Thank you for this information. I will confess that I acted reflexively on this one when I read the single use for which this drug has beeen approved by the FDA. So it's all off-label, okay. Not that it makes it wrong. But I clearly jumped the gun.

I then ran a PubMed search for "low dose naltrexone" and got 358 hits. When I added "pain," it went down to 64, and when I replaced "pain" with "CRPS," the number of articles was reduced to zero. That includes case studies or even any article that might per chance mention the disease at issue in this forum. So when AiKane's doctor said this was "still experimental" s/he wasn't kidding. But at least that disclosure was made.

From what I can see so far, many if not most of the articles used low dose naltrexone as an adjudant to a modest amount of opiods, an option that wasn't given to AiKane. That said, I'm trying to go through all of the abstracts tonight, and see what if any patterns emerge.

Thank you again for the correction. I'll report back as soon as possible.

Mike

I didn't specify....but I take LDN for Multiple Sclerosis. I know others take it for varying reasons and it's used for a multitude of different ailments. I'm not certain CRPS is one of them....just wanted to pass along the links to the LDN threads in the MS forum. Good luck and should you choose to try it I hope it helps!

Kitty -

Thanks. So far I've gotten through 26 of the 64 abstracts, which is to say that I'm back to 2001. They generally fall into three categories: (1) the use of low dose naltrexone (NXT) to potentiate reduced or even very small doses narcotics, e.g. as a "combo drug," (2) as a stand alone drug for diseases such as primary progressive MS or Fibromyalgia when individuals had high sedimentation rates, suggesting that NXT was most effective in the presence of a general inflamatory process, or (3) as an aid in the testing of the true subject of the study, e.g. to determine whether analgesic Substance X worked through opioid receptors.

In light of the fact that AiKane's doctor wasn't giving him an opioid, that would appear to rule out it's use as a potentiator.

More to the point, there has been a substantial amount of research to date suggesting that CRPS has its most active inflammatory components only during the "acute" stage of the illness, typically a matter of 4 - 6 months. See, e.g., Neuropeptides, neurogenic inflammation and complex regional pain syndrome (CRPS), Birklein F, Schmelz M, Neurosci Lett. 2008 Jun 6;437(3):199-202, at 201, free full text at http://www.rsds.org/2/library/articl...in_Schmelz.pdf (noting more overt indications of infalamtory processes during acute stage of disease); Systemic inflammatory mediators in post-traumatic complex regional pain syndrome (CRPS I) - longitudinal investigations and differences to control groups, Schinkel C, Scherens A, Köller M, Roellecke G, Muhr G, Maier C, Eur J Med Res. 2009 Mar 17;14(3):130-5:

ABSTRACT

OBJECTIVES: The Complex Regional Pain Syndrome I (CRPS I) is a disease that might affect an extremity after trauma or operation. The pathogenesis remains yet unclear. It has clinical signs of severe local inflammation as a result of an exaggerated inflammatory response but neurogenic dysregulation also contributes to it. Some studies investigated the role inflammatory mediators and cytokines; however, few longitudinal studies exist and control groups except healthy controls were not investigated yet.

METHODS: To get further insights into the role of systemic inflammatory mediators in CRPS I, we investigated a variety of pro-, anti-, or neuro-inflammatory mediators such as C-Reactive Protein (CRP), White Blood Cell Count (WBC), Interleukins 4, 6, 8, 10, 11, 12 (p70), Interferon gamma, Tumor-Necrosis-Factor alpha (TNF-a) and its soluble Receptors I/II, soluble Selectins (E,L,P), Substance-P (SP), and Calcitonin Gene-Related Peptide (CGRP) at different time points in venous blood from patients with acute (AC) and chronic (CC) CRPS I, patients with forearm fractures (FR), with neuralgia (NE), and from healthy volunteers (C).

RESULTS: No significant changes for serum parameters investigated in CRPS compared to control groups were found except for CC/C (CGRP p = 0.007), FR/C (CGRP p = 0.048) and AC/CC (IL-12 p = 0.02; TNFRI/II p = 0.01; SP p = 0.049). High interindividual variations were observed. No intra- or interindividual correlation of parameters with clinical course (e.g. chronification) or outcome was detectable.

CONCLUSION: Although clinically appearing as inflammation in acute stages, local rather than systemic inflammatory responses seem to be relevant in CRPS. Variable results from different studies might be explained by unpredictable intermittent release of mediators from local inflammatory processes into the blood combined with high interindividual variabilities. A clinically relevant difference to various control groups was not notable in this pilot study. Determination of systemic inflammatory parameters is not yet helpful in diagnostic and follow-up of CRPS I. [Emphasis added.]

PMID: 19380284 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/1...ubmed_RVDocSum

My naive hunch - of the last couple of hours - is that this is the reason why NXT isn't getting as much play in the CRPS medical community as it may be getting elsewhere. Put it another way, three years ago I was trying to run with a study that had come out showing elevated level of IL-6 in the spinal fluid of CRPS patients - others were later unable to replicate the results - but in the meantime, on what was then my annual pilgrimage to Rochester MN to see family and friends and go through the Mayo Clinic, I actively sought an appointment in the Division of Neuroimmunoloy of the Dept. of Neurology, but they catagorically refused to see me. Turns out they didn't regard CRPS as a neuroimmune condition.

Whether the presence of CGRP (p = 0.007!!!) changes that, and in particular provides any possible role for NXT requires going beyond the abstracts and reading the available articles on the use of the drug in MS and Fibro to see what is the hypothisized mechanism of action. And if it's through TNF-alpha, then it's probably safe to assume that it would have as little effect on chronic CRPS as does Remicade. Although potentiating reduced dose narcotics would be a wonderful thing in and of itself, especially with regard to GI motility.

Of course, I didn't know anything about the apparent anti-inflammatory aspect of NXT when I went off half-cocked on Friday. I even assumed that NXT would cancel out the naturally occuring opioids in the body. To the contrary, it may potentiate those as well, which may have been where AiKane's doctor was going in the first instance. But from what little I have read about the use of NXT in MS, the action appears to be in it's anti-inflammatory capacity, as opposed to a palliative effect. That said, if it turns out I got remotely in the ballpark regarding the usefulness of NXT in CRPS (or lack thereof) then I just got lucky, relying on labelling the FDA has yet to update.

Mike

[A very well-respected doc advised my brother that this is the med he would prescribe for rsd. It apparently shows some promise and the apparent lack of side effects makes it that much more attractive.

I really hope they do some clinicals on this for RSD. I've heard it has worked wonders for many people with MS, and if RSD is autoimmune it may help! I tried to get my Dr. to prescribe it but he's a "data" guy and there's zilch out there on this one for RSD! Fortunately, I've recovered and I'm no longer on any meds. But I would have tried this one!