Any Supplement or Medicine That Can Reduce Tinnitus Caused by a "Glutamate Storm"?

I think this is what happened to me that caused almost all of my tinnitus: Glutamate Storm. The following link talks about it. Whether or not its 100% accurate I don't know but as I think more about it, I do think my tinnitus was caused by excess glutamate.

http://nutritionreview.org/2014/07/silencing-tinnitus-new-research-seeks-to-reduce-ringing-in-ears/

Also, I want to add that tinnitus can go down or disappear for people so I don't want anyone scared by reading that article.

 

What makes you think that you had a glutamate storm? You had an infection or an acoustic trauma, or an inflammation of other cause?

 

I was trying to come off benzodiazapines and then came across a loud noise. That is the recent one.

 

Yes yes. I also want to ask that question. Is there any chance to reduce glutamate levels? Mine is benzo induced so it must be related to glutamate storm.

 

Bump

 

It's all very complex and poorly understood. Glutamate is required for the biosynthesis of GABA...

Presumedly, most tinnitus is caused by a glutamate "storm". Excitotoxicity.

 

This is exactly what happened in my case. But, I wonder will this new drugs be efficient in that type of tinnitus? AM-101, Trobalt, SF0034 etc.

 

Time will tell! In the meantime we have benzos, barbiturates and alcohol, just don't go overboard....

 

Are barbituates good for noise induced tinnitus once benzo tolerance happens?

 

Barbs are basically benzos with much more danger attached. They were groundbreaking in 1945, but not very useful in a world that has access to diazepam.

 

I thought it was interesting when I saw that the barbituates had another binding site on this video. Not sure if it means anything though.

The GABA receptor | How does it work?

 

Yeah, they're interesting drugs. The ratio of effective dose to lethal dose is small compared to benzos, though. Caution is advised.

 

@JasonP - I came across a very interesting article that discusses the complex relationship between GABA and glutamate, as well as other factors involved. The article doesn't address tinnitus specifically, but does mention disorders/diseases caused by excitotoxicity damaging neurotransmitters and/or their functions.

It's a long article, and well worth reading. Short link: http://bit.ly/1TNkKXt

Excerpt:

Note: As far as I know, "pandas" in this article refers to pediatric-onset neurological disorders or something similar.

 

One question I keep coming up to is how long does this glutamate storm last? What's the window of opportunity to stop it before the damage is done? Can it be an ongoing glutamate excitotoxicity, or is it a single event?

 

Good question. And I want to add some more to this. I had my T when I quited a benzo abruptly. Is this storm still going on or the damage is done? Why do some people get rid of their Ts after w/d and some not? Does this storm damage to hearing cells or neurotransmitters?

I really do not know why it is so complicated if the cause of this exitotoxicity is known. What are looking for to reverse to damage?

 

A Glutamate storm typically lasts for several minutes to several hours. You will feel it as it hits your face like an XTC pill.

That's not accurate. Glutamate is understood, it mediates the great majority of signals between neurons in the mammalian brain. It is as important to the nervous system as red blood cells are to the circulatory system. There are several institutes that specialize solely in glutamate neurotransmission.


This is a really interesting thread. I'm currently extremely busy but will come back to research the role of glutamate in tinnitus. I was not aware that Benzodiazepine withdrawal had anything to do with the glutamergic system and glutamate metabolism within the brain, this changes things a little bit. Thusfar excitotoxicity causes permanent and conventionally irreparable damage to the neurons it affects.
I see now that Benzo's increase the GABA metabolism which would force the body to produce excess glutamate. Obviously this will lead to excitotoxicity. I don't believe benzodiazepines were ever meant for prolonged use, and they certainly should not be prescribed for long use.

That's not so hard. Benzo's are Roche's primary source of income, between them and the MSG food industry there is several hundred billion dollars working to discourage any link between glutamate metabolism altering drugs, or just glutamate, and brain damage.
There is a doctor I've been wanting to interview on this topic and I should probably work on an interview so that we can publish it on tinnitushub, again I'm really sorry, I'm very busy at the moment.

 

There have been a considerable number of studies about structural brain changes from benzos, which have come to conflicted results. Ashton does not believe that benzos cause what we'd consider "brain damage"; I tend towards taking her word on that until proven otherwise.

The pharmaceutical industry is pretty terrible, as are all multibillion dollar international conglomerates, but these drugs serve a useful purpose.

Personally I don't feel that no one should, or should be able, to elect to use benzos long term... they should just be better educated as to the tradeoffs. It's pretty clear that benzos over time are a lot less caustic to the body than chronic alcohol consumption. That's an easy argument to make because booze is so staggeringly bad for you, but people know that and consume it anyway.

