Is early. Today is 8th day at 1000mg in 2 dose. I don't wante create false hope. Other 6 days i will go on 750 + 750 and after the final step 1000 + 1000. At this time i have "only" a big improvement in hiperacusys (unaspected) and i don't know if it is related to drug.
At this time i have "only" a big improvement in hiperacusys (unaspected) and i don't know if it is related to drug.
I must be only patient and continue on this way.
Thank you for your support
unfortunately my hyperacusis was severe. a simple beep could turn my T from 25db to 100db + headache + nausea + + inability to perform daily activities. Currently I have only floating bilateral tinnitus. I rode the motorbike for 3 days with no consequences. I was in traffic Christmas without problems. I talked this thing to my neurologist, he says he does not know if Keppra can be useful for H. We're trying it in order to low my aberrant T.How bad was your hyperacusis before?
In my mind, T should be lower too if you do have indeed positive results with H...
Carry on!
you will stay on 1000 am monitor creatinine? (3000max)Is early. Today is 8th day at 1000mg in 2 dose. I don't wante create false hope. Other 6 days i will go on 750 + 750 and after the final step 1000 + 1000. At this time i have "only" a big improvement in hiperacusys (unaspected) and i don't know if it is related to drug.
I must be only patient and continue on this way.
Thank you for your support
At a dose of 1000mg is not necessary to monitor liver function or other. This is valid until 3000. It seems to be the antiepileptic less "harmful" currently on the market. I asked the neurologist if I had to do some analysis and he said not.you will stay on 1000 am monitor creatinine? (3000max)
...So in one word, we want ACTIVATION of Kv channel, not INHIBITION....Right?????
... So does LEV enhance or suppress Kv3.1 and/or the "delayed rectification"?????
... Once again, it seemed to me that I could read into this any which way, as either an "inhibitor" or an "activator". Maybe you can see the "truth"?! If so PLEASE TELL ME IN SIMPLE ENGLISH...Maybe the original Chinese would have been as good to me!
Take care, and hoping for some "enlightenment" here....Thanks!
Zimichael
it is referred to KEPPRA XR (extended release) for patients (i suppose) who have the risk of forgot to take the second or third dose. in any case, I heartily thank you for the tip. If I have problems (I hope not) I will keep it definitely in mind.http://www.drugs.com/dosage/keppra-xr.html
here is states depending on kidneys problem that patiens from 500mg-100o mg, so they test ans day what is max dosage.
Dear @Zimichael,
The next documents refers to antiepileptic drugs. The following theory considers the hypothesis that the mechanism associated with tinnitus is similar to seizures.
1) From:
The mechanism of action of retigabine (ezogabine), a first-in-class K+ channel opener for the treatment of epilepsy *Martin J. Gunthorpe, y Charles H. Large, and z Raman Sankar
p 3/13: http://onlinelibrary.wiley.com/doi/10.1111/j.1528-1167.2011.03365.x/pdf
View attachment 4204
LEVETIRACETAM appears to act on reducing SV2A protein wich attenuates the signal at the neurons input while Retigabine acts on potassium channels opener, when they are open, they increase the inhibition of neurons.
This looks like a nightclub. The boss chooses to prevent the most excited subjects to enter (SV2A) or he chooses to neutralize them once they came (Kv) to maintain normal activity in the disco! The first solution seems more manageable! Levitiracetam could works on tinnitus.
2) From:
EXPERIMENTAL AND SIMULATION STUDIES ON THE MECHANISMS
OF LEVETIRACETAM-MEDIATED INHIBITION OF DELAYED-RECTIFIER POTASSIUM
CURRENT (KV3.1): CONTRIBUTION TO THE FIRING OF ACTION POTENTIALS
* C.W. HUANG, J.J. TSAI, , C.C. HUANG, , S.N. WU
p1/11: http://www.jpp.krakow.pl/journal/archive/12_09/pdf/37_12_09_article.pdf
" Therefore, the inhibitory effects on slowly inactivating IK(DR) (KV3.1-encoded current)
may constitute one of the underlying mechanisms through which LEV affect neuronal activity in vivo."
It seems that LEVETIRACETAM reduces the KV3.1 channel. It seems to be the opposite of AUT00063 ( KV3.1 channel opener?).
LEVETIRACETAM seems to be two opposite ways in terms of influence on the activity of neurons. SV2A protein could have the major effect on tinnitus.
To treat Tinnitus, I think we want to INHIBIT abnormal activity of neurons: ACTIVATION of Kv channel to INHIBIT neurons activity could be one answer among many others ...
Am I good?
I wish you all Merry Christmas
WOW MEN!!!
we urgently need a neuroscientist.
Now. If I raise the volume of the stereo and then suddenly make down the tinnitus same far for a few of seconds. Then returns but do not overdo it.
Previously, when i raise the volume of the stereo, I raised the volume of the tinnitus.
It seems that LEVETIRACETAM reduces the KV3.1 channel. It seems to be the opposite of AUT00063 ( KV3.1 channel opener?).
LEVETIRACETAM seems to be two opposite ways in terms of influence on the activity of neurons. SV2A protein could have the major effect on tinnitus.
