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I think I started this general thread last month by asking about
selegiline as a replacement for Amantadine which is/was giving me
unpleasant side effects, especially ankle swelling.  I have not taken any
for over a week now, but I don't know how long it will take to get it out
of my system.

I was especially interested in Ariela's questions and Dr. Romero's reply
about apparently related Rasagiline. I was not encourage by that either.
From all I have heard and read, I have decided Eldepryl is probably not
for me.  I might consider it if it really had the property of slowing
down the progression of PD, but even that seems to have been debunked.

Also, from my reading, I doubt Eldepryl would be  computable with
preparations I take for depression (Welbutrin), Asthma and allergies
(Serevent, Nasocort AQ, Proventil and Pulmicort, all inhaled)
hypertension (Zestoretic) and elevated cholesterol (Provachol).  I also
take Sudafed when I get an upper respiratory infection mild or not so
mild. It helps a lot, but seems to be contra-indicated in combination
with selegiline.  This probably looks like an awful mess, but I have been
virtually free of Asthma symptoms for about 10 years now. The previous
ten were a nightmare!

Also, presently, I am taking only "Suminerole" a new dopamine agonist
still in clinical trial, which seems to be taking care of most of my PD
symptoms, except for fatigue which is occasionally extreme but comes and
goes, "off and on".

Do any of the readers and M.D.s on this list agree with my conclusion or
not?

Nancy K.
You wrote:
>Ariela:
 >You go to the heart of the matter with your questions.
>
>#1  The only PROVEN reason to use a Monoamine Oxidase B Inhibitors
>(selegiline) is to extend the effect of levodopa.  Using selegiline in
>combination with any of the dopamine agonists is not of any proven value.
>The likelihood is that rasagiline will turn out to be the same.  MAOB
>inhibitors are not known to extend the effect of dopamine agonists, and
>there is no theoretical reason why they should.
>
>#2   The use of MAOB inhibitors as FIRST therapy is predicated upon the
>SPECULATION that they may be neuroprotective, and somehow delay the
>progression of the disease.  In the case of selegiline, this proved to be
>wrong in humans with PD.  Given the failure of selegiline in this respect,
>there is no reason to expect that rasagiline would be different, but the
>drug company is proceding with research in this direction hoping that it
>might, and is already beating the drums.
>
>#3   The logic that "any postponement in levodopa start is worth the
>trouble" is highly controversial.  It is promulgated primarily by the drug
>companies who are trying to sell the dopamine agonists - frightening  PWP
>that early use of levodopa causes earlier dyskinesias.  Although many
>neurologists agree, the data are based on incomplete and flawed studies
>designed to promote the use of the agonists.  The final answer with respect
>to this question is yet to come.  In the meantime, some people avoid early
>use of levodopa "just in case."
>
>#4   Many of the ANTIdepressants are reuptake inhibitors - some inhibit the
>reuptake of catecholamines (including dopamine), others inhibit the >>reuptake
>of serotonin.  The antiparkinsonian drugs (levodopa or the agonists) do not
>cause the serotonin syndrome.  With selegiline or rasagiline there may be
>some possibility of precipitating the serotonin syndrome when mixed with
>other antidepressants, but not with the antiparkinsonian drugs.  This is
>unlikely, however, but theoretically possible.
>
>#5  Your observation about the length of studies is very logical.  Indeed,
>we should have learned that lesson well from the DATATOP Selegiline study.
>The initial data (six month follow-up) was initially interpreted as showing
>some neuroprotective effect.  The longer follow-up (five years) showed that
>there was no significant difference.
>
>Jorge A. Romero, MD
>

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