Part of my feeling of improvement, possibly all of it, might well be placebo effect. I know about myself that I am so very hopeful and optimistic that a new and promising remedy will be efficacious for a while. I took vitamin B- 2 and stopped eating red meat, and for a year and a half, my balance was almost restored. When the effect wore off, I could not be sure if B-2 had stopped working for me, or I had stopped believing that it helped.
Curcumin is still helping after two plus years, so I know that it is not just wishful thinking. DM will have to be suspect for a while. In the meantime I will enjoy the little improvements, whether real or imagined.

birte

While the current buzz is about neuroprotection, there was quite a bit of work in the 90s addressing neurofunction. It hasn't been followed up but it did show flames beneath the smoke:

1: Mov Disord. 1998 May;13(3):414-7.

A trial of dextromethorphan in parkinsonian patients with motor response
complications.

Verhagen Metman L, Blanchet PJ, van den Munckhof P, Del Dotto P, Natte R, Chase
TN.

Experimental Therapeutics Branch, National Institute of Neurological Diseases
and Stroke, National Institutes of Health, Bethesda, Maryland 20892-1406, USA.

The effects of the NMDA antagonist dextromethorphan (DM) on levodopa-associated
dyskinesias and motor fluctuations were studied in patients with advanced
Parkinson's disease. During initial open-label dose escalation, 6 of 18 patients
reported a beneficial effect at their individually determined optimal DM dose
(range, 60-120 mg/day). The 12 remaining patients either experienced reversible
side effects, particularly mild drowsiness, or decreased levodopa efficacy, and
were therefore excluded from the study. The six responders entered the
double-blind, placebo-controlled, crossover study with two 2-week arms separated
by 1 week wash-out. On the last day of each arm, motor ratings were performed
every 20 minutes for 8 consecutive hours. In addition, motor complications and
Activities of Daily Living (ADL) were assessed using the Unified Parkinson's
Disease Rating Scale (UPDRS) and patient diaries. With DM, dyskinesias improved
by 25% according to physician's ratings and by 40% according to UPDRS
interviews, without compromising the anti-Parkinson effect of levodopa. Motor
fluctuations and ADL scores also improved significantly. Although the narrow
therapeutic index of DM limits its clinical usefulness, these findings support
the view that drugs acting to inhibit glutamatergic transmission at the NMDA
receptor can ameliorate levodopa-associated motor complications.

PMID: 9613730 [PubMed - indexed for MEDLINE]

1: Neurology. 1998 Jul;51(1):203-6.

Dextromethorphan improves levodopa-induced dyskinesias in Parkinson's disease.

Verhagen Metman L, Del Dotto P, Natte R, van den Munckhof P, Chase TN.

Experimental Therapeutics Branch, National Institute of Neurological Diseases
and Stroke, National Institutes of Health, Bethesda, MD 20892-1406, USA.

OBJECTIVE: This study assessed the effects of the N-methyl-D-aspartate (NMDA)
antagonist dextromethorphan (DM) on levodopa-induced dyskinesias in Parkinson's
disease (PD). BACKGROUND: Recent experimental evidence suggests that increased
synaptic efficacy of NMDA receptors expressed on basal ganglia neurons may play
a role in the pathophysiology of levodopa-induced motor response complications.
METHODS: DM was given to six PD patients with motor fluctuations in a
double-blind, placebo-controlled, cross-over study. At the end of each 3-week
study arm, patients received several brief i.v. levodopa infusions while
parkinsonian symptoms and dyskinesias were frequently scored. Levodopa
dose-response curves for antiparkinsonian and dyskinetic effects were then
compared for each study arm. RESULTS: With DM, average and maximum dyskinesia
scores improved by >50%, without compromising the antiparkinsonian response
magnitude or duration of levodopa, although in some subjects the levodopa
threshold dose was slightly higher with DM than with placebo. CONCLUSIONS: These
findings support the view that drugs acting to inhibit glutamatergic
transmission at the NMDA receptors can ameliorate levodopa-associated
dyskinesias.

