I'm on my second flare since April and just had a Bier Block that didn't work. I have one leg that is the worst of all extremities, but i have RSD on both legs and boths arms and I feel like it might be spreading to my face.

Now my PM prescribed Naltrexone 4.5 mg in addition to Topomax and Despiramine (Norpramin). I have been on Cymbalta (60mg BID) and Mexiletine (total of 1200 mg/daily) but the Mexiletine stopped working.

The Dr. said the Naltrexone is still experimental but with low to no side effects. I don't do well adjusting to new meds and it takes me an avg of 2 months to feel as if i can function again. So I am nervous starting multiple ones at the same time.

Check out Naltrexone on MedlinePlus at http://www.nlm.nih.gov/medlineplus/d...s/a685041.html It's is an opioid antagonist, with it's principle purpose being to prevent folks with dependency issues from getting any pleasant sensation from the use of narcotics.

Maybe you doctor is working off a very controversial theory (but beloved by the WC insurance industry) that where too large a dose of opioids can in fact trigger a pain loop of sorts (called hyperalgesia), no opioids whatsoever - including the natural opioids produced by the body - are even better!

Check out the warnings associated with the drug and what the patient should be advised. I'm betting you've heard none of it. Nor were you advised of the whacky [definitely a poor choice of words on my part] theory your doctor was operating under in the first place. [Consider the following comment withdrawn as premature on my part: Doesn't sound as though you are being well served.]

Mike

ps See following post in response to that of FluteMaker and Kitty.

Hi and Welcome Aikane,
I'm sorry youare having a difficult time. Flares are not a good thing that 's for sure.
I have had RSD for 13 years=full body and have had many flares. A place I go to to check out meds and other medical issues isi www.mayoclinic.com Then it has a medicine section and you just click on N.
My RSD includes my face. I get skin bumps on my scalp, face, outer ears, inner nose I wake up with eye matter, have vision disturbance.
My Dr. generally has the practice of adjusting one med at a time, due to identifying possible reactions. He is a neurologist/psychiatrist/pharmacologist. And most meds he increases/decreases gradually.
It's important to trust your Dr. We are still all different when it comes to reactions to meds. You will get a lot of support here. I'd would encourage you to read a lot of posts here. Also RSDSA on the internet has great information. Also www.rsdrx.com is great place for information. The part of puzzles is a Q&A is very good.
Take care, loretta

Dear Loretta -

I must regretfully and respectfully disagree, and I say this as having grown up in a family of doctors.

In my case, I spent three years in greater agony than I would have been, because a crazy physiatrist decided that I didn't have bi-lateral RSD in my feet and all my problems stemmed from my splayed feet/collapsed arches. Hence I was put into ankle foot orthotics (AFOs), braces that gave my ankles only one range of motion. Then, once it was conclusively established that I in fact had RSD, none of my docs thought about the issue of the immobilization - never good for RSD/CRPS - until I raised it a year or two down the road. I now am in customized prescription orthotics, that look like anything that would be worn by anyone else: I just have to buy my shoes a little larger to accomodate them.

It is always appropriate, IMHO to ask your doctor to explain the mechanism of action of anything s/he is prescribing, even in the most general terms.

And as to all medications, I never take anything until I go online and read the actual FDA approved "Prescribing Information" sheet, the one designed for physicians. (And if that's too technical, go to Medline: there's a reason why that link exists at the top of each page on Neurotalk. The tab is marked "Drugs.") It's surprising how many "contra-indications" I've found that are directly applicable to me. The most common one is glaucoma, even though the list of current meds meds I print out and bring to appointments lists right on it "Xalatan (eye drops) [1 drop each eye/day] [prescribed by ________, M.D., Opthamologist]." Nor do they ask. They just (1) assume it's not an issue or (2) are unaware of the contra-indication in the first place.

I know that my father-in-law died far sooner than he should of because even though he was a bi-polar diabetic, taking large doses of Lithium, none of his far too many doctors ran regular kidney function panels until the point his kidneys essentially failed and he had to go on dialysis. Everyone probably assumed that the other guy was doing it.

But then, I remember where I was standing in my third grade classroom, when I looked up "skeptic" in the unabridged dictionary and realised that was me.

Mike

check out the LDN check in thread here on NT, thousands of people are on LDN (im one of them) and let me tell you,theres nothing wacky about it. there is such great potential in this to help so many people, that its not funny.

I agree! I'm on LDN (low dose naltrexone) and it's been a wonderful experience. Here are the links to the LDN threads. There are two because the first one got too long! You'll find great info on these threads. Good luck to you!

http://neurotalk.psychcentral.com/thread50240.html

http://neurotalk.psychcentral.com/thread71392.html

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