Levetiracetam (Keppra) Worked for My Hyperacusis

@Zechariah Sometimes there are no hard and fast facts with such a tricky affliction. Sometimes all we have to go on is anecdotal evidence. If someone gets relief from a treatment, it is normal to want to share it with others. @Danny Boy is trying to offer his experiences to help others. He has also posted research studies and abstracts. Many people on this forum seem to attack those who want to help. These attacks are not productive at all. This is a "support" forum above all.

@Geo I would use caution on mixing the two until you see how you respond. Just my opinion, though.
 
@Zechariah Sometimes there are no hard and fast facts with such a tricky affliction. Sometimes all we have to go on is anecdotal evidence. If someone gets relief from a treatment, it is normal to want to share it with others.

Yes, but I'm not talking about anecdotal evidence. Danny Boy just states that AUT00063 will be fast tracked even though the authorities haven't said anything which would confirm that. Only thing we have is that Autifony "wishes" it to be fast tracked. And we don't even know if the drug works. These are the facts and therefore you can't say anything like "AUT00063 will be fast tracked".
 
Yes, but I'm not talking about anecdotal evidence. Danny Boy just states that AUT00063 will be fast tracked even though the authorities haven't said anything which would confirm that. Only thing we have is that Autifony "wishes" it to be fast tracked. And we don't even know if the drug works. These are the facts and therefore you can't say anything like "AUT00063 will be fast tracked".

"Fast track designation is designed to aid in the development and expedite the review of drugs which show promise in treating a serious or life-threatening disease and address an unmet medical need.

Serious Condition: Determining whether a disease is serious is a matter of judgment, but generally is based on whether the drug will have an impact on such factors as survival, day-to-day functioning, or the likelihood that the disease, if left untreated, will progress from a less severe condition to a more serious one.

Unmet Medical Need: For a drug to address an unmet medical need, the drug must be developed as a treatment or preventative measure for a disease that does not have a current therapy. The type of information necessary to demonstrate unmet medical need varies with the stage of drug development: early in development, nonclinical data, mechanistic rationale, or pharmacologic data will suffice; later in development, clinical data should be utilized. If there are existing therapies, a fast track eligible drug must show some advantage over available treatment, such as:

  • Showing superior effectiveness
  • Avoiding serious side effects of an available treatment
  • Improving the diagnosis of a serious disease where early diagnosis results in an improved outcome
  • Decreasing a clinically significant toxicity of an available treatment
  • Addressing an expected public health need"
 
"Fast track designation is designed to aid in the development and expedite the review of drugs which show promise in treating a serious or life-threatening disease and address an unmet medical need.

Serious Condition: Determining whether a disease is serious is a matter of judgment, but generally is based on whether the drug will have an impact on such factors as survival, day-to-day functioning, or the likelihood that the disease, if left untreated, will progress from a less severe condition to a more serious one.

Unmet Medical Need: For a drug to address an unmet medical need, the drug must be developed as a treatment or preventative measure for a disease that does not have a current therapy. The type of information necessary to demonstrate unmet medical need varies with the stage of drug development: early in development, nonclinical data, mechanistic rationale, or pharmacologic data will suffice; later in development, clinical data should be utilized. If there are existing therapies, a fast track eligible drug must show some advantage over available treatment, such as:

  • Showing superior effectiveness
  • Avoiding serious side effects of an available treatment
  • Improving the diagnosis of a serious disease where early diagnosis results in an improved outcome
  • Decreasing a clinically significant toxicity of an available treatment
  • Addressing an expected public health need"

*honestly no shown superior effectiveness have been seen from all those people around
*long term side effects (28 days courses)
*dr large said medicine will probably need twitching
*there is no current treatment
*so many have taken pills, strange that only 1-2 forward and said this and this is and those are results. if i was smart i would register myself and say i was there and give you all positive results so now daniel you would gloat until december when they say medicine needs twitching and then quiet 2 phase 2 will be done!

in a way as you are becoming super knowing you remind me of dr daniel negler
@dan
 
@Zechariah Sometimes there are no hard and fast facts with such a tricky affliction. Sometimes all we have to go on is anecdotal evidence. If someone gets relief from a treatment, it is normal to want to share it with others. @Danny Boy is trying to offer his experiences to help others. He has also posted research studies and abstracts. Many people on this forum seem to attack those who want to help. These attacks are not productive at all. This is a "support" forum above all.

