Retigabine (Trobalt, Potiga) — General Discussion

[mmacabre]

I'm pretty sure the pills are coated, and that it also comes in a 50mg dose (mostly for geriatric users, for example someone with liver or urinary problems)

 

[rtwombly]

OK enough on this, though I guess I am at least going to try and decide withing the next few days whether to get some Potiga. For sure though I intend to 'disobey' the instructions and cut 100 mg pills into 50's. I can see no reason why this is given such emphasis by GSK as it is not an enteric-coated pill from what I have found to date or some "multiplex" chemical that needs all parts like can happen in capsules where there are lots of little tiny coloured balls of med making up the 'whole'. Maybe I will phone GSK and try to find out in a roundabout way c/o my "white coat" persona.

We know for sure there's no time-release coating, but I'm unsure about enteric coating. It may just be that the makers of retigabine are concerned you're getting exactly the right dosage: http://www.webmd.com/healthy-aging/news/20040519/cutting-pills-in-half-could-pose-problems mentions problems with dosing.

I'm going back and forth in my mind right now. I lost my health insurance last month, but will have insurance starting September 1, and there are a few different doctors I could ask about Potiga. We're so close to the Autifony trials, though, I don't know if it makes sense to go that route. Just today I watched a video about a little girl had to have an operation to eliminate seizures and was left developmentally challenged. It made me pause because one of the precautions with retigabine is to reduce dosage gradually if you are coming off to avoid triggering "rebound" seizures.

The sensible thing seems to wait until the end of the week and hope we have info on the AUT00063 trial. If we don't hear anything, I may try again for Potiga. I'm sick of living with this ringing if I don't have to.

 

[SoulStation]

That's great news! Be sure to tell your neurologist you will have your eyes examined before and every six months while on the drug to make sure you don't get any eye damage. This way he knows you're on the look out for side effects. Physicians are often hesitant to give drugs with serious side effects, especially with a non-threatening condition. That said, if you present yourself as an intelligent, cautious patient--aware of the risks, but suffering greatly--he may agree to give you a trial run.

You need to do a little savvy salesmanship!

Good luck and tell us as soon as you see your neurologist!

Thanks jazz. I am seeing someone ASAP. Not expecting to get an rx but want will try.

 

[Zimichael]

@rtwombly ..Yeah I hear you about caution, however if i look at the list of side effects at a lot of the meds I have taken over the years they make your hair stand on end! Freaky stuff and usually a list about a mile long.

Regarding cutting the pills...My intention would be to start on 5o mg per DAY total, for a while and taper up really slow. At this level I have no qualms about it being 45 mg or 55 mg if I cut the pill wrong.
I doubt I would ever get close to Matt's dose as I tend to react pretty quickly to nearly any med I have taken no matter what the label says. Also my plasma concentration would be hit at much lower dose than 300 mg TID (the recommendation).

The Canada pharmacy price for 50 mg and 100 mg is almost identical, so I would go for the 100's for that reason.

For me, after all this time, the "ringing" per se as not as bothersome as what it does to my life...On my own, in quiet I can handle it. It's doing almost anything out in the 'world' that is the problem (camping in the wilderness aside). It's too darn noisy out there and thus restricts to a very narrow band of functioning that ain't much of a "life". I don't particularly want "isolation" as a mandate for the next X number of years...But I also have great respect for the screw-ups meds can cause..just look at my T and H as examples!!!

Nothing on Autifony's website yet saying what, when, where the next trails will be...and my chances of getting into Phase II are about zero. My history with T is too long and too complex to be acceptable. If I was a researcher I sure would not take me, unless I wanted to REALLY test if the stuff worked on a tough nut case.

It will most likely have to be "commercial availability" before I can get it...unfortunately.

Best

 

[dan]

Thankyou @Markku , @Johno , for Trobalt prices.

Anybody in UK can check?

 

[Hengist]

The sensible thing seems to wait until the end of the week and hope we have info on the AUT00063 trial. If we don't hear anything, I may try again for Potiga. I'm sick of living with this ringing if I don't have to.

What will you even get from that trial info? Unless you are willing and able to get into the trial there is no reason to delay getting retigabine.

Anyway does anyone have any info on how to get onto AUT00063 trial?

