Hidden Hearing Loss, Tinnitus and Trouble Hearing Conversations in Noise

I never envisaged that also is a possibility. Interesting. It is mechanical vibration after all that also reaches the cochlea.
That would than be instantaneous. Opposed to metabolic stress that could take some time.

I wonder if this also happens in birds.
There is hair cell regeneration in birds, but prior to hair cell damage or even hair cell death, we (mammals) have disconnecting of nerve connections. Is this the same in birds?
If so, does this ability of birds to regenerate damaged hearing includes reconnecting of lost nerve connections?
So not only hair cell regeneration, but also nerve reconnecting ability. I would imagine this is so.

Very interesting.

 

From what I've read and believe me I've read a lot,this is what I've gathered so far.

Noise damages the synapses that underly its corresponding haircell,just because these synapses are damaged doesn't necessarily mean the haircell will die as a result.Its theorised that these neurons disconnecting are what causes T and H,we can still hear the sound as the haircell is still intact but the underlying neuron that brings that impulse to the brain is now damaged and makes us sensitive to noise thus causing pain from what wouldn't normally be a painful sound.There are also noiceptors connected to these neurons and noiceptors only fire when they detect incoming damaging stimuli,they don't fire for any other reason.If someone's voice causes you pain that's the noiceptors telling you that your nerves can't handle this and that this sound is potentially harmful stimuli.The brain will try and protect itself by triggering the middle ear muscle to contract(TTTS)which it does via the facial nerve,also remember the auditory nerve is directly connected to the facial nerve.

It explains to me at least why people recover from H and why others don't.St first the nerves are damaged and then they heal thus stopping the noiceptors from having to react,the nerve is ok now and working well so it's not potentially harmful to you.
For the unlucky ones like me these nerves are still damaged and are still causing the noiceptors to react to alert me that this is potentially harmful to me.

It's also possible to lose haircells without losing the synapse,the haircell dies and glial scars form over where it use to be but the neuron is still in its terminal underneath.This to me explains why some who experience hearing loss don't get T along with it.

After haircell regeneration occurs new synapses stretch out and form connections from what I've read,also they done experiments on mice with auditory neuropathy using Stemcells and they successfully recovered upto 40% of their hearing and that was only a proof of concept study in Sheffield University.The glial scars that form after we lose hearing is actually the very thing that helps us restore hearing,the Stemcells sink into it and begin regenerating the nerves.

There's so much to it really,honestly I'd be here for hours writing about it,but all in all it is totally possible to fix hearing using Stemcells alone,we're just not there yet.I've been reading all the research papers for 12 months straight,every single day at this point lol.

 

I noticed that after my noise incident I am able to hear the little muscles in my middle ear contracting.
(Probably some fluid in the middle ear that makes sound when muscles contract. I will not hear the muscles itself).
(This is an assumption.)
When something slightly louder than average triggers these muscles I hear crackling. When, as an example, I put a plate on the sink I hear this sound of the plate hitting the surface accompanied with a short crackle in my middle ear. And I "feel" this contracting, sort of tugging my ear drum.

I read that after a traumatic noise incident it is possible that the autonomous nerve system gets stuck in high vigilant mode. Lower sound levels that normally would not activate the small muscles in the middle ear will than be activated by the autonomous nerve system. The autonomous nerve system is "stuck in fight or flight mode".
Apparently it is very difficult to get this back to normal.

I acquired hyperacusis without the pain. I wonder if this form of hyperacusis is an overloading of nerves that are still connected to the hair-cells.
It is like using a thin wire for a high current. the wire heats up. Using more wires (braids) makes it easier for the wire to "take" the current.
Also I think the distortion I hear is because of too few nerves connected to the hair-cells.
I notice this distortion when someone talks to me in normal voice. The nerves for higher volumes are not connected any more. So very low level sounds do not distort. This is exactly what I experience.

