Levetiracetam (Keppra) Worked for My Hyperacusis
- Thread starter Danny Boy
- Start date
Member
Large will Win. He's focusing on treating chronic suffers...Large has already created Trobalt which functions on the KV7 channels and can cure tinnitus in the early stages.
Bearing in mind I have been on 10 mg pain killing dose of amityptilyne for 12 years and zopiclone for 6 before my nightmare T&H started. I would now love to come of these but I haven't got a clue where to start and am also worried that having used them long term stopping may actually make things worse.
T&H are making me feel I don't want any drugs in my body at all I want to see if I can cope alone, of maybe melatonine for sleep. Drs just want to give me more drugs ie AD's
I find your posts very informative as (sadly) you have so much experienced of this.
- Dec 24, 2013
- 933
- Tinnitus Since
- (1956) > 1980 > 2006 > 2012 > (2015)
- Cause of Tinnitus
- Ac. Trauma & Ac.Trauma + Meds.
Danny... Oh well...Sigh! Not exactly what I wanted to hear.
Look-it, nothing personal OK, as I remember well when you first got onto TT and were a total train wreck! I mean anyone can go back and look at your posts back then. Just intense and freaked out maxo big time. So to be where you are today and to have gotten here from there, is fantastic. Just not at all what anyone with a modicum of synaptic activity could have guessed back then, at your starts-ville. So BIG KUDOS to you, and for helping so many folks with your posts, attitude, good vibes, and so forth.
However, you are what??? Early to mid 20's perhaps??? Young at any rate. And you have only (sic - yeah I know) had T/H for one year [July, 2014 apparent start date]. To me that says one big thing. You are not as "old a model" as I am. Your T-brain is not as fossilized. Your parts are likely a lot less worn out. Your detox mechanisms have potentially better 'mojo'. You can maybe tolerate a wider spectrum of drug metabolism abuse than I can. Hell I hardly even knew what a doctor was for until age 43 really!
So, given decades more experience with meds shit, and lots of not so fun stuff as a result (badder-arse T and H being part of that package!) I would prefer to have more than the above quote of yours for 'evidence' that "one should take it - Keppra - for three months".
Sorry mate, just not solid enough for me based on the fact that it did not 'hurt' you! It sure "hurt" a few other folks who tried it, and at much lower doses...so it gets down to "subjectivity" instead of "science" (defined simply enough for my tastes as - best of luck facts as we know from human experience at present).
I was hoping for more, as my current head space by afternoons is not so 'cool'. I am struggling to stay conscious by about 3:00 pm, making strategic plans to keep awake until 8:00 pm so that I can collapse into bed and sleep before getting my deep-seated 'second wind' that will keep me awake most of the night if I nap in the afternoons, etc., etc. = a bad spiral if I get even less sleep than am un-graced with).
OK...There you have it. So what do I do now??? I'm staring at my Keppra pills (dwindling fast, as doc dose was 1,000 my total per day and I am at 2,000 mg total per day)...
Pay homage and pain to the Gods of "dose"??? Or pay homage to the Gods of Kronos??? ("Time" - for non classical scholars).
Shit!!!??? (Excuse my French, or Greek, or whatever).
Oh...and the 'disclaimer' re above: All forward looking statements, backwards looking statements, sideways looking statements, upside down looking statements, or verbage of any kind...subject to a brain under the influence, or about to be under the influence...of more, or less, Keppra!
Best, Zimichael
I agree...Gosh I don't even remember those posts? Is there anyway I could look back? Gosh, I would love to see how I was back then? Just to compare. And I get where you are coming from...Keppra doesn't even get me sleepy..Just headaches really and turmeric sorts them out. Well, what do you plan on doing?
- Dec 24, 2013
- 933
- Tinnitus Since
- (1956) > 1980 > 2006 > 2012 > (2015)
- Cause of Tinnitus
- Ac. Trauma & Ac.Trauma + Meds.
Danny... Just do a search c/o your Profile for all your old Posts or Activity. Should be there way back in the beginning. Yeah you were more than climbing the walls mate...A prime example of "initial T freak out" (of which you are not at all alone of course! And of which those of us with SRT/H = sound reactive T and H. can 'meet again' at any time/any day = huge fun!).
