Electrical Stimulation of the Cochlea for Treatment of Chronic Disabling Tinnitus

From the study:

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Agreed. Again, just hypothesising, but if those diseases cause a symptomatic increase in subconscious neural activity, say as a result of inflammation or various misfirings, then these raised levels of activity leaking across the faulty gate to be perceived as tinnitus sounds plausible. This is the thing I like about the gating theory; it doesn't really care much for where the signals originate, just that they reach the gate and leak over it.

Regarding other non-related conditions as an example, this is where I could believe something like schizophrenia originates. I get a sense that there we have 'satellite' personalities, or fragments thereof, orbiting our central-self that for a healthy person cause no issue because of a functioning related gating system. However, if that system were to fail then it seems plausible that just like tinnitus, aspects of 'other' self/personalities could leak over into our main one and cause those horrible symptoms.

Ultimately, if this gating thing holds up, I do believe there'll be a biomarker for it.
Yeah, sure there are many things we don't know about all these brain conditions. In fact, I don't know if there are people with Meniere's, otosclerosis, etc. that never develop tinnitus, because a good gating system protects them by holding off those signals. You would think that that would be possible for a few of those people at least. Someone must have that gating system. But if this isn't happening and in those cases we know that the problem is in their cochlea, then one could say that the gating system doesn't exist or plays no role whatsoever.

Or there is a whole different system that leads to developing tinnitus, be it from such a disease or other things like acoustic traumas.
 
Having said that, what is incredibly encouraging about the Mayo Clinic's early results is the four-fold decrease on standard THI. I reckon with figures like that there can be no mistake that the device is really doing something.
Looks like electrical stimulation is a new avenue to explore. Great that someone is thinking outside the box.
 
Looks like electrical stimulation is a new avenue to explore. Great that someone is thinking outside the box.
Explore? Why can't I personally explore this now at some European clinic willing to take my money? There's plenty of clinics willing to inflict all kinds of unproven but relatively harmless things on you for any affliction you might think of.
 
Totally false. Medical University of Łódź, Poland, where @Mentos was treated, started testing this shit in early 1970s. Basically it is a very old method.
I stand corrected. Thank you for putting me straight. When I think about it, I seem to recall some proponent of acupuncture at some time using electrical stimulation of his needles on the meridian points to up the potential (or something similar). How that worked out I've got no idea but I've read quite a few articles over the years that acupuncture is not much use for chronic tinnitus (It didn't help mine)...

And as for the early onset tinnitus, it has lots of remissions anyway.

Might I ask you the following: If the University of Lódz used electrical stimulation back in the 1970s, why are these latest groups repeating it in the 2020s? It can't just be for old time's sake?
 
- According to the theory of Dr. Susan Shore, tinnitus is the brain's reaction to the hearing loss.

First thing is those phenomena are two separate issues. Second thing is the fact that you don't need to have major hearing loss to get tinnitus.

When you are analyzing the above statements, the logical conclusion is that the statement of tinnitus originating in the cochlea is totally wrong.
Isn't this a bit contradictory, or am I missing something?

The brain reacts to the hearing loss (but not for everyone with hearing loss) by producing a phantom sound. Hearing loss often originates in the cochlea, right? Then how is the tinnitus not related to the cochlea?
 
Isn't this a bit contradictory, or am I missing something?

The brain reacts to the hearing loss (but not for everyone with hearing loss) by producing a phantom sound. Hearing loss often originates in the cochlea, right? Then how is the tinnitus not related to the cochlea?
There's gating areas in the brain that shut down the tinnitus for some people. In people who have tinnitus, those gating areas don't work for some reason. I believe Dr. Rauschecker talks about this in his TED talk.

So, yes, ultimately it starts because of the lack of input from the cochlea but there is something in the brain that makes it permanent.
 
