Lenire — Bimodal Stimulation Treatment by Neuromod

I wonder if Lenire will ever fix a person's tinnitus whose had it for longer than one year.
 
I wonder if Lenire will ever fix a person's tinnitus whose had it for longer than one year.
I will let you know if I am accepted for treatment in November. :) From what I have read about Susan Shore's device she has had better results for people that had tinnitus for longer periods of time. I know it is a different device, but still the same concept.
 
One of the test patients (Patricia) had had her tinnitus for 4-5 years and she had a complete recovery. You can see patient testimonials on this link: https://www.neuromoddevices.com/stories.
Kind of discouraging that of all their participants there's only one where it went completely away. Maybe that's because they only had the device for 12 weeks though? Had they continued even longer maybe it would eventually disappear altogether?

I'm getting antsy about getting my hands on one of these devices as I've just hit two years and it's been bothering me more the past six months than it did the first year and a half. I didn't even look up tinnitus or seek out treatment until this year because it was mild enough that it didn't interfere with my life. Now it's all I think about.
 
Kind of discouraging that of all their participants there's only one where it went completely away. Maybe that's because they only had the device for 12 weeks though? Had they continued even longer maybe it would eventually disappear altogether?

I'm getting antsy about getting my hands on one of these devices as I've just hit two years and it's been bothering me more the past six months than it did the first year and a half. I didn't even look up tinnitus or seek out treatment until this year because it was mild enough that it didn't interfere with my life. Now it's all I think about.
That's the most significant question we don't have an answer too: would continued use of the device reduce tinnitus further?

From the interview, the CEO said that it was a 3 months use because simply there had to be a start and end.

So this question is still up in the air.
 
That's the most significant question we don't have an answer too: would continued use of the device reduce tinnitus further?

From the interview, the CEO said that it was a 3 months use because simply there had to be a start and end.

So this question is still up in the air.
I would assume so, simply because I recall one of the users here state their tinnitus didn't go away until two months AFTER treatment, and I believe they used their device for longer than three months. So, I'm trying to stay positive about it working, but I sure wish they had more testimonials from people who found complete relief instead of just symptom reduction.

That being said, I wouldn't hesitate to buy it once it becomes available because even a chance is better than nothing.
 
I recall one of the users here state their tinnitus didn't go away until two months AFTER treatment, and I believe they used their device for longer than three months.
That could be TOTALLY coincidental.

One person sample size is not enough to draw any conclusions from.
 
I would assume so, simply because I recall one of the users here state their tinnitus didn't go away until two months AFTER treatment, and I believe they used their device for longer than three months. So, I'm trying to stay positive about it working, but I sure wish they had more testimonials from people who found complete relief instead of just symptom reduction.

That being said, I wouldn't hesitate to buy it once it becomes available because even a chance is better than nothing.
Tinnitus at a level of 1-3/10 is completely livable.
You would only hear it at night when you go to sleep, which can be slightly annoying but completely tolerable.
If my 7-8/10 tinnitus was reduced to 3 or 2, I would be so happy and satisfied.

All I want is to watch TV, work in the office or go out and not hear it.
 
It was @kelpiemsp in reference to the device in Minnesota being used for 9 months and from what I gather they've had tinnitus prior to this their entire life.
Ah yes, thank you! And while the other person above said this could be totally coincidental, I hardly think so for someone who has had it for as long as @kelpiemsp. Obviously it's always possible, but very unlikely. So that's encouraging, even if it's only a sample size of one.
 
Based on the PowerPoint presentation most of the benefits showed up at six weeks and then reached a point of diminishing returns which is why they tried changing up the stimulation to drive extra benefits. But even then, it reaches another plateau. So I'm not sure continuing to use it would have much benefit beyond a certain point although I'm sure people will try that regardless. I take 'continued use' to mean preventing the effect from wearing off even though they suggest it should be permanent.
 
That could be TOTALLY coincidental.

One person sample size is not enough to draw any conclusions from.
Did you ever even look at the clinical trial page? @Autumnly was even nice enough to post the info here for you, and you're still not getting it. The inclusion criteria for the trial was up to 10 years. The sample size of their trials are over 500, and clearly not everyone will have complete remission. That was never the claim, but that most will get some relief. It's no wonder your emoji looks all confused.
 