 

[attheedgeofscience]

Nothing on Autifony's website yet saying what, when, where the next trails will be

Mr. Large has already confirmed that the trial information will be made available by the end of August or in September. My other source has confirmed that the reason why that information is still pending is because the study itself ie. phase II has not been approved yet (by the regulatory authorities). I assume that this is only a formality (needless to say) ie. it will happen (of course). But until then, no information will be made available - for obvious reasons (you cannot start recruiting until your are entitled to do so - even if that entitlement is a given).

...So keep watching the Autifony website: I imagine there will be a banner on the main homepage once phase II is started (ie. you won't have to search for the information). My guess...

and my chances of getting into Phase II are about zero.

Quite possibly. The Internet has its strength and weaknesses. One of the weaknesses is that information is universal and instant (in a situation like this) ie. complete transparency (eg. why would you buy an airplane ticket from one supplier when another can provide the same service for $100 less...?).

Last week, when I provided information "to the Internet" that the trial would likely be open to non-UK nationals, I - in a sense - decreased my own chances of getting a "ticket" (given that there are so few "seats" available). Should I have withheld that information to boost my own chances? Does this line of thinking make sense...?

If I was a researcher I sure would not take me, unless I wanted to REALLY test if the stuff worked on a tough nut case.

Either you fit the inclusion criteria or you don't. You won't know until the hard facts are presented.

If you start "shooting up" with Trobalt, you could potentially risk not being eligible for the trial.


Take care.

 

[rtwombly]

For me, after all this time, the "ringing" per se as not as bothersome as what it does to my life...On my own, in quiet I can handle it. It's doing almost anything out in the 'world' that is the problem (camping in the wilderness aside). It's too darn noisy out there and thus restricts to a very narrow band of functioning that ain't much of a "life".

Even with my relatively short history I completely understand what you mean. The worst part of this condition is not knowing what will cause it to spike and being afraid of social situations / hobbies/ whatever that most people don't think twice about participating in.

What will you even get from that trial info? Unless you are willing and able to get into the trial there is no reason to delay getting retigabine.

Anyway does anyone have any info on how to get onto AUT00063 trial?

I'm hoping to get into the U.S. trial. I'm mildly hard of hearing and under 12 months from onset, so think I will be a good candidate.

Even if I did not have this opportunity, though, if I knew we would shortly have more information about the efficacy of AUT00063, it would make me more inclined to be patient. If the first three candidates from on here said, "I took one pill and I'm cured," for instance, it would shrink the difference in my mind between titrating on to retigabine over the course of 4-6 weeks and waiting for phase III/FDA approval, though granted that may be a long ways out.

@ateos good point about starting retigabine now. At best you'd have to go through a 30-day washout before starting AUT00063.

 

[linearb]

I was able to get a potiga prescription very easily, it almost seemed "too easy". My doctor told me to check with a neurologist, the first neurologist I found on google who took my insurance and was able to see me quickly said "oh sure Potiga, this would be an off label use, that sounds fine". He wants me to start at 100mg/day and see what happens.

 

[Hengist]

I was able to get a potiga prescription very easily, it almost seemed "too easy". My doctor told me to check with a neurologist, the first neurologist I found on google who took my insurance and was able to see me quickly said "oh sure Potiga, this would be an off label use, that sounds fine". He wants me to start at 100mg/day and see what happens.

Why is that too easy? You found a doctor that is not conservative go with the treatment.

 

[linearb]

I've been taking a bunch of suppliments and mumbo-jumbo crap, and in general I have a couple drinks a day. I'll probably hold off on starting this for at least a day or to, to wash all that crap out of my system.

 

[Hengist]

Why? The reason you are starting slow is for your body to get used to it, you are not doing this as something that is a special circumstance short term temporary thing. As you can see the others using it are living normally, taking whatever else they took.

 

[linearb]

Because I've been burned by drugs in the past, and only ~10k people in the world have taken this stuff ever as far as I can tell - so there are bound to be bizarre edge case interactions that are not documented yet.

I've also got to do some more soul searching about what I really want to do. I was basically looking for a neurologist's opinion on this, and not expecting to get a prescription so quickly. The other thing I've been considering is just going back on benzos because I know from experience that a pretty low dose of valium (maybe 6-8mg) almost completely silences my tinnitus. So, if I am at the point of wanting to try a drug for this again, then I have to weigh the wealth of data about the long-term risks of benzos, against the lack of data about a novel drug that's only been on the market for 5 years.