@Geo I would use caution on mixing the two until you see how you respond. Just my opinion, though.
The true test will be if the h stays gone after you stop keppra.
Do you plan to stay on it for any extended period ?
 
So, there has been a slight change in my Tinnitus this morning ref. the Keppra.....what the hell do I do with this info??? Which thread do I post it on???

Having two major threads for Keppra, let alone all the other places it pops up is a pain in the arse!

Yesterday I said this:

First up...I am going to now presume two things regarding KEPPRA THREADS:

1. That this, here, is the main thread for reporting on Keppra and its relationship to "Hyperacusis".

2. That this: https://www.tinnitustalk.com/threads...ible-potassium-channel-modulator.7295/page-11 is the main thread for reporting on Keppra and its relationship to "Tinnitus".

Clearly there will be some overlap, but hopefully, we will have more continuity in Keppra reporting than having it spread over numerous places (like in the: "On Retigabine" thread, etc.). I hope that meets with general approval, as I have had a tedious time trying to find it all...Thanks!

So I guess I had better post today's "news" on the other Keppra thread until we have some kind of " Keppra Klub consensus".

Zimichael.
 
@Zimichael maybe you should start a Keppra Klub thread? I agree, it would be nice to have all of the information about Keppra in one place. Is it possible to merge the two Keppra threads? It sounds like you are noticing some effects from the Keppra?
 
@Zimichael I appreciate your difficulty trying to get a "fix" regarding my "situation." It is a complex case for sure, and I have been living it for far too long. I, too, am a stickler for hard proof and controlled data, being a researcher and professor myself. However, I have found that with this affliction, anecdotal evidence is something that one cannot ignore. And often it is all you are going to get.

Before taking Keppra, nothing would touch my hyperacusis. It was severe all of the time. Even the sound therapies made it worse. I was skeptical that the Keppra was making a difference too, given the complexity of my case. So I went without it for 24 hours and had a resurgence of hyperacusis symptoms. Given the short half life of Keppra, I thought that it might have been suppressing the symptoms. My neuropharmacologist friend concurred.

Since being back on Keppra, my hyperacusis is stable, and my tinnitus is extremely fragile (fragility that I attribute to the surgeries). Of course, one size does not fit all, and there is not hard proof data here, or a clinical trial. However, I would not have posted on this thread if I thought Keppra did not have an effect on my hyperacusis. There is mostly anecdotal evidence on many of the threads on this Forum. People are sharing their experience, strength, and hope for others to take or leave as they wish. I have no problem with anyone discounting me, because of lack of hard proof. I am just sharing my experience.

But if I feel better, and it is not the Keppra, I would still take a placebo over hyperacusis any day of the week. My researcher friends, who know me well from being a reviewer for peer-reviewed journals for several decades cannot believe I am saying this. I guess it is hard for me to believe too. I look forward to hearing how Keppra works for you. Best of luck to you!

@svintegrity ...For the record, I have no problem with your report above and using a "gut sense" or "anecdotal evidence"..re your Keppra feelings.
The hard science is nice, but you are clearly no "flip flake" and I trust your judgement on this.

However, one small note, is, that if I am reading your ahhhhhhhhhhhh...very "skimpy" information Profile correctly - you got sudden onset T (and H???) in January of 2014.

