International Tinnitus Journal, Vol. 14, No. 1, 37–41 (2008): Tinnitus — a Philosophical Problem

[MountainCreek]

Keeping cats, after noise trauma, in a high-frequencyenriched environment prevented tonotopic map reorganization and reduced the expected hearing loss due to the noise as contrasted with cats with the same exposure but kept in quiet.

That is to say, high-frequency stimulation maintained normal cortical organization and essentially improved hearing (by reducing expected hearing loss). Noise-exposed cats kept in the high-frequency environment displayed normal spontaneous firing rates. The authors interpreted the perseverance of normal spontaneous firing rates as an indication of the absence of tinnitus.

These are very important observations, because what is implied, at least in the cat model, is that the neural biological responses (see Fig. 1B) to hearing loss can be averted with only postexposure high-frequency sound, suggesting the conclusion that tinnitus is not necessarily an end result of an "exposure" (i.e., not a phantom stimulus). Keeping cats in quiet or providing low-frequency stimulation was not effective in preventing hearing loss and neural map changes.

http://www.tinnitusjournal.com/articles/tinnitus-a-philosophical-problem.pdf

 

[maltese]

Keeping cats, after noise trauma, in a high-frequencyenriched environment prevented tonotopic map reorganization and reduced the expected hearing loss due to the noise as contrasted with cats with the same exposure but kept in quiet.

That is to say, high-frequency stimulation maintained normal cortical organization and essentially improved hearing (by reducing expected hearing loss). Noise-exposed cats kept in the high-frequency environment displayed normal spontaneous firing rates. The authors interpreted the perseverance of normal spontaneous firing rates as an indication of the absence of tinnitus.

These are very important observations, because what is implied, at least in the cat model, is that the neural biological responses (see Fig. 1B) to hearing loss can be averted with only postexposure high-frequency sound, suggesting the conclusion that tinnitus is not necessarily an end result of an "exposure" (i.e., not a phantom stimulus). Keeping cats in quiet or providing low-frequency stimulation was not effective in preventing hearing loss and neural map changes.

http://www.tinnitusjournal.com/articles/tinnitus-a-philosophical-problem.pdf

Oh crap.

This is the exact opposite of what I've been doing.

 

[MountainCreek]

I find it hard to believe that cats are humans though.

Also this is not in agreement with my personal experienes.

Can humans restore hearing by listening to moderate sounds? I find that very hard to believe, and I think one single experiment should be reproduced independently by many research groups, and on different animals.

One can not draw any conclusions from just one experiment carried out by just one research group. They may have made a mistake somewhere in their experimental setup.

 

[MountainCreek]

I would like to carry this experiment one step further and take those tinnitus induced cats and expose them to the same sound background one week after. Would THAT help those cats recover tinnitus. Here I have big doubts.

Sound background may be efficient just BEFORE you got tinnitus. But it may be completely useless after tinnitus has started..?

 

[stophiss]

Interesting but begs many more questions. How soon after acoustic trauma should high frequency sound therapy be administered? What duration? Further, aside from perhaps a stepping stone for scientistics better understanding neural plasticity changes due to acute sound exposure which cause tinnitus, what relevance does this have to the individual who gets exposed to loud sound unintentionally? Why wouldn't high sound exposure effects incrementally erode hearing and contribute to increased tinnitus over time? They do. Tinnitus likely is cumulative...brain changes due to sound exposure and cochlear hair loss each time resulting in brain changes.

An interesting study none-the-less and maybe a form of prevention moving forward say in lieu of taking steroids after actute sound exposure. But is onset of tinnitus too late for example? So many unanswered questions which brings into account the relevancy of how this information could be realistically administered to mitigate brain changes due to acute sound exposure as a form of therapy.

What we really want to know is...how do we put the genie back into the bottle? Once contracting tinnitus, how can the brain be reset as it was before to not create a phantom sound? Beyond daunting of course...brain un-mapping or re-mapping...a lot more difficult than reprogramming an operating system on a computer...and likely why one day robots will take over ....us being pitifully victim of our design and beyond slow adaptation to change for example not accounting for the industrial revolution in the context of hearing resiliency based upon evolution.