Re what to do and my Keppra dilemma. Here's a synopsis of my current thinking:
I could keep climbing to 2,500 mg a day or even 3,000 mg a day, to just hit the "neuronal membrane" harder with higher extra-cellular/inter-cellular concentration??? Or do I figure that maybe by now I should have seen/sensed "some wee change" in my hearing stuff??? I mean, my gut sense is, that a twitch should have happened as I recall (I think) that Cmax is rapid as is absorption...Yes, indeed:
- Absorption of levetiracetam is rapid, with peak plasma concentrations occurring in about an hour following oral administration in fasted subjects. The oral bioavailability of levetiracetam tablets is 100% and the tablets and oral solution are bioequivalent in rate and extent of absorption. Food does not affect the extent of absorption of levetiracetam but it decreases Cmax by 20% and delays Tmax by 1.5 hours.
- The pharmacokinetics of levetiracetam are linear over the dose range of 500-5000 mg.
- There is no evidence that doses greater than 3000 mg/day confer additional benefit.
- Steady state is achieved after 2 days of multiple twice-daily dosing. Levetiracetam and its major metabolite are less than 10% bound to plasma proteins; clinically significant interactions with other drugs through competition for protein binding sites are therefore unlikely.
So...all to say, I should have enough in my inter-cellular neuronal space by now, after 62 hours of taking it at 2,000 mg per day total...AND I am a smallish guy, so may well have a dose equivalent of around 2,500 mg as the 'real' float!
And yes, there is 'expert' advice-evidence c/o a neurologist that "body weight v dose" with Keppra is not "smoke. In other words, it is not something to ignore. So I may have an actual concentration of about 30% more than a person weighing say 200 pounds. Uhhhh...kinda common in America!
Ummmmmmmmmmmmmm!!!
Zim.
Re what to do and my Keppra dilemma. Here's a synopsis of my current thinking:
I could keep climbing to 2,500 mg a day or even 3,000 mg a day, to just hit the "neuronal membrane" harder with higher extra-cellular/inter-cellular concentration??? Or do I figure that maybe by now I should have seen/sensed "some wee change" in my hearing stuff??? I mean, my gut sense is, that a twitch should have happened as I recall (I think) that Cmax is rapid as is absorption...Yes, indeed:
- Absorption of levetiracetam is rapid, with peak plasma concentrations occurring in about an hour following oral administration in fasted subjects. The oral bioavailability of levetiracetam tablets is 100% and the tablets and oral solution are bioequivalent in rate and extent of absorption. Food does not affect the extent of absorption of levetiracetam but it decreases Cmax by 20% and delays Tmax by 1.5 hours.
- The pharmacokinetics of levetiracetam are linear over the dose range of 500-5000 mg.
- There is no evidence that doses greater than 3000 mg/day confer additional benefit.
- Steady state is achieved after 2 days of multiple twice-daily dosing. Levetiracetam and its major metabolite are less than 10% bound to plasma proteins; clinically significant interactions with other drugs through competition for protein binding sites are therefore unlikely.
So...all to say, I should have enough in my inter-cellular neuronal space by now, after 62 hours of taking it at 2,000 mg per day total...AND I am a smallish guy, so may well have a dose equivalent of around 2,500 mg as the 'real' float!
And yes, there is 'expert' advice-evidence c/o a neurologist that "body weight v dose" with Keppra is not "smoke. In other words, it is not something to ignore. So I may have an actual concentration of about 30% more than a person weighing say 200 pounds. Uhhhh...kinda common in America!
Ummmmmmmmmmmmmm!!!
Zim.
I think you're over thinking this? Try keppra 3 months on 2000mg, as per Vikings recommendation and see if it works or not. Anyway, I'll look through my postings.
I can't remember...However he said this
"Small update;
the doctor who prescribed the Keppra on me in december of past year, it being administered to patients who had previously received some relief from the combination of gabapentin + clonazepam. The results seem to be encouraging, especially in the group of patients who suffer from tinnitus unilateral not tonal but white noise, narrowband noise linked with Misophonia or hyperacusis. After 3 months of testing, the maximum dosage of 2000mg per day were obtained the following results:
1) Reduction of tinnitus NOT TONAL from 6 to 3. Disappearance of "tinnitus reactivity". Disappearance of Misophonia (FULL).
Drastic reduction of the headaches associated with iperacusia.The patients have improvement in mood and in their ability to react to their situation of suffering. 2 persons have abandoned the use of SSRIs and are climbing out the use of benzodiazepines.
2) If the tinnitus is tonal, no relevant difference. (not lucky people)
3) If there are hyperacusis or Misophonia, after a month of treatment, the symptoms begin to weigh less on quality of life.
