Retigabine (Trobalt, Potiga) — General Discussion
- Thread starter Mpt
- Start date
Member- Dec 24, 2013
- 933
- Tinnitus Since
- (1956) > 1980 > 2006 > 2012 > (2015)
- Cause of Tinnitus
- Ac. Trauma & Ac.Trauma + Meds.
@dan...Oooops yeah, sorry I spaced out on that one re "GABA" and Glutamate". Both begin with a "G" 
Interesting to know that someone had this thought though, so thanks for that. One article with Shulman (ancient history now = 2002, sums up: http://www.tinnitusformula.com/library/brain-receptors-and-tinnitus/
Whatever the answer, this study supports the concept of a final common pathway for all clinical types of tinnitus, one clinical manifestation of which may be a deficiency of benzodiazepine. It also shows that the GABA/BZ/Cl receptor is a biochemical marker for tinnitus and that treatment of this receptor has resulted in significant, long-term maintenance relief in some patients suffering from severe tinnitus.
But anyhow...Enough on this as I don't want to divert this from Retigabine and hot "K channels", etc.
Thanks for rectifying my brain fry... Best, Zimichael
Interesting to know that someone had this thought though, so thanks for that. One article with Shulman (ancient history now = 2002, sums up: http://www.tinnitusformula.com/library/brain-receptors-and-tinnitus/
Whatever the answer, this study supports the concept of a final common pathway for all clinical types of tinnitus, one clinical manifestation of which may be a deficiency of benzodiazepine. It also shows that the GABA/BZ/Cl receptor is a biochemical marker for tinnitus and that treatment of this receptor has resulted in significant, long-term maintenance relief in some patients suffering from severe tinnitus.
But anyhow...Enough on this as I don't want to divert this from Retigabine and hot "K channels", etc.
Thanks for rectifying my brain fry... Best, Zimichael
Thanks guys, I will look it up.
I agree Dan, although the doctors I've met didn't want to discuss any quote "theories". They wanted me to drop it all and get on with my life. Well, we all know how easy that is when you can't even sleep properly anymore.
I agree Dan, although the doctors I've met didn't want to discuss any quote "theories". They wanted me to drop it all and get on with my life. Well, we all know how easy that is when you can't even sleep properly anymore.
That really is remarkable. I've been wanting to post on here that the real proof of being cured would, for me, to be able to go to a movie or other such loud event without feeling bombarded. As I am right now, my cochlea/DCN can't regulate itself, so when I walk into a loud room, it stays loud instead of me gradually adjusting. If Autifony doesn't post (favorable) inclusion criteria by the end of the month, I'm definitely going to try again to get Potiga.
Yes I understand very well.
Also, it isn't really a "theory" anymore. If a doctor is dismissive of his patient, I would say move on to the next doctor. Unfortunately some doctors are not about healing patients but about making money.
Hi @cdog ,
Thanks for your comment, it's pretty late here in montreal, so I'll be short
(EDIT: I wanted to be short, but I could not resist writing a lot lol, I am such a failure haha)
I think I already covered this question a few weeks ago, maybe this is what you're looking for:
If not we can obviously discuss more in a dedicated thread or in the private chat.
I'll make an additional comment on the action potential:
Basically when you touch your hand you feel it, the nerve is transmiting an electrical message through the spine to your brain.
This is basically the action potential, so when you hear a sound, the information is transmited to your brain in a similar fashion.
Imagine each cell (axone) is closed by a membrane (voltage gated channels):
Outside you have sodium, inside you have potassium, it's a resting state.
View attachment 2640
When you have a stimuli, sodium goes in through the sodium gate and it changes the sign, it's the depolarization
View attachment 2641
Then potassium gate open to let potassium out and change the sign again it's the repolarization
View attachment 2642
Then the sodium potassium pump evacuate the remaining sodium and the cell becomes ready for another cycle
View attachment 2640
The entire cycle looks like this:
View attachment 2643
Now what happens when you have T., the potassium voltage gates don't work very well, and don't let the potassium go out correctly, it means the sign never totally change and a continuous signal is transmited to the brain, in other word Tinnitus.
