Hidden Hearing Loss, Tinnitus and Trouble Hearing Conversations in Noise

I can't be sure. But dealing with the hearing loss and associated discomforts (hyperacusis, distortion, tinnitus and more)
is more difficult if anxiety level is high.
My anxiety level is very high!
It would not surprise me that muscles round the ear(s) and even neck tension up when anxiety is high and make things worse.
Apparently there is also the autonomous nerve system that can make things worse.
Plenty about that on this forum.
I can understand that anxiety and autonomous nerve system will improve over time.
From my own experience I can tell that very, very slowly anxiety level improves.

 

The cochlea is on the HPA axis (https://en.wikipedia.org/wiki/Hypothalamic–pituitary–adrenal_axis). Stress can quite directly affect the earliest stages of your hearing. The two streams (hearing and stress) cross over each other again in more recently evolved regions of the brain (e.g., the cerebral cortex) where sensation is intermixed and contextualized with memory and internal psychological states. Stress is fuel on the fire and hearing in noise (and vice versa).

 

Video segment about hidden hearing loss from ABC 30 News:
http://abc30.com/health/hidden-hearing-loss/1613375/

 

Yes, tracking conversations in noise has become quite the annoyance in my life exactly when I got tinnitus. Not much of a surprise since both conditions underlie the same physical principles of internal cellular and systemic noise cancellation.

It can not, the limit you describe is a physical sensory one. No amount of computer or cerebral processing can restore lost data. One could turn down the severity of tinnitus but only by lowering the hearing threshold but then you would hear even less.

In my opinion the best way is to redesign the ABR and add wavelength dependance. This way the result would be a surface in 3D yielding more information about the hearing i.e area of incurred trauma and wavelength dependent lapses in signal to noise ratios. I was designing this but I'm just out of time.
Furthermore, audiologists generally do track the SNR (signal to noise ratio) but they don't report it to you. As with all measurements at the audiologists, without a before picture you can never be sure about the after picture however a wavelength dependent ABR and DTI MRI could solve this problem because they compare functionality in the same person over different wavelengths.

To paraphrase, this is exactly like measuring a camera's resolution by its ability to detect light intensity. In the end it only takes one pixel and the rest of the camera chip could be utterly destroyed. My bottom line is that this is a very simple principle but all simple principles are often overlooked in groups of people not utterly committed to the correct execution of a cause. It's only hidden because nobody is looking.

Good thread.

 

The cerebrum and the central nervous system are not the same in structure and functionality. Smelling something bad does not strengthen your sense of smell Thankfully.

There's uncertainty (here and in literature) about how the auditory system reorganizes fibers. In principle whenever cells along a pathway die the space can be filled with similar cells but functionality is only marginally restored (0-5%). To make matters worse, as @Vinnitus put it; cells with the wrong functionality could connect and mess up the system.
Human hearing is still the best stereo audio system we know off, but it's not good enough to repair itself after it has been damaged. Fibers do not connect or disconnect on their own, they can die (disconnect), or sprout toward a chemical compound (neural growth factor) and find a connection. The problem is apparently that many new cells have a total lack of any functionality and serve as nothing more than structural reinforcement. This is because they lack the chemical instructions that are available at the formation of the auditory system (i.e birth)

I agree with this statement. Tinnitus is a closely linked to your hearing threshold, when you lower that your tinnitus will become inaudible. I believe the survey we analyzed here showed a slight loss in tinnitus as people aged as well.

 

@Cityjohn Thanks for the explanation.

So al these instructions are stored in our DNA?
DNA is also used when ( as an example) birds inner ears regenerate.
Mapping this process is what Stanford is doing?

 

Ah, but it can! The brain is far more powerful than any computer. True, it cannot restore lost data but it is amazing how much speech information is transmitted to the brain through a damaged ear, albeit in a distorted form. The brain can be trained to 'denoise' this signal and recover intelligible speech information that was previously lost 'in the noise'. (Most of) Our brains are perfectly healthy despite damage early in the auditory pathway. The trick is to leverage the immense processing power of the brain to recover these signals. Here is one example - http://www.pnas.org/content/111/25/E2606.full

 

@Cityjohn so any attempt at recconecting and regrowing cells no matter how effective will onLt result in a functionality of 0.5%?