This stuff (Potiga) has only existed as a prescription since 2009, has been used by a pretty small number of people, and has a black box warning on it. It's known to cause seizures if the dose is reduced too quickly. Anyone who doesn't think it's potentially a very dangerous thing to be messing around with is kidding themselves.

If I was going to be on something long term, I would absolutely, unquestionably, choose valium over Potiga. The thing that is tantelizing to me about Potiga is the theory that it could be used relatively short-term to cause a long-term reduction in the ringing. But, that's a very, very theoretical idea.

 

[Golly]

Because I've been burned by drugs in the past, and only ~10k people in the world have taken this stuff ever as far as I can tell - so there are bound to be bizarre edge case interactions that are not documented yet.

I've also got to do some more soul searching about what I really want to do. I was basically looking for a neurologist's opinion on this, and not expecting to get a prescription so quickly. The other thing I've been considering is just going back on benzos because I know from experience that a pretty low dose of valium (maybe 6-8mg) almost completely silences my tinnitus. So, if I am at the point of wanting to try a drug for this again, then I have to weigh the wealth of data about the long-term risks of benzos, against the lack of data about a novel drug that's only been on the market for 5 years.

This stuff (Potiga) has only existed as a prescription since 2009, has been used by a pretty small number of people, and has a black box warning on it. It's known to cause seizures if the dose is reduced too quickly. Anyone who doesn't think it's potentially a very dangerous thing to be messing around with is kidding themselves.

If I was going to be on something long term, I would absolutely, unquestionably, choose valium over Potiga. The thing that is tantelizing to me about Potiga is the theory that it could be used relatively short-term to cause a long-term reduction in the ringing. But, that's a very, very theoretical idea.

Hi @linearb:

I respect your caution. I, too, am wary of a relatively new drug with serious potential side effects. I just wanted to mention that Benzodiazapines, like Valium, can also lead to seizures if discontinued abruptly. I bring this up only to put that particular risk of Potiga into perspective. Whatever you choose, I hope you find relief.

Best, Golly

 

[linearb]

I know all about benzo risks unfortunately, having been through two different, miserable, protracted tapers. If I ever go back on them, I think I'm more or less going on them for good.

For all I know, the benzos are a big part of the reason that my tinnitus today is so much worse than it was before I was ever on them...

 

[cdog]

I was reading this paper http://onlinelibrary.wiley.com/doi/10.1111/j.1528-1167.2011.03365.x/full on the mechanism of action of Retigabine, and it has a section called "Effects on other K+ channels", which says :

To ascertain whether the effects of RTG/EZG were selective for KCNQ channels over other K+ channels, a range of functional electrophysiological studies have been conducted on exemplar channels from other families that make up the K+ channel superfamily (Alexander et al., 2008). RTG/EZG was shown to be without significant activity at members of the 2TM K+ family of channels (e.g., inward rectifiers KIR 2.1 [IRK1] or KIR 3.1) as well as 4TM family and the 2-pore domain channels, such as K2P1.1 (TWIK1) at concentrations ≤100 μm. Members of the 6TM family e.g., Kv1.5, hERG, which includes voltage-gated [Kv] channels and EAG and Ca2+ activated channels (in addition to KCNQ channels), were also relatively unaffected, with IC50 values of >50 μm and 59 μm, respectively (GSK/Valeant data on file, personal communications). These data emphasize the remarkably selective action of RTG/EZGon a subset of K+ channels, namely KCNQ2–5 over the broader superfamily of K+ channels that occur in humans.

(emphasis mine)

The 6TM family are the voltage gated (i.e. Kv) channels, which they are saying were relatively unaffected, except for the Kv7-5 (aka KCNQ2-5) which the drug targets.

Autifony's AUT00063 targets Kv3, so it would fall in the 'relatively unnaffected' set, according to the above. Still, 'relatively unnaffected' could mean many things - such as, for instance, "affected but only at large drug concentrations".