Now I apologize if I have not read all your posts to fill in the blanks (but that is the beauty of well filled in "Profiles" - they do that job in one click) as have been in my own deep, dark trashville for some time, so missed a lot. But...and I say this gently...You have had tinnitus for a relatively short time = 1.5 years.
From my 6 decades of experience and four levels of this darn affliction, with H appearing at the second level (in 1980), but without me even knowing that at the time (the H part)...Hyperacusis is a rather more malleable animal than my kind of "classic tonal T".

My T never changes, except increased 'objective' volumes I should say. The H has in retrospect has been more variable...The first time I had it for sure (that 1980 period) it went away fairly quickly. Maybe within a year or year and a half. I only know this as I have pictures of me wearing aircraft carrier grade ear muffs digging with my shovel in our stony Missouri Ozarks farm field! The "bing" of my shovel hitting rocks used to "zap" me! I had forgotten, as not long after that I got a high profile job with lots of public exposure, parties, sound, and so forth. T same and stable (no reactivity) and H was clearly "dissipating" or I could not have done that stuff.

Then jump to 2006, when ototoxic cocktail of drugs fried my audile nerves/whatever. The T went up (forever, and became "reactive"...or was that the H???!!!) and the H was the "new" bastard on the block. It took about four years to calm down enough for me to not totally be ruled by it, and 6 years before I could go back to pretty loudish sounds (dancing on stage, etc.) without earplugs.

Now, post the 2012 increase in T and H, there has hardly been any change at all in three years...maybe some lessening in the H by maybe 10% or so. I don't know, as protect in the outside world pretty aggressively.

Conclusion...I think the H "healing" is slowing down with each successive damage assault!

Thus if this is your "first" damage, there could be quite a bit of leeway for changes and so forth over months or a year...BUT, you seem to have all those other things going on (surgery references, and ??? re etiologies) which leave me pretty clueless and unable to warrant much of an opinion worth bean really.

Ummmmmmmm....Not sure if this helps you or just confuses things more. But there's my coffee speech for the morning.

Take care and best of luck. Zimichael
 
Good morning Keppra Klatch participants. I just thought I'd give a weekly update on my Keppra experience. I am still on a low dose of Keppra, and my hyperacusis continues to be greatly reduced, and without the original side effects from the higher dose. I do think that the dose needs to be adjusted according to one's size. It says on the Keppra insert that dosage is dependent on weight in children. It could be possible that this dosage adjustment also applies to small adults. I am a small person.

Before Keppra NOTHING would touch my H, I kid you not! This is coming from someone who could not be in the same room with someone eating toast! We ate off of paper plates, because the sound of the fork touching the plate was excruciating. And I could not handle the sound of an ice cube clinking against a glass. Painful beyond belief!

Yesterday I walked around a busy, bustling village, with church bells chiming, children screaming, and people rolling huge trash bins along the street. There were loud trucks and chairs being scraped across the concrete. My husband immediately put his hands over my ears at every sound, but when I said "no, that sound didn't hurt," his jaw dropped. The only noise that hurt my ears was a high-pitched barking dog in close proximity. Now that really hurt!

I was able to RIDE IN THE CAR to a place I call "my thoughtful spot" just in time to see the Orca whales passing through on their way south to Salmon Banks. I watched a family of otters teaching their young to fish. Keppra has made it possible for me to "boldly go" out to places, where in the recent past I did not dare.

I know that Keppra is not for everyone, nor do I know if the effects will be lasting once I discontinue use. I also know there are many variable involved in this diabolical affliction. For now, I believe that Keppra is playing a role in treating my hyperacusis, and for that I am grateful. It has given me a new lease on life. I am sharing this for anyone who might be interested. I am not claiming a panacea. Take what you like and leave the rest. I am still keeping my fingers and toes crossed for everyone here that you will find some relief from this beast. Best of luck!
 
