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Dr. Boedts, an ENT from Belgium, proposed the ‘Tympanic Resonance Hypothesis in 2020. In his theory, ‘Tympanic Dissonance’ results in multiple local and distant symptoms, most of which can be attributed to activation of the
Trigeminocervical complex. He currenty works at the ‘Listening Clinic’, founded in 2023, exclusively focused on hearing and auditory system issues.
Can you tell us a bit about yourself? What made you decide to pursue a career as an ENT?
I am an ENT doctor who gradually became involved with tinnitus and hyperacusis over the years. My father and grandfather were ENT doctors, and my great-grandfather was a general practitioner. I was interested in every aspect of medicine, so when I had to make a choice, I took the same path and have been very happy with the choice I made. It’s a wonderful job to do.
We’re very happy you made that choice too! What made you decide to use paper patching to treat various symptoms in the ear, and for which symptoms does it help?
So, I started with classical ENT pathology: otitis, grommets, children. Later I moved to sinus surgery and then I moved to otology and ear surgery. I accidentally discovered paper patching around 2006, I think. It’s a technique that has been used for decades, for closing traumatic tympanic membrane perforations.
We had no treatment at the time for autophony. I had read that paracenthesis (making a small incision in the tympanic membrane) sometimes helped, so I tried that in a patient, but to no avail. So I closed the incision with a paper patch, and to my great astonishment, the autophony disappeared at once ! In the next autophony patient, I repeated the procedure, and in the third patient I just applied a patch without making an incision. And strangely, their fullness feeling and slight tinnitus ameliorated too.
Autophony is rare, I saw only one patient with it a month. But a fullness feeling is ubiquitous. As a general ENT, you see several cases a week, often related to muscle tension and anxiety. So, I started to use it in patients with a fullness feeling and no autophony, and it worked in these too.
Then I used it in tinnitus patients. For tinnitus, it works only rarely. For slight, non-disturbing tinnitus, it is efficient. But it is not for most cases of disturbing tinnitus.
Gradually I found that it helps for certain types of vertigo, hyperacusis, pulsatile tinnitus, tension headache, facial pains…
In the beginning, I used patching very much via trial and error. But then I started reading old publications, like the one on Tensor Tympani syndrome by Klockhoff. It is a wonderful observation. And this publication has remained obscure for more than 10 or 20 years! It was not accessible via Pubmed. And the name of the author was misspelled on the publication, so it was very difficult to stumble across. In my opinion, it is a gem.
So, it became clear that the patching was helpful for these patients. But many things remained strange. People suffering from autophony, where the Eustachian tube is supposed to be wide open, also often suffer from tensor tympani complaints. For example, pulsatile tinnitus often responds to paper patching or to treatment of muscle contractions, and it can be related to intracranial pressure problems. And there are many more observations that are difficult to explain.
So, I’ve thought a lot, read a lot, and integrated my patching experiences. And that was then the tympanic resonance hypothesis.
We’re very glad that you have! Can you tell us more about your hypothesis?
It can only be explained if you think of an underlying, regulated mechanism. Evolutionary, a very old mechanism. And because it is old, symptoms are hidden, not obvious. They form clusters. Once you get to recognize them, as did Klockhoff, you cannot unsee them.
I’m getting further on these ideas. I’m at the level of the frogs now: the hearing of the frogs, and how they influence it by contracting and relaxing their lungs and cheeks. So, then there is this link with muscle tensions, with anxiety, etc. And there it starts to get interesting.
There you get to see these old evolutionary links between central and peripheral, between brain and body. So, there you get the insight that the brain and body are not separated, but one machinery. We have been taught that the brain steers the body. But at the same time, the body directs the brain via the gut, via the muscles, via modulation of the senses.
So, it goes like this: when we listen, we contract certain muscles. When you act as if you were listening, you will feel that you contract mimic muscles, jaw muscles, but also your tongue and your palate. Imagine you try to listen to some faint sound on your right side. Most people start to move their tongues. Or when someone is talking on your left side, most people move their face. It is as if you make a triangle, pointing to the sound, or try to shut all sounds out. You feel several muscles.
So, the idea is that the frogs do this to physically modulate the working of their tympanic membranes so as to attract some sounds and repulse some other sounds. They do that (this has been proven by research on frogs), and the hypothesis is that we still do that.