 

[Hengist]

Because I've been burned by drugs in the past, and only ~10k people in the world have taken this stuff ever as far as I can tell - so there are bound to be bizarre edge case interactions that are not documented yet.

I've also got to do some more soul searching about what I really want to do. I was basically looking for a neurologist's opinion on this, and not expecting to get a prescription so quickly. The other thing I've been considering is just going back on benzos because I know from experience that a pretty low dose of valium (maybe 6-8mg) almost completely silences my tinnitus. So, if I am at the point of wanting to try a drug for this again, then I have to weigh the wealth of data about the long-term risks of benzos, against the lack of data about a novel drug that's only been on the market for 5 years.

This stuff (Potiga) has only existed as a prescription since 2009, has been used by a pretty small number of people, and has a black box warning on it. It's known to cause seizures if the dose is reduced too quickly. Anyone who doesn't think it's potentially a very dangerous thing to be messing around with is kidding themselves.

If I was going to be on something long term, I would absolutely, unquestionably, choose valium over Potiga. The thing that is tantelizing to me about Potiga is the theory that it could be used relatively short-term to cause a long-term reduction in the ringing. But, that's a very, very theoretical idea.

Seems to me like you are looking for someone to talk you into taking it as you are scared. This is something made for people with epilepsy and they take it for life so it is not something that is made to be used short duration. That means the drug safety profile must be higher and those people using it are taking it to make their lives normal, not to live under a glass bell. You are worrying too much.

 

[benryu]

Hey guys,

I am kind of off at the moment as I have a lot of work, I see a few discussion around topics that I already covered, maybe it can help to quote some info here! :

I see many questions about the drugs acting on potassium channels.
Here is a technical but clear view on some of those drugs. (Flupirtine, Retigabine, AUT00063)

First and most importantly, potassium channel modulators should not be compared, there is a ton of parameters and subtilities that can change drastically the impact of one drug.

Flupirtine acts mainly on the Kv7.3 , retigabine specifically acts on the neuronally expressed KCNQ2-KCNQ5 (Kv7.2-Kv7.5) channels, AUT00063 will act on the Kv3 channels.

Talking from a neuronal perspective, Kv7 and Kv3 mediate the channels and more precisely the action potential.
The action potential is an electrical signal generated near the cell body of a neuron that propagates along the axon to the axon terminals.

After an acoustic trauma, or after taking some drugs such as quinine there is an interference with the excitability of spiral ganglion neurons (The evil glutamate is guilty ). The membrane potential changes and the modification of the action-potential waveform induced by the problem put the individual in a T. state.

Going back to the potassium channels, Kv7 channels primarily control the interspike interval with a limited effect of the repolarization. Kv3 channels control the repolarization of the action potential and are expected to induce a new state.

The idea is to open the right channels to lead to a neuronal hyperpolarization, thereby stabilizing the membrane potential and decreasing excitability.(No or very little Tinnitus)

Conclusions:

• Despite a drug being potassium channel opener, it has to be very precise to work.
• Flupirtine doesn't act on any sub unit related to T. ( So no possible impact)
• Retigabine acts on interspike interval, meaning less T. spikes and it can possibly repolarize the action potential for some people. But the sub unit range is too wide with numerous side effects. (so it can work to stabilize T. and decrease it to some extent, but is not specific enough to be viable.)
• AUT00063 acts directly on the repolarization and is much more precise, so it's a viable solution providing it works as expected

The impact of retigabine on Kv3 is not necessary related to dosage but more a "physiological response" to the drug, like a positive externality if u will, I don't want to get in the details of this here YET because it would be 3 or 4 pages of explanations with maybe 10 or 15 concepts we did not cover yet together. I promess I'll do it in a dedicated section when the time is right!

I know that @cdog will not have enough of this, so check synaptic calcium ions increase and transporter modulation, I am sure you'll figure out what I meant above <3

Other points for the benzo stuff, this is shit, in a discussion with another member here is what I think:

Drugs such as benzo, lorazepam accelerate brain plasticity, doctors who prescribe it to accute T. patients are idiots.
A well known article demonstrates the following point on other area of the brain, but the idea is the same:
"These findings indicate that a decrease in GABA-related inhibition facilitates practice-dependent plasticity in the human motor cortex, whereas an increase depresses it."
http://www.ncbi.nlm.nih.gov/pubmed/11353733

Lorazepam increased your plasticity and you did not benefit from the time your brain process the information to restructure the brain. In other word, the natural decrease of T. perception thx to plasticity lag.