Same here. What daunts me is that researchers have been reading about this for many, many years before they even became researcher. They still tell us it is a real challenge

 

@Reinier
I think noise induced H with or without pain are exactly the same as one another.

I developed H without pain in January 2014,over two years later and I was 90% cured and back to my old self.I started getting around more noise nothing stupid mind you and the pain started shortly after that and developed from there on out.At first I thought the pain was from middle ear muscle contractions or a tight neck from tensing around sound and my doctors kinda backed me up on this.If I took a bath and relaxed or swallowed a muscle relaxer the pain would go away.The pain was like a burning stinging pain in my neck and scalp that went all the way down my back so naturally I never figured it had anything to do with my ears and was all a result of the"flight or fight response I was having.My T was the same and my sensitivity hadn't increased it was just this random pain that kept showing up and getting worse and worse before finally in January of this year it became unbearable.My ears went crazy and I'm now extremely sensitive to sound and my T has gone through the roof.My ears burn along with a stinging burning pain in my face and scalp that runs down my spine and through my body.If I sit in silence the pain slowly goes away but if I talk I can literally feel a surge through my ears and head,my T goes up with it and along comes the stinging burning pain too

I have seen people get extreme pain from sound when H hits only for it to go away with their H as it heals,I've also seen people get extreme H with no pain that never gets better and some where it does.

What I'm saying is with or without pain it's both the same,there's no difference between the two and they can both get fully healed regardless of there being pain or not.I've read so many stories of people with extremely painful H that got way better after time if not go away completely,I've read about people with no pain who never got better and others that did.Its hard to know why some experience pain and others don't but I don't believe they're separate types of H but more so just two sides of the same damage.

I like your idea of the wires,in a way that's how I picture it.Its like faulty broken wires trying to transport a message to the brain but because the connections are faulty everything is sensitive and or inaccurate hence distortion and over loudness.These connections have a lot to do but when they're damaged its a lot of work for them and of course they can't handle it hence the triggering of noiceptors to tell you to please stop,I can't handle this stimuli and it's potentially harmful.As the nerves heal they can do their job better thus stopping the noiceptors from triggering.If the nerves don't heal you'll continue to have H no matter what you do.

If these nerves can be healed or regenerated I'm absolutely certain,without a question in my mind that H and T that's noise induced will be cured or at least made much much better.I can still hear up to 17,000hz and I have no hearing loss between 0 and 10,000hz so I'm absolutely certain mine is synaptic damage.On that note I have read studies where Stemcells can successfully repair synapse damage in the body and I've also seen studies where the auditory nerve was regenerated using Stemcells.Stemcells make repairing this problem entirely plausible and possible.

 

@bill 112
Sorry to read you have been struck really bad by inner ear symptoms.
I can relate to it.
I read on the internet that a nociceptors a sensory nerve cell is.
I assume we all have the same inner ears. So we al will have nociceptors in our inner ears. Why than get these nociceptors active in some damage and not in other?
And is it related directly to damage or indirectly?
Its is getting too complicated for me.

I also read about people that improve even after 7 years!
If it is healing or brain plasticity, I wonder.
But it is encouraging.

Internet is fantastic. Al this free knowledge. If you are interested, don't have to deal with a deadline and can concentrate, that is. (I sometimes have difficulty concentrating when tinnitus is intrusive again).

 

It's fun to read all this stuff when you literally have not better to do like me,my head spins with all the crap I try to squeeze in there on a daily basis lol.

My T is variable,one second it's silent next thing it's screaming at me and considering I wear earmuffs nearly all day now it's a nightmare.
Anyway I hope with time mine calms down to a bearable level,way too much has happened since the start of the year that makes me question whether this will ever improve.

 

I know.
Tinnitus (and hyperacusis severity) controls my moods.
When my tinnitus is low I think I am almost there . Back to normal again.
When my tinnitus is high I think I will never get a normal life again .
It surprised me to learn how much this condition is able to control my life.

