We can't say for sure yet but FX-322 is designed exclusively for hair cell damage.
If your hair cell damage and corresponding tinnitus is > 6000Hz, I would say very high. As they are doing multiple consecutive dosages in the current study we may see lower frequencies restored with deeper diffusion levels. It may be for some that only a small threshold improvement might be sufficient to "turn off" the brain's maladaption of tinnitus.
Go to the link below and match your tinnitus tone by adjusting the frequency slider of the oscillator. If your sound is hissing or fuzzy it will be difficult to get a matchup though.
Yes, there are tone generators on YouTube and you try to match the region where your tinnitus is. It's harder if your tinnitus isn't a pure tone or if you have lost a lot of hearing bilaterally in the area where your tinnitus is.
Medically defined as loss over 2000Hz which is a useless definition in this context. FX-322 targets higher than that (we should know the exact range at the end of phase 2).
The other way around. It should hit frequencies above 6kHz just fine, but below that is where things are less certain.
I have tinnitus and some pain hyperacusis (mainly discomfort from tinny speakers). I believe that headphones were the cause. I've had a couple of audiograms and they have been very good.
If FX-322 got rid of my tinnitus I would cry my eyes out because I would be able to sleep in peace.
If you have cochlear origin tinnitus, it should come from hair cell damage (inner or outer) or synaptopathy. Unless you have something like hydrops.
When the Tinnitus Talk Podcast happens, Frequency will be asked about how they plan to address the lower frequencies.
I have the same issue - pain hyperacusis has mostly died down but it's still aggravated by tinny speakers. I guess with noxacusis there are still many many unknowns but I speculate that perhaps it's due to damage at a specific frequency (which are amplified through tinny speakers?). Maybe that's our problem so hair cell and corresponding synapse regeneration could help us.
I have submitted it to @Candy for editing and simplifying it to make sure it is clear and easy to understand (that's her wheelhouse more than mine). She has a lot on her plate atm though!Hearing damage is a biochemical process. If you have been exposed to loud sound at sufficient duration (which is exponentially shorter as the sound is louder, for example a gunshot does damage in a second) you have experienced damage.
How deep it penetrates is all about the gel medium they suspend the drug in. There is no inherent quality of the drug that prevents it from affecting hair cells at certain frequencies.
Also, I'm super excited for your upcoming drug summary @FGG, should help quell the banter and confusion on this thread. You're a true gem
The most widely accepted theory of cochlear origin tinnitus (e.g.. Noise, Ototoxins, infections etc) is that the tinnitus is a response to a disrupted signal. So, at the point of the disruption, your brain experiences a phantom sound similar to when a phantom limb pain is still felt when someone loses a leg.
I was referring to a guide explaining what regenerative drugs effect what structures that I was working on, not the Tinnitus Talk Podcast.
Per Liberman, the synapses are the most susceptible to noises but it has been known for awhile that the OHCs are sensitive as well. It may even depend on the individual and the specific exposure. IHC damage seems more prevalent with certain Ototoxins but sometimes noise can damage IHCs more selectively than other structures too for unknown reasons (there was a rabbit study I found awhile ago).There are still so many things I don't get (which may be explained in the layman's guide coming up):
Loud noise seems to cause more damage to the OHCs as they are the first to get hit by it, yet from reading on this forum it seems that when a person suffers ototoxicity that the tinnitus that appears is of a high frequency piercing nature which would suggest damage to the OHCs. So my question is: Why would the OHCs be hit first from ototoxicity instead of the IHCs and auditory nerve? Or are they all getting hit, but for some reason the result is high-pitched tinnitus?
I'm probably missing something very obvious... hence the need for a layman's guide
Also, is it possible that serotonergic drugs, for example, overexcite the part of the brain that is responsible for hearing and raise the gain, so that you hear things you wouldn't normally hear, i.e. that they cause some type of excitotoxicity that alerts the brain to already present hearing loss and the brain, which had ignored previous hair cell damage, all of a sudden becomes aware of it? I'm paraphrasing someone else's words here.
I just wonder if this is what has happened to me, although when I got tinnitus it came with a plugged up feeling in one ear, which I presume means that there has been some (further) cochlear damage occuring due to the drugs, and I have suffered noise trauma since the initial drug-induced onset too.
Not sure if any of that makes sense... like all of us, I'm just really trying to figure out how much FX-322 could help someone in my particular situation.
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