PMID: 9674803 [PubMed - indexed for MEDLINE]

I took my last dose of Sinamet at 11 pm last night..I took my dose of DM at 12:30 am..I was able to put my slippers on with no problem whatsoever and with out using my hands..(SITTING DOWN)..this morning..(BEFORE TAKING MORNING MEDS)..This is no great feat with my left foot, but near impossible with my right foot..Im lucky if I can get my toes into the opening of the slipper with my right foot..I havent been able to accomplish this in more than 2 years, and Ive done it twice since beginning DM..So Im thinking that as I suspected, that because DM is a dopamine reuptake inhibitor, that it works in tandem with Sinamet, and causes the Sinamet to work more efficiently

Prior to this experiment I was taking my last dose of Sinamet at 7 pm, and taking DM at between 12:30 and 2:00 am, when my last daily dose of Sinamet had no doubt worn off, and had run its course, and usually more nights than not I took the DM at, or closer to 2:00 am

So what Im going to try tonight is using Mirapex as a filler inbetween my afternoon Sinamet and an 11 pm dose because I was feeling kinda funky with a 9 hour span inbetween Sinamet doses

I feel absolutely great this morning!..

It has been one week since I began taking my last dose of Sinamet late at night up to 2 1/2 hours or less before taking my daily dose of DM, and it seems that I feel much better the following day if my last daily dose of Sinamet is still active when I take the DM

My daily drug regimens..(I am and have been undermedicated throughout my dx with pd)

My previous med regimen:..

9:00am - 1 Sinamet 25/100...1 Mirapex .25

2:00pm.- 1 Sinamet 25/100...1 Mirapex .25

7:00pm - 1 Sinamet 25/100

1:00am - 1/2 teaspoon DM

__________________________________________________ ______

My new med regimen:..

9:00am - 1 Sinamet 25/100...1 Mirapex .25

2:00pm.- 1 Sinamet 25/100...1 Mirapex .25

7:00pm - 1 Mirapex .25

11:00pm..(or up to 1/2 hour prior to taking DM)..1 Sinamet 25/100

1:00am - 1/2 teaspoon DM

(I use the Mirapex .25 at 7:00pm dose as a filler dose instead of the usual Sinamet)

Ive had a few friends comment on my improved condition, and a couple have asked me if I was on a new medication..My friend Jim who I have fished with since 1978 goes to Florida every winter..He saw me before he left in December..and he just came back and stopped over this morning..He said that he noticed that I wasnt dragging my foot like I was before..that I only stuttered a little bit..that I was more alert, and looked better than I did in December when he left for Fla

It has been about 5 weeks since I began taking DM daily, and there is absolutely no doubt in my mind that it has improved my symptoms drastically..even my memory has improved

but keep an eye on the blood pressure, especially if you use requip. Medline has zero hits on the pair but both requip and DM work through the CYP450 enzymes and mirapex does not. I suspect that that was my real problem. BP was around 200/120 after four days and is just now back down.

But those first days were really good. There is something there, just be prudent.

Thanks for the info Rick..I cant and wont take Requip because it makes me sick..I havent checked my blood pressure yet, and when I do and it happens to be high, the Mirapex is history..actually at this point I dont even really need it anyway..Ill just substitute the 7:00 PM dose with a half tablet of Sinamet

sounds a rather novel use for dextromethorphan--I read about this combo (quinidine and dextromethorphan)being used in Phase 3 trials for ALS patients on another forum--also used for neuropathic pain:

Dextromethorphan-Quinidine Combination Reduces Inappropriate Emotional Episodes in MS





April 18, 2005 (Miami Beach) — A dextromethorphan-quinidine cocktail (Neurodex) effectively addresses the inappropriate laughing and crying episodes experienced by some patients with multiple sclerosis (MS), according to investigators who presented their findings here at the 57th annual meeting of the American Academy of Neurology.