@Zimichael My dose is extremely low. I am taking 250 mg in the morning and 250 mg in the evening. I started at 500 mg once a day and quickly went up to 500 mg BID, and the side effects were driving me into the ground! But I was noticing a change, a real benefit from the drug that I did not want to give up. Quite a dilemma. My neuropharmacologist recommended cutting the dose in half to see what happens. And viola -- I started to accommodate to the side effects. He also recommended titrating up very, very slowly, not a quick jump. I plan to increase by 250 mg after two weeks to see if there is an increase in benefit. I know you are a small person too, so a slow titration may help if you are experiencing side effects. I am 12o pounds and 12% body fat, as a former marathon runner. Not all physiology is created equal! I will be interested in hearing about your progress. Best of luck.
 
@Zimichael My dose is extremely low. I am taking 250 mg in the morning and 250 mg in the evening. I started at 500 mg once a day and quickly went up to 500 mg BID, and the side effects were driving me into the ground! But I was noticing a change, a real benefit from the drug that I did not want to give up. Quite a dilemma. My neuropharmacologist recommended cutting the dose in half to see what happens. And viola -- I started to accommodate to the side effects. He also recommended titrating up very, very slowly, not a quick jump. I plan to increase by 250 mg after two weeks to see if there is an increase in benefit. I know you are a small person too, so a slow titration may help if you are experiencing side effects. I am 12o pounds and 12% body fat, as a former marathon runner. Not all physiology is created equal! I will be interested in hearing about your progress. Best of luck.
knowing that keppra helped someone else gives me great joy... i just want to take it already..too bad i stopped i shouldved just cut the dose like you it probably woulve'd relieved my H by now
 
Good morning Keppra Klatch participants. I just thought I'd give a weekly update on my Keppra experience. I am still on a low dose of Keppra, and my hyperacusis continues to be greatly reduced, and without the original side effects from the higher dose. I do think that the dose needs to be adjusted according to one's size. It says on the Keppra insert that dosage is dependent on weight in children. It could be possible that this dosage adjustment also applies to small adults. I am a small person.

Before Keppra NOTHING would touch my H, I kid you not! This is coming from someone who could not be in the same room with someone eating toast! We ate off of paper plates, because the sound of the fork touching the plate was excruciating. And I could not handle the sound of an ice cube clinking against a glass. Painful beyond belief!

Yesterday I walked around a busy, bustling village, with church bells chiming, children screaming, and people rolling huge trash bins along the street. There were loud trucks and chairs being scraped across the concrete. My husband immediately put his hands over my ears at every sound, but when I said "no, that sound didn't hurt," his jaw dropped. The only noise that hurt my ears was a high-pitched barking dog in close proximity. Now that really hurt!

I was able to RIDE IN THE CAR to a place I call "my thoughtful spot" just in time to see the Orca whales passing through on their way south to Salmon Banks. I watched a family of otters teaching their young to fish. Keppra has made it possible for me to "boldly go" out to places, where in the recent past I did not dare.

I know that Keppra is not for everyone, nor do I know if the effects will be lasting once I discontinue use. I also know there are many variable involved in this diabolical affliction. For now, I believe that Keppra is playing a role in treating my hyperacusis, and for that I am grateful. It has given me a new lease on life. I am sharing this for anyone who might be interested. I am not claiming a panacea. Take what you like and leave the rest. I am still keeping my fingers and toes crossed for everyone here that you will find some relief from this beast. Best of luck!

I'm so happy for you! I'm glad this is working for people! I'm so so happy that me keeping on has brought keppra to everyone's attention. Right, could everyone which keppra is working for email these guys so we can get this to help other people's hyperacusis? http://hyperacusisresearch.org/research-news/ Cheers.
 
knowing that keppra helped someone else gives me great joy... i just want to take it already..too bad i stopped i shouldved just cut the dose like you it probably woulve'd relieved my H by now

I did tell you it could work...I'm sorry it gave you pain...I just wanted you to get better. Is trobalt working?
 
