Botox as a Possible Treatment for Pain Hyperacusis

Fournier and Noreña recently released an interesting paper that somewhat follows up their 2018 acoustic shock study.

In the study, one of the patients reported getting a botox injection into their tensor tympani muscle (TTM) which they described as a "complete success":

"The patient recently received a treatment consisting of a botulinum toxin injection in the tensor and levator veli palatini muscles. One month later the patient reports that the intervention was a complete success: he doesn’t experience pain in the ear after exposition to impulsive sound anymore. Following the intervention, he is not able to voluntarily contract his MEM. These results suggest that some muscle activity in the oro-facial area was responsible for the pain and was deactivated by the toxin." (p. 13)

This is obviously a fantastic result, and it seems to support that TTM hyperactivity (and subsequent inflammation) is a crucial part of pain hyperacusis. The question is whether that leads to sustained improvements. Botox injections don't last forever, so they would likely have to be repeated. I wonder if the injections can either 1) let the TTM rest more deeply, hopefully making it more resilient to injury, or 2) stop the TTM from triggering inflammation altogether, which could prevent setbacks from happening. We don't really know the extent/mechanisms involved in the centralization of pain that likely occur in chronic hyperacusis patients, but it could also give the brain a chance to recalibrate and hopefully drive down central sensitization. I have no idea if that would actually happen. I would happily be a guinea pig, if my circumstances allowed for it.

I'm thinking of contacting Noreña to ask if he has any more insights into potential treatments. If I get a response, I'll let you all know.

 

This is super interesting! How would someone go about getting this done?

 

Any otologist could do it. Specialist ENT.

 

I wonder if anybody on this forum has done it? It does seem a bit risky though, but a relief of the pain hyperacusis would be amazing.

 

I remember reading that traumatized people have enhanced startle response. Sudden loud noise that leads to ear injury certainly can be traumatizing. So it doesn't seem surprising that TTM hyperactivity occurs after such an event and that it leads to inflammation.

 

This makes sense to me in so many ways. I think of the ear/hearing as the surface of a drum. When the tautness of the drum surface is messed up, there are symptoms galore.

Can someone post the full paper?

 

It doesn't seem like anyone here on Tinnitus Talk has done it. I have found some reports of people who got their jaw muscles injected with Botox, but that's another story.

I don't mean to discourage you from trying it, but there's a few things to keep in mind:

1) Fournier and Noreña's model of pain hyperacusis makes a lot of sense, but it hasn't been proven yet, as far as I can tell. There's lots of evidence, but no smoking gun.

2) This is a report from a single patient, and it's not even the main focus of the study.

3) The TTM muscle is responsible for attenuating sounds, including sounds that come from inside your body like chewing. This is a paradox that I'm not sure how to reconcile. Wouldn't paralyzing the TTM make these sounds louder? This is something I intend to ask Noreña when I email him. Sorry I haven't done this yet; I'm in a rough patch with my hyperacusis right now.

 

Perhaps it isn't stopping the TTM, but merely slowing it down so it has a chance to "reset" from its inflammation cycle. So this could mean there is still protection from loud sounds to an extent?

That's just a guess though. I still am trying to understand all of the different stances people have on the origin of this disorder. I'm considering trying the Botox method in the future since I am convinced that all of the pain I get comes from the TTM spazzing out. I don't think I have straight up noxacusis but I do get aches and pain here and there pretty randomly.

 

As far as I know, the TTM doesn't react fast enough to protect against unexpected loud sounds. Unexpected being the key word here (the study shows participants' TTM contracting in response to the anticipated sounds of a pen dropping and a baby crying). This suggests less protection to everyday noise in the case of TTM paralysis (or weakening; it seems that whether Botox completely or partially paralyzes muscles depends on the dose, but I'm not sure).

Here's another relevant bit from this study: one of their patients could contact their TTM at will. This didn't lead to pain, except during noxacusis flare-ups. The authors then speculate that TTM movement isn't sufficient for causing pain on its own; it needs to be accompanied by inflammation.

If this is the case, then maybe it wouldn't matter that the TTM isn't protecting against sounds since the real damage is done by the inflammation; all that matters is stopping the hyperactive TTM from triggering this process. So I think you're right on the money.

I'm still curious about the potential long term benefits of this procedure. It seems great for setback prevention, and perhaps for setback recovery if administered early enough. But can it lead to sustained improvement?

 

I wish we could get some sort of follow up on this particular patient. How are they doing now? If they're still cured from this one procedure then this could be a MASSIVE deal. Even so, the presence of improvement at all is already a huge deal and I hope that researchers explore this potential avenue. If the theory about this being a constant vicious cycle is true within the ear, then it might be a lot easier to treat than we thought. Similar to how it seems to be a growing consensus (from what I've seen) that treating tinnitus might be a little simpler than first hypothesized.

What's funny is I just was thinking about this the other day before your post. If I don't get any better, I might take the plunge and give Botox a shot in the future. I'd definitely post here about it if I did as well.

 

The real tricky part though is that, at some point, the brain becomes involved in the cycle and the pain becomes centralized (a similar process happens with tinnitus). I think that is when treating hyperacusis (and tinnitus) really becomes difficult. Hopefully there might be ways to address this, either through medication or brain stimulation. But we still don't know exactly how that happens, and how much of the pain we feel is due do central sensitization versus the middle ear. My hunch is that "everyday" discomfort is mostly a brain thing, whereas "acute" discomfort (i.e. burning pain, aural fullness, etc) is mostly a middle ear thing, but maybe that's just my experience.

I also think that the brain is to blame for lower thresholds for TTM contractions. I think that's part of the same mechanism that increases central gain and contributes to tinnitus. This makes me think that treating loudness hyperacusis could significantly help pain hyperacusis by increasing the threshold for TTM contractions, hopefully leading to less pain and higher resistance to setbacks. This is, however, total speculation on my part.

Do let us know if you end up getting Botox in the future! There's so little data on all of this, we need every little scrap we can get.

 

Maybe a bit late, but here's the full paper in case anyone's interested.

 

Thank you for sharing. I've had private access to this for a while but was unable to share it with others.

I cannot stress this enough: if you have hyperacusis, you need read to this paper. The TLDR is that the researchers examined 11 patients with hyperacusis using a new ear sensor they developed. The sensor showed that all 11 patients had abnormalities in the way their tensor tympani muscle and/or stapedius muscle behaved. Yes, it's a small sample size, but this to me is the biggest confirmation that what we are dealing with here is a middle ear problem, not a cochlea problem.

 

What was kind of shocking to me was the test itself (tympanometry, exposure to uncomfortable sounds). It sounded like it would be at least painful to many hyperacusis sufferers, if not dangerous in aggravating the symptoms.

 

Tympanometry can be done with sound or with some air pressure. I did it with the air pressure.

 

I looked into Botox before, but of course found reports on forums of it increasing tinnitus. Is it ototoxic or something?

 

The problem with most of the things that can help us right now is that they can also make us worse.