If you look at the document from dr hamann:
http://www2.le.ac.uk/departments/cpp/staff/dr-martine-hamann/hamann-neuroscience-group
This is what they are talking about, the signal become heratic, burst and shit and cannot go in rest mode.
All of this because of a defficient potassium channel: Kv3.1.
The glutamate create what we call otoxicity and this phenomenon affect the potassium channels, it's locked by platicity in a very short time (days, maybe weeks).
They proved that on chicken
http://www.nrronline.org/article.as...olume=7;issue=9;spage=714;epage=718;aulast=Yu
If a drug comes and forces the specific potassium channels to act normally, plasticity will lock in the other way and those axone will be able to go in rest mode, in other words, let you experience silence again.
Hope this help !
Now I go to bed, it's 3am and I give class tomorrow morning haha ^_^
If doctors dont wanna discuss theroies then thats why a cure will never be found. If they pulles the stick out of there ass and actually listen to people instead of saying " you need therapy and you will be okay" then thats not solving the T mystery. Makes me mad.
SteveToHeal
Member
My god. I've heard so many of them say that. I read on a thread here somewhere, that's the point where you strap 2 fog horns to the guys ears and let rip. Then tell him to drop it all and get on with his life. See what he says then.
- Aug 14, 2013
- 2,455
- Tinnitus Since
- Resolved since 2016
- Cause of Tinnitus
- Unknown (medication, head injury)
Try not to explain that to your doctor. He/she wouldn't know the difference in any event.
All he/she needs to know is that it might work (if you want to pursue that option = print documentation). I do not necessarily recommend this approach. If you do consider it, I would suggest agreeing on a time-schedule in advance. It is easy to get "sucked into" the therapy protocol after commencing it (hoping that results will come if "only I continue a little bit longer...").
Yup you are right. I've tried that approach with utter failure as a result.
Great tip on the time-schedule. I will include that in my next attempt. Maybe 6-8 weeks?
And yes, I really do want to try this (Retigabine) as it makes sense from a biochemical standpoint and people here responded positively too it. Also the sooner the better? Or maybe that is a gray area still. Although the question remains, what to print? I understand that I need something rather conclusive but not too lengthy, and it also needs to come from a trustworthy source. Tricky.
@Dedas be careful about that time limit. Benryu posted a suggested schedule on here somewhere, couldn't find it with simple search, but basically, you'll need a week for every 150mg increase, and will likely need to be on 600mg/day or higher before any results are seen, so:
week one: 50mg x 3 = 150mg
week two: 100mb x 3 = 300mg
week three: 150mg x 3 = 450mg
week four: 200mg x 3 = 600mg (this is likely the very earliest you can expect results)
week five: 250mg x 3 = 750mg
week six: 300mg x 3 = 900mg (Mpt's dosage)
You're supposed to stop, absolutely, at 400mg x 3 = 1200mg/day. That's the point at which efficacy is seen to drop off in (epilepsy) patients that do respond. Given how nasty the side effects can be, you won't want to rush it. Plus it takes time to build up in your system. Six weeks could just be the start of your experiment.
week one: 50mg x 3 = 150mg
week two: 100mb x 3 = 300mg
week three: 150mg x 3 = 450mg
week four: 200mg x 3 = 600mg (this is likely the very earliest you can expect results)
week five: 250mg x 3 = 750mg
week six: 300mg x 3 = 900mg (Mpt's dosage)
You're supposed to stop, absolutely, at 400mg x 3 = 1200mg/day. That's the point at which efficacy is seen to drop off in (epilepsy) patients that do respond. Given how nasty the side effects can be, you won't want to rush it. Plus it takes time to build up in your system. Six weeks could just be the start of your experiment.
that is the theory, our only lab rat, mpt has said that after a few days he was "cured"
If you check https://www.tinnitustalk.com/threads/retigabine-trobalt-potiga.5074/page-11#post-57485, you'll note that Mpt started with 100mg x 3 = 300mg/day, then increased slowly until reaching the 900mg level. He experienced some effects after a few days, but did not feel cured until reaching 900mg. Other posters have made the mistake of ramping up too quickly. If you decide to do this, please follow the directions in the information package and expect to take least three weeks or more to reach a therapeutic dose.