In humans, influencing the stiffness of our tympanic membranes (TM) will not physically influence the sound waves as it does in frogs, but it may influence how these reach the brain stem. The idea is: jaw muscles contract -> contraction of tensor tympani muscle -> modulation of TM stiffness -> focusing/zooming in or out to sounds.
There is a system for zooming in or out, based on muscular contraction. Every time you listen (because you want to, or because there is a sound, so you listen without wanting to), you will contract these jaw muscles. Then 2 things happen:
1: an ‘analog’ or peripheral effect: you increase the stiffness of your TM, like the frogs.
2: a ‘digital’ or central effect: you will send some signal to the brain, so the hearing pathways work a bit harder. Your brain‘s hearing pathways are activated. This central effect was discovered by Susan Shore, 20 years ago.
If this ‘tympanic resonance’ system defaults, two thing happen: you cannot correct the stiffness of your TM as you should, and you will continuously activate your hearing pathways in the brain.
You cannot move your hearing system at will as if you were looking at a bright light but were unable to close your eyes or turn your eyes away from the light. Your hearing will be too sharp (or too dull, if it defaults in another way), you will be too sensitive to external sounds, or to internal sounds (pulsatile, autophony).
That is the hypothesis. There may be several stadia:
Stadium 0: This system works continuously in every one of us, daily use.
Next stage: It gets tired. It is what everyone experiences after a long car drive with the radio on or after a party. Slight tinnitus, a dull feeling, some slight headache, and all sounds come in without relief. I mean, flat, as one stream, no separate streams. It can be compared to a tired, aching muscle.
The next stage: In periods of stress, or intense listening effort (e.g., people in a call center, people that continuously use headphones, …) or also when there is hearing loss, this can extend for longer times. This is the tensor tympani syndrome. It can be compared to a muscle cramp, and it can be cured with physiotherapy, tympanic patching, acoustic rest, etc. It continuously sends signals to the acoustic pathways in the brain to activate them, but the process itself is still peripheral, that means, in the body, and it can be cured with peripheral treatments.
Next stage: If this lasts for a certain time, AND combined with stress, emotion, urge: you get central neuroplasticity. The brain has received signals to listen more actively, and now it decides that hearing more actively will be its new default state. Even when everything around calms down, it will remain in this state. So from now on, it does not respond to peripheral treatment.
So can damaged hearing (hair cells) cause the system to enter a long-term state of “tympanic dissonance?”
Not necessarily. Damaged hair cells can cause central plasticity also. Deafferentation plasticity. Tympanic dissonance is different. It can be caused by listening effort, and that can be caused by hearing loss (e.g. damage). But they are separate. So, you see, tinnitus, hyperacusis, … after a blast can be: 1/ damage to hair cells, 2/ acoustic shock and 3/ tympanic dissonance or tensor tympani syndrome. It’s difficult, you need hearing tests.
In my opinion, damage to hair cells causes hearing loss, but not necessarily central symptoms. It is debatable, this would be a subject for a long and arduous debate at a conference.
An acoustic shock is an intense activation of hearing pathways and other central networks. It can cause anxiety, sleeplessness, concentration problems, etc. Westcott described that.
And tensor tympani syndrome, or tympanic dissonance, means that there is no damage. But as the distinction is difficult to make, some people panic: they get a muscle cramp from the loud sound, and because everybody tells them there must be hair cell damage, they continue to cramp their muscles, so the complaints keep going on.
These are easy to cure. Explain this and show that their hearing is fine. Treat them with patching, physiotherapy, a psychologist and some ear rest for a few weeks.
But the problem is these things get mixed. You can have hair cell damage AND an acoustic shock AND muscle tensions. That makes it very difficult.
So, to get back to the resonance hypothesis. At a certain stage, it (tympanic dissonance or tensor tympani syndrome) is still only peripheral, so we can cure it with simple means. But when it becomes central it is more difficult. Often patients tell us: “the fullness feeling is much better; the slight vertigo is better. I was somewhat bothered by sounds but that is now better. But the tinnitus remains.” So, you see, some complaints are peripheral and some central. We can’t tell when we see a patient.
We can only treat and see what happens. The same holds true for hyperacusis. In some patients it is peripheral, unexpectedly! Sometimes the result of a simple patch is astonishing. And then, often, there are no results at all. So, I presume, in these patients it is central.
