[RNcrps2]

Now i am generalized CRPS in all 4 limbs and left side of face and am SIP. 2nd opinion Dr. gave treatment as ketamine coma in Mexico for $50, up front (Germany not doing them anymore) Thats not going to happen, then said i could try 3 day high dose ketamine. I was taking methadone to cover the pain. I tried all narcotics and methadone was the only one working. Dr. didnt agree with narcotics b/c he said if come off them i would go thru withdrawl and flare CRPS or skin becoming more sensative. I had recently read an article about how Methadone is a good choice for tx! My original Dr. said dont worry you are not going to be able to come off them b/c you have a chronic condition. I have read: tx is topicals, lyrica/neurontin, antidepressant-cymbalta, MAO inhib. and opoids! Is this just a ploy for me to come off narcotic and have a coma? Is anyone else on narcotics and how do you feel about it? I do fear my body becoming addicted and getting older being on narcotics but i dont get it. I still feel i missed my opportiunity to get the SCS, but i guess i have to move on. I dont know who to believe anymore. I came out of that Drs office thinking-you know what no one knows. I feel I listened to Drs and now i am general CRPS. I feel like now its my decision to choose my path and i dont know which to take. momof4

[SandyRI]

Not really sure I understand your question completely - the part about the Methadone is a little confusing to me but I might just be missing something...

So many people have had awful outcomes with the SCS that I don't think you missed anything at all there.

You didn't mention the Pain Pump as an option. Why not? Your doctor doesn't do them? Maybe you need to find one that does. Then you could come off the opiates without having withdrawals, and still be painfree. See Lostmary's posts and the new forum. The pain pump sounds like a viable option for many of us that have been sick for a while and have exhausted many of our other options.

Will your insurance company cover the cost of the 3 day ketamine infusions? It's worth a shot before you try the pain pump.

The RSDSA.org website has a wonderful database of articles on these issues.

Like I said above, I wouldn't waste too much time worrying about a missed opportunity with the SCS. After what I have read about them, I wouldn't ever want one - not only because I would be dealing with a rep from the company that sells them after the surgery, instead of a medical professional; when the medical professional that installed likely pocketed a huge kickback from the transaction (remember - I live in RI where this kind of stuff is routine). But also because the SCS can cause infections, leads move and need to be fixed over and over, movement is restricted for the rest of your life, RSD usually spreads from the surgery, etc. They are just very problematic.

Good luck to you.

XOXOX Sandy

[hannah1234]

ketamine, ketamine, ketamine!!!! It is worrrth it!!!!! It gave me my life back, I still have a little pain here and there, and am still taking 2 meds (cymbalta, and remeron to sleep, but then again I have had sleep problems for years prior to rsd)... My answer to everyone is ketamine You pee the ketamine out the next day, so it isnt like putting medicine in you where your body is dependent upon it. It resets your pain transmitters (never did I think I would know this much about ketamine ) It is worth it, for all the side effects we have going through medicine to medicine, why not take a chance on something for 3 days where you dont have to take pills daily!!!!!!!!!!!!! If you have questions feel free to pm me

[RNcrps2]

Hannah, Im glad to hear the ketamine worked for you. Please tell me was your pain well localized or was it spread to other areas? Did you do 3, 5 or 10 day ketamine? How long ago did you have it and have you had boosters? thanks. Heard the Magnesium infusion helps the same but not as dangerous-anyone have that? momof4

[Abbie]

Please know... Because no two of us with RSD are the same, that no medicines will treat us all the same.

Ketamine is not for everyone and will not work for everyone.

I was offered this but after much research with my doctor... including him talking repeatedly with Dr. Schwartzman and Dr. Kirkpatrick it was discovered that since I have severe allergic reactions to narcotic and synthetic pain medicines and my body metabolizes anesthetic medicines at a rapid pace that Ketamine was NOT an option.

Please research as much as you can with your doctor before you rule out or accept this treatment.


Abbie

[AintSoBad]

I've been on methadone for almost 20 years. I'm fine with it.
There is the constipation, if I don't get enough exercise, it's easily dealt with.
Also, if my dose wears off, I DO get pain, and probably some sort of reaction that's over and above the normal CRPS pain. I was told to think of it like Blood Pressure medicine, I'll take it forever, or until something better comes along. It's remarkably inexpensive too.

I do take Cymbalta and diazepam, along with migraine meds.

My pain is more than crps.