4) In patients who did not obtain benefits, was prescribed the Flexiban (Flexeril ... always cyclobenzaprine), with good results on tinnitus tonal, general tension, hyperacusis and headaches. It is noted that these patients have problems related to the neck or jaw or to the structure of the dental arches. Very common side effects that lead patients to abandon the following therapy are excessive sedation or tachycardia. Flexiban has a structure similar to Tegretol. Both are "cousins" of tricyclic antidepressants such as amitriptyline or nortriptyline that already in the past have been shown to have some efficacy in the tensive states, headaches or migraine, hyperacusis, generalized anxiety.
It is hoped that these results are permanent, in view of a future development of Biviracetam (enhanced version of Levetiracetam x10) who @Danny Boy is most active in the research, the suffers may have some help with a drug already tested and without serious side effects, avalaibilty and low price."
Best wishes
- Dec 24, 2013
- 933
- Tinnitus Since
- (1956) > 1980 > 2006 > 2012 > (2015)
- Cause of Tinnitus
- Ac. Trauma & Ac.Trauma + Meds.
Danny...
Well, thanks for the feedback and indeed, without more solid evidence of "Time factor" v. "Dose" factor...(except for linearity of dose for anti seizure applications = more "global firing" c/o a knowledgeable friend's translation of that...which may be very un-similar to T or H if my understanding of all the Kv stuff/Tzounopoulos is worth anything), I am going with my brain and thinking!
When I have not used my thinking, it has generally lead to big time pain. Like trusting the docs re Neomycin and such, without me checking and thinking about it. Too many examples to mention.
So...I took 1,000 mg to give 72 hours total at that dose of 2,000 mg per day total (3 days), then as of tonight's dose am dropping down to...not sure yet, but probably max 1,000 mg per day, or even 500 mg per day and holding it there for a while. My understanding of this drug is clearly that hardly anyone understands it, but that it is NOT a classic Kv modulator in primary action...and to be honest, that is where I have confidence that any T/H action for me, lies.
Otherwise I could just pick any AED drug and give it a shake and may have some luck with it...(which would not be a bad project for TT to assimilate actually! Like a list to date of all those tried, in one easy thread).
And yeah, my "gut" also tells me that if I have not had a "tweak" of a difference or feel in my T or H yet, then I have no particular reason to get more shit-faced right now, versus seeing if a lower dose at longer time exposure (where indeed I got a slight "change in T" action) would be as, or more helpful. I can always get more of this drug, as my doc is fully on board, etc., etc., etc.
OK, there you have it for now. Plus, I may well be getting a bit too wiggy...
Best, Zimichael.
Well, thanks for the feedback and indeed, without more solid evidence of "Time factor" v. "Dose" factor...(except for linearity of dose for anti seizure applications = more "global firing" c/o a knowledgeable friend's translation of that...which may be very un-similar to T or H if my understanding of all the Kv stuff/Tzounopoulos is worth anything), I am going with my brain and thinking!
When I have not used my thinking, it has generally lead to big time pain. Like trusting the docs re Neomycin and such, without me checking and thinking about it. Too many examples to mention.
So...I took 1,000 mg to give 72 hours total at that dose of 2,000 mg per day total (3 days), then as of tonight's dose am dropping down to...not sure yet, but probably max 1,000 mg per day, or even 500 mg per day and holding it there for a while. My understanding of this drug is clearly that hardly anyone understands it, but that it is NOT a classic Kv modulator in primary action...and to be honest, that is where I have confidence that any T/H action for me, lies.
Otherwise I could just pick any AED drug and give it a shake and may have some luck with it...(which would not be a bad project for TT to assimilate actually! Like a list to date of all those tried, in one easy thread).
And yeah, my "gut" also tells me that if I have not had a "tweak" of a difference or feel in my T or H yet, then I have no particular reason to get more shit-faced right now, versus seeing if a lower dose at longer time exposure (where indeed I got a slight "change in T" action) would be as, or more helpful. I can always get more of this drug, as my doc is fully on board, etc., etc., etc.
OK, there you have it for now. Plus, I may well be getting a bit too wiggy...
Best, Zimichael.
Keppra is a very unknown drug in terms of the mechanisms. We may never truly know how it works. I mean, we still don't know how the pill works, but it does? Rather confusing eh? But hey, let's move forward and keep on trying fixing.
no i havent actually for b12 but i had a blood test in november and it came out good..