I did tell you it could work...I'm sorry it gave you pain...I just wanted you to get better. Is trobalt working?
see bro i wasnt lying about the horrific ear aches i should of just dosagged down.. nothing yet..i increased it by 100 today 200-200-100..maybe when i get to a higher dosage ill feel something. no bad side effects
 
see bro i wasnt lying about the horrific ear aches i should of just dosagged down.. nothing yet..i increased it by 100 today 200-200-100..maybe when i get to a higher dosage ill feel something. no bad side effects

You'll get the drunkenness sedation feeling at higher doses and I do believe you about the ear pain, just a shame.
 
so if itll work ill be too high to do stuff??

Well, it'll basically help with sleep...400mg will do that. Just wait until you do, you get that sedated feeling with super low tinnitus. So great.
 
Good morning Keppra Klatch participants. I just thought I'd give a weekly update on my Keppra experience. I am still on a low dose of Keppra, and my hyperacusis continues to be greatly reduced, and without the original side effects from the higher dose. I do think that the dose needs to be adjusted according to one's size. It says on the Keppra insert that dosage is dependent on weight in children. It could be possible that this dosage adjustment also applies to small adults. I am a small person.

Before Keppra NOTHING would touch my H, I kid you not! This is coming from someone who could not be in the same room with someone eating toast! We ate off of paper plates, because the sound of the fork touching the plate was excruciating. And I could not handle the sound of an ice cube clinking against a glass. Painful beyond belief!

Yesterday I walked around a busy, bustling village, with church bells chiming, children screaming, and people rolling huge trash bins along the street. There were loud trucks and chairs being scraped across the concrete. My husband immediately put his hands over my ears at every sound, but when I said "no, that sound didn't hurt," his jaw dropped. The only noise that hurt my ears was a high-pitched barking dog in close proximity. Now that really hurt!

I was able to RIDE IN THE CAR to a place I call "my thoughtful spot" just in time to see the Orca whales passing through on their way south to Salmon Banks. I watched a family of otters teaching their young to fish. Keppra has made it possible for me to "boldly go" out to places, where in the recent past I did not dare.

I know that Keppra is not for everyone, nor do I know if the effects will be lasting once I discontinue use. I also know there are many variable involved in this diabolical affliction. For now, I believe that Keppra is playing a role in treating my hyperacusis, and for that I am grateful. It has given me a new lease on life. I am sharing this for anyone who might be interested. I am not claiming a panacea. Take what you like and leave the rest. I am still keeping my fingers and toes crossed for everyone here that you will find some relief from this beast. Best of luck!
Im happy youre doing so well. Thanks for keeping us updated, Please keep them coming !
 
OK...seeing as this seems to be the most "happening" Keppra thread I am posting this: Questions about the MOA of Keppra here, rather than in the "Tinnitus - Keppra" version thread. (Though it would be nice to keep all of them more clear, and Trobalt stuff in it's camp too. Oh well. Dream on Michael...).

Well, trying to get a handle on MOA of Keppra is a total wildlife park without fences...Just about every "ion" (Ca, Na, K) and numerous 'other pub mates' (GABA, Glutamate, etc.), are regular visitors to the surrounding suburbs/feeding grounds.

The assumption that Keppra is a Kv3.1 modulator is a bit loose to say the least. (Agonist or antagonist by the way??? I can see benefit to both aspects of that voltage gate theory too - depending on if 'stuck' open or, as assumed, maybe,...stuck closed!). I can't really find any newish info on it at all though.

The more recent data (over and beyond the initial definitive stuff in 2008 – 2009) seems to trend towards a "multi-factorial" approach, which to my simple mind means: "Who the hell knows?!"

