Round and Oval Window Reinforcement for the Treatment of Hyperacusis

I just wanted to bump this question for anyone trying to find out about this surgery. I still can't get this answered to any degree that gives me any confidence.

 

Number one reason I wouldn't get this surgery done. Also it's expensive and you need to stay with someone in Florida for 3 weeks.

 

There’s a pretty remarkable success story by a patient that basically got cured from his hyperacusis from this surgery.



Here is his LDL score before and one week after surgery:



A sometimes almost 30 dB improvement in pain/loudness threshold. That’s insane.

Depending on how the FX-322 results turn out, I might take the chance and go do this. It doesn’t affect tinnitus, but my hyperacusis is my biggest gripe at the moment. It’s $8000.

But ideally you would want to get FX-322 first and then if your hyperacusis is not improved by it, go do this surgery afterwards.

 

As a fellow sufferer, I've been following this procedure for a while too. What I find most peculiar about the procedure is that those who see improvements (about 50% from what I gather), see improvements in both ears. This is at odds with our current models of hyperacusis and it would suggest, as much as it pains me to say it, that there may be some kind of centralised mechanism involved in these specific patients. Assuming it's a middle ear issue, the peripheral changes from the operation may lead to some kind of positive feedback loop in the brain that causes the other ear to behave normally again.

This whole incident makes me think again about my own hyperacusis. For example, my hyperacusis started in both ears at the same time. What is interesting to note is that one ear was closer to the acoustic event that set it off than the other. To add to this, I don't think ear health degrades uniformly between both ears. This is evident in many people who have hearing loss in one ear but not the other. So with all this mind, I don't see how any theory that proposes some kind of "threshold" of damage that needs to be reached for one to develop hyperacusis is plausible, given that most of us will have inconsistent damage between both ears. I wonder then if hyperacusis is multifactorial, in that you need not only extensive peripheral damage but also some kind of centralised damage as well.

 

But how long did the guy suffer from hyperacusis before having the surgery?

We must remember that many cases of hyperacusis naturally gets much better over time. Usually the first year or two.

 

To be fair none of what you said precludes a damage threshold, it's just not uniform across both ears. I say this because it's important when thinking about reversing damage that we have a threshold we can cross back over.

 

I think a lot of people's hyperacusis is middle ear related. Hyperreflexive tightening of the associated muscles to lower thresholds is bilateral because the normal reflex is also bilateral.

 

Can you please clarify though how this explains benefit in both ears when only one ear has been operated on? Perhaps it was self-evident but given my non-medical background I'm a bit too dumb to read between the lines sometimes.

What I find interesting is that although Silverstein's own paper states at the outset that the etiology of hyperacusis remains unknown, it does seem to concede, or at least suggest, that the procedure is a band-aid in nature, and that the true culprit is still the inner ear:

"These observations reinforce that the dampening procedure may have rendered the inner ear less sensitive to the effect of sudden changes in sound and pressure, therefore decreasing the hypersensitivity of the inner ear"​

So what I'd like to understand is this: in the cases where Silverstein's surgery clearly works, is this because the middle ear was compromised and the otherwise healthy cochlea was left "unguarded", or was it because the cochlea had become sensitive due to whatever mechanisms are at play in the inner ear when it comes to hyperacusis? Given the wording of this quote - specifically the reference to "hypersensitivity of the inner ear" - it would suggest to me that it's the latter.

I also found it interesting that there are other middle ear procedures that see benefits in both ears when only one ear has been operated on, the other being a stapedotomy, even in cases of bilateral otosclerosis. Again, the Silverstein paper says:

"Similar phenomena where greatest benefit occurs after the first ear surgery has been observed in subjects who underwent bilateral stapedotomies"​

I've tried to find an explanation as to why this is also the case but no luck so far.

 

Simply put, the damage is in one (inner) ear but as the normal reflex is always bilateral, so is the hyper-reflex.

 

I'm still not sure if I'm following correctly. When you say the reflex is bilateral, are you saying that the brain needs to receive a "noxious" or "dangerously loud" signal from both ears, as opposed to just one ear, in order for the brain to say "ok, this is dangerous, we're tightening muscles in both ears", to put it in layman's terms?

If so, how would this understanding fit into cases of unilateral hyperacusis?

 

What I mean is, in the case of the pain coming from middle ear spasms in particular (versus sensitized type 2 fibers which can just be in one ear or both), the normal Stapedius, and Tensor Tympani reflexes are over sensitive. This reflex isn't a unilateral reflex even in healthy individuals. Your middle ear muscles don't tend to respond to sound on just one side just like if someone flies towards your left eye, both eyes tend to blink together unconsciously.

 

I see. But to take that analogy a step further, if someone was blind in one eye and someone flew towards them, that wouldn't mean they wouldn't blink at all, surely? Both eyes would still blink, right?

Which is why I'm still very confused and just trying to get my head round this. Given the reflex is bilateral, would it not be the case that even after the surgery to reinforce one ear, both ears would still need to be reinforced to dampen the reflex, presumably because one ear is still being exposed to loud enough sounds to induce the reflex in both ears, albeit one is now reinforced and therefore less prone to tightening and pain?