To treat Tinnitus, I think we want to INHIBIT abnormal activity of neurons: ACTIVATION of some Kv (or KCNQ) channels to INHIBIT neurons activity could be one answer among many others ...
Am I good?
I wish you all Merry Christmas
I am so happy for you @Viking. My tinnitus behaved exactly as you describe before starting the Trobalt. With @Zimichael, I discovered that this is defined as: reactive tinnitus.
I'm confused by the two arguments (and related mechanisms of action) "increased At inhibition" - "decreased At excitation".
Thank you for your "mechanical explanation". I really appreciate it.It's a major gain mechanism to increase the accuracy of neuronal responsiveness. By balancing the excitation drive with inhibiting inputs it increases the range of excitation that the neuron can work with.
Think of it like the brakes and the accelerator of a car. You can slow down by easing off the accelerator but the brakes provide an inhibitory input to slow you down quicker and vice versa. Using both brakes and accelerator you can control the speed of a vehicle far more accurately.
If you decrease the inhibition (the brakes) then the car speeds out of control (an epileptic fit) unless you also decrease the excitation (the accelerator)
The mechanism here is like getting some huge ceramic brakes for your car and fitting a speed limiter too. Potassium is your brake cable and sodium your throttle cable.
Hope that makes sense.
It's a major gain mechanism to increase the accuracy of neuronal responsiveness. By balancing the excitation drive with inhibiting inputs it increases the range of excitation that the neuron can work with.
Think of it like the brakes and the accelerator of a car. You can slow down by easing off the accelerator but the brakes provide an inhibitory input to slow you down quicker and vice versa. Using both brakes and accelerator you can control the speed of a vehicle far more accurately.
If you decrease the inhibition (the brakes) then the car speeds out of control (an epileptic fit) unless you also decrease the excitation (the accelerator)
The mechanism here is like getting some huge ceramic brakes for your car and fitting a speed limiter too. Potassium is your brake cable and sodium your throttle cable.
Hope that makes sense.
haven't had time to digest this thread, just wanted to say that i recall reading on a few epilepsy forums, at least on two occassions, that some people were taking retigabine as an add-on drug with keppra.
Lucky this morning, after a really bad day and night i wake up after only 3 hours of sleep with 5db T instead yesterday 80db. Today i will see my neurologist and shows to him the papers that ypu have found about keppra and try to take more explanations about his mechanism of action. Thanks @Zimichael . Thanks to all soldiers!@Viking ... Hang in there my friend, as long as things do not get too bad of course. As it seems to be evident now that these KV drugs may have to "fight the brain/plasticity fighting back" so to speak. Like changing old habits perhaps. It is not easy.
Of course I don't know for sure, but I would imagine that the "brain patterns" of my same tone of T after 58 years (an E-flat Eeeeeeeeeeeeeeeeeeeeeeeee) must be incredibly entrenched. So changing that would be very hard. If it were to change I suspect it would be a "mobile" process, like has happened with @rtwombly.
When I took retigabine I got absolutely zero change in tone, or 'location feeling' of my T...just the increased H. So I think that maybe it is good that anything is changing in your T as it shows the drug is affecting the stuck/messed up neuronal signals that are causing the tinnitus.
How it will end up, I have no idea, but to me, if I would have had a "change" it would have given me hope.
However, I know how easy it is to talk from the side-lines, but unless things get bad for you and volume goes up a lot or H increases a lot, I would assume there may be a "fight" to find a new homeostasis.
Also, though...personally I would NOT expose myself to any degree of louder sounds, even to test how much you can tolerate. It feels unwise and risky to me. I would wait until the action of the drug is clear and then take it slowly into "sound". Motorcycles and so on....Ahhhhhhhhhhhhhhh???
My two cents. Good luck and hope things calm down for you.
Zimichael
Generally my T is bad since i wake up at morning and go worse during the day. In this days i'm experiencing (over the big improvement in H) a constant fluctuation. For example...now i'm up by 3 hours and took keppra... waked up with lower t on left side...now is gone to the right side. Lucky same tone lower. Without meds the T was more marked on left side with apyke on right side. Now are 3 days of continuos changing in lateralization and tonality. Today will be the first day of 1500mg divided in 3 doses. Also i will see the neurologist. On the telephone conversation he sayd that transient worsening is normal in his clinical experience and he advice me to wait and resist. Also i have cutted clonazepam from 2.5mg to 1mg. Probably there is a miscellaneous of consequences in the brain.Good news Ivan, nice to hear it. Perhaps yesterday was just a bad day. Is your T generally better, or just better than yesterday and simply came to the state it was?
DO NOT MIX! If a drug is working for you off-label, there is no reason to add another without any certainty. The only certainty we have is that you can have serious side effects and unpleasant in your situation prevents...
I myself would try it, perhaps I will, but I am currently under Gabapentin (Neurontin) for 1 month. No results yet, will discuss it with my doc if I will go on with it. Other options are:
1) Tegretol (mvc signs in my MRI)
2) Keppra
3) Trobalt
Yeas, unluky (and it is not only my experience/opinion) LLLT does do exactly nothing. It is all suggestion.But he also promotes laser therapy, which makes me skeptical since this LLLT therapy is believed to be scam by many.