 

@bill 112 I'm also on board with the synapse theory. Do you think this is also why some people have good days and bad days? If T is supposed to be based on the theory of hair cell death, then if the cells are dead, wouldn't the T levels always remain the same? But if we're talking about neurons and them being hyperactive/damaged or unpredictable this would explain fluctuations in T, H, volume and even pain. I also agree it's why stem cells have the potential of working. With stem cell therapy, everyone is looking at the hair regrowth but it may actually be the neuronal repair that's making the difference.

 

Thats pretty much how I see things,for years I thought it was mainly a brain thing but this year I have completely changed my entire stance on the entire thing due to my new symptoms.

My symptoms would point at something damaged or overactive in the inner ear mainly synaptic damage or neuron damage.It explains reactive or fluctuating T and why people's T gets louder after moderate normal sounds,if the nerves are no longer connected or dead then why are they still reacting to stimuli?Why are the nerves hurting from sound if they're no longer there?Why does my T go up and down with every single sound along with accompanying pain?

I've seen where people had LLLT years after trauma only for them to see huge improvement in their symptoms,LLLT doesn't grow new cells so what exactly is happening then?Looks to me like it's repairing damaged cells or neurons that are very much still alive but heavily damaged.This is why I see SC's as a viable option,I may not be right in Whst I'm saying but it's the theory I'm sticking with for now as it makes the most sense to me.

 

The most plausible explanation for why T severity bobs up and down relates to changes in the physiology and chemistry in your brain, not changes in the ear. The consensus view is the brain is dynamically changing the amount of gain (i.e., amplification) that is is imposing on the reduced signal arriving from the damaged cochlea and nerve. Too little gain, neurons within the central pathway become hypoactive. Adding more gain allows neurons to compensate for the loss of input from the ear and reach their activity set points. This comes at a cost. With the gain up too high, neural circuit operations become hyper-synchronized and unstable. We hear tinnitus.

Going back to the root of this thread, a loss of cochlear nerve synapses reduces the earliest wave of the sound evoked potential. This is the report from the Liberman & Maison paper that started this thread. Paradoxically, a loss of wave 1 amplitude is associated with an enhanced amplitude of later waves.
Brainstem auditory evoked potentials suggest a role for the ventral cochlear nucleus in tinnitus. Gu JW, Herrmann BS, Levine RA, Melcher JR. J Assoc Res Otolaryngol. 2012 Dec;13(6):819-33.

The loss of early input is over-compensated by hyper synchronized, hyperactive responses in the brain. This central gain is adjusted up and down. The input from your ear is just down (without interventions, at least). It's the physiology and chemistry of your brain that causes the day-to-day fluctuations.

 

What is your view on TRT ? Do you think listening to broadband noise and sound enrichment at night would help the brain to better know the damages in the ear and therefore adjust the gain in the correct way which would in the end reduce T and H?

 

Can we than conclude "repairing" this wave 1 output has a high probability to reduce tinnitus (or even better)?

What I do not yet understand is the influence of the cochlear amplification function.
My hearing threshold is up. So I could conclude outer hair cells partly are not working any-more. On top of that there appears to be loss of synapses to the inner hair cells. (tinnitus and distortion at levels 70 dB and higher ). That is my situation at the moment.

Before my noise incident I had a slightly elevated haring threshold (40 dB at 4 kHz). But I experience tinnitus and distortion.
But in that situation the wave1 should also have been lower than original.
Why than did I not have tinnitus?
Could it be that tinnitus especially develops when connections on inner hair-cells are damaged?

