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Hi, could you please tell me where you got the intratympanic steroid injection done? I'm in NYC and I can't seem to find any doctors that would do it...

As to the $$$ side of things, have you looked at the online Canadian pharmacies?

Hmmm, this seems to go against Prof. Tzounopoulus's paper Pathogenic plasticity of Kv7.2/3 channel activity is essential for the induction of tinnitus where he says: KCNQ channels, often KCNQ2 and KCNQ3, mediate the native neuronal M-type current. M currents are strongly inhibited by activation...

Can this neural signature be (strongly statistically) correllated with the subjective perception of tinnitus intensity? If so, has there been any study conducted (with a decent sample size) that demonstrated such a correlation? And by correlation I mean both a binary "signature existence...

Well, if he has no symptoms, and will continue to have no symptoms, for some time x in the future, then I think we can all agree that fits the definition of the word "cure". The question is what x should be - is it "the rest of his life", is it "five years (as in five year survival rate)" or is...

My theory is that the key may be to replace the 'normal level target' that homeostatic mechanisms 'go back to'. It could be that the changes which cause tinnitus, such as noise exposure, cause things like calcium (Ca+) concentration levels in the DCN to become really low (because of lack of...

Thank you for finding the paper, @locoyeti ! Just a question on the data bolded above - if the effective therapeutic concentration is 7.4um and at 1200mg/day you only get to 2.0um, it seems that it would require 7.4/2.0 * 1200 = 4320 mg/day of retigabine to get the the therapeutic concentration...

Very interesting...Does anyone have the full text of this article?

I agree too... Time for a flupirtine thread! And willing volunteers..

There are many hypotheses as to the mechanisms that cause and maintain tinnitus. These few pages...

I'm surprised this even needed FDA clearance. I mean, it's just an ipod with an app. Isn't that at odds with both the study it's supposed to be based on and the supposed mechanism of action? The study abstract says "All patients decreased their tinnitus intensity in the first month of...

Right, but if input from the cochlea to, say, the DCN, was truly lost for some specific frequency, then how would you be able to 'fill in' for it using any external sound generating device at that frequency? The cochlea simply would not be capable of transmitting any signal for that frequency...

Nice paper, but I have two comments/questions : 1. Perhaps the decrease in tinnitus intensity was due to better sleep quality, induced by the generated sound (acting as a masker). In other words, perhaps a better study should have had a control group receiving a regular masking sound (e.g...

Purposeful malpractice would cost him much more than just his career...

This portion of the video says the stem cells are attracted to chemokines released near the area of injury : But what are the chemokines released near damaged/defunct inner hair cells? Are they still released years after inner hair cell destruction?

Has the Aspartame - Tinnitus connection been firmly established? Or is it yet another unverified rumor or myth regarding the "dangers of aspartame".

What's the subject name, if you don't mind (just curious)?

I think this is an important bit. Look at what @SoulStation said : I suspect many others who have tried Retigabine share this view. It seems that all previous drugs and treatments tried for tinnitus have not had this level of the perception of a 'real effect', of the perception that the drug...

I was talking about esketamine (hydrochloride), which is what they inject in AM-101 trial (if you're not getting a placebo). Esketamine is a form of ketamine.

I would think alot would depend on the rate that ketamine gets metabolized at - or rather, for how long does it stay attached to the NMDA receptors, until it is either dislodged (via thermal motion perhaps, or by some competitor molecule like, say, glutamate), or broken down by something else...

Not really. Many people are routinely ordering illegal drugs online via the darknet. It comes to them by mail and they receive it just fine.

I think the connection to the DCN is not through the drug diffusing there but rather through the cessation of aberrant signaling from the cochlear neurons. [The 'aberration' here could, for example, be a lack of signals, or an excess of them]

I don't see how that necessarily follows from the definition you gave. From the definition, plasticity is not about recovery (to some 'normal' homeostatic level), but rather simply the stregthening of synaptic response in response to increased activity, and weakening in response to decreased...

Yeah, but most if not all drugs are like that before a Phase I trial on humans - no one knows how humans will respond. (Although I guess more careful experimentation is done on animals prior to that). On the other hand (and I brought up this example before), there are people like Alexander...

If you go to that link and select the country (e.g. USA), it says it's available and you can buy either 10mg or 50mg of it. Mpt was asking about it here : https://www.tinnitustalk.com/threads/bms-204352-maxipost-—-modulating-potassium-ion-channels-decreases-tinnitus-in-rats.258/ I guess that...

Has anyone looked into Maxipost? Is it obtainable anywhere? (Perhaps here : http://www.tocris.com/dispprod.php?ItemId=383718 )?

I think the medicine is 'controlled' in the sense of the FDA not permitting GSK to just sell it without a prescription. But the chemical compound itself is not controlled - if you want you can synthesize it in your basement (ignoring any patent/copyright issues for now) and no DEA agents are...

@attheedgeofscience : Any results to update about your experience with flupirtine?

Unless it's on a controlled substance list, I don't think there is any problem importing it, without any kind of license or governmental permission. If you're saying that it breaks the patent on Retigabine, then perhaps GSK can sue the Chinese manufacturer, but I don't think can sue (or enforce...