In 2014, some good soul must have got frustrated, and like me, asked the question: "Can someone explain exactly how Keppra (levetircetam) works?"

http://www.researchgate.net/post/Can_someone_explain_exactly_how_Keppra_levetiracetam_works

After the SV2A, Calcium and Glutamate are mentioned, one reply goes to this later source from 2014:

http://journal.frontiersin.org/article/10.3389/fncel.2014.00164/full

Whereupon this part, (inserted below), is intriguing...Almost inferring that a Keppra induced "construction remodel" happens where the action potential is basically deferred by kicking the can down the axonal road! Like, hey, the further away it all happens from the synaptic cleft, the less likely (the gates, activating the neronal transmission) are to fire as much! This could be akin to saying it's harder to hit a target with a sub-machine gun (aka, 'hyper firing of epilepsy') if it is further away. Any soldier will tell you this is true. Actually it's pretty hard to hit someone even super close up if over hyped up on adrenaline... or synaptic Glutamate perhaps?! Etc., etc.

Don't take my word for it read it here, or on the link!

Because transmitter release is controlled by action potential-(AP)-triggered calcium influx in the synaptic terminal, regulation of ion channels which shape the axonal AP and terminal depolarization is an effective mechanism of presynaptic plasticity. With this definition, the AP initiation zone (AIZ) could be viewed as part of the presynaptic equipment. A striking form of homeostatic plasticity has been documented for the AIZ: this entire subcellular structure including voltage-gated Na+(Nav) and K+(Kv) channels can be shifted along the axon (Figure1), thereby counteracting hyperexcitation by increasing thresholds for AP generation (Grubb and Burrone, 2010). Such axonal remodeling may be facilitated via ion channel trafficking regulated by alternative splicing, as shown for "shaw-related" Kv3 channels (Gu et al., 2012).

Cool idea huh?! Just get rid of T or H by booting it down the hill...Sigh!

Anyway, as you can probably tell by now...I am giving up on trying to see if Keppra is a Kv3 regulator. Either it works for us or it does not. Or for some of us, and not for others.

Same old tinnitus guessing game.

Best, Zimichael
 
I know...But this is what we need to do for tinnitus/hyperacusis to not drive us crazy.
damn i guess
OK...seeing as this seems to be the most "happening" Keppra thread I am posting this: Questions about the MOA of Keppra here, rather than in the "Tinnitus - Keppra" version thread. (Though it would be nice to keep all of them more clear, and Trobalt stuff in it's camp too. Oh well. Dream on Michael...).

Well, trying to get a handle on MOA of Keppra is a total wildlife park without fences...Just about every "ion" (Ca, Na, K) and numerous 'other pub mates' (GABA, Glutamate, etc.), are regular visitors to the surrounding suburbs/feeding grounds.

The assumption that Keppra is a Kv3.1 modulator is a bit loose to say the least. (Agonist or antagonist by the way??? I can see benefit to both aspects of that voltage gate theory too - depending on if 'stuck' open or, as assumed, maybe,...stuck closed!). I can't really find any newish info on it at all though.

The more recent data (over and beyond the initial definitive stuff in 2008 – 2009) seems to trend towards a "multi-factorial" approach, which to my simple mind means: "Who the hell knows?!"

In 2014, some good soul must have got frustrated, and like me, asked the question: "Can someone explain exactly how Keppra (levetircetam) works?"

http://www.researchgate.net/post/Can_someone_explain_exactly_how_Keppra_levetiracetam_works

After the SV2A, Calcium and Glutamate are mentioned, one reply goes to this later source from 2014:

http://journal.frontiersin.org/article/10.3389/fncel.2014.00164/full

Whereupon this part, (inserted below), is intriguing...Almost inferring that a Keppra induced "construction remodel" happens where the action potential is basically deferred by kicking the can down the axonal road! Like, hey, the further away it all happens from the synaptic cleft, the less likely (the gates, activating the neronal transmission) are to fire as much! This could be akin to saying it's harder to hit a target with a sub-machine gun (aka, 'hyper firing of epilepsy') if it is further away. Any soldier will tell you this is true. Actually it's pretty hard to hit someone even super close up if over hyped up on adrenaline... or synaptic Glutamate perhaps?! Etc., etc.

Don't take my word for it read it here, or on the link!

