You present a pretty convincing case; one I have heard repeated almost verbatim. You said:: "All of these behaviors COMPLETELY went away when I stopped taking the agonists. There is no way they are part of advancing disease, at least from my perspective." I suppose the only way of obtaining further evidence that the dopamine agonists (DA'S) are indeed the culprit, would be to have advanced PWP in the control group. I didn't do my homework - has this been done? How else can they determine if advanced PD folks that have been on levadopa (Sinemet) along with the DA's would have these symptoms? But it iidoes seem likely that if your symptoms totally stopped, it must have some correlation.

There's one poster here who has studied this at length. I think I'll get in touch with her and ask for her input. I cannot see that many "long" longitudinal studies have been done.

And the symptoms you mention (increased dystonia) are one or the major reasons that I am not as motivated to drop the agonists. The agonists prevent or help lower my pain level. I know this because I have tried to wean myself from them before, slowly titrating down, as my neurologist suggested.

Additionally, although not a proven fact, agonists have shown some merit of being neuroprotective. Azilect (an MAO-Inhibitor) has also made this claim.

Paula, now I want to address your question as to how this "new" theory or way of assessing Doamine Agonist Withdrawal Syndrome (DAWS), differs from Neuroleptic Malignant Syndrome (NMS). It appears that the symptoms very similar to NMS have been applied to a scale, but it's very similar (although I haven't really dug into it all that much).

Time will tell.

Peggy
Peg