@Cityjohn , what I meant by "it's complicated" is the link between dietary glutamate, GABA synthesis, stress and neurology. It's all connected, and much more complicated than "avoid glutamate".

 

I don't know why but I begin to think my case is not curable. The "permanent damage" makes me feels so depressed. So does it mean that the upcoming drugs are not for drugs induced tinnitus?

 

The same case can be made for leaded gasoline, and nuclear deterrents. I'm not so much interested in it's usefulness as how to deal with it's misuse and the complications that arise.

In the Netherlands benzodiazepines use is restricted. I'm very glad I was not able to elect more use of Oxazepam.

Thank you for your input.

 

I assume you are talking about your symptoms from the poisoning. How do you know the amount of MSG that you consumed?

But what about glutamate excitotoxicity triggered by acoustic trauma? From my understanding acoustic traumas can immediately kill the hairs or nerve connections in extreme cases like an explosion, but more often the connections to the nerves weaken and begin to die off over days to months.

For me, I suffered a short duration acoustic trauma that I knew right away affected my hearing, but the loud ringing did not set in till several days later. In hindsight, I'm pretty sure it affected my ultra high frequency hearing and that's where my tinnitus lies.

Auris put out an interesting video touching on the subject of this: http://media.corporate-ir.net/media_files/IROL/25/253572/webcast/Marlies Knipper v2.mp4

 

No I'm not. It's called a storm for a reason. It typically happens suddenly in large parts of the brain and results in what could be seen as catastrophic damage. The word storm has been chosen to make the analogy to something that comes in fast and wrecks havoc.

As I understand it Benzo's drive up the production of GABA. Should you suddenly stop to provide the brain with artificial incentive to metabolize that glutamate into GABA, which is the only thing that can save you from all that glutamate, you're going to have a severe problem with elevated levels of intercellular glutamate. I'm pretty sure it says in the pack booklet that you can not stop taking benzo's cold turkey if you've taken them for a longer period.

The acute symptoms of MSG ingestion are well known, both with my academic internist, and in literature. There is a physical lower reaction, and a clear visual upper, limit to the dose. And finally the brain barrier permeability that was taken into account to calculate the systemic dose, and ingested doses.

This is not colloquially known as a storm.

You've mixed up three different things here; Acoustic trauma that kills hair cells, acoustic trauma that does not kill hair cells allowing them to excite the axon to death, and an unspecified form of neuronal degeneration over time. I'm not familiar with a mechanism of action in which acoustic damage could cause neural degeneration over time.

Tinnitus does not result because of hearing damage per se. The problem lies in the signal processing of the CNS. The CNS periodically monitors the signal coming from the ears and eyes and cleans it up by setting a threshold of hearing per frequency to mask sounds not coming from the outside world.
When the synapses in the cochlea or anywhere in between the cochlea and other filtering centers go nuts, the signal will no longer be interpreted as internal noise because a sufficient number of synapses are giving the same signal at the same time. This is why we get a relatively high volume of tinnitus suddenly as opposed to gradually increasing.
The mechanism here is not as sophisticated as it may seem, it emerges naturally from the way the circuit is hooked up. The reason I know this is because as an amateur astronomer and neurology hobbyist I had simulated the optical nerves and calculated the thresholds because we wanted to learn about our limits with the naked eye.

According to that presentation the CNS filters signals by proportion, meaning that when 5% of the signal is a high pitched noise you're fine. Until you lose 90% (arbitrary) of the other synapses, in which case 50% of what is left is creating a noise that your CNS no longer interprets as noise to be filtered.

There are multiple ways solve this problem, AM-101 attempts to inhibit the signal being produced at the synapses, it is a targeted non competitive neural inhibitor. The doctor also mentioned that repair of the ribbons would help, the question is whether we can repair them so long after damage. The problem is that the glia clean up the dead cells and you're left with a very clean loss of neurons. The question here is whether BDNGF can cause the synapses that are left to sprout new dendrites to increase the population on which to base the signal filtering. Another way is to change the threshold of noise filtering in the brain stem by means of devices like the mute button, or the vagus nerve stimulator.

That's a very interesting presentation. I believe I can very easily develop a way to do Auditory Brainstem Response Audiometry. I'll look into that.

To summarize, whatever your cause, the end result is the same for all tinnitus sufferers, and so are the solutions. To remain relevant to the thread, if you're expecting a glutamate storm, the best thing you can do, the same that an ambulance would make you do, is to ingest large amounts of vitamin C, anything above 2 grams is fine.

 

I got my T when I was 6 weeks out of the drug. It sounds weird this storm took place this late. But I know it is the case because I got very severe vertigo attacks two nights in a row before T came. I think it was when the storm took place in my brain.

