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thanks for your response, dr. romero. alas, here's (of course) the inevitable 'follow up': #1. it’s been my experience that in spite of the studies -- DATATOP and the subsequent, controversial british PDRG-UK (which concluded that selegiline was responsible for a 57% increase in a patient's mortality odds over those who received levodopa only) -- the medical establishment opts for selegiline as soon as pd is suspected. my PWP was prescribed the drug first by a (very) general neurologist, and then by a succession of better and finer-tuned movement disorder specialists. i hope i'm not being indiscreet when I say dr. fahn of columbia-presbyterian recommends selegiline together with a dopamine agonist as the initial line of defense, then maintains this basic regimen for as long as one's symptoms are manageable. which makes me wonder -- if selegiline does not extend the effect of dopamine agonists, does not delay the need for starting levodopa (or its effect once it’s started), and does not slow neuron degeneration, does it really matter if it "only" relieves the symptoms of pd? for an incurable, difficult disease, I’d say this ain’t too shabby…. #3. when faced with a "just in case" scenario, I think I become a lemming – just count me in! it seems to me that the controversy over how long can levodopa be administered without causing or accelerating dyskinesia is inherently unsolvable. as with cancer studies, it would be impossible to design a model where the natural progression of the disease could be factored in as a constant, finite variable. now if the received perception is that of a limited treatment-period (I understand 5 to 10 years before levodopa’s effectiveness begins to fail and side effects become intolerable), then why not err on the side of caution, especially if a patient is doing all right? #4. oops, my mistake. Of course there are many ANTI depressants that are reuptake inhibitors (not the least of which is the SSRI group...). however, i'm afraid that error made my query rather unclear. i should have asked two separate questions: a) do all dopamine agonists have depressant- or barbituate-like properties? and b) if so, would they not, when combined with selegeline (an MAO-B inhibitor), cause a "shock" reaction similar to that of prozac (SSRI) when given with selegiline? #5. and last but not least, speaking of selegiline being such an 'iffy' drug (even as a simple anti-oxidant), how do you explain the great popularity and following it has among anti-aging enthusiasts? thanks very much, ariela ---- Jorge A Romero MD <[log in to unmask]> 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 thatit 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 respectto this question is yet to come. In the meantime, some people avoidearly 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 maybe 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 __________________________________________________ FREE voicemail, email, and fax...all in one place. Sign Up Now! http://www.onebox.com ---------------------------------------------------------------------- To sign-off Parkinsn send a message to: mailto:[log in to unmask] In the body of the message put: signoff parkinsn