Two things can happen to this ‘listening system.’ The first, I just described. It is oversollicited. We call it ‘strain’. The second problem is ‘sensitization.’ So there the system works just fine. No muscle contractions.
In strain, there is an increased input. In sensitization, the input is normal, but there is increased output. The dual response (the contraction of the tensor tympani and the signal to the brain to spur it to hear more intensely), is exaggerated.
So, a sound that will cause a small muscle contraction in most people, will cause an exaggerated contraction in these patients, and an exaggerated message to the brain. This is very nicely shown by Arnaud Noreña and Philippe Fournier.
Interesting. Can you tell us a bit more about your results using tympanic patching for hyperacusis patients? Do you notice differences in the results between those with pain vs loudness hyperacusis? Any differences between patients who present early vs late?
Hyperacusis is a big name for several things that are difficult to pinpoint, you know that better than I do. Pain hyperacusis seems to be ‘sensitization’, an exaggerated response to a normal input. Loudness hyperacusis is difficult. I’m not sure. It is in most cases an exaggerated response, I think. Now there are people who tell me: “I don’t have hyperacusis, but my hearing is too good. I hear the fridge, I hear electricity, I hear lamps. I am the only one in the house hearing those things”. That, in my opinion, is strain. It is the listening system that does not succeed in shutting off. Also patients that cannot escape from unwanted sounds and have a flat soundscape: that appears to be strain. And the latter two react well to patching.
Then there are the interpreters in Canada. They have suffered from symptoms since Covid. They use headphones all the time. Philippe Fournier found that moderate sounds, such as speech, are louder for them than for others. But this is not called hyperacusis, rather chronic acoustic shock. not because of hair cell damage, but because of listening fatigue due to continuous headset use.
Is the pain in pain hyperacusis likely a result of the middle ear muscles contracting too much? What exactly creates the pain?
Actually, I’m not sure. Middle ear muscle contraction is certainly a part of it. But what exactly causes it… it is complex. It is in the middle of it, that is sure. Everything connected to middle ear muscle contraction is worth investigating and treating. So, I’d say, probably yes.
So, what is related? Middle ear muscles are like other muscles. Football players get cramps, so they have to stop playing, get massages and slowly start again. The more they use their muscles, the harder they cramp. You see that at the World Cup. You’d think they’ll never play again when you see them lying on the grass. But they do. So, I think it is similar.
Could the burning pain be similar to delayed pain in your legs after a long run?
Maybe yes, interesting idea. Arnaud suggested something like that in his publication. That it is inflammation, local inflammation.
And what about the trigeminal nerve?
The trigeminal nerve and occipital (C2) nerve are the central driveways for the whole system. The trigeminal nerve is the nerve of the antennae: ears, whiskers, skin, etc. All our antennae.
So, evolutionarily: the trigeminal nerve is activated when there is anxiety because of possible danger. This nerve innervates the jaw muscles, so these will contract. They make the tensor tympani contract, so the hearing is sharpened. And from these muscles, signals go to the hearing centers and the centers of alertness in the brain, making one more alert.
So there is an activation of this alert-system. What is interesting: complaints due to this activation may thus be intensified by pre-existing anxiety, but also: many people who were not anxious at all, become more and more anxious as these complaints go on, because of the maintained activation of this system. Egg and chicken, you’ll never know.
It is one big system, that is activated. We try to determine the inputs and outputs and try to treat as much as possible of these. In one person, it is about muscles, e.g. because of dental problems. In another, it is about anxiety and stress. In yet another person, a part of the tympanic membrane is floppy so he will activate the system in order to stretch it. In a fourth person, it is his job (headphone use or others) and so on.
Sometimes it is the Eustachian tube. I am convinced this plays an important role, but it is not so easy to reach. I think we should look more at the Eustachian tube.
What are your experiences with using paper patching for treating various symptoms, including hyperacusis?
Sometimes we get good results (with patching), often no results at all, for patients with similar complaints. Patching for pain hyperacusis can modify it, but it does not influence strong pain, but mollifies it.
For hearing too well, patching works very well. But that is not an important complaint. Sometimes people tell me: “I do not understand my husband sitting in front of me in the restaurant, but I am obliged to listen to the conversation to the right, 3 tables further.” That is a zooming problem, and often reacts very well to patching.
In your paper, you mention “unpublished clinical experience.” Are you planning any new clinical trials regarding patching?