The brain reacts to the hearing loss (but not for everyone with hearing loss) by producing a phantom sound. Hearing loss often originates in the cochlea, right? Then how is the tinnitus not related to the cochlea?
Hearing loss leads to reduced electrical activity down the auditory nerve. This causes changes in the DCN, where cells fire spontaneously, and this is then transmitted further through the auditory parts of the brain. Sounds are then processed in the auditory cortex. By stimulating the cochlea, you are increasing that electrical activity again and this causes adaptive changes in the brain, much in the same way a cochlear implant does.
 
I think it's safe to say that the cochlea isn't the root cause of tinnitus, for the most part. What should be targeted is the brain stem (DCN), which has been shown in numerous studies, to be the epicenter of tinnitus generation (at least in noise-induced tinnitus cases), like in Susan Shore's papers.
This is what this technique does:

Using Extracochlear Multichannel Electrical Stimulation to Relieve Tinnitus and Reverse Tinnitus-Related Auditory-Somatosensory Plasticity in the Cochlear Nucleus
 
I am super curious how this whole electrical stimulation to the cochlea method would affect reactivity and/or hyperacusis. A part of me thinks it would drive my reactivity crazy! But I could be wrong. Although reactivity very much feels like it is in the inner ear, anything I have read on it more mentions neural networks in the brain gone awry. I just need my reactivity to STOP. I so envy those with "normal" tinnitus that does not spike or change to external sound stimuli.
 
All tinnitus will be cured, or tinnitus from loud noises, or tinnitus from neck/jaw, etc?
Good point. One approach can't address every cause or form of it. Similarly, when I read posts saying "there is no cure, nothing works" I think "...except for everyone who's cured."
 
I think those theories are BS. Chronic tinnitus usually fluctuates and we have moderate and severe days, so it can change.
Tinnitus setting in the brain is BS. I had had tinnitus for 5 years. I got a cochlear implant and my tinnitus is much better as a result. It takes time for the brain to adjust but it filters and adjusts to hearing sound again.
 
Tinnitus setting in the brain is BS. I had had tinnitus for 5 years. I got a cochlear implant and my tinnitus is much better as a result. It takes time for the brain to adjust but it filters and adjusts to hearing sound again.
Seems to indicate that -- in your case -- the tinnitus and the remedy are situated in the ear/cochlea.
 
Possibly relevant to this discussion:

Sensory gating functions of the auditory thalamus: adaptation and modulations through noise-exposure and high-frequency stimulation in rats

The study demonstrated that the medial geniculate body (MGB), a part of the auditory thalamus, acts as a filtering relay station in auditory processing, and its functions may be impaired by noise exposure. While high-frequency stimulation could ameliorate some of these effects, it was not successful in fully restoring sensory gating.

Helpful at least!?
 
My God, I can't wait until they figure this out. I'm so tired of this back and forth. Why can't they just keep tinkering with it until they get the right results?
 
My God, I can't wait until they figure this out. I'm so tired of this back and forth. Why can't they just keep tinkering with it until they get the right results?
It's so frustrating for sure. I'm not sure why they always stop short during these experiments. I don't know if they just want to do the bare minimum, or they just end up running out of money so they can only do so much, I'm not really sure.
 
Dr. Carlson's trial at Mayo Clinic in Rochester, MN is active/no longer taking participants and they updated the estimated study completion time to December 2023. Sample size of 9, but given the strict "rules" around the study and also people being willing to have the device implanted in mastoid bone, I'm not surprised at the low sample size. In any case, I will be very interested to see these outcomes.

Novel Tinnitus Implant System for the Treatment of Chronic Severe Tinnitus
 
Dr. Carlson's trial at Mayo Clinic in Rochester, MN is active/no longer taking participants and they updated the estimated study completion time to December 2023. Sample size of 9, but given the strict "rules" around the study and also people being willing to have the device implanted in mastoid bone, I'm not surprised at the low sample size. In any case, I will be very interested to see these outcomes.

Novel Tinnitus Implant System for the Treatment of Chronic Severe Tinnitus
Nice find @ErikaS.

Does this mean they don't exclude severe-profound hearing loss at 4 kHz and above?