 

No, not really. Putting more sound into the ear (i.e., masking noise) allows the brain to turn down it's gain somewhat and disrupts the hyper synchronized volleys of spontaneous electrical events that likely cause the phantom percept. But it is most effective while the sound is on, or for short intervals after it is turned off. In fact, it can make tinnitus worse because 1) even low sound levels, when presented constantly for a very long time (i.e., days) can exacerbate cochlear synapse loss, 2) work in animals shows that passive sound exposure to narrowband sound can decrease GABA tone in the cortex. You really really really don't want to decrease GABA tone any further if you have tinnitus. 3) suddenly removing the constant sound can lead to large fluctuations in central gain (like a car fishtailing on an icy road).

I think there are ways to "reprogram" the central amplifier and decrease tinnitus severity even if the input from the ear and cochlear nerve remain depressed. But there is no proof of it yet. It's something we are working on in my laboratory. The most effective way to tap into the plasticity of the adult brain is to engage neuromodulatory systems (e.g., dopamine, acetylcholine, noradrenaline, oxytocin, serotonin etc.), either by stimulating certain peripheral nerve afferents directly (e.g., vagus nerve), neuromodulatory brain centers directly, or, better yet, by recruiting their natural activation through structured training/learning paradigms. Passively listening to sound does not engage these neuromodulatory system. Without them, there is little hope for driving lasting, positive plasticity in the adult brain.

 

So everyday noises at low volume can increase synaptic degeneration?

 

Yes, it would be logical to conclude that restoring a normal wave 1 amplitude would lead to a lasting decrease in tinnitus severity. Easier said than done. Certainly, this is the focus of many biotech companies like Decibel. It is interesting to consider whether wave 1 amplitudes can be recovered by a clever hearing aid programming algorithm. Most hearing aids are programmed without any consideration of wave 1 amplitudes. Most audiologists don't measure ABR or Eletrocochleography at all. If they do, they only measure threshold and don't consider using this signal as feedback to program their hearing aids. They say amplitudes are too noisy to make meaningful measurements but the Liberman & Maison paper (and others) shows they were wrong about this, just as they have been wrong and short-sighted about so many issues related to hearing health. ...but that's a different rant for a different thread.

Everyone with cochlear synapse loss and/or outer hair cell loss presumably has a reduced wave 1 amplitude. But not everyone with a reduced wave 1 amplitude has tinnitus. That is because tinnitus does not arise directly from the cochlea, but rather from how the brain interprets the reduced signal from the cochlea. Presumably, the gain control in your brain was able to offset the cochlear loss with your threshold shift without causing tinnitus. The subsequent noise exposure drove intense activity throughout the auditory pathway followed by a sudden, sustained drop was additional cochlear synapses were loss. This added insult may have caused your central amplifiers to go haywire. This is one of many explanations, so don't put too much stock in it. I was just trying to explain why you had a threshold shift without tinnitus before your subsequent noise exposure.

 

In mice, yes. Maison, Liberman and colleagues exposed adult mice to an octave wide band of noise at a very moderate sound level (just 84 dB SPL). But they did it for a week straight. They found wave 1 amplitude loss and inner hair cell cochlear synapse loss. Look at Fig. 7 and 8 of this paper. It's the Exposure Alone group. The other groups have damage to their efferent cochlear feedback, which is not directly relevant to your question.

Efferent feedback minimizes cochlear neuropathy from moderate noise exposure.
Maison SF, Usubuchi H, Liberman MC. J Neurosci. 2013 Mar 27;33(13):5542-52.

 

Interesting read,thank you for that.

So this raises a question,if these noise levels can damage these nerves after damage has already occurred,does that mean that a H patient will slowly but surely progress downward from even moderate sound exposures over time?It seems to be the case with a lot of H sufferers that I've spoken to,that they've slowly but surely gotton worse and worse from small noise exposures over time which would correlate with Libermanns findings.This year alone I have progressed down hill from the smallest of noises,like someone laughing suddenly or something hard being dropped etc.

It's basically a neuro degenerative condition,that it slowly progresses once it's been set in motion?The more noise these damaged nerves are put through the more they will continue to degenerate?They can no longer handle noise like they could pre trauma thus the roof for noise is now significantly lower than before making them much more susceptible to damage,nerves that could once handle 85db all day long before damage may occur can now only handle let's say 60db for 40 minutes before damage occurs.