Last (and maybe least) haha, I think I saw some of u talking about lidocain:

This is just a much more elegant way to say what I wrote above, Lidocaine or Phenytoin are strongly linked to sodium / potassium channels. Lidocaine is a sodium blocker and Phenytoin reduces the amplitude of sodium-dependent action potentials through enhancing steady state inactivation of sodium channels.
In simple words they close the sodium valve in the brain, and here in our case in the auditory system. By doing so, sodium channels are at the level of the defective potassium channel common to chronic T. sufferers. (THis is why it turns off the T. for a moment, but it's not the good philophy, and it's not targeting the specific P channel).

In fact, as soon as the drug is gone sodium become dominant again and prevent the auditory system to go back in a resting state. (Turn on big speakers and turn the sound up without any music or noise, you will hear a continuous buzz in the speaker. THis is pretty much what happens for us).

The big difference with the AUT00063 is that it doesn't try to reduce sodium channels to a defective state, but it helps potassium channels to go back to a normal state of activity. Over the time it's going to train it again to work normally because the circuit itself is not damaged as demonstrated in this article:

http://informahealthcare.com/doi/abs/10.3109/14992027.2013.846482

It's like a manual car that stalled, it's nothing more than to protect the engine that it does so, it doesn't mean your car is broken, you just have to turn the key to start the engine again. It's pretty much what AUT00063 is trying to do.

 

[rtwombly]

Seems to me like you are looking for someone to talk you into taking it as you are scared. This is something made for people with epilepsy and they take it for life so it is not something that is made to be used short duration. That means the drug safety profile must be higher and those people using it are taking it to make their lives normal, not to live under a glass bell. You are worrying too much.

To be fair, linearb is right that the drug has only been around since 2009, and despite the best intentions of doctors, it has produced some potentially lifelong side effects, possibly only after long-term use (4+ years). I went to a neurologist's office, and was told by the doctor and his PA that they don't prescribe retigabine after the problems their patients had while using it.

On the other hand, they did say that it was a decision reached on balance. Retigabine didn't work well enough for their epilepsy patients compared to the frequency and severity of side effects. We are in a different situation, trying to test the efficacy against a condition for which there are no medicines (epilepsy is a much worse condition, but at least there are a variety of pharmaceutical approaches). Personally, my goal is either to wait for AUT00063, or if the wait seems like it will be long, to use retigabine as a stop-gap until it is available. I would not favor retigabine as a long-term solution.

@benryu thanks for those reminders. I think I'm a bit clearer on the mechanisms of action and how these drugs differ.

 

[Hengist]

I have also read about complaints of epilepsy patients and their problem was that although retigabine did help their epilepsy it did not remove it completely, they would have weird body movements still although not full epileptic attacks. However since reading the side-effect profile of retigabine it seems rather mild compared to most of the usual drugs which usually include life-treathening stuff like bleeding etc. Most of antibiotics can destroy your tendons (got mine destroyed by some) permanently alter your immune system etc. None of this is present with retigabine but people seem to freak out over it because it influences THE BRAIN (dramatic music).

 

[linearb]

I'm not cautious about it because it's a "brain drug" per se, most of the good drugs are brain drugs in some capacity. When I was much younger and foolish I took more than my share of acid/dmt/etc, and much more recently I've attempted various things for tinnitus treatment that include a chunk of the classic seizure drugs (carbazepine analogs) as well as weirder things like amiltryptaline.

The pigmentation and retinal effects are unique, poorly understood, and off-putting. I'd rather have blue lips and blurrier eyesight than have tinnitus, but there's a real risk of ending up with all three.

I'm not trying to dissuade anyone. I may well end up trying this myself -- after all, I sought out and filled a prescription for it. I'm just trying to keep a balanced view of it. Probably there will not be any serious side effects associated with using it at a relatively low dose for a relatively short period, but there are no guarantees.

And for the record, I am equally cautious about everything, definitely including antibiotics. I think fluoroquinolones are scary and overused, and I don't even take stuff like amoxicillian if I can avoid it. I'm looking at a shelf full of amoxicillian bottles that I was given for one minor malady or another and never opened.