Is this all not pretty pointless then?

 

I've read somewhere that the possible synapse therapy does not work on people who have had damage for over 24 hours. Is this true, or is this just the time it took to regenerate slight damage within a test?

 

I cannot edit my post so please forgive my double posting as I'd like to make an update and prevent anyone from going through hassle of answering my question.

According to this, at the bottom, they do not know the window length of opportunity. However, 24 hours has been confirmed to be effective. http://www.nature.com/articles/srep24907

 

I'm afraid I was not talking about the same thing. The paper you quoted doesn't claim one can improve hearing or physical signal processing. When we say noise in science (not the same as a noisy environment) usually we mean no computer no matter how powerful can ever de-noise whatever the signal is hidden in. Let me illustrate;



When you introduce a bias of two electrons into a 2D field measurement you can subtract it. When one introduces noise which is by definition random no series of action can ever remove it. When the noise is larger than the signal nothing useful can be recovered. In this case one could apply a kernel (contrast or brightness increase) to increase the contrast between the noise and the signal however when you don't have a 2D field, but just a 1D signal (auditory) you can't increase contrasts. There is no clever signal processing that could ever restore the signal.

We can train a rat or a human to "extract information from weak signals in noisy backgrounds" but the limits here are obvious. Firstly the sound must be heard in the first place and thus already above the noise levels, there is only a slight improvement (not a recovery), and "learning does not typically generalize to untrained stimuli" which means that this research is actually highlighting conditioning, not a signal processing improvement, hence it's pretty much useless.

My problem is that often I can not hear the entire sentence. I can't even hear myself breathe in a silent room because of my decently loud tinnitus. The general rule is that x/sqrt(x) is the amount of poisson noise in any signal x. If you mix a signal with some tinnitus (and it's noise) you're going to have more noise and so be less able to understand what is being said. Maybe conditioning can reduce the severity slightly by improving your 'perceptual salience', but the physical problem remains severe and the actual auditory system that is causing the problem is not being altered by the conditioning.

 

No that is what the body can manage on its own without any help.

If you would introduce a genotherapy that reprograms the cells to revert to an earlier state they would repopulate the entire system (or give you terminal brain cancer).
LLLT works by introducing a power surplus and initiating the production of neural factors that should stimulate dendritic sprouting but it hasn't been as effective in practice as we had hoped.
Stem cells also stimulate the production of neural growth factors and more over they completely replace the damaged parts with a cell in an "early" state.

There perfectly valid and logical ways, but none are being properly explored at length right now.

You can also introduce Direct Current stimulation onto the brain to reduce tinnitus which is quick, easy, and simple. The only downside is that it reduces your intelligence and I'm not willing to give that up.

 

Figure 4c shows that recognition of words in noise increases after training. Thanks anyway for the math lesson.

 

Nerve regeneration related articles.

https://www.sciencedaily.com/releases/2016/10/161007084632.htm

https://www.sciencedaily.com/releases/2016/11/161114105712.htm

https://www.sciencedaily.com/releases/2016/04/160420151828.htm

https://www.sciencedaily.com/releases/2016/06/160629095603.htm

https://www.sciencedaily.com/releases/2016/09/160916132053.htm

https://www.sciencedaily.com/releases/2016/10/161004085256.htm

https://www.sciencedaily.com/releases/2015/05/150521120919.htm

Judging from these links alone, I think the ribbon synapse issue is much more likely to be dealt with by science sooner than haircell regeneration, which is already close to being addressed. The question that needs answering is whether or not treatment can be given after significant time is passed. However, based on what I have seen, that seems plausible. Neurogenesis is an amazing science.

 

Well it was meant as a public respons, but you're welcome

4c shows words comprehension in lower SNR, but nowhere near low enough to be lost in noise to the extent of losing the data. You had stated:

however, 'lost in the noise' means unrecoverable per definition.