Or am I picking this up completely wrong?

 

That is the implication, yes. You can count on your ears degenerating as you age, even if you are very careful about not exposing yourself to noise. Age-related hair cell loss is slow but synapse loss will begin earlier. If you damage the synapses through noise exposure it will hasten their age-dependent demise and perhaps even increase their susceptibility towards additional acoustic insult. This is true in mice, with supporting evidence in other species as well. This paper lays it out and others have followed.
Acceleration of age-related hearing loss by early noise exposure: evidence of a misspent youth.
Kujawa SG, Liberman MC. J Neurosci. 2006 Feb 15;26(7):2115-23.

 

@Sen

 

@HomeoHebbian Thanks for taking time to answer questions.
I think it is quite an opportunity to have someone on this forum so knowledgeable and willing to put energy and time in answering questions.
I follow this thread with interest.
It increased my (very basic) understanding of hearing processes considerably.
Some good news (researchers finding out a lot about hearing lately). Sometimes not good news (NIHL renders the cochlea even more susceptible for "wear and tear").
I do hope plenty good news will come from Massachusetts (Liberman and researchers) in 2017.

 

I feel like our generation is screwed when I read things like that. There are so much things going on in the cochlea (and the brain of course)...

It's "funny" because sometimes, when I have to explain quickly what I have, I say that my ears suffer from a degenerative condition. And now I read that that's what it is.

Anyway, thank you for your contribution @HomeoHebbian.

 

Does this mean we are all screwed and there is nothing we can do about it except never leaving home?

Seems like trying to live my old live minus clubs, bars, headphones and parties might still not be enough lol.

Quite depressing, really.

 

These have been my thoughts too for quite a while. But that doesn't explain how you could recover from H the first time around. It also doesn't explain why some people can recover from the use of LLLT, TRT and other sound therapies, different medications etc.

 

What we learn from HomeoHobbian is actually huge. We can put a name and some facts on our condition, we can understand better why it gets worse if it gets worse. My H is not under control at all and I can see why more clearly now. It's depressing but at least I know I'm not crazy, this is a real condition.

But I was hoping some sort of treatment would be possible in the next few years, which doesn't sound very realistic now...

 

My ears went through a period a few months ago where they got extremely irritated around noise, everything was slightly muffled sounding etc. Now they are back to "normal" ie not irritation/hyperacusis flare ups in everyday life and it actually doesn't feel like there is anything wrong with my ears. But tbh I am very wary about anything setting them off again.

Especially at this time of year what with Xmas parties etc. Even my parents aren't greatly understanding about it - e.g. I often have to ask them to turn down the volume slightly on the car radio and they get annoyed at me etc, same with the TV. Like I'm not doing this to be difficult I don't want to be this way either.

As for a cure/effective treatment, it can be hard to stay optimistic. My knowledge is v rudimentary compared to many on here but I'm still hopeful. It was about 30 years ago that scientists discovered that birds regenerate their hearing and there has obviously been a lot of progress since then. Another 30 years from now and who knows? Being 20 years old with this sucks because you're so young but then on the other hand, it makes me hopeful about the treatment options that could be available within my lifetime.

 

Maybe their hearing just recovered with only minimal damage,nearly undetectable by themselves.

That the ears need a long time to recover from the initial sound trauma and that slowly over time the nerves in the ear become less inflamed from the insult.This recovery varies from person to person,one might recover 90% whilst the next might recover only 10%.
If we were to stab a nerve in 20 people every one of them would recover to varying degrees,one persons nerve might repair fully whilst the others simply don't.

I think TRT is useful for phonophobia after a noise trauma,it lets people realise what their ears can handle and that these volumes aren't hurting them so they become less and less anxious thus it is hailed as a miracle treatment.