Wish you luck with your decision!

Pete

[RNcrps2]

Pete, Thanks so much for replying because that is similar to what my regular pmDr. said about methadone- that its like a diabetic needing to take insulin. It's also good to hear that you have been on it for that long and it still works. Out of all the narcotics that is the only one that didnt mess with my head and all of them cause constipation. My sister feels if I finally found something that stops the pain why would i stop taking it and with the medical advances I might not have to be on it forever. Like Abbie said, different things work for different people. Thanks. momof4

[fmichael]

RNcrps2 -

There is a variation/combination of ketamine (or other NDMA-receptor antagonists and some other drugs as well) along with the pump that should be considered as well. But some background is in order. For a long time, we've known obout "opioid-induced hyperalgesia," defined in open-source (and freely useable, thank you) Wikipedia as follows:

Opioid-induced hyperalgesia[1] or opioid-induced abnormal pain sensitivity[2] is a phenomenon associated with the long term use of opioids such as morphine, hydrocodone, oxycodone, and methadone. Over time, individuals taking opioids can develop an increasing sensitivity to noxious stimuli, even evolving a painful response to previously non-noxious stimuli (allodynia). Some studies on animals have also demonstrated this effect occurring after only a single high dose of opioids.[3]

Although tolerance and opioid-induced hyperalgesia both result in a similar need for dose escalation, they are nevertheless caused by two distinct mechanisms.[4] The similar net effect makes the two phenomena difficult to distinguish in a clinical setting. Under chronic opioid treatment, a particular individual's requirement for dose escalation may be due to tolerance (desensitization of antinociceptive mechanisms), opioid-induced hyperalgesia (sensitization of pronociceptive mechanisms), or a combination of both. Identifying the development of hyperalgesia is of great clinical importance since patients receiving opioids to relieve pain may paradoxically experience more pain as a result of treatment. Whereas increasing the dose of opioid can be an effective way to overcome tolerance, doing so to compensate for opioid-induced hyperalgesia may worsen the patient's condition by increasing sensitivity to pain while escalating physical dependence.

Notes
1. Angst, MS & Clark, DJ: Opioid-induced hyperalgesia: A qualitative systematic review. Anesthesiology 2006; 104:570–87
2. Mao J: Opioid-induced abnormal pain sensitivity: Implications in clinical opioid therapy. Pain 2002; 100:213–7
3. Celerier E, Laulin J-P, Corcuff J-B, Le Moal M, Simonnet G: Progressive enhancement of delayed hyperalgesia induced by repeated heroin administration: A sensitization process. J Neurosci 2001; 21:4074–80
4. Chu LF, Angst MS, Clark D. Opioid-induced hyperalgesia in humans: molecular mechanisms and clinical considerations. Clin J Pain. 2008 Jul-Aug;24(6):479-96. PMID 18574358

Opioid-induced hyperalgesia, Wikipedia, the free encyclopedia, http://en.wikipedia.org/wiki/Opioid-...d_hyperalgesia (last accessed February 10, 2010)

And in that regard, we have numerous peer-reviewed articles, such as the following by Sanford M. Silverman, M.D., Opioid Induced Hyperalgesia: Clinical Implications for the Pain Practitioner, Pain Physician 2009; 12:679-684 FREE FULL TEXT AT http://www.painphysicianjournal.com/...12;679-684.pdf:

Abstract
Opioids have been and continue to be used for the treatment of chronic pain. Evidence supports the notion that opioids can be safely administered in patients with chronic pain without the development of addiction or chemical dependency. However, over the past several years, concerns have arisen with respect to administration of opioids for the treatment of chronic pain, particularly non-cancer pain. Many of these involve legal issues with respect to diversion and prescription opioid abuse. Amongst these, opioid induced hyperalgesia (OIH) is becoming more prevalent as the population receiving opioids for chronic pain increases. OIH is a recognized complication of opioid therapy. It is a pro-nocioceptive process which is related to, but different from, tolerance. This focused review will elaborate on the neurobiological mechanisms of OIH as well as summarize the pre-clinical and clinical studies supporting the existence of OIH. In particular, the role of the excitatory neurotransmitter, N-methyl-D-aspartate appears to play a central, but not the only, role in OIH. Other mechanisms of OIH include the role of spinal dynorphins and descending facilitation from the rostral ventromedial medulla. The links between pain, tolerance, and OIH will be discussed with respect to their common neurobiology. Practical considerations for diagnosis and treatment for OIH will be discussed. It is crucial for the pain specialist to differentiate amongst clinically worsening pain, tolerance, and OIH since the treatment of these conditions differ. Tolerance is a necessary condition for OIH but the converse is not necessarily true. Office-based detoxification, reduction of opioid dose, opioid rotation, and the use of specific NMDA receptor antagonists are all viable treatment options for OIH. The role of sublingual buprenorphine appears to be an attractive, simple option for the treatment of OIH and is particularly advantageous for a busy interventional pain practice.