Inclusion criteria:
  • Normal to moderate SNHL (≤70 dB HL; based on PTA of 0.5, 1 and 2 kHz) and WRS ≥ 75%.
 
Nice find @ErikaS.

Does this mean they don't exclude severe-profound hearing loss at 4 kHz and above?

Inclusion criteria:
  • Normal to moderate SNHL (≤70 dB HL; based on PTA of 0.5, 1 and 2 kHz) and WRS ≥ 75%.
I guess not, @Nick47? Good question.

As much as I am looking forward to see where this goes, I just don't know how this would benefit reactivity. Let's just say reactivity in those with SNHL is a very enhanced central gain in the brain. Unless this could help reset that in some way, I feel like any extra stimulation to the actual ear itself would possibly do the opposite and aggravate noise sensitivity. When I was in communication with Nicole, I asked her if reactive/sound sensitive tinnitus (tinnitus that changes, spikes, and/or worsens in pitch, intrusiveness, etc. in the presence of external sound stimuli) is an exclusion criteria for participants. She responded "It's not ideal but isn't specifically an exclusion criteria." I would really love to get Dr. Carlson's input/thoughts on reactivity and sound sensitivity and what could be expected with this device.
 
I think it's safe to say that the cochlea isn't the root cause of tinnitus, for the most part. What should be targeted is the brain stem (DCN), which has been shown in numerous studies, to be the epicenter of tinnitus generation (at least in noise-induced tinnitus cases), like in Susan Shore's papers.
I've had a rethink on this, after reviewing the evidence, the highly significant pilot studies on these extracochlear implants, cochlear implants, and a conversation with Prof. Peter McNaughton.

Currently it points to aberrant activity in the DCN as the first part of the tinnitus brain network, but that the activity starts peripherally in the auditory nerve as tinnitus can, without doubt, be modulated by extra and intra implants. Add this to the elimination of tinnitus in guinea pigs with the HCN2 blocking drugs, which according to Prof. McNaughton, cannot penetrate the BBB, supporting the hypothesis of a peripherally driven phenomenon. He did say he has been wrong before and will be wrong again, and was very modest and humble, but that he now had some evidence to support his hypothesis. He also said if his hypothesis was right, it would be much easier to treat, rather than designing a drug that crosses the BBB and causes side effects.

He said his hypothesis and early findings support the role of the DCN being involved.
Prof. McNaughton said:
The cochlear nucleus is the first stop for signals originating in the auditory nerve. The increased activity that the Shore group have identified in cochlear neurons lines up nicely with our views that in fact abnormal activity originates in the auditory nerve itself. The auditory nerve is a more promising place to look for pharmacological targets because it is in the peripheral nervous system – targets in the CNS almost inevitably involve psychotropic effects which may be very undesirable. We are trying to develop peripherally restricted drugs which will not have CNS effects.
What do you think so far?
 
I've had a rethink on this, after reviewing the evidence, the highly significant pilot studies on these extracochlear implants, cochlear implants, and a conversation with Prof. Peter McNaughton.

Currently it points to aberrant activity in the DCN as the first part of the tinnitus brain network, but that the activity starts peripherally in the auditory nerve as tinnitus can, without doubt, be modulated by extra and intra implants. Add this to the elimination of tinnitus in guinea pigs with the HCN2 blocking drugs, which according to Prof. McNaughton, cannot penetrate the BBB, supporting the hypothesis of a peripherally driven phenomenon. He did say he has been wrong before and will be wrong again, and was very modest and humble, but that he now had some evidence to support his hypothesis. He also said if his hypothesis was right, it would be much easier to treat, rather than designing a drug that crosses the BBB and causes side effects.

He said his hypothesis and early findings support the role of the DCN being involved.

What do you think so far?
Honestly it's all speculation. We can't know for sure unless more research is done. I never thought that tinnitus is solely DCN, just that, possibly, catastrophic tinnitus has significantly more somatic crossfire which causes insanely more hyperactivity specifically in the DCN.
 

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