Hidden Hearing Loss, Tinnitus and Trouble Hearing Conversations in Noise

Maison and Liberman recently published an interesting paper on hidden hearing loss in humans (not mice). http://dx.doi.org/10.1371/journal.pone.0162726

Additional press coverage here (and many other places too)
http://www.wsj.com/articles/cant-hear-in-noisy-places-its-a-real-medical-condition-1474909624

It has been made clear in a variety of animal models that synapses of the auditory nerve, not hair cells, are the most vulnerable elements in the ear to the effects of environmental noise exposure. Damage to nerve fibers isn't detected by standard hearing tests and thus this type of damage is said to "hide" behind an otherwise normal audiological report. This has been published and discussed already. The trouble has been finding an objective test in humans that is sensitive to this hidden nerve damage and might explain why people with normal thresholds struggle to follow conversations in noisy background conditions (and also explains why they might have tinnitus).

This paper identifies such a measurement, the AP:SP ratio, that correlates with difficulty understanding words in noise in young musicians that are at substantial risk to develop tinnitus and hyperacusis despite their normal thresholds. This measure comes from the very first bumps on the auditory brainstem response. The SP is the summating potential and is thought to be generated by electrical current in the hair cell. The AP is the action potential, the volley of electrical activity that goes through your auditory nerve en route to the brain. In people that struggle to hear speech in noise, ratio of the SP:AP amplitudes is closer to 1.0 (equivalent).

There are a few important ramifications: 1) The standards for "safe" noise exposure levels are probably way off because they are based on a test of hair cell integrity, not nerve fiber loss. 2) Audiologists better should find a way to measure the thing that relates to people's primary complaints, difficulty hearing speech in noise and tinnitus. Maybe this is it. 3) The SP:AP ratio might be a better predictor of tinnitus (and tinnitus relief) than other measures.

Thought you might like to know about this. The paper has some caveats and shortcomings too and I would be happy to describe it's limitations as well if that would be useful.

BUT I also have a question for those of you with tinnitus who are still reading this long post: what is your experience tracking conversations in noise? Is it particularly difficult for you? Did it get worse around the time that your tinnitus became more invasive? I know that was true for me. I think they are closely connected...

 

I have been saying for some time that the OSHA PEL levels for noise exposure are too high. Mostly basing on Lieberman's earlier work on mice. Still, most ENTs and audiologists swear by them as the gold standard for what is safe.

Would an ABR show this nerve degeneration? I had one done, but because of my hyperacusis they could not get a good wave I. Still, with no apparent wave I they deemed it good.

As far as tracking conversations in noise, yes it is harder now. Before my acoustic trauma I was able to pick up conversations from across a noisy room.

 

I deem it useful!

Regarding your question, yes I experienced the described difficulties as soon as my T set on. The moment I got my 'perfectly fine' audiogram I knew something was wrong with what we perceive as 'safe'.

In fact, if you think about it. As soon as you take away everything that is 'man-made', you can't find any regular happening situation wherein we, as humans, would be exposed to 85 dB+ for a prolonged time (8 hours +). The likelihood of such a situation decreases as the dB amount hypothesis rises. Thus, evolutionary speaking, it is not natural for us to be in loud surroundings.

Side note, if we take a look at the species that can regenerate hearing (eg. bird and fish species). We can presume that, again evolutionary speaking, they need a regenerative hearing.
Fish live in water, and as physics teach us, sound 'travels' louder underwater. So they would be exposed far more often and not for a prolonged time (except for rapid-current fish) to sound levels that reach a lot higher dB level.
Birds on the other hand, fly a lot and if we look at them in an evolutionary way, they always did. It is established that the mere sound of wind (eg. on a motorcycle) can damage our hearing A LOT. So birds are exposed for prolonged times to fairly high sound levels generated by the wind.

