Comparison of Otoacoustic Emissions in Tinnitus and Hyperacusis Patients with Normal Hearing

Juan

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Dec 15, 2016
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Comparison of otoacoustic emissions in tinnitus and hyperacusis in adults with normal hearing sensitivity
Conclusions: The reported non-significant differences in DPOAEs in individuals with tinnitus and/or hyperacusis do not support a peripheral mechanism or an interaction between peripheral and central mechanisms underlying tinnitus or hyperacusis. Our findings, however, suggest the need to assess basal cochlear function (e.g. EHF thresholds) for a better understanding of differences in DPOAE measures in tinnitus and/or hyperacusis.
It is a pity that the full article is not available for free.

If I understand the conclusions well, it seems to point to a cochlear dysfunction or cochlear damage as the main cause of tinnitus and hyperacusis.

I had myself the distortion product otoacoustic emission (DPOAE) test and results were normal, I think. It was a long time ago. Did you guys have this test too? What were the results?
 
Oh saw this paper this morning! I had the cochlear test too a few years ago. I can't remember the results, but they said it confirmed that some of my cilia had died off, and that confirmed by tinnitus. Interesting to see these results in light of this study.
 
Oh saw this paper this morning! I had the cochlear test too a few years ago. I can't remember the results, but they said it confirmed that some of my cilia had died off, and that confirmed by tinnitus. Interesting to see these results in light of this study.
Does tinnitus caused by noise exposure always mean that those hair cells have died off?
 
Love to see this. This is the kind of research we need, moving away from the brain and "all in your head" and more towards the ear.

Makes me want to try to get an OAE test, though I'd fear worsening.
So why does it fade over time/disappear for some people (who had tinnitus from noise damage)? I'm just curious :)
Nobody knows.
 
So why does it fade over time/disappear for some people (who had tinnitus from noise damage)? I'm just curious :)
Maybe the brain ignores the tinnitus signal... that's my guess. It has been compared to the phantom limb phenomenon sometimes.
 
So why does it fade over time/disappear for some people (who had tinnitus from noise damage)? I'm just curious :)
So, as @Shizune said, we don't really know. My hunch is that for some people, their brain resolves the issue and moves on, ending the ringing. Other people probably just get used to their tinnitus which causes it to fade in their perception. There's probably some sort of genetic/environmental factors at play as well. Like if you go to a concert, get tinnitus, but overall live a quiet life, you probably have a better chance of recovering. That's just speculation on my end though.
 
So why does it fade over time/disappear for some people (who had tinnitus from noise damage)? I'm just curious :)
There is a Ted Talk about this. There is a "gating" system in the brain. It seems to turn on in people with chronic tinnitus.
 
I believe so, because the ringing is triggered in your brain from loss of auditory information from hair cells.
Yes, but hair cells die off in everyone - it comes with age, and is why our hearing thresholds deteriorate. I had something in my OAE test at 4-8 kHz, but my hearing was good up to the 12 kHz limit on the audiogram. No speech-in-noise issue either.

So I do not know what conclusions you draw from OAE tests.
 
Love to see this. This is the kind of research we need, moving away from the brain and "all in your head" and more towards the ear.

Makes me want to try to get an OAE test, though I'd fear worsening.
Is it just me or have you interpreted it wrong @Shizune? This is saying it's not a peripheral mechanism.
do not support a peripheral mechanism or an interaction between peripheral and central mechanisms underlying tinnitus or hyperacusis.
That said, it may certainly be triggered by hearing damage but the actual mechanism is no longer generated by the inner ear or its interplay with the brain. It seems more a brain derived mechanism after loss of input.

@Travis Henry, you may find this useful.

It's a shame we can't see the full publication.
 

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