No, not on patching in se. We are working on a tool to measure what happens, so we can objectivate. With this device, we’ll certainly publish. But without it, it is difficult. People just don’t believe it. Arnaud made a good device for sensitization, ours will be more for strain. They’ll measure the same things from a different perspective.
We are looking forward to reading about the device and the results.
I will keep you posted!
We have heard you recently started injecting Xylocaine and Botox to treat pain hyperacusis. What caused you to start this form of treatment? Where do you inject the Xylocaine or Botox? Is there anything you can share about the results with hyperacusis?
Arnaud’s device taught us a lot about the connections, which regions trigger Tensor Tympani contractions. So, I started injecting bupivacaine (similar to Xylocaine) in these regions. Often with good results. Mostly in tinnitus patients, but of course, some of them suffer from hyperacusis as well.
The thing is: there is a great variability in these locations, in their power to trigger tensor tympani and complaints. Migraines, which share some features with tinnitus/hyperacusis, are caused by sensitization of another branch of the trigeminal nerve. Botox works well here.
In migraine, Botox is injected in a standard series of locations. There are similarities (between migraine and hyperacusis) in the mechanisms involved. If we identify the exact locations for tinnitus/hyperacusis, we could develop a protocol to use Botox for these symptoms. So, my idea is, if we can identify them in a gentle, safe way by injecting bupivacaine, that may be a path to a Botox treatment. And I think there are two possible paths:
1/ inject all locations that we identify, as is done for migraine;
2/ make a personalized map of a specific patient and inject Botox only for locations that matter for that patient.
I think we are now at the level of making that map. I injected Botox in some patients, but at a low dose.
How do you identify the locations for a specific patient?
Via a clinical examination: trigger points. And experience: patients tell me where they can influence their complaints, some locations keep coming back. I have high hopes that Arnaud’s pressure measurement device may help us for that. It is astonishing to see the TM move on the screen when you touch a certain muscle, or when there is a sound.
But then, some locations give a TM movement in a healthy person, so we’ll have to make a “map” in healthy persons first, and then compare with patients. We are talking about that. And then we can trial with bupivacaine. These together would allow us to make such a map, with the people treating these symptoms.
That’s wonderful! Speaking of measuring the muscular contractions in the middle ear, is it possible for the tensor tympani (TT) to contract in time with the heartbeat? Several patients have experienced this. We are sometimes told it is likely vascular, but it really does not seem to be.
Using the pressure measurement device, we see a heartbeat in one ear only in most people, not in everyone. Arnaud thinks that it is an artefact (the arteries). I think it is a TT contraction in everybody, to eliminate the sound of the heartbeat. The TT contracts to eliminate disturbing body sounds. If that does not function properly, you get pulsatile tinnitus, etc., which rather often responds to patching, physiotherapy and now also injections.
You only treat patients with Botox injections if they react positively to a Xylocaine injection first. Why is this?
Because I am new to Botox, and I like to play safe. And I want to get insight into what I do. Botox often gives results only after a few weeks, gradually. Local anesthetics do so after 5 minutes, full-blown. So, I can try six localizations in an hour. The patient goes to the waiting room, comes back for an injection, goes to the waiting room, etc. This gives an incredible lot of information in a short time. You’d need months or years for that with Botox.
I honestly think this is a good way to learn fast and in a safe way how to proceed with Botox treatment. Of course, we cannot be sure that Botox will work if bupivacaine works.
Can you tell us your thoughts about injecting Botox in the tensor veli palatini (TVP)?
I believe that it may lead somewhere, but it is too early to tell. I think, in a year or so, we’ll know more about the use of Botox. The TVP should be a good fit. In my hypothesis, the TT, TVP and medial pterygoid form one system, with receptors all over the tympanic membrane, TT, on the palate (a lot!) and next to the Eustachian tube. In the ‘pharyngeal recess,’ these receptors may be the key, and we try to deactivate them.
Which receptors are you referring to?
TRPV receptors. They work with CGRP, a very interesting molecule.
We assume you are gathering data about the results with Botox? Are you planning to publish these in a journal?
Yes, certainly. But not right now, I want to be more certain. I would not like to create a buzz about something we are not sure about. All this is only a first step, not certainty at all.
Is it possible to inject the tensor veli palatini muscle on both sides simultaneously? If so, would this not present issues with swallowing?