Regardless of semantics; using the brain to battle tinnitus and loss of hearing is like trying to reprogram the brain to deconvolve an image with a custom kernel for the purposes of curing lens related eyesight problems. Regrowing the central nervous system seems easier.

 

www.youtube.com/watch?v=IOb5ic9oOmg
I watched this and found this really interesting.
Somebody on this forum place this link, but I could not find which thread it was any-more.
Anyway, it is all about hidden hearing loss and neurotrophins.
Professor O' Leary explains it very good, I think.

 

I'm not sure you got that one right... My hearing threshold at 6000Hz is 60dB and I can tell you my 6000Hz tinnitus is louder than ever.
No study has found a link between hearing thresholds and severity of tinnitus.

 

Hehe good catch But I was refering the situation wherin one lowers the action potentials of all neurons at the same time everywhere in the auditory system, thereby reducing tinnitus (and all other brain or auditory activity). The problem with that is that you also lose more hearing.
Say you have a 60db threshold, and you did something like direct current stimulation, it would increase your hearing threshold even further, but also increase your tinnitus hearing threshold. However DC brain devices also reduce working memory and alertness, and are not yet tested properly.

My point here was that it's impossible to reduce the perceived level of tinnitus unless you reduce the level of perception, and that this would reduce the level of perception in the entire auditory system, also affecting hearing. (and perhaps even balance)

 

Watched the entire thing with great interest. How lucky we are; the synapses do not seem to grow back to the IHC in the case of a noise incident as apparently the IHC is affected in some way as well. In excitotoxicity due to chemicals however, the synapses seem to be able to regenerate and reconnect to the IHC.

It seems there really appears to be a difference in the way the damage came to be.

 

This isn't entirely true. Tinnitus (it's more and more looking like) is a dysfunction in the peripheral nervous system / auditory cortex and has a very different mechanism than what drives actual hearing. If the current model of errant signals to the brain continues to hold, turning off those errant signals (though they be perceptive in nature) may have little or no effect on hearing as a whole.

This principal is what is leading research with NDMA inhibitors with companies like Auris and Novartis. Particularly noted with Keyzilen™:

 

Yes I noticed that too. Positive is that this is now known (although I believe this is still an assumption).
The contents of this video clip made so much sense to me and was so well explained.
Apparently up to 60dB is most likely outer hair cells (loss of cochlear amplifier function).
Difficulty understanding people in noisy surroundings could be loss of connection from inner hair cells. I think there was also the suggestion that this loss of connections to the inner hair cells could be the reason for tinnitus and hyperacusis.
I read this a lot. So this could be really what is happening.

I would already be ecstatic when my tinnitus and hyperacusis would be past tense in 5-10 years.
Than the next step is outer hair cells to improve hearing threshold

 

I just wondered.
When the connections on the inner hair-cells remove themselves because of a partly damaged inner hair cell, what happens if reconnecting attempts using neurotrophins are successful?
It would not be surprising that these new connections made, are not sustainable because of the (partly) damaged hair-cell.

 

You are right, there isn't much use in connecting a nerve terminal to an inner hair cell that is damaged or missing. The idea here is that the nerve synapses are far more vulnerable to the effects of noise than the hair cells. This has been shown in many species. In cases where threshold sensitivity is normal (i.e., hair cells are working fine) but difficulties are noted tracking speech in noise or with tinnitus, the culprit is most likely the loss of cochlear synapses and related changes within the brain itself. In this situation, it would conceivably be helpful to reconnect the nerve terminal to the base of the inner hair cell.

 

But are hair cells really working fine when treshold sensitivity is normal? The way an audiometric test measures this is way too crude. Aside from that, maybe damage is possible to hair cells while this doesn't affect the treshold sensitivity directly or at least not in the crudely measured frequencies? (One could have damaged hair cells at 1.5khz but those are never measured)

If this is not the case, then what is the reason that synapses do not reconnect to IHCs after noise damage specifically, like claimed in the video? Is this ANY noise damage or only noise damage where treshold sensitivity is affected?

