I've gone back and read about dextromethorphan and naltrexone, which I take as low dose naltrexone or LDN, and was surprised to learn that they are both dopamine agonists like Mirapex which I also take. My reason for taking naltrexone, off label, for the past 32 months is to hopefully slow or halt PD progression. I can't say I have seen the movement benefit that Steve has seen because I wasn't looking for it when I first began LDN (maybe I saw an improvement in balance). I can say that I don't seem to have progressed but I don't know why. The point of taking either of these drugs (opioid receptor agonists) at a low dose, is to slow or halt progression.
The research done by Dr. Zagon and Dr. Hong emphasize that somehow these opioid drugs work within a low dose window and that to exceed the dose level could make the disease worse. Dr. Hong believes PD is the result of activated microglia cells which cause inflamation and the loss off dopamine cells (he has shown that femtomolar doses of naloxone protect rodent brains against this inflamation). So in the case of naltrexone, which has been used daily at doses of 50 to 100mg for substance abuse, it would not be a good idea to take a 50mg pill for PD (LDN has to be compounded as 4.5mg capsule).
If there is a doctor here or neurologist, are you aware that the drugs mentioned above are dopamine agonists like Mirapex and have they been used to treat PD? These are pretty inexpensive drugs compared to Mirapex. Do you have any comment on the use of these drugs at a low dose to slow PD progression other than not to take them? People mention liver damage but so far there has been no news of people on LDN or DM having this problem at these levels.
Ashley

dopamine agonist definition:
http://www.parkinsonsdisease.com/pcp/PCP7D.HTM

naltrexone: note, can be Rx by doctor, Revia, if you have a substance abuse problem and then you can make you own LDN.
http://www.intelihealth.com/IH/ihtIH...91/339954.html
Naltrexone has been used for the treatment of alcoholism since its 1994 approval by the federal Food and Drug Administration. Naltrexone acts as an opioid antagonist within the opioid neurotransmitter system, which is a part of the brain's reward system. When opioids are stimulated, levels of a neurotransmitter called dopamine are increased. Dopamine activity is thought to be key to experiencing the "high" of a variety of different drugs, including alcohol. Naltrexone achieves its effects by "blocking" this domino-type chain of events that lead to the desire to continue drinking. In short, naltrexone decreases the rewarding effects of drinking and reduces the craving for alcohol that often leads people to relapse.