PMID: 19461836 [PubMed - indexed for MEDLINE]

Thus, much can be gained by just tinkering with the medications, including opioid rotation and using the opioid with drugs that strengthen the opioid analgesic effects (a “potentiater”) to the point that you are actually taking lesser amounts of the narcotic – with all of its side effects – or by otherwise using an opioid or “partial opioid” that also interferes with pain signaling between the brain and the spinal column. From what I understand, the principal drugs that are either “full” or “partial” opioids, while at the same time interfering with pain path signaling are Methadone and Buprenorphine (Subutex).

And interestingly, Buprenorphine has been combined with trace amounts (millionths of a gram) of a powerful anti-opioid drug developed to treat overdoses, Nalaxone HCL (Narcan), which can act as a powerful potentiater. For a good recent article in the area - and one of hundreds - check out, Abul-Husn NS, et al., Augmentation of spinal morphine analgesia and inhibition of tolerance by low doses of mu- and delta-opioid receptor antagonists, Br J Pharmacol. 2007 Jul;151(6):877-87, FREE FULL TEXT AT http://www.ncbi.nlm.nih.gov/pmc/arti...3/?tool=pubmed

Abstract
BACKGROUND AND PURPOSE:
Ultralow doses of naltrexone, a non-selective opioid antagonist, have previously been found to augment acute morphine analgesia and block the development of tolerance to this effect. Since morphine tolerance is dependent on the activity of micro and delta receptors, the present study investigated the effects of ultralow doses of antagonists selective for these receptor types on morphine analgesia and tolerance in tests of thermal and mechanical nociception.

EXPERIMENTAL APPROACH: Effects of intrathecal administration of mu-receptor antagonists, CTOP (0.01 ng) or CTAP (0.001 ng), or a delta-receptor antagonist, naltrindole (0.01 ng), on spinal morphine analgesia and tolerance were evaluated using the tail-flick and paw-pressure tests in rats.

KEY RESULTS: Both micro and delta antagonists augmented analgesia produced by a sub-maximal (5 microg) or maximal (15 microg) dose of morphine. Administration of the antagonists with morphine (15 microg) for 5 days inhibited the progressive decline of analgesia and prevented the loss of morphine potency. In animals exhibiting tolerance to morphine, administration of the antagonists with morphine produced a recovery of the analgesic response and restored morphine potency.

CONCLUSIONS AND IMPLICATIONS: Combining ultralow doses of micro- or delta-receptor antagonists with spinal morphine augmented the acute analgesic effects, inhibited the induction of chronic tolerance and reversed established tolerance. The remarkably similar effects of micro- and delta-opioid receptor antagonists on morphine analgesia and tolerance are interpreted in terms of blockade of the latent excitatory effects of the agonist that limit expression of its full activity.

http://www.ncbi.nlm.nih.gov/pubmed/17502848

The one drug on the market that actually combines the two is called Suboxone and is marketed to treat drug dependence. I’m not sure if the proportions of the two drugs in Suboxone are perfect for its use as a potentiated analgesic, but if you do a term-search for “Suboxone” in this forum, you will find some people who swear by it.

But the problem is that Suboxone (for FDA approved prescribing information, see http://www.suboxone.com/pdfs/SuboxonePI.pdf ) is that it's titrated to assis in the weaning off of narcotic dependency, not necessarily for maximum analgesis effect, which could in theory vary slightly from person to person.

The pump could moot the questiion, putting a good pain specialist in the driver's seat, lawfully administering a combination of FDA approved drugs in a pain pump, and notwithstanding which recipe is chosen (full/partial opiod plus either a potentiated such as micro-doses of nalaxone or an NDMA-receptor antagonist, ranging conceivably from low, low dose ketamine to the over-the-counter cough suppressant dextromethorphan) all in what may be the very near future.