There has been 4 months since the damage is done. I wonder if it is still too late to do something for it.

 

@Cityjohn - researchers at the university of Michigan have observed in animals, that following severe acoustic trauma, there is a decrease in auditory fibers in the dorsal cochlear nucleus... and in tinnitus animals, a subsequent increase in signaling in sensory fibers.

Do you know enough about the neurology to speak to how this observation relates to what you've already said in this thread? UofM believes there is a path towards a novel and noninvasive treatment in this work; a preliminary human trial was recently completed.

 

@Cityjohn - relevant video with regard to previous post:

"The Neural Bases and Neuroengineering of...

 

Of the top of my head I can see how there could be a decrease there but for it to have any meaning there would have to be a comparison to the cochlear post synaptic neurons, the ribbon synapses, and the ventral cochlear nucleus. Signaling would follow from sound i.e tinnitus but unless there is increased signaling in the DCN without any signaling before that we can't say if it originates in the DCN.
I don't see how that knowledge yields a novel and noninvasive treatment.

I had not yet viewed the trigeminal system in a way that could be used to mask sound stimulation.

 

Thanks for the explanation @Cityjohn.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2812055/

That makes sense. That better explains what I have been assuming for some time.
This may be veering a little off topic, but I wonder if certain people are more susceptible to getting tinnitus, or rather not being able to filter out internal noise. I for one have always had a difficult time filtering out external 'noise' long before I ever got tinnitus. Hearing things like a CPU fan going out or a cracked transformer would irritate me especially if I was stressed. That's another good question, can stress interfere with the brain reacts to a change in input or sudden sensory loss?

The thing I don't understand is why is this cascade of changes so permanent once they occur and why can't the brain relearn to filter out this errant signal?
People tend to lose their ultra high frequency hearing with age, but the vast majority never get ultra high frequency tinnitus.

 

@Cityjohn if you get a chance to watch or skim the video, I'd be curious to know your reaction. I think you have a much better grip on the neuro side of this; I'm just a web hacker and everything I know about signal processing and neuronal communication, I've learned on the side...

 

@Cityjohn , first just let me say, AGAIN , that your presence and input on this site is a gift. I enjoy reading your mind (ha ha - I mean: reading the CONTENTS of your mind) and am grateful for your posts.

With regard to AM-101 and its theorized mode of action, I am curious about something. In one of their published research papers, Auris has a chart which shows that the people who respond well to this drug begin to show their decrease in tinnitus volume somewhere between 25 - 35 days AFTER the injections are administered. For the first 25 days (in general, I suppose, as individual responses may have varied), their sound perception is the same (and also note: the study participants often get a week or two of increased tinnitus from the procedure itself, blocked ears, etc. But between about 14 days to 25-30 days, the chart still shows the same tinnitus volume perception level.).

Any particular reasons you can surmise/intuit as to that timeline?

Thanks!

 

@Alue I agree with this! If only about 10% of the population gets tinnitus, and we KNOW that many more have hearing loss, whether age-related or other, then there MUST be some predisposing factors for the "tinnitus susceptible." After all, this can also relate to stress, and who gets the ulcer, and who the heart attack, and etc. So our neurological systems are probably susceptible. And like you, I have had a lifelong hard time with extraneous irritating environmental noises. I'm also acutely sensitive to many types of stimuli, from visual to tactile.

 

I'm going to answer very succinctly because I have a metric ton of maths to absorb before 6 pm.

This is a very good paper and I had read it a few months ago. There's a slight problem in their premise though as a big load of glutamate at the nerves would also be perceived as very loud tinnitus, and the body very quickly metabolizes glutamate, within hours it would have to be gone.
Then there's another thing, they don't specify if the loss of neurons over the course of several months are alive or dead before being lost. It's obvious they should be lost if they're damaged because the glia around the neurons clean up dead cells, and that could indeed take several months.

According to this study there is such a thing as resilience to tinnitus. https://www.sciencedaily.com/releases/2015/08/150827121921.htm

Yes, furthermore extended periods of stress will damage the glia making your neurons much more susceptible to glutamate damage or general excitation.

I did watch, the video provides a good insight into the use of the trigeminal nerve to mask tinnitus which is quite interesting. The trigeminal nerve is easily accessible for therapies and it also explained why there is such a thing as somatic tinnitus. Basically the nerve for motion and touch that goes to your cheek is interlinked with the cochlear nerves and it can be used to influence it.

None other than the brain is a very slow organ and perhaps the dose they use is very small.
I'd like to point out that I haven't closely looked at AM-101 other than to see that its a ketamine derivative. Ketamine is a horse tranquilizer and can cause consciousness altering effects. I have no idea how it would help.