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Thread: Keppra

  1. #1
    Forum Member Barry52's Avatar
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    Keppra

    Hi all,

    I read about this today on a forum and thought it might be of interest. I don't know about availability in the UK. I know Dr. Bedlack is well respected in the US.

    Here's an interesting alternative to Baclofen for those of you that don't do well on that drug when it comes to spasticity (or functioning). If you would like the complete article, ask for KEPPRA FOR MND BEDLACK 2009 and the diminutive but peppy Lisa Dang will make that happen. Here's a bit of a description:

    Back in the late 2000's, Dr. Bedlack [whom some of us might worship just a bit] did a study on the use of Keppra in a SMALL SMALL group of 20 people with MND [14 had ALS (4 FALS and 16 sporadic), 3 had PLS, 3 had PMA (this is the opposite of PLS--all LMN)].

    "They were instructed to begin taking 500 mg twice daily either in tablet or solution form. After day 7, the dosage was increased to 1000 mg twice daily, and after day 14 the dosage was increased to 1500mg twice daily. If a patient was unable to tolerate a dosage increase, they were asked to resume taking the highest tolerable dose."

    I want to again point out this was a VERY SMALL STUDY. But. It worked--at least in terms of reducing spasticity and muscle cramping. It is not enough to say YES, DO IT--but it is perhaps (depending on you) enough to say, "Hmmm. I might ask to try that out" if your spasticity is not responding to Baclofen. Keppra is also sedating but not as bad as Baclofen in many people. There are also reports of psychological reactions (e.g., "Keppra rage") which happen in a smaller number of people. IF YOU ASK YOUR DOCTOR TO TRY THIS, KEEP A CLOSE EYE ON EMOTIONAL REACTIVITY!!!

    "In this small, open-label study, levetiracetam treatment was temporally correlated with a large drop in cramp severity, cramp frequency, and phasic spasticity. The size of the drop in cramp severity, the primary outcome measure, was larger than was seen in the placebo group in previous cramp studies (21). The mismatch between an effect on phasic spasticity and none on tonic spasticity is similar to what was seen in a previous study on subjects with multi- ple sclerosis (5). Levetiracetam treatment was associated with a significant increase in adverse events, but few of these were serious or associated with discontinuation of study drug. The increase in adverse events may well have been due to disease progression."

    PLEASE NOTE: There was a difference in how it worked between two kinds of spasticity (tonic and phasic--doesn't work on tonic and does on phasic). Same effect was found in a study looking at Keppra for spasticity in MSers. I don't know what the difference is between those two kinds of spasticity but if you do know, please explain below!
    Iím going to do this even if it kills me!

  2. #2
    Forum Member Ellie's Avatar
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    Hi Barry,

    Spasticity, in simple terms, can be tonic or phasic in response to the stretch reflex.

    Tonic refers to spasticity associated with high muscle tone i.e. that which affects most of us here. It is continuous and is controlled by drugs such as Baclofen and Tizanidine.

    Phasic refers to spasticity which occurs in phases, rather than continuous. Clonus is an example of this. Phasic spasticity is controlled by drugs such as Diazepam and Levetiracetam (brand name Keppra)

    I have awful clonus and myoclonus at night in my feet in particular, and my knees, to a lesser extent. I took Keppra for 10 days and found it intolerable! It's a strong anti-epileptic drug and even though I only took it at night, it made me zombie-like. Maybe that's just me?

    Hopefully I've kind of explained it to you?

    Love Ellie.
    ​Diagnosed 03/2007. Sporadic Definite ALS/MND Limb Onset.
    Eye gaze user - No working limbs - No speech - Feeding tube - Overnight NIV.

  3. #3
    Forum Member Barry52's Avatar
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    Thank you Ellie for your concise summation of a lengthy report.

    Barry x
    Iím going to do this even if it kills me!

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