And the best part is, not only is the "augmented" opioid a much better analgesic, but the patient gets far less of it, ergo fewer complications. Potentially a whole new world, right around the corner. (Seroiusly, if you search "Augmentation of spinal morphine analgesia and inhibition of tolerance by low doses of mu- and delta-opioid receptor antagonists" on PubMed, you'll pull up the abstract I've quoted above, then go to the right hand side of the page a click "See all" under related articles, and you will get 2.603 hits, of which 548 will be freely avaiable in full text!)

For those whose pain is at the point where it boils down to the choice between a ketamine coma or a dilaudid pump, it's worth a conversation with your pain dr. in any event.

Mike

[SandyS]

thanks Mike for this post...when I took my daughter to Dr. Kirkpatrick, After she had the Ketamine treatments, he took her off of all opiads for this reason. Thank you for posting this, because I really could not quite understand why he would take her off of these pain meds. Now I truly get what he meant. Thanks again Mike!

??????? Have you thought about MED School????

Sandy

Originally Posted by fmichael

RNcrps2 -

There is a variation/combination of ketamine (or other NDMA-receptor antagonists and some other drugs as well) along with the pump that should be considered as well. But some background is in order. For a long time, we've known obout "opioid-induced hyperalgesia," defined in open-source (and freely useable, thank you) Wikipedia as follows:

Opioid-induced hyperalgesia[1] or opioid-induced abnormal pain sensitivity[2] is a phenomenon associated with the long term use of opioids such as morphine, hydrocodone, oxycodone, and methadone. Over time, individuals taking opioids can develop an increasing sensitivity to noxious stimuli, even evolving a painful response to previously non-noxious stimuli (allodynia). Some studies on animals have also demonstrated this effect occurring after only a single high dose of opioids.[3]

Although tolerance and opioid-induced hyperalgesia both result in a similar need for dose escalation, they are nevertheless caused by two distinct mechanisms.[4] The similar net effect makes the two phenomena difficult to distinguish in a clinical setting. Under chronic opioid treatment, a particular individual's requirement for dose escalation may be due to tolerance (desensitization of antinociceptive mechanisms), opioid-induced hyperalgesia (sensitization of pronociceptive mechanisms), or a combination of both. Identifying the development of hyperalgesia is of great clinical importance since patients receiving opioids to relieve pain may paradoxically experience more pain as a result of treatment. Whereas increasing the dose of opioid can be an effective way to overcome tolerance, doing so to compensate for opioid-induced hyperalgesia may worsen the patient's condition by increasing sensitivity to pain while escalating physical dependence.

Notes
1. Angst, MS & Clark, DJ: Opioid-induced hyperalgesia: A qualitative systematic review. Anesthesiology 2006; 104:570–87
2. Mao J: Opioid-induced abnormal pain sensitivity: Implications in clinical opioid therapy. Pain 2002; 100:213–7
3. Celerier E, Laulin J-P, Corcuff J-B, Le Moal M, Simonnet G: Progressive enhancement of delayed hyperalgesia induced by repeated heroin administration: A sensitization process. J Neurosci 2001; 21:4074–80
4. Chu LF, Angst MS, Clark D. Opioid-induced hyperalgesia in humans: molecular mechanisms and clinical considerations. Clin J Pain. 2008 Jul-Aug;24(6):479-96. PMID 18574358

Opioid-induced hyperalgesia, Wikipedia, the free encyclopedia, http://en.wikipedia.org/wiki/Opioid-...d_hyperalgesia (last accessed February 10, 2010)

And in that regard, we have numerous peer-reviewed articles, such as the following by Sanford M. Silverman, M.D., Opioid Induced Hyperalgesia: Clinical Implications for the Pain Practitioner, Pain Physician 2009; 12:679-684 FREE FULL TEXT AT http://www.painphysicianjournal.com/...12;679-684.pdf:

Abstract
Opioids have been and continue to be used for the treatment of chronic pain. Evidence supports the notion that opioids can be safely administered in patients with chronic pain without the development of addiction or chemical dependency. However, over the past several years, concerns have arisen with respect to administration of opioids for the treatment of chronic pain, particularly non-cancer pain. Many of these involve legal issues with respect to diversion and prescription opioid abuse. Amongst these, opioid induced hyperalgesia (OIH) is becoming more prevalent as the population receiving opioids for chronic pain increases. OIH is a recognized complication of opioid therapy. It is a pro-nocioceptive process which is related to, but different from, tolerance. This focused review will elaborate on the neurobiological mechanisms of OIH as well as summarize the pre-clinical and clinical studies supporting the existence of OIH. In particular, the role of the excitatory neurotransmitter, N-methyl-D-aspartate appears to play a central, but not the only, role in OIH. Other mechanisms of OIH include the role of spinal dynorphins and descending facilitation from the rostral ventromedial medulla. The links between pain, tolerance, and OIH will be discussed with respect to their common neurobiology. Practical considerations for diagnosis and treatment for OIH will be discussed. It is crucial for the pain specialist to differentiate amongst clinically worsening pain, tolerance, and OIH since the treatment of these conditions differ. Tolerance is a necessary condition for OIH but the converse is not necessarily true. Office-based detoxification, reduction of opioid dose, opioid rotation, and the use of specific NMDA receptor antagonists are all viable treatment options for OIH. The role of sublingual buprenorphine appears to be an attractive, simple option for the treatment of OIH and is particularly advantageous for a busy interventional pain practice.

PMID: 19461836 [PubMed - indexed for MEDLINE]

Thus, much can be gained by just tinkering with the medications, including opioid rotation and using the opioid with drugs that strengthen the opioid analgesic effects (a “potentiater”) to the point that you are actually taking lesser amounts of the narcotic – with all of its side effects – or by otherwise using an opioid or “partial opioid” that also interferes with pain signaling between the brain and the spinal column. From what I understand, the principal drugs that are either “full” or “partial” opioids, while at the same time interfering with pain path signaling are Methadone and Buprenorphine (Subutex).

And interestingly, Buprenorphine has been combined with trace amounts (millionths of a gram) of a powerful anti-opioid drug developed to treat overdoses, Nalaxone HCL (Narcan), which can act as a powerful potentiater. For a good recent article in the area - and one of hundreds - check out, Abul-Husn NS, et al., Augmentation of spinal morphine analgesia and inhibition of tolerance by low doses of mu- and delta-opioid receptor antagonists, Br J Pharmacol. 2007 Jul;151(6):877-87, FREE FULL TEXT AT http://www.ncbi.nlm.nih.gov/pmc/arti...3/?tool=pubmed

Abstract
BACKGROUND AND PURPOSE:
Ultralow doses of naltrexone, a non-selective opioid antagonist, have previously been found to augment acute morphine analgesia and block the development of tolerance to this effect. Since morphine tolerance is dependent on the activity of micro and delta receptors, the present study investigated the effects of ultralow doses of antagonists selective for these receptor types on morphine analgesia and tolerance in tests of thermal and mechanical nociception.

EXPERIMENTAL APPROACH: Effects of intrathecal administration of mu-receptor antagonists, CTOP (0.01 ng) or CTAP (0.001 ng), or a delta-receptor antagonist, naltrindole (0.01 ng), on spinal morphine analgesia and tolerance were evaluated using the tail-flick and paw-pressure tests in rats.

KEY RESULTS: Both micro and delta antagonists augmented analgesia produced by a sub-maximal (5 microg) or maximal (15 microg) dose of morphine. Administration of the antagonists with morphine (15 microg) for 5 days inhibited the progressive decline of analgesia and prevented the loss of morphine potency. In animals exhibiting tolerance to morphine, administration of the antagonists with morphine produced a recovery of the analgesic response and restored morphine potency.

CONCLUSIONS AND IMPLICATIONS: Combining ultralow doses of micro- or delta-receptor antagonists with spinal morphine augmented the acute analgesic effects, inhibited the induction of chronic tolerance and reversed established tolerance. The remarkably similar effects of micro- and delta-opioid receptor antagonists on morphine analgesia and tolerance are interpreted in terms of blockade of the latent excitatory effects of the agonist that limit expression of its full activity.

http://www.ncbi.nlm.nih.gov/pubmed/17502848

The one drug on the market that actually combines the two is called Suboxone and is marketed to treat drug dependence. I’m not sure if the proportions of the two drugs in Suboxone are perfect for its use as a potentiated analgesic, but if you do a term-search for “Suboxone” in this forum, you will find some people who swear by it.

But the problem is that Suboxone (for FDA approved prescribing information, see http://www.suboxone.com/pdfs/SuboxonePI.pdf ) is that it's titrated to assis in the weaning off of narcotic dependency, not necessarily for maximum analgesis effect, which could in theory vary slightly from person to person.