Instead of cutting the nerve, is it possible to 'disable' it temporarily - like anesthesize it with lidocaine or the likes? This will enable one to see if tinnitus is eliminated or not.

Modern medicine, like almost any scientific discipline nowadays, has its theoretical underpinning in biology, which in turn has its base in chemistry and that in turn in physics. (Reductionism is firmly established in the sciences). The directions that medical research (and from it, practice)...

Hopefully the amnesia is not permanent! :unsure: (that is, if you go off the drug, you have pre-drug levels of mind clarity). Also, perhaps the amnesia effects will lessen over time? Who knows.

I'm taking NAC (2000mg/day). Is that much different than ALA (i.e. do you think I be taking ALA instead, or in combination with it)? Do you think atlas orthoganol would potentially help with noise induced tinnitus (being that atlas is about spine related correction)? Also, what's SOTO?

Why is that?

Surely some island nation or something like that would do.

On that note, why wait for UK approval at all? Just manufacture it in a country that has no drug approval policies, and order it from there :)

Perhaps it is possible to activate that enzyme only in the neurons responsible for hearing (like the spiral ganglion neurons). One way is to make the enzyme dependent on something (co-enzyme, etc.) that is specifically expressed by inner ear/spiral ganglion neurons. Here is where nanotechnology...

One interesting section from the article : To summarize (according to how I understood it) - the molecular mechanism of why Kv7 channels close in the first place, is thought to be caused to the decreased levels of the PIP2 (a phospholipid component of the membrane). When they increased those...

Hearing clicking/crackling sounds in the ears when swallowing happens (I guess) to everyone sometimes. But does Tinnitis make you hear this clicking loudly and on every swallow? The loudness seems to be proportional to the loudness of the tinnitus at the time.

Yeah, but on the other hand, some people try street drugs without knowing what's in them, and couldn't care less. Still others, like Alexander Shulgin, experimented with completely new, synthesized drugs, never feared, and lived a long life. I guess it all depends on your mindset and risk taking...

I don't think it's so much that it's different systems rather than completely different conditions/causes. In case of MS, it seems like it's the immune system attacking cells and creating lesions - so this has a genetic component and a (progressive) damage (lesions) to neurons component. In the...

It could also be that aut00063 will prove in fact prove ineffective, and retigabine will prove effective. That, for instance, would give us a clue that we should be focusing on Kv7 and not Kv3 channels. But my point is that if even one substance is proven effective for completely (or nearly...

Well, there are things like, say, white-noise generators that mask the tinnitus. So that fits the "alleviate the symptoms temporarily" criteria. But, of course, no one wants to be walking around with a white noise masker in their ear all or most of the time. On the other hand, if Retigabine is...

Sorry, I don't know if I could have made it more clear. I'm just trying to get to the bottom of things in terms of understanding. I'm not trying to challenge just for its own sake. Retigabine works on improving 'locked' Kv channels. I was trying to understand exactly how Kv channels get...

The bolded part above is what requires explanation. Here we have a neuron, and the subcellular location of Kv channels Figure 5. Subcellular localization of voltage-gated K+ channels Somatic Kv channels include Kv3 and ERG, but the major part of the conductance arises from channels in the...

Fun reply with graphics, but I'm still not sure it answered the question it posed : So the question is : what's the link between glutamate release and Kv channel abnormality? So what I'm getting from above is : glutamate excitotoxicity -> destruction and regrowth of synaptic bouton -> during...

Nanotechnology is the most obvious (but perhaps hard to implement right now) method - you just have nanobots attach to synapses and measure firing rates, and destroy the cells firing abnormally. But there are many others conceivable methods - for example some molecular compound or protein that...

How about this little idea - instead of fiddling with the Kv channels to control the firing of the cell, find a way to DESTROY the haywire cell completely. Fight it like a cancer - chemo kills the cancer cell, it doesn't try to repair its dna,etc. back to normal. If that can be done selectively...

I don't think blanket statements like this are true. It really depends on the details and specifics. In particular, it may depend on whether the underlying mechanism which causes the Kv channel down regulation is reversible or not. It might be the case that there is no real 'damage', but that...

This is still where I'm very unclear. What is the nature of the interference with the excitability of spiral ganglion neurons? Here's a chain of causes : 1. Glutamate excitotoxicity in the hair cell, or even possibly further downstream in spiral ganglion neurons, leads to 2. ???, leads to 3...

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 : (emphasis mine) The 6TM family are the voltage gated (i.e. Kv) channels, which...

That section ("KATP channels in glutamate mediated synaptic degeneration", page 11, http://tinyurl.com/mrgwnxz) simply mentions that activating Katp channels (and thus hyperpolarizing the membrane) helps reduce (dampen) the excitotoxicity caused by glutamate. It does not suggest that the...

Hey, thanks for the graphical explanation :) After reading some more wiki, I think I more or less understand now - IF the potassium channel is blocked, repolarization takes longer than usual (it still occurs via the sodium/potassium pumps), and therefore the membrane remains depolarized for...

Are you saying that there is some causative link between glutamate excitotoxicity and blocked Kv channels? I tried to find this in some articles you linked, but wasn't able to. [According to one of them ('Katp channels are key modulators of glutamate receptor"), "Increase in glutamate release...