But that's just me, wondering why birds and fish regenerate hearing. It is 'interesting' (or rather frustrating) to see that all the research regarding 'hearing regeneration in birds and fish' focuses solely on the regeneration of the hair cells. This while we know that 1. the synapses connect the hair cells to the auditory nerve 2. it is likely that the synapses take a lot more and faster damage than the hair cells 3. hair cells without their connection to the auditory nerve are like an unplugged coffee machine, they are there and you can signal them, but they do shit (generally speaking that is). I think it is established that viable synapses are a conditio sine qua non (vital) to the working of the hair cells. Also, I find it not hard to believe that it works like this in birds and fish. So, why on earth would a bird regenerate its hair cells without regenerating the synapses in some kind of way? It wouldn't.

Even if they find a way of regenerating hair cells, it will help only as much as there are viable synapses left. And if synapses truly 'die' before hair cells, then there will be not much left.

Concluding, I think they should prioritize some of the research to synapse regeneration and preservation or allocate funds to 'liaison-research' between synapse and hair cell regeneration research.

 

I have experienced Tinnitus first andafter developing hyperacusis my hearing in noise abilities worsened significantly.

 

Good question. Yes, they use the ABR to identify a pathology "hiding" behind a normal threshold audiogram. BUT, no surprise here, you have to look at the ABR in a different way than the current audiology standards. When Audiologists (or neurologists) measure your ABR they are just looking at the lowest sound level that can produce the characteristic bumps in the electrical recording. Thresholds don't pick up this kind of injury. You have to look at the wave amplitudes. Conventional wisdom is that wave amplitudes are too 'noisy' to provide any useful information. This study says otherwise. They find that the ratio of amplitudes of the earliest waves in the ABR are significantly correlated with your ability to correctly recognize a word in noise.

 

Well, be sure to keep your eye on Decibel Therapeutics then. They are probably developing compounds to increase cochlear synapse repair. But that years and years away, best case scenario. I myself am more interested in how the immense processing power of the brain can be trained to improve its ability to identify words that were previously buried in noise and to turn down central gain to reduce the severity of tinnitus and hyperacusis. I have my fingers crossed for a cellular inner ear therapy down the road, but if you are looking for a realizable solution in the here and now I think your attention might be better focused on brain-based therapies that are just beginning to come into focus.

 

Like VNS ?
Do you think virtual reality could be useful if the right games are developped ?

 

Since the beginning of tinnitus (mild), barely manageable when normal speech in noise but far from before tinnitus, and huge difficulties with speech in noise when there is noise + reverberation like factories, under the rain etc , and much less punch and sparkle when listening to music, all of this came immediately after tinnitus appeared, even at this quiet low amount of damage it is very debilitating so I can a very little bit imagine the nightmare for moderate and severe case

 

Don't you guys think that this discovery plays a part too?

Link: http://www.hopkinsmedicine.org/news...y_new_contributor_to_age_related_hearing_loss

That those considered to have "age-related hearing loss", could quite possibly be experiencing the same thing as what is now deemed "hidden hearing loss"? So if synapses were to be repaired, there is a difference in the two nerve fibers belonging to our auditory processing system. Could these lost out-going nerve fibers be causing tinnitus? And the many in-going nerve fibers that take their place be causing the change in hearing threshold?

I don't see just regenerating nerve fibers as restoring better hearing. There needs to be a balance between the two opposite functioning nerve fibers/spiral ganglion neurons.

 

Yes, I do. That is something that we are working on (audio training in virtual reality). Vagus nerve stimulation is powerful, no doubt. I think the challenge will be to make it precise and lasting. Stimulating the vagus nerve is a more direct but less precise way to activate the same neuromodulatory brain area that we are targeting with our immersive software training games.

 

That's interesting. There are four kinds of nerve fibers in the cochlear nerve: Type I afferent, Type II afferent, MOC efferent and LOC efferent. Very early in development, the MOC efferents sit on the inner hair cell but then get bumped over to the outer hair cells once the Type-I fibers take their position on the inner hair cell. When the Type-I fibers are damaged through noise trauma etc., the MOC efferents creep back towards the inner hair cell. As this paper says, they shut down signaling so it really is adding insult injury: losing the Type-I cochlear nerve synapses invites the MOC fibers back and they shut down the signal from the ear to the brain even further. Thanks for bringing this article to my attention. I know the authors (they do excellent work), but this paper escaped my notice.