The pump could moot the questiion, putting a good pain specialist in the driver's seat, lawfully administering a combination of FDA approved drugs in a pain pump, and notwithstanding which recipe is chosen (full/partial opiod plus either a potentiated such as micro-doses of nalaxone or an NDMA-receptor antagonist, ranging conceivably from low, low dose ketamine to the over-the-counter cough suppressant dextromethorphan) all in what may be the very near future.

And the best part is, not only is the "augmented" opioid a much better analgesic, but the patient gets far less of it, ergo fewer complications. Potentially a whole new world, right around the corner. (Seroiusly, if you search "Augmentation of spinal morphine analgesia and inhibition of tolerance by low doses of mu- and delta-opioid receptor antagonists" on PubMed, you'll pull up the abstract I've quoted above, then go to the right hand side of the page a click "See all" under related articles, and you will get 2.603 hits, of which 548 will be freely avaiable in full text!)

For those whose pain is at the point where it boils down to the choice between a ketamine coma or a dilaudid pump, it's worth a conversation with your pain dr. in any event.

Mike

[loretta]

Originally Posted by RNcrps2

Now i am generalized CRPS in all 4 limbs and left side of face and am SIP. 2nd opinion Dr. gave treatment as ketamine coma in Mexico for $50, up front (Germany not doing them anymore) Thats not going to happen, then said i could try 3 day high dose ketamine. I was taking methadone to cover the pain. I tried all narcotics and methadone was the only one working. Dr. didnt agree with narcotics b/c he said if come off them i would go thru withdrawl and flare CRPS or skin becoming more sensative. I had recently read an article about how Methadone is a good choice for tx! My original Dr. said dont worry you are not going to be able to come off them b/c you have a chronic condition. I have read: tx is topicals, lyrica/neurontin, antidepressant-cymbalta, MAO inhib. and opoids! Is this just a ploy for me to come off narcotic and have a coma? Is anyone else on narcotics and how do you feel about it? I do fear my body becoming addicted and getting older being on narcotics but i dont get it. I still feel i missed my opportiunity to get the SCS, but i guess i have to move on. I dont know who to believe anymore. I came out of that Drs office thinking-you know what no one knows. I feel I listened to Drs and now i am general CRPS. I feel like now its my decision to choose my path and i dont know which to take. momof4

Hi Momof4, I totally agree with Sandy on the SCS. I also have generalized RSD full body SIP. My Dr. is a neurologist, psychiatrist, and pharmacologist. He is very conservative and I have been seeing him 6th year. He is against Methadone. I have been taking vicodin for years. About 6 months ago I was able to go down from 6 a day to 4 . My Dr. believes in muli meds to minimize the opiads. I also take Lorazepam also reduced from 6 to 4. I take 2 blood pressure meds. Cymbalta 120 mg. and a sleeping pill. I used to take 3200 mg neurotin but was able to slowly go off and the electric jerk and jolts did not come thru. I hated that med-weight gain. I have a window of time to drive. I am totally mobile with the exception of one hand 50% range of motion. It was 4 years before I was diagnosed and had delay of treatment of the hand.
I did go thru 150 physical therapy treatments for both frozen shoulders, but got full range of motion back- that was before diagnosis of RSD. I had a year remission after each shoulder
My third round with RSD came while water skiing. I pulled a nerve in one hand getting up out of the water. Misdianosed as RA- Changed Drs. and diagnosed with RSD in one min. confirmed with nuclear med. equipment.
My Dr. just built two clinics with HBOT and I'm going to try the HBOT. I also have trigeminal nerve disorder-feels like an ice pick in temple. loss of feeling down left side of face. I also have internal pelvic RSD If the HBOT doesn't work, I'll consider Ketamine.
How are you doing? I was devasted when a new neuro said I had generalized. He suggested seeing a psychiatrist. I didn't like his two suggestions, in fact I didn't like him. So I found one on my own. The first visit I knew he could help me. He is a gem. I had already had over 2 years of counseling with a psychologist when my parents died. and that helped. but as we both know, this is a different animal.
Are you mobile? have you had pt. I found massage therapy very good. I started right away. and had it each time just before the pt. This is all before I was diagnosed with RSD. Now, I find swimming pool 86 degrees, very helpful in keep mobile and even reversing my toes that were curling. They went back to touching the floor in 4 months in the pool.
Really hope the best for you. please let us know how you are doing? Your friend, loretta with soft hugs