 

No. Only the damaged ear needs to be reinforced and then the reflex (which happens bilaterally) will normalize.

And yes, I believe both eyes still blink if one eye is blind and something is thrown at the good eye.

 

But that's my entire point. We are seeing resolution of hyperacusis in both ears, in people who have the same compromised LDLs in both ears pre-surgery, despite getting round and oval window reinforcement in only one ear! At the risk of repeating myself, why would the bilateral reflex normalise in the presence of another damaged ear? I'm sorry if I'm being annoying but this is very confusing.

 

It wouldn't. If only one ear was damaged and then normalized to sound, the reflex normalizes in both ears because the reflex is bilateral.

Maybe I misunderstood your original point because central damage was discussed and I thought you meant the fact that the reflex was bilateral meant there was central damage and I was just pointing out that the reflex is always bilateral and in the case of hyperacusis it just has a lower threshold.

 

Yeah, there's definitely been a misunderstanding.

My initial reply was to @Philip83 concerning someone who had resolution of bilateral hyperacusis despite treatment of only ear, which is standard procedure for the Silverstein surgery. I suppose this isn't something one would know unless one is familiar with the procedure, especially as the photo doesn't make it obvious either, but in any case I was trying to press a question on the hive mind that I've had for a while now, which is: how can this be possible?

The Silverstein paper I linked to makes reference to this phenomenon across most of his patients and after all these years he and his team still have no explanation for why this happens either, which is why I asked about what other central mechanisms could potentially be at play here, because surely if it was strictly peripheral we would see benefits in only ear, not both. At least we've established that a change in the acoustic reflex isn't one of them. But I also wanted to give the hive mind some food for thought, because this bilateral benefit following treatment of only one ear isn't limited to the Silverstein surgery, because as Silverstein also notes, there are cases of bilateral improvements following stapedotomies in only one ear.

So with that out of the way, I also want to repeat my second question, which is whether those cases of hyperacusis that are resolved by Silverstein's surgery can be explained as having a middle ear or inner etiology. Silverstein says that:

"These observations reinforce that the dampening procedure may have rendered the inner ear less sensitive to the effect of sudden changes in sound and pressure, therefore decreasing the hypersensitivity of the inner ear"​

So again, in the cases where Silverstein's surgery clearly works, does the hive mind think this is because the middle ear was compromised and the otherwise healthy cochlea was left "unguarded", or was it because the cochlea had become sensitive due to whatever mechanisms are at play in the inner ear when it comes to hyperacusis? Given the wording of this quote - specifically the reference to "hypersensitivity of the inner ear" - it would suggest to me that it's the latter.

 

From what I gather, after the procedure the person has improved hyperacusis but less sensitivity to naturally loud sounds. This mechanism is what protects us from dangerous levels of noise, so in the long run we would lose some of the capability designed into our auditory system for safety.

 

This is what I am seeing:

One cochlea damaged -----> increase central gain ----- > loudness hyperacusis + added complication of middle ear muscle having enhanced reflex to the louder sound, which adds to both loudness hyperacusis because of reduced dampening effects and middle ear pain. This would be bilateral since the normal reflex is bilateral.

You fix the "bad side" and you dampen sound reaching the damaged ear and the brain has a different sound setpoint and it improves the reflex in both ears.

Now if for some reason, you are saying you could do either ear and it doesn't matter when only one was initially damaged then I really have no idea.

 

It would appear to be either ear, although I remember reading Silverstein's early success rate was 60% and has since improved to 80%. I'm wondering though whether you may be on to something and whether the lack of a 100% success rate can be attributed to the chance involved in "picking" the correct ear for surgery. I know there are some with bilateral hyperacusis who tend to have it worse in one ear than the other (personally speaking mine fluctuates), so it would make sense if those types of patients opted for the worse ear, which I would imagine also happens to be the ear with the most cochlea damage (and therefore more often than not "luck out" in their choice).

As a thought experiment, and assuming your theory is correct, I wonder what implications this may have for regenerative treatment, given that it would arguably be doing the very opposite of "dampening" sound. I suppose if we look at your flow chart, one could argue that increased peripheral input would turn down the central gain and in turn the middle ear would calm down as well. This would tie in with some of the hyperacusis models @100Hz has been a proponent of. I'm going to be making a post on hyperacusis and FX-322 soon and this is something I'm going to give some thought to. Although it wasn't my field of study, I have some knowledge and background in audio engineering and the more I study the auditory human system the more similarities I begin to find, and this is something I'm going to be writing about soon, because I feel this could be an area of medicine where a multi-disciplinary collaboration could be quite useful.

 

Since the round and oval reinforcement surgery is a common procedure that can be done by most otologists, I’m curious about any improvements Silverstein might have made to the surgery to make it more effective. I know that Silverstein also fixes hyper mobile stapes, but I’m wondering if he has also refined the technique of reinforcing the round and oval windows as well.

 

Now that FX-322 at least in the short term is a bust, I'm planning to have this surgery done by the end of the year if my recently worsened hyperacusis doesn't get better.

These testimonials are just a tad bit better than the ones I saw from for ex. Lenire.

