Residual Inhibition Combined with Neuroinhibition

[The Red Viper]

Here's a working theory and I'm not sure if anyone has thought of this yet. But before I go into it let me lay down some relatively well-known facts:

• There are people with hearing loss but no tinnitus.
• There are people with tinnitus but no measurable hearing loss (there may or may not be what people have termed "hidden hearing loss).
• Residual inhibition works to completely eliminate tinnitus in many people with tonal tinnitus at a single frequency, albeit it only lasts for a few seconds up to a few minutes for most.
• There are drugs known to eliminate tinnitus, such as lidocaine, trobalt, etc., in many people.
• The current theory among many researchers is that tinnitus always accompanies hearing loss, even if the loss isn't measurable.
• The current theoretical speculation also points to neuronal hyperactivity, hence why some drugs that calm down neurons seem to help tinnitus.

So here's what may possibly be happening. Perhaps in those of us that had a sudden onset of T, there may have been a hearing loss for whatever reason (acoustic trauma, ototoxicity, etc.) but it happened too quickly for the neural pathways to adapt. Hence why it may be that in other individuals with gradual hearing loss, there is no T. In those people it may have been the case that the neural plasticity was able to adapt and inhibit noise from lost signals at a more "natural" pace (I admit I'm not sure if that's really a thing).

Thus a potential therapy could be to expose a person to sounds that trigger residual inhibition (e.g. acoustic neuromodulation) for enough time for the effect to be appreciable (say at least 30 minutes if that's possible, heck I'd take 10 minutes). Immediately following the triggering of residual inhibition, administer a drug that calms down the neural pathways (e.g. GABA, trobalt, lidocaine, whatever...). Adjusting the timing here would be critical, as you'd want the drug to take effect immediately after the residual inhibition starts and before the T starts to come back. My shot in the dark theory is that this would allow the neural pathways to calm down permanently, or at least reach a point of relative equilibrium.

I know @JasonP mentioned this with respect to supplements, so what do you guys think?

 

[The Red Viper]

Basically imagine finding your T frequency, listening to the General Fuzz ACRN for 30-60 min. straight, and before the ACRN is over, place a lidocaine patch or pop a GABA pill so that it is timed to kick in towards the tail end of the ACRN.

 

[Alue]

I have had similar thoughts with regards to the etiology of tinnitus:. sudden hearing loss that the brain overreacts to resulting in extreme hyperactivity in certain parts of the brain, but I'm not sure this would be easy to reverse. I have heard one theory that these change take place almost instantly which would indicate synaptic plasticity, but there appears to be involvement in ion channels as well and I'm not sure how long those neuroplastic changes take. (I have a very limited understanding of neurology, so I could be off base.)
I wish I knew more about neurochemistry or knew someone whose brain I could pick.

O' and residual inhibition does absolutely nothing for me.
Can someone explain to me why residual inhibition works in the first place and why it only works on some people.

 

[The Red Viper]

Yeah the hearing loss thing is very mysterious. I mean a 13 year old can hear higher frequencies than a 30 year old. If hearing loss was really the end all be all cause, then everyone would get tinnitus as they age. Yet they don't. This would also call into question the effect of cumulative hearing damage as well (think going to loud concerts for years and then only getting tinnitus after one particular concert). Again I'm not sure, but I'd like to give this a try personally. Maybe I'll mess around with ACRN and gaba tea.

 

[JasonP]

Here's a working theory and I'm not sure if anyone has thought of this yet. But before I go into it let me lay down some relatively well-known facts:

• There are people with hearing loss but no tinnitus.
• There are people with tinnitus but no measurable hearing loss (there may or may not be what people have termed "hidden hearing loss).
• Residual inhibition works to completely eliminate tinnitus in many people with tonal tinnitus at a single frequency, albeit it only lasts for a few seconds up to a few minutes for most.
• There are drugs known to eliminate tinnitus, such as lidocaine, trobalt, etc., in many people.
• The current theory among many researchers is that tinnitus always accompanies hearing loss, even if the loss isn't measurable.
• The current theoretical speculation also points to neuronal hyperactivity, hence why some drugs that calm down neurons seem to help tinnitus.