I'm not a doctor and am not offering any advice, but i suspect (for H) keppra seems to work better at lower doses and the results seem to present themselves relatively quickly.
@swc5150 and @svintegrity both had good results at 500mg per day.
I dug this post up from Viking as well:
" I'm not an expert in chemistry and are only on the sixth day of treatment with Keppra (500 + 500 in the morning in the evening). The only thing I can say is that by the third day my hyperacusis is drastically gone. I have no more problems with loud noises. I think it is not a placebo effect. Hyperacusis is an ugly beast. I have no more abnormal reaction to loud noises. The brain response is changing. Yesterday and today I could go out with my very noisy motorcycle without getting headaches and increased tinnitus. I will try to better understand this study together with my neurologist. Thank you so much for your always immense contribution.
Best wishes"
I would stick between 500mg and 1000mg for a couple of weeks to see if there are any improvements. Does anyone have any additional thoughts?
I would stick to a low dose if i was trying keppra.
We don't know the Keppra dosing information to treat H (or T for that matter), but its fairly easy to find for Epilepsy (as that is the intended purpose for this AED, not for treating H or T). Theres someone on this forum thats saying go up to 2000mg or 3000mg (for treating H) without ANYTHING to back these statements, i would steer well clear of advice from that person.
That being said, we have some anecdotal evidence here that it works for H at (relatively) low doses.
Good afternoon Keppra Klatch fans,
I was going to wait a couple more days before posting an update on this thread, but so much is happening on this "happening" Keppra thread, thanks to @Zimichael @Geo @Danny Boy @Rube @Telis and @swc5150 that I decided to chime in with a Keppra update.
I have been on Keppra for a little over a month now. After my initial dose increase resulting in intolerable side effects for a "lightweight" like me, I have remained at a considerably low dose -- 250 mg. BID. Again, I am a small person, with a high metabolism and low body fat.
At present, my hyperacusis is still much diminished. Is it cured? No. Is it completely gone? No. Am I going hog wild and exposing myself to every loud sound imaginable? No. But I have seen noticeable results in reduction in my hyperacusis since being on Keppra. Yes. I swear, before the big K nothing, and I mean NOTHING, touched my big H!
Now @Telis don't get me wrong . . . I am not exposing myself to sounds that could cause further damage. I am talking about crumpling up a plastic bag, an ice cube hitting a glass, a fork touching a plate, switching off a light -- EVERYDAY sounds that used to be painful, but abnormally so. I still use hearing protection when I use my vacuum cleaner, run my blender, or use any household appliance/power tool. I will, however, go above decks on a ferry when I didn't dare before. Ride in a car, or sit on a street corner for a few minutes. Do I go totally unprotected? No. I keep my noise canceling headphones very close at hand, and there is still the reflex of hands over the ears, which is ever present.
Okay then, questions about mechanism of action have run rampant on this thread. Understandably so, we're talking about a complex drug here. Most of the work on MOA for AEDs (let's all talk in acronyms now!) has been focused on the anti-seizure effects for epilepsy. Thus medicine for these drugs for OTHER symptoms remains an art form, taking an empirical approach to find which drug or combination of drugs works best and at what dose! Many AEDs have numerous mechanisms and may affect neurotransmitters by acting on numerous targets.
For example, Levetiracetam (interesting I should use that example, no?) blocks VSSC, blocks T-type Ca++ channels, and increases GABA. Side effects can include dizziness, IRRITABILIY (have you noticed on this Keppra thread?!?), behavioral changes, but no significant pharmacokinetic drug interactions.
@Zimichael Keppra is not considered to be primarily a Kv3 drug, but may involve another of almost 100 of other K channel subunits that have been identified. So I do not think this to necessarily be a " knock down the door" drug (dose), but one based on "time," taking into consideration the best dose for efficacy while reducing side effects. But this is just my armchair opinion, kind of like the person in the space simulator pulling levers and pushing buttons, but not really flying the machine, right?!? My experiment is still a work in progress.
Keppra may not be for everybody, nor is it one-size-fits-all. And I am not saying it is a cure-all by any stretch of the imagination. I am a case study, N = 1, but I have always thought that it only takes one case to prove a possibility!
I was going to wait a couple more days before posting an update on this thread, but so much is happening on this "happening" Keppra thread, thanks to @Zimichael @Geo @Danny Boy @Rube @Telis and @swc5150 that I decided to chime in with a Keppra update.