Johno
Member
- Jan 8, 2014
- 231
- Tinnitus Since
- 6/07/2012
- Cause of Tinnitus
- acoustic trauma
What if Tsufferer stops retigabine? Not suddenly of course. Will T return back? Can it be even worse than before retigabine experiment? What do you think about it?
Mpt stated earlier that he is still taking his 900mg/day dose, but is considering reducing it gradually.
Here's the summation of what benryu's already explained, supported by Dr. Large of Autifony (not sure the reference). In theory what has happened to us all is that a sodium-gated potassium channel in our auditory processing system has become dysfunctional. Instead of rapidly opening and closing as it should, it's become stuck. Think about a dripping faucet in your sink. You're supposed to be able to open and close the valve, getting water only when you want it, but when you have a faulty valve, you get leakage: drip, drip, drip.
What retigabine does is "open" a set of potassium channels that include the one that's gone wrong. Opening all the way and then closing again is what the channels are supposed to do, but the faulty one has started bouncing, never quite opening or shutting all the way, creating this whine in our heads. When you force the channel open, it closes again, because of the way it's made. So there you get one full cycle of proper functioning. So long as the drug is active in your system, it will continue to open the channels for you, and nature will continue to close it. In theory, if you continue this cycle long enough, the brain's plasticity (tendency to repeat certain states) will make opening and closing properly a normal part of its cycle, as it should be, and you'll no longer need the drug to do the job for you.
Now, the big difference between retigabine and AUT00063 can be seen here, as retigabine opens a whole family of sodium-gated potassium channels - Kv2 through Kv5 - and AUT00063 moderates exactly one - Kv3.1. It's always preferable to do as little meddling with the brain as possible, and retigabine is known to have some ugly and mysterious side-effects. So AUT00063 is preferable.
Benryu also had a post some time back about spike inhibition vs. whatever AUT00063 does better. That part was over my head. The point was that AUT00063 is more likely to lead to that desirable state of plasticity taking over (or the gates being properly polarized, whatever makes sense in this context). I'd have to re-read it to get more than that. Suffice it to say, AUT00063 has a good chance of being a cure in a fairly short time, while retigabine is something you may have to take for an extended period of time. Think 4+ months. Either or both may eventually be something you can stop taking, AUT00063 probably faster than retigabine. At this point it's a bit too early to say. Personally I have no problem taking a pill or three every day for the foreseeable future. I take all kinds of vitamins now, and none of them cures my tinnitus!
Here's the summation of what benryu's already explained, supported by Dr. Large of Autifony (not sure the reference). In theory what has happened to us all is that a sodium-gated potassium channel in our auditory processing system has become dysfunctional. Instead of rapidly opening and closing as it should, it's become stuck. Think about a dripping faucet in your sink. You're supposed to be able to open and close the valve, getting water only when you want it, but when you have a faulty valve, you get leakage: drip, drip, drip.
What retigabine does is "open" a set of potassium channels that include the one that's gone wrong. Opening all the way and then closing again is what the channels are supposed to do, but the faulty one has started bouncing, never quite opening or shutting all the way, creating this whine in our heads. When you force the channel open, it closes again, because of the way it's made. So there you get one full cycle of proper functioning. So long as the drug is active in your system, it will continue to open the channels for you, and nature will continue to close it. In theory, if you continue this cycle long enough, the brain's plasticity (tendency to repeat certain states) will make opening and closing properly a normal part of its cycle, as it should be, and you'll no longer need the drug to do the job for you.