With TRT for H I believe it's applied along side whatever natural recovery is happening,if the persons nerves make a full recovery then its attributed to TRT when it wasn't actually TRT at all,as this paper shows playing noise like that into your ears can actually exasperate the problem and further degrade the nerves if the trauma that instigated the H was bad enough.If someone's trauma wasn't that bad and the ears are going to recover this noise won't worsen them,the damage was minimal and they are going to recover great regardless of this noxious noise being played into their ears.If TRT doesn't work then it's your fault according to them but this paper kinda proves that it very much isn't their fault,their trauma was more than say the guy that fully recovers with TRT and thus it can't possibly help them,if anything it's worsening the condition and haulting any further healing that was going to happen.Like I said above,nerve damage and it's recovery will vary from person to person,no two people will be the same,so applying the same set of TRT rules to everybody is absolute insanity.

After recovery has hit its peak susceptibility will always remain,just how susceptible you are all depends on how well the nerve recovered from the trauma that caused the whole thing in the first place.

If you look at Adams story on YouTube,his ears recovered after ten months,he done TRT alongside it and of course credited that to his recovery,but I quarantee you it was just natural healing and all TRT did was remove his fear of noise in the way I posted above.He still has tinnitus so that means permanent damage was done but yet he still follows the same rules as a healthy hearing individual,85db for 8 hours is ok and that our ears aren't anymore susceptible etc.As we know from that study into Tinnitus patients,nearly all T patients LDLS are less than someone without T but this lack of sound tolerance simply isn't noticeable by the patient,that is until it becomes worse from more noise that the ears"should"not get damaged by.

We have no idea what a damaged ear can now take and applying the same rules as before is wrong,this paper shows that they can indeed be damaged by less volume than they were before the trauma.

As for LLLT it makes more sense why it would help,according to posts of studies on the H research page a noise trauma to these nerves instigates an inflammatory response in the cells,the inflammation causes these cells to degenerate and how much they degenerate all depends on how bad the response is.Even after recovery has occurred that susceptibility still remains,if someone experiences hot burning pain from a car horn that's the nerves getting inflamed by the noise,keep doing this and the nerves will continue to degenerate.
They reckon that LLLT reduces inflammation and that's why I believe it can actually help H.

Wanna know something funny?
Last year if I heard a sharp sound my ear would go hot and stuffy,my audiologist assured me it was the muscle in my inner ear causing it and not to worry,that once I had desensitised my nervous system that this would stop.I was then put on strong anti-inflammatories for an arm injury and I remember getting hit by a sharp noise and there was zero stuffiness,zero ear pain absolutely nothing came after the insult where it most certainly would have come normally.

People ask for proof?Where is Jastrebroffs proof?There isn't any it's just a good theory that gives people hope that this condition isn't permanent and that it's just their brain causing all this,once they calm their nervous system down they will be back to their old selves again.
But he has zero proof,I ask these people for actual proof that it's the flight or fight response and they can never really give that to me,I'm yet to see any hardcore definitive proof in his theory.

How can these people argue with this paper?And these studies?Its proof set right down in front of them but they refuse to acknowledge it,they don't want to hear it and would rather talk about your anxiety.

 

Yet one would say that if the issue is of such magnitude, fragility, permanence and ever-deteriorating nature as proposed here, everybody would at least suffer from it to some degree. We are all exposed to loud sounds on a daily basis, making auditory damage an inevitable fact of life apart from any damage inflicted by ageing alone. Even then, the misunderstanding of our condition by others is so widespread, it doesn't make sense to believe this problem is so great as portrayed in statistics. It kind of doesn't add up.

Almost everywhere I mention Tinnitus or Hyperacusis, I get presented with misunderstanding facial expressions or behaviour which makes clear I'm not taken seriously. They mention my condition is probably "annoying" (thats put lightly in my opinion), but no one seems to suffer from it. This is even so while being around "outgoing" people exposed to a whole lot more noise than the average person. It is almost like living in some kind of alternate reality with this condition. I can understand the isolation and desperation T&H sufferers might feel. It makes me question the reliability of the statistics sometimes.

