Hyperacusis Case Study: "A Case of Acoustic Shock with Post-trauma Trigeminal-Autonomic Activation"

[lymebite]

A new research paper on a case study of hyperacusis. The patient is a doctor so the descriptions of symptoms are quite precise.

http://journal.frontiersin.org/article/10.3389/fneur.2017.00420/full

 

[Reinier]

@lymebite That looks interesting. Have you read it?

I see there is also talk about the middle ear.

"Second, the functional integrity of the middle ears was also investigated using multifrequency tympanometry and direct examination of the eardrums."

In my case I am still not confident that there is no change (damage?) in my middle ear after experiencing my acoustic shock injury.

I will download the article and see what they say about this.

 

[lymebite]

That looks interesting. Have you read it?

@Reinier

I have read it. While I will look to you and others for more insightful thoughts, my perspective is that this article is an excellent addition to a rather sparse collection of literature on hyperacusis. The detailed descriptions of the symptoms are especially helpful I think in conveying the experience of this particular patient. I would love to see one hundred additional similar high quality articles about other H case studies with different groups of symptoms, but for now am grateful to see this article published.

 

[lapidus]

The mention of rhinorrera as a symptom is interesting to me considering I've had a runny nose (without any other flu or cold-like symptoms) almost every morning since my hyperacusis started. I have never really thought about it being connected in any way.

 

[lapidus]

@japongus it would be interesting to read your thoughts about this.

 

[PaulBe]

Not really so nowadays, but in the beginning I would experience some sounds (particularly fairly percussive or unexpected sounds) as traveling in a sensory manner across my maxilla. When I found an intelligent GP we talked about it and kind of agreed that cross-talk between nerves packed closely together could result in transfer of stimulus where a sound would be converted to a tactile sensation if that was the proximal nerve pathway that was picking up the misdirected impulse. In a way this paper validates my theory of what was happening to me at the neurological level. This paper also finally places some real-world physiology behind some of the limbic-based assumptions that drive current therapeutic models of care, which up to now have been based largely on educated guesswork and treasured theories. It also suggests a cascading injury process occurs that can potentially be blocked at some point.

This paper also shows what is possible as far as basic research (that still hasn't been seriously done) could go, and is one of the most significant I've seen, hence I expect it will get buried and forgotten by the Medical establishment, unless Brian Pollard can get to it.

My thanks to the vigilant @lapidus

 

[Lex]

The mention of rhinorrera as a symptom is interesting to me considering I've had a runny nose (without any other flu or cold-like symptoms) almost every morning since my hyperacusis started. I have never really thought about it being connected in any way.

I was just going to start a thread about this! I noticed that every time after I feel the tingling in my earlobes and stabbing in my ear canals, my nose would run, and I would also have post-nasal drip down my throat. I've always felt they were connected but I didn't know how or why.

My T and H were both caused by an acoustic trauma I got 1.5 months before onset, I'm sure of that. But one week before onset, I remembered having a really bad sinusitis case where my face and cheeks hurt and my nose ran.

 

[lapidus]

My thanks to the vigilant @lapidus

I think you meant @lymebite and not me. He's the authour of this thread and the finder of the article. Pollard probably already knows about this article, otherwise I think Lymebite could inform him.

 

[Reinier]

"We suggest that these symptoms may result from a loop involving injury to middle ear muscles, peripheral inflammatory processes, activation and sensitization of the trigeminal nerve, the autonomic nervous system, and central feedbacks."
That is almost everything
Also, how do you influence the autonomic nervous system?
How long can something remain inflamed? Not indefinitely is suppose?
My ASI happened two years ago.
Although the "I" in ASI could in my case be incident instead of injury. I don't know if my middle ear is injured.
But I often wondered if it was (is).

 

[PaulBe]

Er, yeah. Sorry vigilant @lymebite

 

[PaulBe]

@lymebite

Umm yeah, Lapidus was in the two posts above me, and you know how it is when someone's on top of you. Its the first thing you see when you dare to open your eyes. A pussy in a space-suit. Why not?

 

[japongus]

@japongus it would be interesting to read your thoughts about this.

Very important piece of work in the purposefully forgotten world of the middle ear. I said acoustic trauma could cause otalgia over at chat-h last winter, to the derision of the local sound therapist, and this guy goes and says it's part of the parcel. He compared one ear with the other to see changes, and one ear was worse off than the other, so once again not objectively visible like we've always been told, but only when comparing a healthy ear with a troubled ear. He speculates on a bunch of possibilities, like ear deformation, and notices high tension and high hyperemia comes with high frequency tinnitus whereas low tension comes with low frequency tinnitus, he notices easier admittance in the ear that's worse off, and speculates about the existence of ossicle deformation as a result of tonic tension of the middle ear muscles.

 

[japongus]

"We suggest that these symptoms may result from a loop involving injury to middle ear muscles, peripheral inflammatory processes, activation and sensitization of the trigeminal nerve, the autonomic nervous system, and central feedbacks."
That is almost everything
Also, how do you influence the autonomic nervous system?
How long can something remain inflamed? Not indefinitely is suppose?
My ASI happened two years ago.
Although the "I" in ASI could in my case be incident instead of injury. I don't know if my middle ear is injured.
But I often wondered if it was (is).

In the fb TTTS group we found a german eustachian tube doctor diagnosing PET without autophony in cases of my type of hyperacusis where apparently ''the tube is not always open''. As of now we only know he did it by acoustic reflex decay testing. I can only combine that with info I posted here last spring about certain people with autophony and PET who only had it when they lie down. It was from a french site that said the oxygen flow from the eustachian tube changed the inflammatory process in the mucosa by changing the amount of CO2 present and that this caused low frequency tinnitus. I suspect between middle ear tension and eustachian tube issues that are hard to diagnose. I am also immensely suspicious of how someone in the H and T research group got exactly my type of H in one ear by having bioplastique injected into his other ear's patulous eustachian tube. See where I'm going with this...

 

[japongus]

Everyone should be over at libgen reading the bibliographies in articles like these to get a sense of what a fucking mess the world of the ear is and what little consensus there is in it, for the next time you're told some crummy-ass narrative by the local technician.

By the way, if you read Jastreboff's neuroshitological vision of the ear, he discards that the middle ear has any issues with a simple test that this paper proves to be outdated. I'm sure that won't stop him trying to rewrite another edition in 10 years time, I bet like the 90s, when he was treating the yet to be discovered dehiscent ears with sound therapy lol