Yes, you can have some swallowing problems and that lasts for a few months. It’s very annoying. It has been done for palatal spasms, but I’m not sure if it’s been done bilaterally. It may depend where you inject the TVP: on the palate, via the nose, near the Eustachian tube…
Could injecting Botox into the TVP worsen symptoms or create new symptoms? Would it have any negative effects on the function of the Eustachian tube? Could it possibly cause or worsen patulous Eustachian tube (PET)?
I think Botox is quite safe. As for PET, I have the impression that, in some patients, it may be related to the contraction of the muscles, and we do not know exactly which ones. I imagine that, if you weaken the TVP, you might increase the effect of the LVP or another one, but that is just an idea, and cause PET symptoms for a few months. I have only seen one or two patients who had it done, so I cannot say.
A question we’ve heard from a lot of patients: can muscles in the middle ear be reacting inappropriately to sound and cause immediate or delayed pain even if you don’t seem to feel them contracting frequently?
Yes, they contract when you want to listen to something, when your organism wants you to shut down body sound and pay attention to the outside world, as part of the startle reaction, as part of anxiety reactions, that is, and spontaneously, on certain sounds.
And when you contract other muscles or stimulate facial regions, these things make the TT contract. And it can be impressive to see on the screen, a muscle contracting just because a train in the background is passing. A train that I hadn’t even noticed. So that is sensitization, of course, an exaggerated response.
It contracts in everybody, but not to the same degree, or not for the same sounds, and not similarly for the same stimuli.
Have you heard of the inner ear type II afferent theory of pain hyperacusis? If so, what are your thoughts on that?
No sorry, I’ll have to read about it. Several mechanisms may exist in several people. The cochlea for me is difficult, as I have no tools to treat it. In my setting, as a clinician, I try to steer towards things I can treat. So, I tend to leave cochlear pathology aside and focus on the middle ear. I suspect several mechanisms may exist. In some patients, it may be like this: you get symptoms only if several factors are at play simultaneously. Both may be correct and have their importance.
That makes sense. Other than bupivacaine, Botox injections, and patching, what are the most important recent research developments that help you in your practice to treat pain hyperacusis patients?
Neuro-inflammation is an important one. But still early, it will get more important, and not only for hyperacusis! We are also currently using transcutaneous electrostimulation of the trigemino-cervical region, but mostly for tinnitus. We have very limited experience with hyperacusis using it.
For tinnitus, we also use bimodal stimulation, in order to re-calibrate the central auditory pathways.
We actually had a question related to that. Do you think a neurostimulation device that stimulates the trigeminal and occipital nerves could be helpful for pain hyperacusis given the involvement of the trigeminal nerve? Such devices have proven effective for migraine and there are early positive results for mood as well.
Very interesting. You have central vs. peripheral neuromodulation, or modulation of the brain through the skull, vs modulation of brain via the incoming peripheral nerves. This device says it targets periperhal nerves.
I get the impression that up to now, central neuromodulation acts on central complaints: anxiety, exhaustion, depression, etc. When these central mechanisms play a role in hyperacusis, it can help via these mechanisms. I have the impression that it does not actually work for tinnitus/hyperacusis specifically. But as often in medicine, you often don’t get results as long as you treat a whole group. And you get more results as you start dividing into subgroups. So, it might be interesting in the future.
But, it appears that tDCS (transcranial direct current stimulation), which is seen as central neuromodulation for anxiety and depression, works at least partially via modulation of peripheral nerves. And we often hear patients who get peripheral electrostimulation (trigeminal) tell us that it calms them down. In these cases stimulation of peripheral nerves does something to the brain.
So, the distinction between central and peripheral is … not a real one. You know that sometimes people get calmer or more able to concentrate after patching. It is about inputs, outputs, and finding the right mechanism. So yes, I don’t know this device but the idea seems right.
Do you think the Shore device or something like it could possibly be effective for loudness or pain hyperacusis?
It has been studied and is marketed for tinnitus. I think time will tell if it may work for hyperacusis. At this point, we do not use bimodal stimulation for hyperacusis.
Sometimes patients tell us that transcutaneous electrostimulation did not help for their tinnitus, but it did for their migraines. And the same, but opposite, exists in Botox treatment for migraine: tinnitus disappears, but not systematically. Some mechanisms overlap, and some don’t.