 

Yeah I wonder if this is along the lines of what you mean. I figure that partially damaged haircells/neuron connections may produce false positives in hearing tests, and produce "reactive tinnitus" "distorted hearing" symtoms in sufferers. Since they produce that frequency but not correctly, this is especially relative to people that describe hearing distortion, or reactive tinnitus. For instance, my reactive tinnitus, is always at certain frequencies, it's like if a fan is running, or cars are driving by, or listening to music etc, I will not hear the sound at certain frequencies, but will instead hear a whistling/resonance/pure tone/feedback like sound at that frequency, and it is always significantly LOUDER than the source sound. What could biologically could cause this? And this is something I have heard other members of the forum say they experience as well. @VRZ78 @Tom Cnyc to name two.

 

@SilverSpiral that has thankfully stopped happening. Lately it seems I'm mostly fine or I have a hissy electric sound in my head. I still hate it.

 

@HomeoHebbian
I was just wondering if it is known what makes the nerve synapses disconnect from the hair cell?
Is it possible that the hair cell is not "healthy" any more?

How certain is this idea?
If it is possible for the hair cell to get damaged and not provide the correct proteins to the nerve synapses, reconnecting will perhaps work. But than the nerve synapse will disconnect again.
I understand it is possible for a hair cell to damage, but not die. But is that damage limited to the stereocilia only?
Is it possible that the nerve synapses disconnects because the hair cell is not able to keep the nerve synapses "fed" any more. I read that also the hair cells "feed" the synapses with neurotrophins.
Sorry for the rudimentary descriptions.

 

This is the value of research on animal models. I have seen evidence from five different types of mammals all showing that auditory nerve synapses are lost before there is any evidence of hair cell pathology. This is called synaptopathy without permanent threshold shift. Whereas we only have relatively blunt instruments in humans, we can actually scrutinize individual hair cells in animal models. Again, there is no evidence of pathology. Of course, one cannot prove the negative. There could be hair cell pathology that we have not yet detected.

But I doubt it. I'm certain that auditory nerve synapses are eliminated without any evidence of threshold shift or inner/outer hair cell pathology. The next most vulnerable cellular element is the outer hair cell. Outer hair cells are mechanical amplifiers and as soon as you lose outer hair cells you see a demonstrable increase in pure tone thresholds and otoacoustic emissions. So, thresholds are terrible for lots of reasons but they are a reasonably sensitive marker of hair cell dysfunction. This thread originated with the paper from Maison and Liberman. They are on their way towards developing an objective test for synaptopathy.

As for your last point about not measuring responses at cochlear frequencies positioned between the test frequencies (at least I think that is what you were driving at), that's not the case. A tone will cause a region of the basilar membrane to vibrate, not a point. The size of this region depends on the sound level (and other factors). At high sound levels, a tone will activate the corresponding region of the basilar membrane but also regions around it, which would include frequencies between those used during the audiogram. So, it does test the health of intervening regions of the cochlea even though it samples at discrete points. Hope that makes sense.

 

We aren't exactly sure why the nerve terminal pulls off the hair cell during intense noise exposure. It could be purely mechanical forces that physically separate them. It could be activity-dependent, as you suggest, wherein an inner hair cell that 'goes silent', even temporarily, will induce the nerve terminal to disconnect. Or it could be a third option wherein a hair cell undergoing metabolic stress sends out a chemical 'distress signal' that causes it to scrutinized by the cellular sanitation crew (macrophages, microglia) and it ends up getting functionally disconnected. This is a hot topic these days.

Much like a magnet, the nerve terminal will stay "stuck" on the inner hair cells unless one or more of the above factors occurs. Therefore, it is not folly to think that reconnecting the nerve terminal to the hair cell could provide a lasting fix (assuming that one limits their noise exposure thereafter).

 

And that would be possible one day ?
I don't get it, hair cells die or are just out of function (waiting for a fix) when you have visible hearing loss ?