I would like to know how everyone is doing with it. I know Steve is doing well and wondered about the others.

Ran across a clue to its action or, at least, more data. It is an NMDA antagonist, which means that it blocks the receptors that are involved in the role of glutamate which can be harmful.

I got to wondering what other NMDA antagonists were around and found that magnesium was one.

I am doing remarkably well..Two things that may play into the scheme is, that Ive been seeing a Chiropractor once a month since around August

Ive also tweeked my med regimen a little bit..My former regimen was:.

Sinenet 25/100 x 3 daily

Mirapex .25 x 2

1/2 teaspoon DM Daily before bed


My new regimen since about October is:..

50/200 Sinemet CR x 2 daily

Mirapex .25 x 2

1/2 Teaspoon DM Daily before bed

So basically Im taking 100 mg more of Sinamet daily in the form of CR

My blood pressure went from an average of 140/93 - 130/80..last check in Oct was 120/70

I have more movement, less fatigue..but have some dystonia in my right leg and foot..not serious, but uncomfortable sometimes..The Chiropractor has been experimenting with additional adjustments on the nerves that control those muscles, to see if he can relieve the spasms..I have no results to report about that yet..I havent had as many dystonia flare ups lately, but havent been as physically active as I was when it was at its worse..So it would be inaccurate at this time to make a judgement call concerning it

People who know me have made comments on my condition, all positive..Ive had a few of them ask me what I did to change it?..People have stopped asking me if I need help..At AA meetings people were constantly asking me if they could get me a cup of coffee..if I needed a ride..Not lately though..I figure that since my first symptoms, Im about to enter my 6th year with pd, and Im doing better now than I was 2 years ago, when I met some of you at the WPC..MY gait is almost normal..the limp is all but gone..I sleep well, my face doesnt mask, and I dont find my self uncomfortable sitting/standing for longer lengths of time..putting my coat on/taking it off is easier than last winter..As a matter of fact, I dont even think about it now..I have stopped looking in the mirror to buckle my belt..Driving has been easier, and more confident..and theres been a few times lately that I forgot to take my 2nd dose of meds at 4:00 pm, and one night I didnt realize it untill 11:00 pm, and didnt bother taking them untill the next morning, at 9:00 am at the usual time

Do I believe that DM has something to do with all this?..I think it does, but Im going to give it some more time before I am certain beyond a reasonable doubt..If I dont have to make any significant med changes within the next 2 years or so, and am reasonably as physically active..fishing etc, as I am now..then I think that is a fair rule of thumb..But for now..one of the 3 things that Ive been doing, or a combination of them, has something to do with the success Ive been experiencing

One other thing to note..My life is more peaceful than its ever been, and I have about zero stress..From my past experiences, I know that has something to do with the way Ive been feeling

I have progressed very little, if any, since I began taking DM in 2002.

I was diagnosed in April 2001 at a very ealy stage of motor involvement. I began 3 tablets per day of generic sinemet carbi/levo 25/100. That eliminated the mild motor symptoms of dragging my left foot and some bradykinesia. Later in 2001 I started 200mg amantadine, later decreased to 100mg to relieve leg and ankle swelling. After reading about CoQ10 early in 2002, I began taking 3x300mg of that per day.

A few months later I learned about an already FDA-approved drug naltrexone, introduced by forum member AshleyK as potentially neuro-protective at very low doses. AshleyK was/is apparently taking naltrexone, hoping thereby to achieve arrest of PD progression. She was aware that some PD patients were experiencing symptom non-progression similar to the elimination of further exacerbations of multiple sclerosis that many of those patients have experienced with LDN (low dose naltrexone) treatment. I seriously considered LDN for myself.

I subsequently discovered that experiments by Dr. Hong's research group at the National Institute of Environmental Health on protection of mouse midbrain dopamine neurons from inflammation was achieved by extremely low concentrations of a group of drugs that included naltrexone, naloxone, and dextromethorphan. Being aware that dextromethorphan is available over the counter in several antitussive preparations (cough syrups), and that a prescription is required for naltrexone, I decided to add a nightly 3-4mg dose of DM to my other meds. That is the amount of DM in a half teaspoon of Pedia Care Cough. Recommended dose for cough supression in a 6-12 year-old is 2 teaspoons (14mg) every 6-8 hours.

The history of this saga can be found by searching the old neurotalk post archive under dextromethorphan or DM.

Finally, I can report that I have experienced little progression of PD motor symptoms since adding DN to my other meds, although I have developed the tendency to shuffle-walk after arising in the morning before taking meds. Any changes in my cognitive functions are minimal, mostly slow recall of names of persons and of some objects on occasion.

Like Steve, when I occasionally forget my afternoon sinemet (half a regular and a cr) I have little or no loss of function. I simply wait until the next morning to take the regular daily round. Also, like Steve, I think the decreased stress achieved by my retirement last December has really worked to my advantage.

Current daily meds:

2x50/200 generic sinemet cr, two half tablets 25/100 generic regular sinemet
(total 500mg levodopa)
100mg amantadine
900mg CoQ10
150mg Welbutrin
30mg Cymbalta
*Shaklee Vitalizer (multivitamins plus dietary supplements) daily pack
*Shaklee HerbLax (herbal laxative preparation) 3-4 tablets
82mg aspirin

*my wife is a distributor of Shaklee products.

My neuro has no problem with my taking DM. Whether it is actually providing neuroprotection or my case of PD is just a slower progressing type is still unknown. At any rate, I intend to continue taking it indefinitely, or until I am convinced that there is something more effective.