 

Yeah, I agree with a lot of things you said. Seems logical to me alas the TRT school of thought more and more comes off as Jastrebroff's and Hazel's wild ramblings. There are some research suggesting that H pain might be because of inflammation. If this is the case, would it be easier to treat than tinnitus and hearing loss?

http://hearinghealthfoundation.org/blog?blogid=246
http://hyperacusisresearch.org/an-md-summary-of-the-2016-aro-hyperacusis-symposium/

 

And then what about this guy, who said after sound exposure, his symptoms worsened for years, and then as far as i can gather from his description in the article, made a complete recovery around 10 years after his onset? http://www.irishtimes.com/news/health/my-life-was-a-war-against-noise-1.517024

 

Thanks @Foncky and @Reinier . I'm learning a lot from everyone in this community as well. It's really a 2-way street. My end of the 2016 outlook is as follows:

Long-term developments (5-15 years) - It is hugely encouraging that so many reputable, well-funded biotech companies are working on hearing. I think that we will see exciting new drugs for 1) hearing protection (i.e., squirt this behind your ear drum before going into battle), 2) gene therapy for certain forms of congenital deafness, 3) inner-ear repair immediately following damage. I am skeptical that we will be able to repair/rebuild/rejuvenate an inner ear with age-related decline or chronic sensorineural hearing loss. At this point, medicine has not been able to achieve this high bar with any organ system. You can bet that the inner ear will not lead the charge as it is so small, intricate and inaccessible. It makes me sad and frustrated when I read about people lining up to have stem cells or inner ear therapies from various quacks promising the impossible. Believe me, nothing would make me happier than news from a reputable source that stem cells etc. could rebuilt the auditory nerve or inner ear. This just seems implausible to me.

Short-term development (1-5 years) - I'm actually optimistic that we'll make good headway on new types of tinnitus relief in the near term. We haven't even scratched the tip of the iceberg with possible brain-based therapies. The interesting thing is that - with the exception of Mike Kilgard (MicroTransponder) and a few others - there have been exceedingly few tinnitus interventions made available from people who actually understand brain plasticity. Tinnitus is an outcome of brain plasticity gone awry. I have the utmost respect for engineers, acousticians, and ENT docs, but their expertise just isn't terribly helpful for understanding the root causes of tinnitus in the brain. I think we've had enough maskers, electrical/optical stimulation regimens, and passive listening "therapies" to prove this point. True, a few people do benefit from these (and, for the most part, there is little harm in trying). But the benefits are modest, to be charitable, and most people are just wasting their time.
As neuroscientists with backgrounds in brain plasticity get interested in tinnitus, I think we will see a new class of therapies creep into research journals and - eventually - the marketplace that combine immersive auditory training with drug therapies and brain stimulation. In fact, this is something we are working on in my laboratory. We haven't published our biggest findings yet, but I am sitting on a manuscript that describes improved perception of speech in noise for older, hearing aid users through training in an immersive "action audio game" that we programmed. These kinds of therapies are used routinely to treat central visual impairments like amblyopia but the auditory field has been slow to pick up on this. I don't have anything definitive to share with this community on tinnitus at this time, but we are actively working on this and have had some encouraging early results for speech in noise processing and tinnitus relief.
Hopeful eyes for near-term tinnitus relief should be focused on brain-based therapies, not cellular repair of chronically damaged ears. Sadly, there really isn't a thread for research on brain-based therapies, because a definitive paper has yet to be published. That means there is lots for us to do in 2017. We'll be working hard to develop objective biomarkers of tinnitus and then start clinical trials for brain-based interventions. In the meantime, I'm very glad to be able to log in to TT and learn from all of you (even if I play the role of wet blanket most of the time).