Is Recruitment a Myth?

A decade ago, Marsha Johnson said that the largest tinnitus clinic in the USA a decade ago, so 20 years ago, wasn't testing for hyperacusis in tinnitus patients. When they started testing for hyperacusis, they suddenly discovered half of the tinnitus patients had hyperacusis. I assume once they made this amazing discovery they got busy publishing in a journal and happily marched home to watch reruns of Friends. Tinnitus clinics have a penchant for professional solipsism and that's a great example. What if even though we're being told by these self-anointed experts that hyperacusis and recruitment are different, when recruitment could just be hearing loss + hyperacusis?

@AnxiousJon said he saw Harold Kim say the middle ear could be involved in magnifying certain pitches. Now, I certainly haven't read all the recruitment literature out there, and Kim could just be an incompetent or he could be at the top of the game, we don't know because nobody bothers to read and everyone just prefers to pay 500 bucks for conferences spilling with pretension over at Baltimore or London. What I have seen from the ''recruitment is a thing'' camp is thoroughly unconvincing, given that embarrassing anecdote uncovered by Johnson, and given that it's usually told in the manner of thoroughly outdated hyperacusis dot net manual. When I was on the phone with Peter Franz six months ago, he said Meniere's patients have recruitment, not hyperacusis, and that stopped me in my amateurish ambitious plans to interview him for a Tinnitus Talk topic. But now I wonder, is he really testing for hyperacusis? Could it just be his patients of the Meniere's variety, all have hearing loss plus hyperacusis? How deep does the amateurish grapevine go-- Look at this thread where a patient claims to get cured from something that looks like recruitment and the expert pulls out enough TRT rationalizations to make a feminist look like a quantum magician from Planet Uranus B12.

 

Yikes, I should never have mentioned his name anywhere.

Harold Kim never spoke to me about hyperacusis, period. The only thing we spoke about was what I visited him for: surgery to removed the tensor tympani and stapedius.

The only thing he told me was the effectiveness of the surgery being only a majority of the time because sometimes a third muscle is responsible sometimes for the myoclonus.

I will be getting the surgery when I get the money or insurance that will cover it.

 

Why not mention him? I'm not saying he is talking about hyperacusis. What I am saying is that he's unknowingly talking about hyperacusis. Big difference. All it takes to get written up as a hyperacusic is to say you have discomfort with sound (on an LDL test), and AFAIK those requirements are filled when you say the middle ear can imitate external sounds, and I get a thump with every new signal over noise.

However, what if the thump isn't followed by other thumps. That could be real hyperacusis and tenotomy would make it worse as we'd have things like hypoxia inside the cochlea. If it is followed by other thumps, that could be merely middle ear issues. If the thumps are merely heard and not felt, that could be merely tinnitus. See what I mean? If doctors like Kim have seen a thump from setting a coffee cup on the table- that isn't followed by other thumps- get cured from tenotomy, then hyperacusis and reactive tinnitus would fall under suspicion of being something in the middle ear.

 

Serious people know hyperacusis is in the middle ear. To have a kind of hyperacusis in inner ear, Boston guys have to put mice in 120 dB during 2 hours. None of us had this treatment with continuous sound, more often is just a quick trauma.

 

I don't think people are aware of the little legitimacy the word hyperacusis has. They talk about it like there's a grand tradition behind it but there isn't. At what point does reactive tinnitus become ''hyperacusis'', when the tinnitus becomes loud enough to be felt rather than heard, at least in my case. Then there is little difference between reactive tinnitus and hyperacusis. Also I'm amazed by the lack of shits given by patients but that's mostly because they're all encouraged not to think for themselves by TRT experts.

Yours was sudden, mine wasn't, mine went over minutes or hours in night clubs there are plenty of people like that here. Anyway, there are lots of angles of it being in the inner ear too, both sudden and prolonged. Inner ear hypoxia doesn't need hours as far as I understand and that's just one of a number of theories. Or even the inner ear affecting the middle ear. What is this mouse study you're talking about?

 

Remember that acoustic damage (whether spike or prolonged exposure) isn't the only possible source of damage for the inner ear. There's a few illnesses and conditions that could lead to the inner ear being somehow damaged and creating hearing conditions like tinnitus & hyperacusis. Cochlear otosclerosis is one of them for example.

 

Together with a stupid sound discomfort test in a sound booth, the modified Khalifa Questionnaire is all hyperacusis is. A bunch of tendentious stupid questions in addition to unspecified discomfort in a sound booth. These large tinnitus clinics of ever so recent creation don't bother looking into exactly what type of discomfort the patient is feeling because doing so would be like admitting that there are different types of hyperacusis from different injuries, and that it isn't a discipline on its own that comes out of a protection mechanism in the limbic system where the specifics don't matter and the only thing that matters is the limbic system.