I have been on Keppra for a little over a month now. After my initial dose increase resulting in intolerable side effects for a "lightweight" like me, I have remained at a considerably low dose -- 250 mg. BID. Again, I am a small person, with a high metabolism and low body fat.
At present, my hyperacusis is still much diminished. Is it cured? No. Is it completely gone? No. Am I going hog wild and exposing myself to every loud sound imaginable? No. But I have seen noticeable results in reduction in my hyperacusis since being on Keppra. Yes. I swear, before the big K nothing, and I mean NOTHING, touched my big H!
Now @Telis don't get me wrong . . . I am not exposing myself to sounds that could cause further damage. I am talking about crumpling up a plastic bag, an ice cube hitting a glass, a fork touching a plate, switching off a light -- EVERYDAY sounds that used to be painful, but abnormally so. I still use hearing protection when I use my vacuum cleaner, run my blender, or use any household appliance/power tool. I will, however, go above decks on a ferry when I didn't dare before. Ride in a car, or sit on a street corner for a few minutes. Do I go totally unprotected? No. I keep my noise canceling headphones very close at hand, and there is still the reflex of hands over the ears, which is ever present.
Okay then, questions about mechanism of action have run rampant on this thread. Understandably so, we're talking about a complex drug here. Most of the work on MOA for AEDs (let's all talk in acronyms now!) has been focused on the anti-seizure effects for epilepsy. Thus medicine for these drugs for OTHER symptoms remains an art form, taking an empirical approach to find which drug or combination of drugs works best and at what dose! Many AEDs have numerous mechanisms and may affect neurotransmitters by acting on numerous targets.
For example, Levetiracetam (interesting I should use that example, no?) blocks VSSC, blocks T-type Ca++ channels, and increases GABA. Side effects can include dizziness, IRRITABILIY (have you noticed on this Keppra thread?!?), behavioral changes, but no significant pharmacokinetic drug interactions.
@Zimichael Keppra is not considered to be primarily a Kv3 drug, but may involve another of almost 100 of other K channel subunits that have been identified. So I do not think this to necessarily be a " knock down the door" drug (dose), but one based on "time," taking into consideration the best dose for efficacy while reducing side effects. But this is just my armchair opinion, kind of like the person in the space simulator pulling levers and pushing buttons, but not really flying the machine, right?!? My experiment is still a work in progress.
Keppra may not be for everybody, nor is it one-size-fits-all. And I am not saying it is a cure-all by any stretch of the imagination. I am a case study, N = 1, but I have always thought that it only takes one case to prove a possibility!
I'm just glad you are getting better mate! I really hope it does work out for you in the long term.
That's VERY encouraging news, for sure! "Much diminished" would be a great relief for people that suffer from severe H.
That said, thanks for taking the time to write the update on your positive experience with Keppra.
On a personal level, I'm really glad for you!
- Jun 26, 2014
- 2,264
- Tinnitus Since
- 11/2013
- Cause of Tinnitus
- Drugs barotrauma
Well that's good to hear, glad you are getting some relief and not going nuts out there in the noise
2000 to 3000 mg is the max dose tolerated for epilepsy...
As for T and/or H there is no data at all. We're all completely in the dark.
Anyone's guess is as good as anyone's at this point in time.
- Dec 24, 2013
- 933
- Tinnitus Since
- (1956) > 1980 > 2006 > 2012 > (2015)
- Cause of Tinnitus
- Ac. Trauma & Ac.Trauma + Meds.
Note: For the non 'research oriented' but interested in Keppra, you may want to just skip down to the "key take-aways" in part 2. of this post...as yes, I do tend to drone on. Not changing my 'spots' now, sorry.
@svintegrity ...Ta much for add on info. post as indeed backs up the stuff I seem to be finding as dig deeper. Also much thanks to @111 down under, for two excellent tomes on Keppra (and Brivaracetam) which for the die-hards will get the 'links' below.
1. ~ OK...so for all you could ever want to know about Keppra (& Briv.) here is a link from a more than exhaustive study out of Germany in 2012. And don't get put off by it being in German to start with as the main text is in English. However, do be put off with the fact that it is 170 pages long before the 'references' start!!!
http://hss.ulb.uni-bonn.de/2012/3068/3068.pdf
I did not review it all. No way! However I did skim, and also looked for (search/find) key things of interest to me re. my whole initial approach to taking Keppra...that it was a Kv3.1 drug, like Autifony's famous star - or at least that Keppra had strong elements of Kv3.1 possible modulation.