 

Thank you for giving me a much more detailed explanation of the nerves involved in our auditory processing system. The Johns Hopkins article gives a very simple explanation and I've been wanting to understand what is really involved. What are the MOC efferent and LOC efferent? If I'm correct, the efferent nerves extend from the hair cell towards the brain and the afferent nerve come directly from the brain towards the hair cells?

I know this is somewhat off topic, but I came across this article yesterday talking about the auditory cortex and the amygdala. Link: http://www.news-medical.net/news/20...between-the-auditory-cortex-and-amygdala.aspx

To go along with the link, my brain processes sound is a very odd way now. I've pushed through depression without taking antidepressants, but a holistic route instead. I've pushed and I'm still pushing through severe anhedonia. But the way my brain hears sound is almost too "logical". I'm associating the depression/anhedonia with how my brain now processes noise. Take your average rock/indie/alternative song. I can hear the drums, the guitars, the bass, the vocals.....but I hear them as if I was standing in a room while they were being recorded next to me. Or in other words, I hear them as if I were the microphone picking them up. The high frequencies sound very distorted too. Especially vocals from music.

From that, what I've been wondering is if I've lost all of a certain type of nerve fiber. I'm still hearing a good bit of the frequency range, but the rich quality is completely gone. So if my brain is still processing noise, then a certain of type or nerves are still attached. Except there has to be one or even types missing.

I've been on the hunt to learn more about how I felt such strong emotions from my hearing before my incidents and ringing.

 

Let me make sure I am understanding this right, because I think it may be relevant to my case.

For over a year now I've been noticing that my hearing feels muffled, that music doesn't sound as crisp, and in particular I've had trouble hearing people over conversation more than what I remember being normal. However, on multiple hearing tests I was told that my hearing was great. I have no other problems that could cause this muffled sound (everything is "clinically" normal with me). And for the past few months, I've had tinnitus, which is progressively getting worse.

This research is saying that standard hearing tests aren't entirely accurate in measuring hearing loss, because they don't measure damage to nerve fibers? Why is it that they don't measure damage to nerve fibers, and what sort of hearing test that did measure this damage could be administered? Is there any way for me to take such a test so I have a clearer sense of what my condition is?

 

hopkinsmedicine.org/news/media/releases/found_a_likely_new_contributor_to_age_related_hearing_loss

It is always good news that there is better understanding of the inner ear. So it is good to know that new connection form.
Quote: "We don’t know why the new connections form, but it might be as simple as a lack of competition for space once the outgoing nerve cells have retracted.” End quote

And than there is research from Maison and Liberman suggesting regenerating/repairing lost connections could improve hearing. (the hidden hearing loss).

Are these two research findings not "clashing"?
Simply said: In order for regenerating/repairing lost synapses do you need to "remove" the new formed connections?
The newly formed connections appear to be "counter productive".
I just wonder: If these findings from hopkinsmedicine are correct, will it make regenerating much more difficult?

 

Yes, you are understanding the situation correctly. The "gold standard" test of hearing measures the faintest sounds you can detect. This is called an audiogram. It is sensitive to hair cell damage. Various government agencies use the audiogram to determine the safe acceptable noise exposure levels. A given exposure intensity x time is judged safe or not based on whether it causes a permanent shift in the audiogram. Now we know that nerve the nerve fibers that connect the brain and the ear are most sensitive to the effects of noise than hair cells. The audiogram doesn't directly measure the health of nerve fibers and, by extension, exposures deemed safe are not based on the must delicate parts of the ear. When you lose nerve fibers without losing hair cells, your sensitivity to faint sounds is not necessarily affected but your ability to track conversations in noise may suffer and tinnitus can occur. In this way the damage is said to be "hiding" behind a normal audiogram.

There are no established tests for auditory nerve fiber damage. Hearing scientists like MC Liberman, C Plack and others are hard are work on developing these tests. Even so, many audiologists are slow/reluctant to incorporate this knowledge into their clinical practice. Government safety agencies haven't seemed to take notice yet (at least not to my knowledge).