So here's what may possibly be happening. Perhaps in those of us that had a sudden onset of T, there may have been a hearing loss for whatever reason (acoustic trauma, ototoxicity, etc.) but it happened too quickly for the neural pathways to adapt. Hence why it may be that in other individuals with gradual hearing loss, there is no T. In those people it may have been the case that the neural plasticity was able to adapt and inhibit noise from lost signals at a more "natural" pace (I admit I'm not sure if that's really a thing).

Thus a potential therapy could be to expose a person to sounds that trigger residual inhibition (e.g. acoustic neuromodulation) for enough time for the effect to be appreciable (say at least 30 minutes if that's possible, heck I'd take 10 minutes). Immediately following the triggering of residual inhibition, administer a drug that calms down the neural pathways (e.g. GABA, trobalt, lidocaine, whatever...). Adjusting the timing here would be critical, as you'd want the drug to take effect immediately after the residual inhibition starts and before the T starts to come back. My shot in the dark theory is that this would allow the neural pathways to calm down permanently, or at least reach a point of relative equilibrium.

I know @JasonP mentioned this with respect to supplements, so what do you guys think?

That is some interesting stuff! If anyone tries this let me know what happens.

 

[DebInAustralia]

Here's a working theory and I'm not sure if anyone has thought of this yet. But before I go into it let me lay down some relatively well-known facts:

• There are people with hearing loss but no tinnitus.
• There are people with tinnitus but no measurable hearing loss (there may or may not be what people have termed "hidden hearing loss).
• Residual inhibition works to completely eliminate tinnitus in many people with tonal tinnitus at a single frequency, albeit it only lasts for a few seconds up to a few minutes for most.
• There are drugs known to eliminate tinnitus, such as lidocaine, trobalt, etc., in many people.
• The current theory among many researchers is that tinnitus always accompanies hearing loss, even if the loss isn't measurable.
• The current theoretical speculation also points to neuronal hyperactivity, hence why some drugs that calm down neurons seem to help tinnitus.

So here's what may possibly be happening. Perhaps in those of us that had a sudden onset of T, there may have been a hearing loss for whatever reason (acoustic trauma, ototoxicity, etc.) but it happened too quickly for the neural pathways to adapt. Hence why it may be that in other individuals with gradual hearing loss, there is no T. In those people it may have been the case that the neural plasticity was able to adapt and inhibit noise from lost signals at a more "natural" pace (I admit I'm not sure if that's really a thing).

Why some people respond to residual inhibition (myself included) and others do not is obviously related to the heterogenous nature of tinnitus. I just wish I could understand this also. My t is not tonal, but some of my white noise (that can also be modulated somatically) can be inhibited by listening to white noise. The central headnoise seems quieter too after I listen to white noise for a short time, but I cant get rid of it entirely. sigh.

I just wonder how many of those who can take advantage of RI also have white noise which is somatic in nature, as this might point to its causation?

Have you guys tried the above yet? Unfortunately, I think that the neuronal plastic changes have occurred and is probably not simply a case of taking a supplement whilst listening to ACRN. Worth a try though I guess. Anyone game?

Thus a potential therapy could be to expose a person to sounds that trigger residual inhibition (e.g. acoustic neuromodulation) for enough time for the effect to be appreciable (say at least 30 minutes if that's possible, heck I'd take 10 minutes). Immediately following the triggering of residual inhibition, administer a drug that calms down the neural pathways (e.g. GABA, trobalt, lidocaine, whatever...). Adjusting the timing here would be critical, as you'd want the drug to take effect immediately after the residual inhibition starts and before the T starts to come back. My shot in the dark theory is that this would allow the neural pathways to calm down permanently, or at least reach a point of relative equilibrium.