Retigabine didn't work well enough for their epilepsy patients compared to the frequency and severity of side effects.

do you know what side effects in particular worried them, and if the side effects persisted longer than the drug? Stuff like dizziness and sleepiness doesn't faze me too much because it's common with all the seizure drugs and many other things, and is self-limiting. (In fact I like being sleepy, generally, because I'm wired to be too alert by default). The urinary retention stuff doesn't sound pleasant, but isn't super alarming to me. The skin and eye effects are more or less unique to retigabine, and concern me more because no one seems to know if they're permanent.

If I could get my hands on a vial of AUT00063 tomorrow, I'd probably just eat it :-p

 

[linearb]

Drugs such as benzo, lorazepam accelerate brain plasticity, doctors who prescribe it to accute T. patients are idiots.
A well known article demonstrates the following point on other area of the brain, but the idea is the same:
"These findings indicate that a decrease in GABA-related inhibition facilitates practice-dependent plasticity in the human motor cortex, whereas an increase depresses it."
http://www.ncbi.nlm.nih.gov/pubmed/11353733

Can you expand on what you mean here? Do you think using benzos for acute tinnitus literally makes it more likely to become a chronic condition?

I suspect that my history of benzo use may have made my tinnitus more significant; at this point I've been off of them for about 16 months, with no real change in the ringing. But, I have read accounts of people with no preexisting tinnitus who developed it as a result of withdrawal from benzos and did recover from it, but in some cases it took 3-4 years after withdrawal from the benzo. One of the big reasons I'm reluctant to just go back on valium now to deal with this, is that if I do I will never know if I might have improved on my own, given more time. I'm curious what you think about all of that.

edit: err - the way I read that is, that benzos decrease plasticity, not increase it? Benzos increase the action of GABA, doesn't that mean that the presence of a benzo causes an increase in GABA-related inhibition, which would decrease the specific kind of plasticity being studied here? Also, how applicable is this to sensory nerves?

 

[Hudson]

Is there a list of the people who have taken retigabine in here? I would like to compile a list of people.

@Mpt, @Christian78 ? Am I missing others?

 

[jazz]

Is there a list of the people who have taken retigabine in here? I would like to compile a list of people.

@Mpt, @Christian78 ? Am I missing others?

@Viking is another one; he had good results, but had to quit due to side effects.

 

[111]

So i tried to get trobalt to trial it out. My dr had no issues with me taking it at all off label, she was even pleased to try to help me out, as long as i saw her each week in the first month or so so she could monitor its progress she agreed to me being on it. Then when she went on the system to get it for me, turns out the med has been approved by this countries medical board for release over a year ago but GSK havent marketed it yet here... frustration.. ?

So given the fact that i cannot get this yet, she is more than happy for me to try something else out, so, as i am very very down at the moment in myself, has anyone tried the below med, just wondering if this could help me out ?


Carbamazepine

Abstract
Objectives: There is strong evidence in the literature about the effect of local anesthetics such as lidocaine in controlling tinnitus; these agents act by stabilizing hair cell membrane and cochlear nerve fibers. However, the effect of intravenous lidocaine is transient, and its oral analog (tocainide) does not have the same efficacy for long-term treatment in patients with tinnitus. Some oral anti-epileptic drugs (carbamazepine, for instance) have been used alternatively in several studies.

The mechanism of action of carbamazepine and its derivatives is relatively well-understood. Carbamazepine stabilizes the inactivated state of Voltage-gated sodium channels, making fewer of these channels available to subsequently open. This leaves the affected cells less excitable until the drug dissociates.[citation needed] Carbamazepine has also been shown to potentiate GABA receptors made up of alpha1, beta2, gamma2 subunits.[27] This mechanism may contribute to its efficacy in neuropathic pain and manic-depressive illness.

 

[Zimichael]

Can you expand on what you mean here? Do you think using benzos for acute tinnitus literally makes it more likely to become a chronic condition?