Hyperacusis Testimonials: How Dr....

Does anyone have a good reason why I shouldn't do it? I have pretty crippling hyperacusis, including pain and TTTS, all which seems to be resolved by this procedure according to the Silverstein Institute and the testimonials.

 

I hate the idea of the blocking the round window without any good indication that it can be successfully reversed if need be (I've been trying to find out for a while, even Silverstein Institute never got back to me when I emailed them twice about reversal possibility). There's enough of a challenge getting a drug into the round window as it is by the looks of it.

Having the stapes part of the procedure only however, seems good though for TTTS though and would leave the round window in its natural state for the future.

 

It was my understanding that it is reversible? Although it’s only what I have sporadically picked up from some random googling so far, and I don’t remember where I read it. But of course it would be necessary to also have this information officially from Silverstein. I will try to write them as well.

Securing the Stapes bone to help with TTTS though, like you said, does seem like a good middle ground if the round window re-enforcement is not reversible.

Do you think this would also have some positive effects on the loudness/pain component of hyperacusis?

 

What makes you say that the stapes part is good for TTTS specifically?

 

I would think the stapes reinforcement wouldn't need to be undone for any reason; in the longer video (linked below), it appears to be a worn-out joint like you would see in an elbow and knee. It makes me wonder how many of us experiencing hyperacusis partly just have worn out stapes from long-term noise exposure (myself included.)

Round and Oval Window Reinforcement for...

 

I'm sure this has been shared here, but just read through this paper from 2016:

Minimally Invasive Surgery for the Treatment of Hyperacusis

And this from 2018:

Stapes hypermobility as a possible cause of hyperacusis

I have one bad ear with hyperacusis that causes most of my problems, I may look into this. Does anyone know of anyone on here that has had the operation? Seems like there might be some trade-offs. I'd love to pick their brains about it.

 

As far as I can tell, the only drawback seems to be potential minor loss of hearing in the higher frequencies. But it's minor to the point that subjects don't notice it unless they take a PTA, i.e. no subjectively perceived loss of hearing. Also, I'm pretty sure this only applies to the round window reinforcement, and not the stapes reinforcement.

However, as has been stated here before, the RWR could potentially hinder future hair-cell medicines to enter through it (?). I emailed Silverstein Institute today with the question if the procedure is reversible. I'll post it here if I get a reply.

I'm thinking maybe it's possible to only do the stapes reinforcement and skip the RWR. Although, it seems that they can only assess wether the stapes is "loose" while you are being operated on, so maybe they won't agree to skipping the RWR and put you to sleep just to check your stapes? So many questions...

 

Yeah, the idea of the stapes reinforcement doesn't bother me, neither does the slight HF hearing loss that looks like may occur. Its unclear what the effects of tinnitus are? It appears that many patients have tinnitus, but they don't do a TFI. However, afterwards nearly all QoL scores improve; so I guess less hyperacusis is a better trade-off even if tinnitus doesn't change or gets slightly worse.

The RWR is an issue. I'm curious if its thin enough that an intratympanic injection will still be able to penetrate through it and into the cochlea.

 

Yes, both eyes blink. I have a friend who has one eye. He flinches with both eyes.

 

I've managed to correspond with the Silverstein Institute and a number of patients who have had the surgery over the past two years. I actually took their Hyperacusis Assessment, and plan to set an appointment with Dr. Silverstein or one of his associates.

I learned that nearly all patients had a "hypermotile" stapes joint, which was reinforced during the surgery with tissue. I also learned that multiple layers of tissue are applied to the oval and round window to reinforce + reduce vibration. It is the vibration from the combination of hypermotile stapes joint and activated nerves at the base of the cochlea which presumably causes some level of hyperacusis / pain irritation.

It appears that a few early patients actually returned to Silverstein to have additional layers of skin added. It looks like initially, they did 4 layers, in later patients it was increased to 6-8 layers.

In the patients I corresponded with / read posts on, history and outcome was a mixed bag:

Almost all of them had a history of some type of music / noise exposure / acoustic trauma that led to their hyperacusis. Many had lived with hyperacusis / tinnitus for many years (2+ years). They also seemed to have the most positive outcomes. Many have sustained their outcomes from following up on social media 2 - 5 years later.

There were a few that had hyperacusis for a surprisingly short time (6-9 months) before getting the surgery, which surprised me. Seems too soon; as I know personally that the disorder takes about a year to really stabilize. Some of those specific patients have not had as good as outcomes. From what I gather, they continued to go back to their pre-noise damaged ways, and re-injured their ears.

A couple had hyperacusis from medication. Really mixed bag here in terms of long-term recovery from the surgery.

Just wanted to share my findings. I am interested in the surgery, and will proceed with an appointment for Q&A. The multiple layers of tissue applied to the round window does give me pause, so I will ask about it.

I suspect that the procedure is not reversible, and if it is, there would have to be some scarring remaining. No patients that I could find have ever mentioned that they were told it was reversible.

Perhaps though, these intratympanic drugs like OTO-413, PIPE-505, & FX-322 will still be able to pass through a reinforced cochlea? I cannot find specific evidence to show that any of these drugs will pass through it.