We (hearing scientists) are working hard to secure government funding to build the tests. It's a very hot research area. We can only hope that clinicians will take the necessary steps to perform these tests. Many audiologists are "old school" and consider pathology that lies after hair cell transduction (i.e., anything to do with nerves or neurons) to be an issue for neurologists to deal with. I sincerely hope that a few forward-thinking audiologists are thinking about how they can advance their practice to address this growing need.

 

Thanks for recommending the paper. I'll give that a look. Just to clarify, efferent nerves carry signals from the brain to the ear. Afferent nerves carry signals from the ear to the brain. There are two kinds of afferents (Type-I and Type-II) and two kinds of efferents (MOC and LOC). MOCs protect the ear from damage and sharpen cochlear frequency tuning. LOCs are poorly understood but seem to adjust gain on the Type-I afferents. Type-I afferent convey the bulk of acoustic signals from the ear to the brain and are the primary concern for issues related to tinnitus and hidden hearing loss. Type-II are basically pain fibers and are only activated by very intense noise. Some think there is a connection between Type-II fibers and hyperacusis.

 

Good points. We don't really know. There is likely a chemical signals that keeps them away from the inner hair cell as long as the Type-I fibers are in their normal place. When the Type-I fibers are stripped off the inner hair cell tt could take days, weeks, even months before the MOC fibers creep back towards the inner hair cell. If you apply NT-3 it is really anyone's guess as to what would happen. It could very well increase the number of MOC terminals (NT-3 doesn't select for fiber type) and make matters worse. It could bring the surviving Type-I fibers back into position and the MOCs could slink back to the other side of the cochlear tunnel where they belong. At this point, they have only published findings from NT-3 applications that occur immediately following noise exposure, before the MOCs have shifted over. Repairing Type-I cochlear synapses with NT-3 is going to be much harder with every day that passes after the injury. These questions are being pursued by just a few labs across the world because the ear is a very complicated, specialized system. Hence, progress is slow.

 

This is happening to me. May you explain more? While listening to music, I can hear my tinnitus. Nothing can mask my T.

 

Thanks again for explaining the auditory nerve in a more sophistaced matter. I've understood that glutamate is involved with the Type-1 Afferents. Glutamate seems to cause subjects' ringing to "spike". I've read about users on here eating food containing MSG and having their ringing become much louder. But then, you also have coffee which has spiked the ringing for some and has lowered the ringing for others.

What I really want to understand is are there other chemicals involved in the auditory system like acetylcholine or dopamine. I feel like the auditory cortex being involved with the amygdala would support that question.

 

Are you in the field of audiology (hearing scientist)?

 

Could one develop tinnitus by straining to hear voices in a somewhat loud environment that would be otherwise non-damaging? For example, if I was in the weight room with music playing and I was straining to hear what people were saying, could that straining to hear in itself be damaging? Or is the causal relationship reversed: you only developed the strained hearing in loud environments because your hearing has already been damaged, and the strain in itself cannot cause any further damage?

 

Now I wonder if it could be an advantage if haircells are not there any more. So the audiogram indicates loss of hair cells could be an advantage for restoring hearing?
Perhaps "easier" to fix than the hidden hearing loss, where according to Hopkinsmedicine research new counter-productive connections are made.

Quote: "Fuchs and his team say there may be ways of preventing the incoming nerve cells from forming new connections with inner hair cells, a technique that could help maintain normal hearing through old age." End quote.
So this is perhaps a silly thought from me. No hair cells no connections. I suppose the new connection are still made to remaining haircells anyway. Just not to non existing haircells.


In the brain new connections are made all the time.
https://www.sciencedaily.com/releases/2013/10/131010205325.htm
So I could easily understand that this could also happen in and around the inner ear. When new connections in the brain are made it is productive. Learning a new skill strengthens and generate new connections in the brain. Why than are the new connections in the inner ear not productive?
Could this making of new connection be similar to the mechanisms in (as an example) birds inner ears? Or is it similar to the making of new connections in the brain when learning a new skill? Or are these two mechanisms the same (inner ear regeneration in birds and making new connections in the brain.)?