I know @JasonP mentioned this with respect to supplements, so what do you guys think?

 

[Pleasure_Paulie]

The latest theory is that tinnitus starts due to stress + acoustic trauma combined. When cortisol is present glutamate is released the tinnitus starts.

 

[stophiss]

Good theories Red Viper. What do I suggest? You try it and get back to us. If it solves your tinnitus it may help others.
Please keep us posted.

 

[The Red Viper]

@stophiss

So my T is weird. TL;DR I think my issue the whole time was a neck injury and I'm not trying anything until I get a diagnosis with confirmation.

Here's a quick lowdown (I'll be as brief as I can): in January I got a cold and it went away like normal, but I still had a residual cough. With that residual cough, I went sledding and everything seemed fine. I hit a ramp while riding a tube and ate it, but felt fine the next day. Following the sledding, my right ear just wouldn't pop. No fluid, but there was a dysfunction in the Eustachian tube. About a month after I went sledding (end of Feb.) I began to get really bad headaches around my right temple, along with a feeling of dysequilibrium and fogginess. I saw an ENT and a neurologist and they didn't see any glaring issues. I took ibuprofen for ten days as directed by my GP for the headaches and I woke up with T after the tenth day.

An MRI (head), CT (sinus), CTA (neck) later and nothing wrong. Several blood tests (including Lyme and Epstein-barr, i.e. the mono virus) as well and nothing. Two hearing tests that both checked out as well.

So I attribute my T, which is relatively mild btw, to Eustachian tube dysfunction (ETD). I initially thought it might be ototoxicity due to the ibuprofen, but I've had days where I've had no tinnitus. I've also had a lot of days where it's relatively nonexistant. Now what caused the Eustachian tube dysfunction? I believe it was mild inflammation leftover from the infection I got in January combined with a neck muscle injury. I think my initial neck injury was mild, but because I didn't know about it I continued to aggravate it by doing things such as weight lifting and indoor rock climbing. This would explain why I didn't get headaches until about a month later.

Now the cause of my ETD is likely residual inflammation combined with some swelling in my neck muscle that makes it more difficult for regular swallowing to open my right Eustachian tube. Every morning I wake up with negative ear pressure only in my right ear but never in my left ear. I also wake up with T, but it goes down throughout the day. It has also been getting relatively milder for the past twenty days because I have realized that my neck might have been the culprit the whole time and I've been applying a heating pad to my neck at least three times a day for about 20 minutes or so on each application.

As to why residual inhibition works for me, I'm not sure. I don't think I have hearing loss, even hidden hearing loss. At least not anything that's not natural for my age. I do know that it works, but as soon as I listen to another noise, such as a Youtube video, the T kicks back up again. In that sense it is reactive, but only once it's been inhibited and even then it'll just kick back up to it's "normal" level.

I threw out the residual inhibition combined with medication idea initially because I hadn't pinpointed the likely root cause of my issues, namely my neck. I'm working on confirming my suspicions with an imaging modality better suited for neck muscles such as MRI or ultrasound. So at this point I'm not willing to experiment until I get any possible neck issues properly diagnosed and confirmed.

 

[JasonP]

Here's a working theory and I'm not sure if anyone has thought of this yet. But before I go into it let me lay down some relatively well-known facts:

• There are people with hearing loss but no tinnitus.
• There are people with tinnitus but no measurable hearing loss (there may or may not be what people have termed "hidden hearing loss).
• Residual inhibition works to completely eliminate tinnitus in many people with tonal tinnitus at a single frequency, albeit it only lasts for a few seconds up to a few minutes for most.
• There are drugs known to eliminate tinnitus, such as lidocaine, trobalt, etc., in many people.
• The current theory among many researchers is that tinnitus always accompanies hearing loss, even if the loss isn't measurable.
• The current theoretical speculation also points to neuronal hyperactivity, hence why some drugs that calm down neurons seem to help tinnitus.