Because transmitter release is controlled by action potential-(AP)-triggered calcium influx in the synaptic terminal, regulation of ion channels which shape the axonal AP and terminal depolarization is an effective mechanism of presynaptic plasticity. With this definition, the AP initiation zone (AIZ) could be viewed as part of the presynaptic equipment. A striking form of homeostatic plasticity has been documented for the AIZ: this entire subcellular structure including voltage-gated Na+(Nav) and K+(Kv) channels can be shifted along the axon (Figure1), thereby counteracting hyperexcitation by increasing thresholds for AP generation (Grubb and Burrone, 2010). Such axonal remodeling may be facilitated via ion channel trafficking regulated by alternative splicing, as shown for "shaw-related" Kv3 channels (Gu et al., 2012).

Cool idea huh?! Just get rid of T or H by booting it down the hill...Sigh!

Anyway, as you can probably tell by now...I am giving up on trying to see if Keppra is a Kv3 regulator. Either it works for us or it does not. Or for some of us, and not for others.

Same old tinnitus guessing game.

Best, Zimichael
thats all chineese to me bro lol does this mean your not going forward with keppra? or are you saying that theres no data on how it actually works for H but your trying anyways ..
 
thats all chineese to me bro lol does this mean your not going forward with keppra? or are you saying that theres no data on how it actually works for H but your trying anyways ..

Geo... Well, no sweat if the axonal synaptic Keppra dance is Chinese to you, as it is to me too after trying to "translate" it. All to say, the key thing that counts is if it works.

However, one of my reasons for going into it in more detail was to see if it had genealogical ties to AUT00063, as then there could be some relevance to "time frame" and "dose" guesses...Well for me anyhow. *[Recall that we Kv fans were somewhat chuffed to find out that when Autifony first published the trial info, that it was a zap, straight on max dose pill from the get go...no taper. Thus reinforcing the "Marines at the door - overwhelming force" theory v. the "Medieval slow siege" theory].
I was hoping to bring more of my own 'understanding' to that aspect, but as reported, ended up in a wild suburb with no street signs. Thus the guessing game...As look, here we have "results" from @svintegrity at 250 mg BID = 500 mg total/day...yet potential doses of up to 3,000 mg total/day (or more). So...Ummmmmmm???????????

Your other question. No, I mean "yes"...I am continuing with Keppra as before, but just without much of a plan. Currently I am at 1,500 mg total per day (750 mg BID) and was going to ramp to 2,000 mg today, but decided to wait a few more days due to the complete "unknowns" (see above conversation and lack of MOA discovery on my part) on the "temporal v. dose" question.

Also, before I go and give myself a bigger headache in the mornings (my main side effect right now, though good organic coffee seems to obliterate it :coffee: ), maybe I should actually "evaluate" my H first???!!! Like: "Oh, how do I know if my H has changed unless I expose myself to some known levels of 'hurt' sound???!!" Which of course, I have not been too keen on in the past few years. Thus I need to go to town and seek out some free range kids in the natural foods store, or stand outside the library until one of those redneck trucks with fat tyres and a big exhaust sticking out the side goes past...And see what happens if my earplugs are not in, or half in...Basic medical science stuff, etc., etc.

My 'tinnitus' has not changed. That one time blip in volume or tone change from Eeeeeeee to Ddddddd, on the second day, did not hold or repeat. Though my T is not as loud as it can be (aka "deafening"), but that can just be because it has not been 'amp-triggered' by sticking earplugs in, or going to said 'town' for many days. If I stay home and be in my general 'open ear canals noise control zone' my T hits baseline (quite loud enough thank you!). So no cigar there either.

Ummmmm...That's about it I guess....Oh! Maybe this is relevant, though is actually relevant for a lot of the AEDs (anti-epileptic drugs), I reckon Keppra is somewhat of an "upper". Not as much as Trobalt for sure (where a lot of trialees have been high as kites), but my general levels of energy and attitude are better since starting it. BUT...that could also be just because I am doing something, instead of just sitting in a T/H prison watching the bars go by.