Now, the big difference between retigabine and AUT00063 can be seen here, as retigabine opens a whole family of sodium-gated potassium channels - Kv2 through Kv5 - and AUT00063 moderates exactly one - Kv3.1. It's always preferable to do as little meddling with the brain as possible, and retigabine is known to have some ugly and mysterious side-effects. So AUT00063 is preferable.
Benryu also had a post some time back about spike inhibition vs. whatever AUT00063 does better. That part was over my head. The point was that AUT00063 is more likely to lead to that desirable state of plasticity taking over (or the gates being properly polarized, whatever makes sense in this context). I'd have to re-read it to get more than that. Suffice it to say, AUT00063 has a good chance of being a cure in a fairly short time, while retigabine is something you may have to take for an extended period of time. Think 4+ months. Either or both may eventually be something you can stop taking, AUT00063 probably faster than retigabine. At this point it's a bit too early to say. Personally I have no problem taking a pill or three every day for the foreseeable future. I take all kinds of vitamins now, and none of them cures my tinnitus!
i'm fairly certain that @Mpt stated that he tapered up very quickly, it was the reason that @Christian78 initially went up quickly. it is probably a good idea to taper up slowly though.
I think you mean voltage-gated potassium channels. Retigabine targets Kv7.2 - Kv7.5. I am not a neuroscientist, but I have been doing my best to absorb as much of this science as I can, and am humbled by the complexity of these phenomena. That being said, I am fairly certain that your characterization is not very accurate, and though well intentioned, is not exactly helpful in simplifying this.
Christian78
Member
- Dec 17, 2013
- 965
- Tinnitus Since
- (Sep 2013)
- Cause of Tinnitus
- progressive tinnitus, time of expiring in next 3-6 months
I did try as Mpt , he wrote me use 3 day 100, 3 days 200, and then 300 times 3 per day. second time i tried much slower than Mpt, he used it extremely fast and he is on higher dosage.
- Dec 24, 2013
- 933
- Tinnitus Since
- (1956) > 1980 > 2006 > 2012 > (2015)
- Cause of Tinnitus
- Ac. Trauma & Ac.Trauma + Meds.
So..."To Potiga or Not to Potiga ~ That is the question?!"
Is anyone else taking Potiga/Trobalt/Retigabine yet?????????????
I am unfortunately starting to come down off my "mountains high" (as expected) and having to face the normal mundane aspects of chores, bills, Tinnitus isolation, 'what the hell to do next with my life', etc., etc., etc.
Before I went away the Potiga trial was pretty much top of the list and I was considering by-passing the local CVS pharmacy (and their 'full box' requirement = > $$$$$) and going via the Canadian pharmacy my doc's assistant recommended.
Other options to Potiga were some suggestions by my doc to modulate "hyperneurosensitivity-reactivity" via Lidocane injections close to the ganglia in upper spine/neck...Plus a few other less exotic ideas. These now seem unlikely to help as I suspect from all of @benryu has so elaborately explained, that those hyper-reactivity elements are Glutamate related and that train left the station many years ago at the "onset" period of damage. Not for sure of course, as I do believe neuro-excitation can be ongoing with specific chronic infections (like endotoxicity c/o mold say, that can trigger all kinds of crap including anxiety, insomnia, 'wired-yet-tired' stuff...which all sounds like 'neuro-excitation' to me! By the way, very simply speaking, I consider the "excretions" of toxic microbes - be they bacterial, or fungal, to be potential neurotoxins. Kinda like pissing and shitting in a stream...contaminates the water so it has to be purified ('detoxed' - by Cytochrome P450 pathways and their kin) before use. Not sure if viruses "excrete"...Mmmmmm ).
Anyway, as I seem to have an unfortunate history of reacting badly to many meds (though surprisingly not to some that are generally poorly tolerated - so it is inconsistent) I was really hoping more "guinea pigs" would be out there doing this before I stepped in. I realize that AUT00063 is the way to go, as Retigabine is a shotgun approach and the scatter is going to hit more than just the potential Kv3.1 channel. As most folks probably know..."side effects" are almost by definition, crap getting hit that is not the intended target but gets caught up in the artillery barrage. I guess collateral damage would be the term and is part of the cost/benefit equation.