I want to see a cellular level explanation of exactly how this would work. If there is hyper activity in the DCN, I want to know why the hyperactivity is there and why electrically stimulating it with noise and shocks would fix that, and why the timing matters etc.

I have noticed that there is zero explanation for that.
 
I want to see a cellular level explanation of exactly how this would work. If there is hyper activity in the DCN, I want to know why the hyperactivity is there and why electrically stimulating it with noise and shocks would fix that, and why the timing matters etc.

I have noticed that there is zero explanation for that.
I watched a presentation from Susan Shore where she explains that. If you dig a bit, you'll find it.
 
I want to see a cellular level explanation of exactly how this would work. If there is hyper activity in the DCN, I want to know why the hyperactivity is there and why electrically stimulating it with noise and shocks would fix that, and why the timing matters etc.

I have noticed that there is zero explanation for that.
It is an inherent assumption of the model. You would have to go back to neuromodulation theory, and we are discussing applied methods. It wouldn't make any sense to talk about it in that detail. But page two, paragraph one, bullet point three gives you a layman's example.

https://www.researchgate.net/public...ynchronized_activation_of_multimodal_pathways
 
I want to see a cellular level explanation of exactly how this would work. If there is hyper activity in the DCN, I want to know why the hyperactivity is there and why electrically stimulating it with noise and shocks would fix that, and why the timing matters etc.

I have noticed that there is zero explanation for that.

Behold, molecules and stuff:
https://stm.sciencemag.org/content/10/422/eaal3175

Synaptic plasticity has been suggested as a foundation for network-level homeostatic adaptation (37). In the fusiform cell circuit, glutamatergic inputs to the granule cell–parallel fiber circuit are up-regulated after hearing loss (38–40), resulting in increases in LTP (41). This homeostatic mechanism in response to altered input is not exclusive to the auditory pathway (42). After light deprivation, visual-cortical neurons exhibit expansion in STDP due to increased N-methyl-D-aspartate (NMDA) receptor activation (43). Blocking NMDA receptors in the fusiform cell circuit reduces neural synchrony (44). Muscarinic acetylcholine receptors, whose expression is up-regulated after noise exposure (45), also contribute to STDP (46, 47).

STDP can affect intrinsic membrane excitability by altering ion channel conductance. Maladaptive changes to fusiform cell plasticity that decrease inhibition through reduced hyperpolarizing currents could also contribute to increased synchrony and spontaneous activity. Reduced potassium channel activation and reduced glycine and GABA (γ-aminobutyric acid) receptor activation of fusiform cells have been demonstrated in tinnitus models. A major source of GABA input and glycinergic input to fusiform cells arises in cartwheel cells (fig. S1). These DCN interneurons, which receive parallel-fiber synapses that exhibit STDP, provide recurrent inhibitory synapses onto fusiform cells. Cartwheel cells, therefore, may play an essential role in generating fusiform cell synchrony. Another potential player, the Golgi cell in the marginal region of the cochlear nucleus, provides feedback modulation of granule cell output, which may entrain parallel fibers into synchronized firing. These network components are likely to work together to increase synchrony in fusiform cells, thus potentially playing important roles in tinnitus.

Because the human cochlear nucleus contains all of the cellular elements present in the DCN of rodents, we reasoned that the same bimodal protocol might suppress tinnitus in humans. In both the animal and the human studies, bimodal but not unimodal auditory stimulation effectively suppressed tinnitus. The documented failure of unimodal auditory stimulation to produce long-term changes in fusiform cell firing rates predicted that unimodal auditory stimulation would be inefficient at reducing tinnitus. The significant reduction in tinnitus in animals and tinnitus loudness and distress in humans suggests that the bimodal treatment was successful at inducing frequency-specific LTD, reversing the pathological neural activity responsible for the generation of tinnitus.
 
I want to see a cellular level explanation of exactly how this would work. If there is hyper activity in the DCN, I want to know why the hyperactivity is there and why electrically stimulating it with noise and shocks would fix that, and why the timing matters etc.

I have noticed that there is zero explanation for that.
It's the same concept Dr. Shore is working on, and she seems to have it down better than Neuromod. She explains some of it here in this interview with the ATA:

https://www.ata.org/news/news/tune-atas-brand-new-podcast-dr-susan-shore
 
Well, with Neuromod's track record of communication I doubt we'll ever get one.
They cannot just communicate whenever they feel like it.