And lastly, @Danny Boy, if you have any decent papers/reports giving the skinny on Keppra and the "dose saturation efficacy v. temporal" debate, do please let me know. *[I have the three main ones we all reviewed ref. 2008 - 2009].

Best, Zimichael
 
Geo... Well, no sweat if the axonal synaptic Keppra dance is Chinese to you, as it is to me too after trying to "translate" it. All to say, the key thing that counts is if it works.

However, one of my reasons for going into it in more detail was to see if it had genealogical ties to AUT00063, as then there could be some relevance to "time frame" and "dose" guesses...Well for me anyhow. *[Recall that we Kv fans were somewhat chuffed to find out that when Autifony first published the trial info, that it was a zap, straight on max dose pill from the get go...no taper. Thus reinforcing the "Marines at the door - overwhelming force" theory v. the "Medieval slow siege" theory].
I was hoping to bring more of my own 'understanding' to that aspect, but as reported, ended up in a wild suburb with no street signs. Thus the guessing game...As look, here we have "results" from @svintegrity at 250 mg BID = 500 mg total/day...yet potential doses of up to 3,000 mg total/day (or more). So...Ummmmmmm???????????

Your other question. No, I mean "yes"...I am continuing with Keppra as before, but just without much of a plan. Currently I am at 1,500 mg total per day (750 mg BID) and was going to ramp to 2,000 mg today, but decided to wait a few more days due to the complete "unknowns" (see above conversation and lack of MOA discovery on my part) on the "temporal v. dose" question.

Also, before I go and give myself a bigger headache in the mornings (my main side effect right now, though good organic coffee seems to obliterate it :coffee: ), maybe I should actually "evaluate" my H first???!!! Like: "Oh, how do I know if my H has changed unless I expose myself to some known levels of 'hurt' sound???!!" Which of course, I have not been too keen on in the past few years. Thus I need to go to town and seek out some free range kids in the natural foods store, or stand outside the library until one of those redneck trucks with fat tyres and a big exhaust sticking out the side goes past...And see what happens if my earplugs are not in, or half in...Basic medical science stuff, etc., etc.

My 'tinnitus' has not changed. That one time blip in volume or tone change from Eeeeeeee to Ddddddd, on the second day, did not hold or repeat. Though my T is not as loud as it can be (aka "deafening"), but that can just be because it has not been 'amp-triggered' by sticking earplugs in, or going to said 'town' for many days. If I stay home and be in my general 'open ear canals noise control zone' my T hits baseline (quite loud enough thank you!). So no cigar there either.

Ummmmm...That's about it I guess....Oh! Maybe this is relevant, though is actually relevant for a lot of the AEDs (anti-epileptic drugs), I reckon Keppra is somewhat of an "upper". Not as much as Trobalt for sure (where a lot of trialees have been high as kites), but my general levels of energy and attitude are better since starting it. BUT...that could also be just because I am doing something, instead of just sitting in a T/H prison watching the bars go by.

And lastly, @Danny Boy, if you have any decent papers/reports giving the skinny on Keppra and the "dose saturation efficacy v. temporal" debate, do please let me know. *[I have the three main ones we all reviewed ref. 2008 - 2009].

Best, Zimichael

Levetiracetam (LEV) is predominantly (66%) excreted unchanged by the kidneys, with a smaller amount (27%) metabolized to three inactive compounds.94 It does not bind to plasma proteins. The pharmacokinetics of LEV are not affected by mild to moderate liver impairment.95 In patients with severe liver cirrhosis (Child–Pugh Class C) total clearance was reduced by 57% and a reduction in dose by 50% is recommended.96 We did not come across any report of LEV-induced hepatotoxicity on a Medline search.

http://onlinelibrary.wiley.com/stor...gr&s=fcf2e04c729afcc1183b00f211b1a82406c75434

http://www.jscimedcentral.com/Psychiatry/psychiatry-2-1011.pdf
 

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