So..."To do or not to do???!!!" Ha, ha...Yeah i know what the response out there will be, seeing as I have a scrip and a source! But...boy I am not too keen on getting trashed without any on the ground support.
Mmmmmmmmmmmmmm....So back to my question. Is anyone else close to getting on board with this stuff??? Matt's new-found life in the auditory world is sure good news and very encouraging. And AUT00063 could be many years off still until it is available to the general public.
Best, Zimichael
Is anyone else taking Potiga/Trobalt/Retigabine yet?????????????
I am unfortunately starting to come down off my "mountains high" (as expected) and having to face the normal mundane aspects of chores, bills, Tinnitus isolation, 'what the hell to do next with my life', etc., etc., etc.
Before I went away the Potiga trial was pretty much top of the list and I was considering by-passing the local CVS pharmacy (and their 'full box' requirement = > $$$$$) and going via the Canadian pharmacy my doc's assistant recommended.
Other options to Potiga were some suggestions by my doc to modulate "hyperneurosensitivity-reactivity" via Lidocane injections close to the ganglia in upper spine/neck...Plus a few other less exotic ideas. These now seem unlikely to help as I suspect from all of @benryu has so elaborately explained, that those hyper-reactivity elements are Glutamate related and that train left the station many years ago at the "onset" period of damage. Not for sure of course, as I do believe neuro-excitation can be ongoing with specific chronic infections (like endotoxicity c/o mold say, that can trigger all kinds of crap including anxiety, insomnia, 'wired-yet-tired' stuff...which all sounds like 'neuro-excitation' to me! By the way, very simply speaking, I consider the "excretions" of toxic microbes - be they bacterial, or fungal, to be potential neurotoxins. Kinda like pissing and shitting in a stream...contaminates the water so it has to be purified ('detoxed' - by Cytochrome P450 pathways and their kin) before use. Not sure if viruses "excrete"...Mmmmmm ).
Anyway, as I seem to have an unfortunate history of reacting badly to many meds (though surprisingly not to some that are generally poorly tolerated - so it is inconsistent) I was really hoping more "guinea pigs" would be out there doing this before I stepped in. I realize that AUT00063 is the way to go, as Retigabine is a shotgun approach and the scatter is going to hit more than just the potential Kv3.1 channel. As most folks probably know..."side effects" are almost by definition, crap getting hit that is not the intended target but gets caught up in the artillery barrage. I guess collateral damage would be the term and is part of the cost/benefit equation.
So..."To do or not to do???!!!" Ha, ha...Yeah i know what the response out there will be, seeing as I have a scrip and a source! But...boy I am not too keen on getting trashed without any on the ground support.
Mmmmmmmmmmmmmm....So back to my question. Is anyone else close to getting on board with this stuff??? Matt's new-found life in the auditory world is sure good news and very encouraging. And AUT00063 could be many years off still until it is available to the general public.
Best, Zimichael
- Aug 14, 2013
- 2,455
- Tinnitus Since
- Resolved since 2016
- Cause of Tinnitus
- Unknown (medication, head injury)
That's probably not a bad description. I would, however, go one step further and say that the shotgun is pointed in the wrong direction...
At this very particular moment in time, you should wait one or two weeks and see if by some miracle you get admitted onto the AUT00063 trial. Depending on the outcome of that, you can then decide whether to become a Trobalt-guinea pig or not.
My suggestion.
Christian78
Member
- Dec 17, 2013
- 965
- Tinnitus Since
- (Sep 2013)
- Cause of Tinnitus
- progressive tinnitus, time of expiring in next 3-6 months
first day without tinnitus, i had in morning took pill and some sound that help rewire brain, and i painted a room, been to sop, anyway today without tinnitus after one year. i hope it last longer.
That is great news Christian! I'm so happy for you and I hope it continues to get better and better
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