I recently was prescribed namenda for chronic pain of Fibro. and RSD and neuropathic mouth pain. I read where it was used for Parkinsons but also for FM - off label. My Dr. read the same literature I guess. I have taken all the meds (over 35) usually prescribed for pain with no success. Thus he is trying another route. I started it today.
However, now I googled it and found it is only used for Alzheimers. I'm confused.
Anyone try this drug?
Sydney

Dear Sidney -

There is a substantial body of evidence that show's the chronic pain alone can lead to the loss of gray matter in the brain. Please see, "Chronic Back Pain Is Associated with Decreased Prefrontal and Thalamic Gray Matter Density," A. Vania Apkarian, et al, The Journal of Neuroscience, November 17, 2004 • 24(46):10410 –10415. The abstract of the article is as follows:

The role of the brain in chronic pain conditions remains speculative. We compared brain morphology of 26 chronic back pain (CBP) patients to matched control subjects, using magnetic resonance imaging brain scan data and automated analysis techniques. CBP patients were divided into neuropathic, exhibiting pain because of sciatic nerve damage, and non-neuropathic groups. Pain-related characteristics were correlated to morphometric measures. Neocortical gray matter volume was compared after skull normalization. Patients with CBP showed 5–11% less neocortical gray matter volume than control subjects. The magnitude of this decrease is equivalent to the gray matter volume lost in 10 –20 years of normal aging. The decreased volume was related to pain duration, indicating a 1.3 cm3 loss of gray matter for every year of chronic pain. Regional gray matter density in 17 CBP patients was compared with matched controls using voxel-based morphometry and nonparametric statistics. Gray matter density was reduced in bilateral dorsolateral prefrontal cortex and right thalamus and was strongly related to pain characteristics in a pattern distinct for neuropathic and non-neuropathic CBP. Our results imply that CBP is accompanied by brain atrophy and suggest that the pathophysiology of chronic pain includes thalamocortical processes.

For a free, full text copy of the article, click here: http://www.jneurosci.org/cgi/content/full/24/46/10410

The tie-in piece to RSD/CRPS is “Decreased Levels of N-Acetylaspartate in Dorsolateral Prefrontal Cortex in a Case of Intractable Severe Sympathetically Mediated Chronic Pain (Complex Regional Pain Syndrome, Type I),” Igor D. Grachev, et al, Brain and Cognition, Vol. 49, Issue 1, June 2002, Pages 102-113. And the abstract of the article is as follows:

In our previous in vivo proton magnetic resonance spectroscopy (H MRS) study we found reduced levels of N-acetylaspartate in dorsolateral prefrontal cortex of chronic back pain patients. This study tests whether these chemical abnormalities can be detected in other pain states. Using H MRS, we measured levels for N-acetylaspartate and other identifiable chemicals relative to creatine in four bilateral brain regions, including dorsolateral prefrontal cortex, orbitofrontal cortex, cingulate, and thalamus, in a case of intractable severe sympathetically mediated chronic pain [complex regional pain syndrome (CRPS) type I]. The subject's chemical variations in the brain were compared to the same regional chemicals in 10 normal subjects (age- and sex-matched). Univariate statistics showed reduced levels of N-acetylaspartate in bilateral dorsolateral prefrontal cortex and increased levels of myo-inositol in left orbitofrontal cortex of the patient with intractable severe CRPS type I. These data support our original hypothesis that depletion of N-acetylaspartate in dorsolateral prefrontal cortex is a chemical marker of chronic pain, indicating for neuronal degeneration. Unpredicted changes of orbitofrontal myo-inositol may be related to the specific mood/affective state in an extreme pain perception. This is the first report, which identifies chemical markers in the prefrontal cortex for objective measurement and monitoring of CRPS type I. This information might lead to valuable insights into diagnosis and future effective interventions of CRPS type I (e.g., prefrontal brain stimulation).

A copy of the Grachev article is attached to this posting

For this reason, my doctors put me on Namenda (mementine), a so-called NMDA receptor antagonist – like ketamine – that was approved by the FDA a couple of years ago for the treatment of mild to moderate cases of Alzheimer's disease. I now take 30 mg. a day, along with all of my other medications. While it isn't perfect, I can tell the difference in terms of my conversational abilities and the like, on the days in which I miss taking the meds in my haste to get out of the door in the morning, where I still drive kids to school 5 days a week.

That said, I share the opinion of Dr. Robert Schwartzman, when he saw me 3 years ago in Philadelphia for my RSD/CRPS, that Namenda really isn't stong enough to have an effect on the pain as such.

I hope this is at least kind of, sort of helpful.

take care,
Mike

Attached Files

Decreased Levels of N-Acetylaspartate in Dorsolateral Prefrontal Cortex in a Case of Intractable Sev (111.8 KB, 622 views)