Dextromethorphan for dyskinesia?
 

I know that RLSmi and others are using low dose dex as a protection, but has anyone tried it for dyskinesias?


1: Amino Acids. 1998;14(1-3):75-82.

Blockade of glutamatergic transmission as treatment for dyskinesias and motor
fluctuations in Parkinson's disease.

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

National Institute of Neurological Diseases and Stroke, National Institutes of
Health, Bethesda, Maryland, USA.

In animal models of Parkinson's disease (PD), glutamate antagonists diminish
levodopa (LD)-associated motor fluctuations and dyskinesias. We sought to
investigate if these preclinical observations can be extended to the human
disease, by evaluating the effects of three non-competitive NMDA antagonists
(dextrorphan, dextromethorphan and amantadine) on the motor response to LD in
patients with advanced PD. In four separate trials, adjuvant therapy with these
drugs reduced LD-induced dyskinesias and motor fluctuations. These findings
support the view that drugs acting to inhibit glutamatergic transmission at the
NMDA receptor can ameliorate LD associated motor response complications.


PMID: 9871445 [PubMed - indexed for MEDLINE]

Rick, this is a pretty old study, and I have not tried to look up the entire article yet. My guess is that the dosages were well in excess of that of the DM i am taking (approx. 4 mg/ day (night).

Thanks. A drawback to my current "kitchen sink" approach has been some dyskinesia, especially in bright sunlight. So today I took approximately one teaspoon just before going out. Had some DK at first but had faded pretty much completely within 30 min. I'm not going to add dex on top of everything else until I sort things out a little, but given what a bas*ard DK can be someone might want to try it, particularly to see just how low a dose can be.

Robert, I had been wanting to ask- why the importance of taking the low dose dex at bedtime?

The bedtime dosing
 

has to do with timing the exposure of the receptors (opioid, I think) to a brief "shot" of the drug prior to the normal circadian timing of maximum endorphin release, which is apparently between 1:00 and 4:00 a.m. The brief inhibition by the drug apparently stimulates enhanced release of endorphin and production of additional receptors. The enhanced endorphin effect apparently has a regulatory effect on the intrinsic immune system.
This is the explanation given by Dr. Ian Zagon, the Penn State researcher who has done most of the work on the mechanism of low-dose naltrexone. There is a more complete description of this by Dr. Zagon on the LDN web site.
Robert