Short answer...There is absolutely zero back-up or mention of that in this German paper. There is small reference to generalized Potassium channels within epileptic MOA ideas...and yes, in relation to our old comrade in arms (or hell, perhaps to some), Retigabine.
Conclusion on all that, to me OK, is that Keppra is not a Kv drug of any significance.
Thus I am no longer thinking of it in those terms, and no longer acting on it in those terms. Results, are as prior stated...I'm dropping off and not heading for 'break the doors down' dose effective inter-extra cellular neuronal saturation levels. *[And yes, Keppra is considered 'dose linear' but I consider that more relevant for the epilepsy model not the 'model' I had in mind. Also the Australian TGA paper next makes me wonder a bit WTF is going on with "dose" anyhow...or my concentration perhaps!].
2. ~ OK...the second paper, c/o the Australian TGA (which does some good work indeed...as per our research efforts on Retigabine, etc., etc.). This one is shorter and more readable, with some easier 'take-aways' that could be of interest to some here considering Keppra, or already taking it. *[And yes, I need to re-read it again (and maybe again!) to see what the hell is going on re the different "studies" quoted. That there is hardly any difference between doses of 1,ooo mg total v. 3,000 mg total, and that maybe Europeans act in a hugely different manner to Americans at even lower dose differentials???!!! Ummmmmmmm...must be me! Though the issue could just be that these 'problems' are all within the "Add-on AED Therapy" department, where more than just one AED...than just Keppra, is involved!. Plus they do not indicate which prior AEDs were actually used...So this could all be a red herring for us anyhow].
http://www.medicines.org.au/files/txplevet.pdf
Key take-aways, summarized in short (thus incomplete) sound bytes:
- Due to its complete and linear absorption, plasma levels can be predicted from the oral dose of levetiracetam expressed as mg/kg bodyweight. Therefore, there is no need for plasma level monitoring of levetiracetam.
Translate as: Body weight and size matter! (Also noted c/o @svintegrity).
- Following single dose administration (20 mg/kg) to epileptic children (6 to 12 years of age), the half-life of levetiracetam was 6.0 +/- 1.1 hours. The apparent body clearance was approximately 30% higher than in epileptic adults.
Translate as: Yeah you younger folks with less 'wear and tear' on your body parts are likely to unload Keppra faster and better than us more 'matured' (screwed over by various sundry health insults) folks.
- Monotherapy (i.e. = just Keppra, no other AED add-ons)...The recommended starting dose is 250 mg twice daily which should be increased to an initial therapeutic dose of 500 mg twice daily after two weeks. The dose can be further increased by 250 mg twice daily very two weeks depending upon the clinical response. The maximum dose is 1,500 mg twice daily.
Translate as: The Aussies seem to believe in classic titration - both in and out of Keppra use. Mmmmmmm...
- Overdosage: The highest known dose of levetiracetam received in the clinical development program was 6,000 mg/day. Other than drowsiness, there were no adverse events in the few known cases of overdose in clinical trials.
Translate as: Go wild! Compared to Trobalt, "Twinkies" may be more harmful to your health than this stuff. Well, as usual, not everyone is created equally and treat accordingly.
Ummmm... OK think that's about it for my Keppra 101. Now just observation and reflection...Wunderbar! Or possibly..."Shit, that is a bit of egg in the face!" could be more appropriate, depending on your disposition.
Best, Zimichael
@svintegrity ...Ta much for add on info. post as indeed backs up the stuff I seem to be finding as dig deeper. Also much thanks to @111 down under, for two excellent tomes on Keppra (and Brivaracetam) which for the die-hards will get the 'links' below.
1. ~ OK...so for all you could ever want to know about Keppra (& Briv.) here is a link from a more than exhaustive study out of Germany in 2012. And don't get put off by it being in German to start with as the main text is in English. However, do be put off with the fact that it is 170 pages long before the 'references' start!!!
http://hss.ulb.uni-bonn.de/2012/3068/3068.pdf
I did not review it all. No way! However I did skim, and also looked for (search/find) key things of interest to me re. my whole initial approach to taking Keppra...that it was a Kv3.1 drug, like Autifony's famous star - or at least that Keppra had strong elements of Kv3.1 possible modulation.