Robert

There is one thing I will say about progression in my case..I started DM almost 3 years after dx, and I was progressing at a moderate rate..What I have noticed is that since last March I havent gotten any worse, and after switching to Sinemet CR in October Ive improved

Your experience represents more definite positive results than mine. It appears that you actually dimished in motor symptoms rather than just arresting progression. Overall, i'm convinced that low dose DM shows the best promise in neuroprotection.
A few weeks ago I emailed the local movement disorder specialist, who is also a member of the Parkinson's Study Group, complaining that I felt the NIH is wasting its money with neuroprotection studies on things like creatine instead of more promising drugs like dextromethorphan and naltrexone that have already shown some effectiveness. I told him of my experience since beginning DM, and he replied that PD is so inherently variable in it's rate of progression that my experience was hardly significant in the overall big picture. My own neuro is not so dismissive, and could be described as cautiously optimistic about DM.

I would like to hear from others who are using DM or naltrexone in an attempt to achieve neuroprotection and progression arrest.

Robert

The thing that baffles me about PD is how the symptoms can vary so much and so often. I keep watching for things that may seem to make it better or worse, but so far, as so many have said before, stress is the one thing that clearly makes a difference. Retirement may be the best medicine.

But just for a minute. If we want to go deeper let's start another...

For me, the statement "stress is the one thing that clearly makes a difference" is probably the most important clue we have. It leads to several interesting points:
1) Stress reactions lie within the domain of endocrinology, not neurology. That alone means trouble for us. We fall between the cracks.
2) Stress research reveals a picture of a balancing act built around a lifelong pursuit of homeostasis ("health" or "balance"). It is like balancing on one foot, even for normal folk.
3) Certain things can make it harder to balance on that foot. The prenatal bacterial toxin hypothesis incorporates one.
4) As time goes on it gets harder and harder as the system fatigues. As we age we encounter secondary insults such as pesticides. Where a healthy system might be able to maintain balance, we start to wobble.

Since each of us is at a different point in that continuum and since we encounter different secondary insults, each of us is different in presentation.

Except for the response to stress. There is something unusual about our relationship to it. As we discovered earlier, a heck of a lot of us had high stress childhoods, jobs, etc. and held up well (or seemed to). Somewhere along the line we crossed a threshold.

One interesting thing is that this view makes room for other theories as "secondaries". The BBB idea fits in well, for example. Stress increases inflammation which increases BBB permeability and so on.

So, if we want to get into that let's jump to its own thread. In fact, I will paste this over for a starter.

I have been wondering how the people who are taking Dextromethorphan have been doing lately. It's good to see Steven and Robert think DM is halting or slowing down their PD progression. It seems to be true that PD is variable and it's difficult to determine if any of these supplements make a difference in progression.
I have been taking 4.5 mg of naltrexone, LDN, for 42 months now and I have not had to increase my mix of Sinemet and Mirapex since starting LDN ( I also take 600 mg of Q10). My major symptom was tremor which became progressively worse until I started Sinemet (it's gone for now) which also confirmed PD. My neuro thinks I could be in that "lucky" group that's slow progressive (she still doesn't know I take LDN, she told me not to take it when I asked for an LDN Rx). So that's the big unknown for me, am I lucky or does LDN (and DM) work as studies at the NIH in rodents show it should. Does anyone have any thoughts on how long a PD'er can stay on a constant lower dose of Sinemet before symptoms reappear/get worse and you have to move up the Sinemet dosage?
Also for Steve, maybe naloxone (and DM?) is protective for HBP and hardening of the arteries.

A novel inhibitory effect of naloxone on macrophage activation and atherosclerosis formation in mice.
http://www.ncbi.nlm.nih.gov/sites/en...t=AbstractPlus

Ashley

at least with the dextromethorphan. What about naloxene (sp?) Is it an NMDA blocker too, or is there two different things going on?

And has anyone besides myself had major motor problems from MSG ingestion? Such an encounter should set the NMDA receptors firing like the Fourth of July and it sure does ruin a good half a day when it happens.


1: Pharmacol Ther. 2004 May;102(2):155-74.

Rationale for and use of NMDA receptor antagonists in Parkinson's disease.

Hallett PJ, Standaert DG.

MassGeneral Institute for Neurodegenerative Disease, Massachusetts General
Hospital, Harvard Medical School, 114 16th Street, Charlestown, MA 02129, USA.

N-Methyl-d-aspartate (NMDA) glutamate receptors are a class of excitatory amino
acid receptors, which have several important functions in the motor circuits of
the basal ganglia, and are viewed as important targets for the development of new
drugs to prevent or treat Parkinson's disease (PD). NMDA receptors are
ligand-gated ion channels composed of multiple subunits, each of which has
distinct cellular and regional patterns of expression. They have complex
regulatory properties, with both agonist and co-agonist binding sites and
regulation by phosphorylation and protein-protein interactions. They are found in
all of the structures of the basal ganglia, although the subunit composition in
the various structures is different. NMDA receptors present in the striatum are
crucial for dopamine-glutamate interactions. The abundance, structure, and
function of striatal receptors are altered by the dopamine depletion and further
modified by the pharmacological treatments used in PD. In animal models, NMDA
receptor antagonists are effective antiparkinsonian agents and can reduce the
complications of chronic dopaminergic therapy (wearing off and dyskinesias). Use
of these agents in humans has been limited because of the adverse effects
associated with nonselective blockade of NMDA receptor function, but the
development of more potent and selective pharmaceuticals holds the promise of an
important new therapeutic approach for PD.

PMID: 15163596 [PubMed - indexed for MEDLINE]

If you mean MSG as in Chinese food?..Doesn"t affect me, as a matter of fact, it hasn't mattered what I eat, and even protien around med time hasn't made a difference in motor syptoms for me