There is a process and they can only communicate on milestones. They can't just make a statement without having a justification released in place, like data to back it up.

They will release the results of their third trial at one point.

Remember the company has been in business for 10 years and they did communicate on milestone events.

Be patient.
 
What I've been able to glean from all this is that the underlying mechanism is poorly understood to the point where they have to sort of fumble around via trial and error with the parameters. Now, if you read a research paper it will be all dressed up in scientific lingo but at the end of the day they don't really know whether it will work until they test it... i.e. trial and error.

Because of this, I really don't find the theoretical end of the equation to be what inspires confidence but rather the statistical results of the trials. The theory makes for an interesting intellectual exercise but no matter how rigorous the science, theory is still ultimately theory. It's a mental trap you can fall into where latch onto and dig deeper and deeper into a theory based on how rational it sounds only to discover that it simply doesn't work.
 
What I've been able to glean from all this is that the underlying mechanism is poorly understood to the point where they have to sort of fumble around via trial and error with the parameters. Now, if you read a research paper it will be all dressed up in scientific lingo but at the end of the day they don't really know whether it will work until they test it... i.e. trial and error.

Because of this, I really don't find the theoretical end of the equation to be what inspires confidence but rather the statistical results of the trials. The theory makes for an interesting intellectual exercise but no matter how rigorous the science, theory is still ultimately theory. It's a mental trap you can fall into where latch onto and dig deeper and deeper into a theory based on how rational it sounds only to discover that it simply doesn't work.
The underlying mechanisms of how many medical things work are unknown. Antidepressants notoriously are not known how they work. I agree their conclusions are based on the results of the experiments rather than on understanding the mechanism.

I believe Lenire is a very credible device and what I can conclude from following Lenire is the following.

- The company changed its name from MuteButton ("Mute") to Lenire (which means to soothe). The company doesn't claim that it can cure your tinnitus and it made it very very clearly. It claims that in majority of patients in can achieve a reduction. (In the medical world, rarely we have complete cures, most of disorders/illnesses are "treated"/lessened. So it's not a surprise that a Lenire is a possible treatment and not a cure).

- Results show that some reductions are in fact significant and noteworthy and some reductions are "slight".

-Testimonials on their website range from impressive (great reduction to almost cured) to "I got a slight improvement". Some scams would only filter the greatest results and put them as testimonials and create false promises. Neuromod chose intentionally a testimonial of someone saying I got a "slight reduction" in order not to give false promises.

- Even if I don't benefit from Lenire, I would not regret the 2500 euros spent as this certainly is not a scam. I would just consider myself unlucky and wish others benefit.
 
Progressively fade.
See the strange thing is, with Lenire this doesn't seem to be the case.
What I've been able to glean from all this is that the underlying mechanism is poorly understood to the point where they have to sort of fumble around via trial and error with the parameters. Now, if you read a research paper it will be all dressed up in scientific lingo but at the end of the day they don't really know whether it will work until they test it... i.e. trial and error.

Because of this, I really don't find the theoretical end of the equation to be what inspires confidence but rather the statistical results of the trials. The theory makes for an interesting intellectual exercise but no matter how rigorous the science, theory is still ultimately theory. It's a mental trap you can fall into where latch onto and dig deeper and deeper into a theory based on how rational it sounds only to discover that it simply doesn't work.
That's how I feel about it, bimodal stimulation will work for a lot of people, but I think it's the 'first' treatment of it's kind that's 'poked it's head out of the ground first'.

The good news is actual treatments are on the way for once. I more or less still hold the position that tinnitus will be cured in the 2020s.
 
I'm getting antsy about getting my hands on one of these devices as I've just hit two years and it's been bothering me more the past six months than it did the first year and a half. I didn't even look up tinnitus or seek out treatment until this year because it was mild enough that it didn't interfere with my life. Now it's all I think about.
How did it get worse?
 
How did it get worse?
Good question. I was exposed to some chemicals at my (now former) workplace and things just started going haywire in my body from there. I've had nerve pains in my head and all other sorts of stuff going wrong ever since. Then the tinnitus just started bugging me more. Since then I've had ear issues on and off for months and no ENT can see a reason for it. Test results show I have reactivated Epstein-Barr virus. Not sure if that's what giving me all these issues but I have not felt well in many months.
 

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