Short answer...There is absolutely zero back-up or mention of that in this German paper. There is small reference to generalized Potassium channels within epileptic MOA ideas...and yes, in relation to our old comrade in arms (or hell, perhaps to some), Retigabine.
Conclusion on all that, to me OK, is that Keppra is not a Kv drug of any significance.
Thus I am no longer thinking of it in those terms, and no longer acting on it in those terms. Results, are as prior stated...I'm dropping off and not heading for 'break the doors down' dose effective inter-extra cellular neuronal saturation levels. *[And yes, Keppra is considered 'dose linear' but I consider that more relevant for the epilepsy model not the 'model' I had in mind. Also the Australian TGA paper next makes me wonder a bit WTF is going on with "dose" anyhow...or my concentration perhaps!].
2. ~ OK...the second paper, c/o the Australian TGA (which does some good work indeed...as per our research efforts on Retigabine, etc., etc.). This one is shorter and more readable, with some easier 'take-aways' that could be of interest to some here considering Keppra, or already taking it. *[And yes, I need to re-read it again (and maybe again!) to see what the hell is going on re the different "studies" quoted. That there is hardly any difference between doses of 1,ooo mg total v. 3,000 mg total, and that maybe Europeans act in a hugely different manner to Americans at even lower dose differentials???!!! Ummmmmmmm...must be me! Though the issue could just be that these 'problems' are all within the "Add-on AED Therapy" department, where more than just one AED...than just Keppra, is involved!. Plus they do not indicate which prior AEDs were actually used...So this could all be a red herring for us anyhow].
http://www.medicines.org.au/files/txplevet.pdf
Key take-aways, summarized in short (thus incomplete) sound bytes:
- Due to its complete and linear absorption, plasma levels can be predicted from the oral dose of levetiracetam expressed as mg/kg bodyweight. Therefore, there is no need for plasma level monitoring of levetiracetam.
Translate as: Body weight and size matter! (Also noted c/o @svintegrity).
- Following single dose administration (20 mg/kg) to epileptic children (6 to 12 years of age), the half-life of levetiracetam was 6.0 +/- 1.1 hours. The apparent body clearance was approximately 30% higher than in epileptic adults.
Translate as: Yeah you younger folks with less 'wear and tear' on your body parts are likely to unload Keppra faster and better than us more 'matured' (screwed over by various sundry health insults) folks.
- Monotherapy (i.e. = just Keppra, no other AED add-ons)...The recommended starting dose is 250 mg twice daily which should be increased to an initial therapeutic dose of 500 mg twice daily after two weeks. The dose can be further increased by 250 mg twice daily very two weeks depending upon the clinical response. The maximum dose is 1,500 mg twice daily.
Translate as: The Aussies seem to believe in classic titration - both in and out of Keppra use. Mmmmmmm...
- Overdosage: The highest known dose of levetiracetam received in the clinical development program was 6,000 mg/day. Other than drowsiness, there were no adverse events in the few known cases of overdose in clinical trials.
Translate as: Go wild! Compared to Trobalt, "Twinkies" may be more harmful to your health than this stuff. Well, as usual, not everyone is created equally and treat accordingly.
Ummmm... OK think that's about it for my Keppra 101. Now just observation and reflection...Wunderbar! Or possibly..."Shit, that is a bit of egg in the face!" could be more appropriate, depending on your disposition.
Best, Zimichael
I'd like to hear @Danny Boy s take on this specific point. I bet that he knows what he is saying because earlier he said that Brivaracetam is Kv3.1 modulator as well?
@Zimichael thanks for the valuable fact based insight.
- Dec 24, 2013
- 933
- Tinnitus Since
- (1956) > 1980 > 2006 > 2012 > (2015)
- Cause of Tinnitus
- Ac. Trauma & Ac.Trauma + Meds.
@Zechariah ...Yeah, well we may all be doing our best in a very murky and turbulent pond with god knows which way is up...Not jumping DB's response as I too am interested in whatever/whenever on all this stuff, but dig this (2008):
Brivaracetam was also devoid of effect on high- and low-voltage activated calcium currents (Kostyuk et al., 2004), and on voltage-gated potassium currents (Margineanu et al., 2004) in isolated rat hippocampal neurons.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2518465/
Sigh!
Brivaracetam was also devoid of effect on high- and low-voltage activated calcium currents (Kostyuk et al., 2004), and on voltage-gated potassium currents (Margineanu et al., 2004) in isolated rat hippocampal neurons.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2518465/
Sigh!
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