So here's what may possibly be happening. Perhaps in those of us that had a sudden onset of T, there may have been a hearing loss for whatever reason (acoustic trauma, ototoxicity, etc.) but it happened too quickly for the neural pathways to adapt. Hence why it may be that in other individuals with gradual hearing loss, there is no T. In those people it may have been the case that the neural plasticity was able to adapt and inhibit noise from lost signals at a more "natural" pace (I admit I'm not sure if that's really a thing).

Thus a potential therapy could be to expose a person to sounds that trigger residual inhibition (e.g. acoustic neuromodulation) for enough time for the effect to be appreciable (say at least 30 minutes if that's possible, heck I'd take 10 minutes). Immediately following the triggering of residual inhibition, administer a drug that calms down the neural pathways (e.g. GABA, trobalt, lidocaine, whatever...). Adjusting the timing here would be critical, as you'd want the drug to take effect immediately after the residual inhibition starts and before the T starts to come back. My shot in the dark theory is that this would allow the neural pathways to calm down permanently, or at least reach a point of relative equilibrium.

I know @JasonP mentioned this with respect to supplements, so what do you guys think?

Do you think the drug Riluzole could work? There is info about the drug here:

https://www.tinnitustalk.com/threads/residual-inhibition-combined-with-neuroinhibition.17265/

 

[The Red Viper]

@JasonP The link doesn't seem to go anywhere but this thread. I haven't messed around with this idea directly since I started this thread, but I do have some important updates. So I figured that my headaches, ear popping, ear whooshing, and tinnitus may have been from a neck injury I unwittingly sustained earlier this year. So I got an MRI of my neck soft tissue earlier this month. It was with contrast. Now the interesting and scary thing about it is that two to three days later I started developing this weird neuropathy all over my body. Specifically, I had a numbing sensation (but not tingling) wherein my pain sensation and deep touch seemed to dull. This is known as paresthesia. It was troubling to say the least. However, any residual pains I was used to feeling from past injuries suddenly disappeared. The tinnitus also disappeared as well. I saw my GP and neurologist, as well as an infectious disease doctor. Infections were ruled out, and I don't think it was a spinal cord injury as it also affected the sensations in my gums (which are controlled by nerves that bypass the spinal cord). I decided on a hunch that it must have been a B12 deficiency. The reason I say that is because for the two months or so prior I had switched from soy milk that was fortified in B12 to almond milk that had none. I also skipped out on vitamins for a while as well. So I decided to take sublingual B12 (methylcobalamin, it's more readily absorbed than cyanocobalamin) and I regained my pain sensations after about a week. I continued taking B12 for another week and then stopped and switched to a regular multivitamin as I figured I was topped off. However, the paresthesia is starting to come back, so perhaps while my B12 blood serum (I had it checked and it was about 750) is good perhaps it hasn't settled into my cells yet. I'll keep you guys posted.

TL;DR Some weird stuff happened where my whole body got numb/dull and I loaded up on B12 and it seemed to fix the problem. While I was somewhat numb my T disappeared.

 

[JasonP]

@JasonP The link doesn't seem to go anywhere but this thread. I haven't messed around with this idea directly since I started this thread, but I do have some important updates. So I figured that my headaches, ear popping, ear whooshing, and tinnitus may have been from a neck injury I unwittingly sustained earlier this year. So I got an MRI of my neck soft tissue earlier this month. It was with contrast. Now the interesting and scary thing about it is that two to three days later I started developing this weird neuropathy all over my body. Specifically, I had a numbing sensation (but not tingling) wherein my pain sensation and deep touch seemed to dull. This is known as paresthesia. It was troubling to say the least. However, any residual pains I was used to feeling from past injuries suddenly disappeared. The tinnitus also disappeared as well. I saw my GP and neurologist, as well as an infectious disease doctor. Infections were ruled out, and I don't think it was a spinal cord injury as it also affected the sensations in my gums (which are controlled by nerves that bypass the spinal cord). I decided on a hunch that it must have been a B12 deficiency. The reason I say that is because for the two months or so prior I had switched from soy milk that was fortified in B12 to almond milk that had none. I also skipped out on vitamins for a while as well. So I decided to take sublingual B12 (methylcobalamin, it's more readily absorbed than cyanocobalamin) and I regained my pain sensations after about a week. I continued taking B12 for another week and then stopped and switched to a regular multivitamin as I figured I was topped off. However, the paresthesia is starting to come back, so perhaps while my B12 blood serum (I had it checked and it was about 750) is good perhaps it hasn't settled into my cells yet. I'll keep you guys posted.