Could it be quicker to see if stem cells can do the job?
Stem cells have all the information. Instead of trying to understand step by step all the different processes and interactions.
I guess we could need both.
Questions, questions

 

If you consider there are two directions in which the synapses work, brain to ear and ear to brain, couldn't it be possible that if the IHC acquires more of the wrong MOC-type connections (brain to ear), the remaining Type 1 afferents will perceive signals "coming from the brain", possibly explaining (some types of) Tinnitus? The MOC-typed connections are used to sharpen cochlear frequency tuning or protect from damage, according to @HomeoHebbian above, so signals from the brain are being sent over these connections. These signals might perhaps be intercepted by the remaining type-1 afferents and be perceived as "noise" or "static".


(blue being type-1 afferent, red being MOC-efferents).

These MOC-efferents should actually only be connected to the OHC's (outer hair cells) if I understand correctly, as these outer hair cells regulate protective reflexes and tuning. Apparently there is a chance they spawn new branches and connect to the IHC, while the IHC should only have connections to LOC-efferents and type-1 afferents.



This raises some interesting questions for me...

• Is it possible that increased connections by MOC-efferents to the IHC are perceived by the remaining type-1 afferents as Tinnitus due to the brain signaling over these MOC-efferent connections?
• If the LOC-efferent connected to the IHC regulates the "gain" with signaling from brain to ear, could a disconnection of this LOC cause the gain to remain "stuck" at a certain level, possibly causing the perception of Tinnitus?
• Is the MOC-efferent-typed connection made to the IHC after trauma a matter of pure chance? What determines a MOC-typed efferent reconnects to the empty space at the IHC left by the disconnected type-1 afferent (is this pure chance)? This might perhaps explain why for some people Tinnitus resolves after some time (the right type of synapses reconnected), while for others it becomes a chronic experience (the wrong-typed MOC-efferents connected instead of the type-1 afferents). Of course this latter part assumes my first question is true.
• Is finding an intermediary compound which binds NT-3 solely to type-1 afferents currently a subject of research? Is this even possible?
• Does death of the IHC cause cessation of the signaling of connected synapses (including the wrong MOC-efferents) and thus, cessation of Tinnitus? This might perhaps explain Tinnitus-cessation after many years for some people due to the normal aging process? This question also assumes my first question to be true.

For chronic sufferers maybe the MOC-efferents need to be disconnected from the IHC's first before type-1 afferents can be reconnected. Or at least some kind of balance needs to be restored. This will be a very localised task as you do not want to cause disconnection of MOC-efferents from the OHC's...

 

My tinnitus started one month after a noise incident.

Why does a type-1 Afferent disconnect from the inner hair cell and not reconnect, but an MOC-efferent does connect?
Is the Hopkinsmedicine the only research that see these processes? To me this looks like an important discovery. So I wonder if there is a follow up on this research.

Can we assume that these different connections are inputs and outputs and processing in the brain is the amplifier?
Than if an output gets connected to an input we will have feedback.
That is probably to simply putt. Must be more complex.

That sound more plausible than my feedback theory (-;
Is there only one type-1 Afferent fibre connection for one inner hear cell?

 

From what I read, there appear to be multiple type-1 afferent connections to a single IHC, which have a possibility to increasingly get replaced by MOC-efferent connections upon trauma and/or aging. Whether this MOC-connection process (instead of a type-1 afferent reconnecting) is a matter of chance or not is not sure.

Maybe Tinnitus resolves/reduces in either of five situations?:

• The IHC only has MOC-efferent connections left (all type-1 afferent connections got replaced by MOC-efferent connections and thus send no signals to the brain, there are only brain->haircell connections). This effectively renders the IHC useless for hearing. I'm not sure if this situation can occur.
• The IHC has no MOC-efferent connections, but only type-1 afferent connections (and a LOC-efferent connection) like it should (normal situation).
• Over time more type-1 afferents manage to reconnect to the IHC, pushing back the "noise" caused by the MOC-efferents resulting in a reduction of Tinnitus (more "outside sound" gets processed in the IHC).
• The IHC dies, no signaling is possible anymore by both type-1 afferent connections as MOC-efferent connections for that hair cell.
• The LOC-efferent connection is restored to the IHC if disconnected, potentially restoring the ability for the brain to adjust the gain for the IHC (and maybe this gain restoration resolves tinnitus).