The incongruous laughing and crying episodes, also called "emotional incontinence," are due to pseudobulbar affect (PBA). Dextromethorphan, the active ingredient in most over-the-counter cough suppressant syrups, also binds to the sigma-1 and N-methyl-D-aspartate neuroreceptors and therefore had the potential to address PBA.

"If we gave patients a sufficient dose of dextromethorphan alone to penetrate the central nervous system, the trade-off would be nausea and vomiting," principal investigator Hillel Panitch, MD, said during a press briefing. "However, because quinidine prevents systemic metabolism of dextromethorphan, we can use less dextromethorphan that is yet sufficient to address PBA." Dr. Panitch is a professor of neurology at the University of Vermont College of Medicine in Burlington, where he is the director of the Multiple Sclerosis Center at Fletcher Allen Health Care.

The investigative formulation, also known as AVP-923, consists of 30 mg each of dextromethorphan and quinidine sulfate. In a double-blind, placebo-controlled study, the investigators recruited 150 patients with MS at 22 community and university-based centers to be treated either with the study drug or placebo every 12 hours for 12 weeks. The patients completed a diary and recorded the number of episodes of inappropriate laughing, crying, or both that occurred each day and indicated the medications they took, the times they took them, and any adverse events. The patients had scored at least 13 on a validated self-assessment tool used to evaluate PBA.

The investigators saw the patients in follow-up clinic visits on days 15, 29, 57, and 85. At those times, they obtained patients' clinical chemistry, vital signs, physical examinations, and electrocardiograms. The investigators compared the change in self-assessment score between the treated and placebo patients and also assessed individual change from baseline to the date of each study visit. They also compared the number of laughing and crying episodes and used separate visual analog scale scores for overall quality of life, quality of relationships, and pain intensity.

Treated patients had a clinically and statistically greater reduction in their self-assessment scores than did those who received the placebo (P < .0001). Treated patients also had fewer laughing and crying episodes (P = .0002), a higher quality of life and relationships (P < .0001 and P = .0001, respectively), and less pain (P = .027).

When the investigators evaluated response rates, they found that 84% of treated subjects responded to treatment compared with 49% of placebo patients (P < .0010). The number of emotionally inappropriate episodes per week was 46% lower in the treated group than in the placebo group, with treatment effects observed the first week of treatment.

The rate and severity of adverse events were similar in the two groups, although more patients in the treated group reported dizziness (P = .01). Eleven treated patients (14%) discontinued treatment due to adverse events, as did eight placebo patients (11%). The investigators documented no clinically significant changes in other safety measures.

"I treat many patients with MS and it's refreshing to see a new treatment strategy that appears to have a low rate of side effects," said Michael E. Batipps, MD, who commented on the presentationin an interview seeking outside comment. "We've seen many drugs developed for MS that eventually have been found to have substantial side effects. PBA is a concerning development that we would like to prevent from happening, and the potential to treat it is encouraging. However, although the dextromethorphan-quinidine combination appears to show promise in a subset of MS patients, we will need to see whether these results are confirmed in further studies." Dr. Batipps is a neurologist in private practice in Washington, D.C., with a focus in MS.

The study was funded by Vainer Pharmaceuticals, the maker of Neurodex.

AAN 57th Annual Meeting: Abstract S46.001. Presented April 14, 2005.

Reviewed by Gary D. Vogin, MD

....riight...hit me with it. Which cough medicines contain this elixir/Have been like a whirling dervish,obsessed with cough medicines.Am reading all the labels. My kids don`t get chance to take any medicine cos I`ve whipped it from their hot little hands,eager to read the label before they`ve even had chance to get the top off ...and have still not hit on the ingredient yet.

Are certain ones more effective than others.Forgive me if someones listed them somewhere in this thread.No time to wade through it all.just want the stuff. eek. Can it be bought in another form?

gagging...

From page 9 I think, a post from RLSmi:

I am now convinced - 1/2 tsp Robitussin (adult) at bedtime helps me turn over in bed with a little more ease, and helps me sleep longer. I THINK it is still helping my balance. I hate the taste of it.

birte