TL;DR Some weird stuff happened where my whole body got numb/dull and I loaded up on B12 and it seemed to fix the problem. While I was somewhat numb my T disappeared.

Wow, it stinks that sometimes the things that might help lower our T end up causing other problems. I hope you get everything as well as it can be. I apologize for the link. The correct link is here:

https://www.tinnitustalk.com/thread...iluzole-ignorant-stupid-or-worth-a-try.17437/

My question is, would taking a drug and then doing something like taking a shower or listening to whatever will cause residual inhibition (of course it would have to be at safe level) right before, during, and after the onset of action for a drug that lowers glutamate or something similar would cause a lowering of tinnitus?

 

[JasonP]

Here's a working theory and I'm not sure if anyone has thought of this yet. But before I go into it let me lay down some relatively well-known facts:

• There are people with hearing loss but no tinnitus.
• There are people with tinnitus but no measurable hearing loss (there may or may not be what people have termed "hidden hearing loss).
• Residual inhibition works to completely eliminate tinnitus in many people with tonal tinnitus at a single frequency, albeit it only lasts for a few seconds up to a few minutes for most.
• There are drugs known to eliminate tinnitus, such as lidocaine, trobalt, etc., in many people.
• The current theory among many researchers is that tinnitus always accompanies hearing loss, even if the loss isn't measurable.
• The current theoretical speculation also points to neuronal hyperactivity, hence why some drugs that calm down neurons seem to help tinnitus.

So here's what may possibly be happening. Perhaps in those of us that had a sudden onset of T, there may have been a hearing loss for whatever reason (acoustic trauma, ototoxicity, etc.) but it happened too quickly for the neural pathways to adapt. Hence why it may be that in other individuals with gradual hearing loss, there is no T. In those people it may have been the case that the neural plasticity was able to adapt and inhibit noise from lost signals at a more "natural" pace (I admit I'm not sure if that's really a thing).

Thus a potential therapy could be to expose a person to sounds that trigger residual inhibition (e.g. acoustic neuromodulation) for enough time for the effect to be appreciable (say at least 30 minutes if that's possible, heck I'd take 10 minutes). Immediately following the triggering of residual inhibition, administer a drug that calms down the neural pathways (e.g. GABA, trobalt, lidocaine, whatever...). Adjusting the timing here would be critical, as you'd want the drug to take effect immediately after the residual inhibition starts and before the T starts to come back. My shot in the dark theory is that this would allow the neural pathways to calm down permanently, or at least reach a point of relative equilibrium.

I know @JasonP mentioned this with respect to supplements, so what do you guys think?

@Cityjohn and I had a "conversation" on a thread and here is what was said:

Me: Hey John, I was just curious does residual inhibition caused partly by affecting glutamate or is it caused by something else?

Him: As I understand it, it shortly depletes the supply of glutamate in the synapses and it takes a second before the same synapses can fire again.

The drug Riluzole is supposed to remove excess glutamate or lower glutamate. Is it possible that the residual inhibition could be used for a small amount of time (say tinnitus maskers - safe volume level of course) and then take a Riluzole and wait til the drug's onset of action? Would this work? I don't really understand the brain that well, so residual inhibition may not even matter but I figured I would ask.