If the LOC-efferent connection is involved in Tinnitus generation (this might also be just the sole reason, maybe the MOC-efferents aren't even involved in this), maybe reconnecting a disconnected LOC-efferent to the IHC might resolve Tinnitus. @HomeoHebbian mentioned the LOC-efferent might possibly be responsible for "gain adjustments" in the IHC. This might be a clue the LOC-efferent (or the lack thereof upon disconnection) could be involved in Tinnitus or Hyperacusis generation. Maybe the LOC disconnects after a certain intense noise trauma, leaving the IHC in a certain unadjustable "gain" status?

 

Maybe the type-1 afferent is able to reconnect, but the MOC-efferent grows into place at a faster pace by nature. Maybe it depends on the severity of the noise trauma and are the type-1 efferents "swung away" from the IHC further than a nearby MOC-efferent if the trauma is severe enough? Maybe some chemical is involved in determining or suppressing which type of synapse is allowed to connect (and maybe this chemical balance is disturbed)?

Maybe the type-1 afferents reconnect to the IHC at a later time, resulting in Tinnitus-reduction due to the already connected MOC-efferents (explaining the case "Tinnitus reduction after a while but not really resolved (got more into the background)" like often described)?

Lots of "maybe's", I know, but interesting stuff to think about. A lot of different combinations in connections are possible and it seems these connections and the status of each individual IHC changes a lot throughout life (similar to the brain-synapse connection analogy), making Tinnitus in its current form and intensity not necessarily permanent in that way, but ever changing. I wonder if MOC-efferents are able to disconnect or be disconnected in any way after connecting to the IHC...

I heard about the odd story of people's Tinnitus being resolved after a new noise exposure, maybe the disconnecting MOC-efferents is what happened in that case. Seeing all the possible combinations/outcomes, I wouldn't recommend trying to replicate that, because it seems like playing russian roulette with the synapses. It might however be a (rare) possibility if this is true.

 

Hey Baxter,

Hidden hearing loss is really just starting to be recognized. There is a test out to measure the brain's response to noise called an "Auditory Brain Response". I had one done around the winter of last year. It unfortunately showed no issues in my hearing even though I had such gigantic changes in my hearing over the past two years. So something is missing. Homeohebbian posted at the top of this thread about a test supposedly being developed to measure hidden hearing loss.

Hope this helps.

 

I have some hearing loss in the high frequencies but my hearing is otherwise relatively "normal". If I'm in a loudish restaurant or other place where there's tons of background noise I have a REALLY hard time understanding people.

 

Wow. That is weird and could be very important in this whole reconnecting process, if that is what is happening. Are these cases documented or anecdotal?
Very difficult to see what is going on because of brain involvement.

I agree.

 

Those cases are unfortunately anecdotal. If one of my theories has any truth to it however, it shouldn't be an impossible outcome (albeit a very rare one seeing the possible combinations). If loud noise can "eject" the synapses from the haircell after which random synapses reconnect again, why couldnt that happen more often and even with more beneficial results? It's like rolling dices, because as far as I know there is nothing but chance which decides what synapses ultimately reconnect (unless the MOC-efferents have some advantage I don't know of now). Maybe some suppressed chemical(s) or gene(s) arranged the correct organization during development of the fetus in the womb, after which it is not active anymore and the synaptic reorganization is left to environmental factors during life.

Maybe the ejection of synapses is part of the natural ageing process as well. In our brains reorganization takes place all the time, why wouldnt that happen in the auditory system?

It could also explain the various pitches people can hear in Tinnitus and the randomness of hearing new pitches, depending on the amount of wrong synapses connected to a haircell and the frequency that haircell is responsible for in the cochlea. Of course, the higher frequencies at the base of the cochlea would be affected first for this kind of noise-induced synaptic damage.

But I'd like to remind everyone that I am speculating here and I'll be happy to see my speculated theories kicked and smashed to smithereens if anyone has some other, perhaps more logical, ideas or facts. It just sounds sensible to me based on the currently known data.