I suspect that my history of benzo use may have made my tinnitus more significant; at this point I've been off of them for about 16 months, with no real change in the ringing. But, I have read accounts of people with no preexisting tinnitus who developed it as a result of withdrawal from benzos and did recover from it, but in some cases it took 3-4 years after withdrawal from the benzo. One of the big reasons I'm reluctant to just go back on valium now to deal with this, is that if I do I will never know if I might have improved on my own, given more time. I'm curious what you think about all of that.

edit: err - the way I read that is, that benzos decrease plasticity, not increase it? Benzos increase the action of GABA, doesn't that mean that the presence of a benzo causes an increase in GABA-related inhibition, which would decrease the specific kind of plasticity being studied here? Also, how applicable is this to sensory nerves?

I'm on a similar same page as @linearb, @benryu ...Sorry, I know you have tons of stuff to do, but at some point would be nice to clarify, as one way I could read what you said would be that taking Retigabine or AUT00063 with a Benzo may actually help to grease the wheels of 'plasticity' and give a potentially higher chance of rectifying the T screw up state.

..."Drugs such as benzo, lorazepam accelerate brain plasticity"...and then..."These findings indicate that a decrease in GABA-related inhibition facilitates practice-dependent plasticity in the human motor cortex, whereas an increase depresses it."
As Benzos increase GABA I don't quite see how they 'accelerate brain plasticity' yet an 'increase (of GABA) depresses it (it being 'GABA-related inhibition practice-dependent plasticity').

Maybe I have all this arse-about-face, as there are double negatives involved and my brain is "negatively polarized" by trying to understand it all...Ha, ha. Oh Geeez, too late for some coffee to get those neurons firing.

Take care, and as always this stuff is GREAT! Hey am I giving my doc an education on about to use "Glutamate de-excitation" and "Lidocaine-induced neural ganglia bathtub soaking".

Bedtime... Zimichael

 

[Hudson]

@Viking is another one; he had good results, but had to quit due to side effects.

So we have @Mpt, @Christian78, and @Viking. Who else should be on the list? I think it will be helpful to compile some of this information about experiences so people will not have to comb through such a large thread.

 

[Zimichael]

MODERATORS... Hey have a question, or two actually.

This thread is getting so huge that it is becoming quite a chore to find stuff I know is in it but has been gobbled up in all the fantastic discussion. Like just getting hold of benryu's picture of gated channels took me forever to find (page by page, as a search with his name produced a deluge and it did not help)...Plus I thought it maybe had been in the Autifony thread as could not locate it so spent ages in that too.

So...being still kind of new to the Forum is there a way you deal with this for 'ease of use' purposes??? Obviously, we can all do our best to keep it on track and focused on Retigabine for one, (like Carbamazepine discussion should be brief and directed to a new thread, etc. if gets wordy). However this thread is also now indelibly stamped with Kv channels as an integral part of the discussion. And should be even though it is not just "Retigabine" related.
As mentioned, when you add all this to the main Autifony Thread and I start to cross reference...my brain goes into a homeostatic state between depolarizationa and hyperpolarization = "high potential for confusion and a grinding halt"!!!

Sorry, I don't have any brilliant ideas on how to help here (see above 'condition'!)

Next up...is there a way to open up all of @benryu 's posts alone in one sequence??? I can of course get all the 'titles' of his posts in a search, but then have to open up each one, one at a time. Which is no better than scrolling through the whole thread really. I am beginning to shudder at what this is going to be like when this has 50 pages or more in it!!!
I guess, this question is sort of like a filter thinggie, but probably not possible on my end of the chain...but thought I would ask as I sure would like a summary of all benryu's posts in an uninterrupted sequence to study for instance.

Thanks much... Zimichael

 

[111]

The issue i find is that this thread just generates so many questions and points of view from many people that i lose track of what is being discussed, people will ask a question for example, then the next 4 posts dont answer that question as they are discussing other points, and away it goes on a different tangent and that persons question didnt get answered.
Maybe split this thread up somehow to have the people on this med reporting how they are doing, daily / weekly / monthly and dosage levels etc and questions directed at them only, medical information about this med on another thread, and general questions on another, at least that way if more people manage to take this med we can all see how they are progressing, i have lost track who is even on this stuff and i have tried to get it myself recently.

 

[Viking]

@Viking is another one; he had good results, but had to quit due to side effects.

I've solved problem of kidney stones. On 30 August i will retry starting with 50x3. Hoping...
Ivan