies in sensorineural hidden hearing loss and synaptopathy. Btw, I'm quite sure their claim used to be SNHL without being hidden at all, because ''dude you know tinnitus is hearing loss and the H is the central gain to compensate for it'', but then someone paid attention to the nonsense and they had to attach the ''hidden'' part to it. Someone might want to read this thread if they're planning on buying their way into this year's London Hyperacusis conference. Talk about the world being upside down.

 

Maybe the problem of hearing damage is multi-factorial, and there is some blending of conductive and SN issues that existing testing doesn't have the sensitivity to interpret. Greg's story is interesting because it combines apparent SN sound interpretation issues originating from a conductive issue. If I'm reading him correctly it sounds like the issue was within conduction but the impact was a mix of conductive and SN symptoms. Would that be fair comment Greg?

 

To be honest I don't think anyone has a good explanation for all my symptoms. I've asked a few experts (as in leading scientists in the field) and they have different opinions. If you're interested in the details, read on.

What I do know is that when my surgeon opened my ear on suspicion of otosclerosis, he did confirm the diagnosis visually (it is actually visible to the naked eye - you just have to push the ear drum to the side to see it), and there were 4 doctors present during surgery so I think I can trust the report.

However, I really don't fit the mold: otosclerosis is normally a slow progressing disease. It takes years if not decades to degrade your hearing to the point that you start thinking about hearing aids or surgery. In my case, a few weeks is all it took to create a 50 dB air bone gap. My initial SNHL was sudden, overnight. In addition to this, nobody in my family has this (it is supposed to be hereditary), and also I'm a male (it is supposed to hit females twice as much).
The other part of the puzzle is that I originally showed symptoms of sensorineural losses, which then progressed to mixed losses (sensorineural + conductive). Mixed loss are typically indicative of problems with both the middle ear and the inner ear. I also suffered from bad hyperacusis at that point.
I did the surgery and H went away almost completely. My air bone gap closed and I'm now left with sensorineural losses in the high frequencies.
If my problem was only in the middle ear, I should not have sensorineural losses.

When I try to make sense of all the info from the various doctors and neurotologists, I think that what may have happened to me is that a pathological focus (i.e. a bone remodeling site) started damaging the area where the middle ear and the inner ear connect, which is around the stapes bone (it's the most common area where damage starts in otosclerosis). This, unfortunately, created damage on both sides of the "border", creating the mixed loss. The middle ear side was fixed with surgery: no more conductive losses and H. The inner ear side did not get fixed and may actually have been hurt a bit more during surgery: it is not uncommon to have high frequencies take a toll after a stapedotomy. The area where the prosthesis gets inserted is where the footplate of the stapes is which is at the base of the cochlea. That is where the high frequency hearing apparatus resides.

My guess is that the disease hasn't progressed into the inner ear far enough to be clearly visible in a CT scan, but it is doing enough damage at the periphery of the cochlea to impact the high frequencies.

So to go back to your question, I think there was (and still is) a component of my issue that is related to the inner ear, even though the most common cases of otosclerosis are pure middle-ear issues.

 

The SN loss is one thing, and probably inevitable under the circumstances, but the resolution of hyperacusis after surgery is interesting. If I may, how did your hyperacusis present itself? Was it purely a pan-volume thing, or did it split into uneven frequencies?

 

Interesting is just the tip of the iceberg. Both the cochlea theory and the central gain theory make no sense to explain @GregCA recovery, and yet they're mainstream. @GregCA had crackling, I have thumping and vibration, and joe schmoe has a banana in his ear. ''Hyperacusis'' is the bastard son of real conditions in otology, I bet if the hyperacusis questionnaire that doesn't bother to ask what sensations we're having started to ask the questions, ''hyperacusis'' as a separate discipline would disappear and each of these types of symptoms would have a far better definition today, they'd each belong in their own real diagnosis from the real fcking world.

 

Then maybe actual research would start.

I wonder what the acute appendicitis distress questionnaire reads like?

 

Re-reading your account, @GregCA I can't remember if I asked you elsewhere what exactly did your hyperacusis feel like and to what sounds were you sensitive to?

 

It was a weird sensation. Not like a stabbing or burning, but something I had never felt before, very bad discomfort, like when your speaker can't take the amount of power you send to it and it starts crackling.

It wasn't that normal sounds were amplified greatly. It's the that the faintest sound would trigger it. For example, typing on my keyboard would be enough to trigger it (with everything else being quiet). The other triggers were things like crumpling paper or plastic bags.

The odd thing is that there were other sounds with much higher volume that didn't seem to trigger H.

 

So on a single instance of keyboard type you would have a single pop or a series of pops, and it was until the end of the sound or beyond the end of the sound?

 

I don't remember with high accuracy how many pops I had, but I want to say a series of pops, and it would stop at the end of the sound. It didn't "bleed over".

 

Preop when you had conductive hearing loss and H, did you also have a low frequency T? Or only the high-pitched T that remained postop?

And just to be clear, no echoing, no thumping. The H was just popping?

 

Pre surgery I had - in addition to the high frequency T - another sound that wasn't constant (it was cyclic, but I'm not sure it matched my heartbeat): it would go up and down in frequency (so it would get into the low bands as part of its cycle), and feel a bit like if you were to throw a can of soup into your dryer and start the program, so the can starts making noise as it bounces around in the drum.

After surgery I was left with the high pitch T, and a sporadically would get low frequency T like a fog horn. It would visit me mostly when I'd lay down, and then stay for a couple of days, and go away for a couple of weeks. Unfortunately as of a few months ago, this low frequency T has decided to stay so it's now there 24x7. Thankfully it's not bothering me during the day because its volume is low compared to ambient noise and the high pitch screech T, so I barely notice it during the day.
The other "fun" T that has visited me every once in a while post surgery is pulsatile T, especially when I would do something strenuous. Thankfully that one hasn't visited in 6+ months. Maybe some parts of the middle ear have healed to the point that this isn't an issue anymore.

Correct. Just popping/crackling.

 

Greg your description at 1:38 could be of my sound intolerance. I've never demonstrated low frequency loss on an audiogram, but in the real world, my low frequencies drop out every seventy-two hours and slowly return for a day or two only to drop out again. This pattern has been more or less consistent now for three years. The feeling it causes is worse than the sound, which is bad enough.

 

I've had ocd since very early childhood along with anxiety and depression. I was actually told as a kid I could stop this anytime if I really wanted to. It caused much difficulty because I believed them. People treat this stuff - along with many other things like T or H - as if you have a character flaw or something. I think it just makes others feel more secure because people want a simple reason. What's easier than blaming the person with the issue.

And I've only begun looking into all these things so I don't know my h on the research. However I've had very sensitive hearing all my life long before the T. I don't think I have a formal diagnoses of H yet but the ENT mentioned it to the assistant taking notes during the exam. I even show one sided HF hearing loss but there is no acoustic trauma I can pinpoint. The noise that drove me crazy and aggravated this was a common noise that didn't bother anyone else. To me it was inescapable and was like an icepick. So can normal sounds cause trauma to overly sensitive ears?

 

Blaming the patient is last refuge of Medical ignorance.