Basically, we have no diagnostic tools and limited insight. We need, in my opinion, to learn from trial treatments, preferably safe ones. This is from my point of view, as a clinician of course. The results of trial treatments may then allow us to define subgroups. The ones that respond to a treatment, and the others. And that may lead to more knowledge or subtler treatments.
Severe pain hyperacusis is not recognized as a disability in many countries. What could be done to raise awareness and help hyperacusis sufferers?
I don’t know. A high-profile thing, like the interpreters of the international institutions? And then go to the newspapers? The problem is, always, you cannot show results and graphs. People need to see something and then it becomes real for them. They need to see a graphic on a screen.
The device of Fournier and Noreña is showing things for the first time, no?
Yes, it does. But it shows TM movements in healthy persons also. We need to make this map for normal people first. And even there, there is a lot of variability. And then compare them to patients.
You know, I get the impression that the trigeminal nerve is like a tree. It grows differently in different people, with some branches more and others less active. And then something changes, and it relocates its activity.
That seems consistent with what we see in pain hyperacusis patients, with different distributions of pain in different patients.
It seems to be a living, adaptable thing. When I apply patches, sometimes the TM is hypersensitive. After two weeks, it is much less so. Same for palpation of the palate. So, it redirects its activity
depending on the needs. We are back to the receptors. These are the things that make that redirecting happen. Nature is wonderful!
Do you have any theories of how throat pain might arise in pain hyperacusis patients? Many of us have throat pain or strange sensations in the throat. I was wondering if this could involve the glossopharyngeal nerve.
Yes, vagus/glossopharyngeal, pharyngeal plexus, connected with auricular branch of vagal nerve, and with muscles of Eustachian tube. I coined the term ‘tympanic dissonance’ because I found two groups of patients. One with ‘tensor tympani syndrome’, and one with ‘sensory laryngeal neuropathy’.
Do you think a glossopharyngeal block might also help some of these patients?
It might. I’ve never thought of it. Maybe with vagal stimulation at the pinna also.
Pain hyperacusis patients are often worsened by some audiological tests (like LDL tests). How could we raise awareness in the medical community about the existence of several types of hyperacusis and the need to treat them differently?
I never do it. If you are not specifically treating these patients, it is difficult to get to an understanding of different types of hyperacusis. I only got to know the difference long after I started treating tinnitus. As a doctor, you’re only human, you want to see a graph, something real. But I think the added value in any type of hyperacusis is so limited that it does not weigh up to the inconvenience and risk of making it worse.
Right, hopefully, we will have more “evidence” soon. Related to glossopharyngeal involvement: Some ENTs, including Dr. Bance in the UK, have had success treating pain hyperacusis with tympanic neurectomy (cutting Jacobson’s nerve). What are your thoughts about this?
I’ve treated only one patient with a neurectomy (both Jacobson’s and the sensitive branch of the facial nerve). My experience is limited. I went the path of patching/electrostimulation/psychologist/physiotherapy, etc. I try to avoid cutting the tendon of the TT although I am told by colleagues that it seems to work in many cases. There is not a lot of information on this. But for some complaints, even a small success rate may be interesting. Cutting the Jacobson’s nerve is a small thing after all.
Some think if the TVP Botox works, it’s more likely that cutting the tensor tympani muscle will work but that seems to be based on very little data.
That is often the case with these things. I think Botox is a more interesting path to follow, in a coordinated way. Bringing our individual experiences together, brainstorming. And then, in the next stage, if it appears to lead to something, working out a formal study and formal protocols. But as I said earlier: it is promising, but too soon to tell if this will really lead to something.
One patient’s noxacusis symptoms were improved by a sphenopalatine ganglion block (SPG block). In your opinion, what would be the mechanism of this improvement?
That is in my opinion just one more possible location of the many ones. But it Is an interesting one. I would then try to anesthetize it in my next hyperacusis patients and see if something happens, and then include it in a ‘test battery’ or not. In my view, that is anesthetizing very simply via the nose.
But again: I have the impression that locations are variable and may shift. So, there is a possibility that you extinguish the fire at one branch, and that it doubles at the level of another branch. These are things we don’t know as of yet. Let’s hope it does not work that way.
This was a fantastic interview! We learned a lot. We appreciate your time and the work you are doing.
Thanks to you too.