1. Long term effects of rsd/crps
2. Living with rsd / crps - When the only constant in your life is pain
3. Living together with rsd/crps
4. Having sex & dealing with rsd/crps also Q & A's
5. Conditions we treat
6. Studies being done on rsd/crps people
7. New rechargeable SCS systems
8. Two new studies support neurologic bases for chronic pain
9. Epidemiological studies of rsd/crps
10. Objective correlates of rsd/crps
11. NINDS rsd/crps information page
12. Chronic pain drains the brain
13. Rsd/Crps How much can it take over your body
14. Pain & Depression
15. Four tips to help cope with chronic pain & depression
16. Stress & Pain
17. Its not in my head !
18. Facing the storm
19. Put your stress into perspective & lower your pain
20. Prescriptions recall's
Long Term effects of RSD/CRPS
Dr's getting together to learn how to treat RSD / CRPA people . This is about rsd / crps . Meds . Side effects and long term use of meds .
Take Care & Soft Hugs
is on a plane right now. So, what we're going to do here is focus a little bit on the research that Dr. Schwartzman has been doing in collaboration with investigators in Germany, looking specifically at use of Ketamine in low doses and high doses.
ADVERSE EFFECTS OF OPIOIDS (NARCOTICS)
And fortunately, we have here with us today, our first speaker.
Our first topic is Adverse Effects of Opioids.
I cannot think of someone more qualified to discuss this topic than Dr.Thomas Kiefer in Germany and as I've noted, Dr. Kiefer has been collaborating with Dr. Schwartzman, so we're going to see some very cutting-edge research that's going on in trying to find, hopefully, a potential cure, or at least a way to put these patients in some type of partial remission. The reason I can say that Dr. Kiefer is an expert on Adverse Effect is because his colleague, Dr. Rohr and he have been doing this research at their University the Eberhard-Karls University Medical School in Germany. Their research with the NMDA-antagonist Ketamine shows great promise in the treatment of advanced RSD.
Welcome Dr. Kiefer!
Thank you for offering to discuss with us the adverse effects of opioids at this late date. Would you just please give us a nice succinct presentation on some of the important things physician's need to know about the adverse effects of opioids and after you do your presentation we're going to have a discussion among experts here in the United States and elsewhere in the world, and I would like you to stay available to us because then I want to come back to you after those discussions; and I'm sure there's going to be some questions for you. Dr. Kiefer, welcome. Please tell us what you know about the adverse effects of opioids.
Dr. Kirkpatrick! Thank you very much for your kind introduction and above all the great opportunity to participate in today's event. Now, let's get to our presentation, which is concerned with the adverse effects of opioid treatment.
A few days ago we performed a Medline search from 1966 up to today to review the existing evidence in treating RSD / CRPS with narcotics. We found a total of 2,788 Medline-referenced articles concerned with RSD / CRPS. Combining this research with the term "Opioids" resulted in only 32 articles. Out of those, only 2 articles were randomized controlled trials, thus high quality of evidence.
One of those articles by Dr. Harke and colleagues, published in Anesthesia and Analgesia in 2001, investigated the effect of either carbamazepine or morphine after a primary successful treatment of spinal cord stimulation, in a mixed population of 43 patients with neuropathic pain. While carbamazepine showed significant delay in pain increase after successful spinal cord stimulation, morphine did not. Only 2 (two) patients of the carbamazepine and 1 (one) patient of the morphine were reported to be pain free. Concerning morphine, they concluded that probably the dosage of 90 mg (ninety-milligrams) a day was insufficient for neuropathic pain states.
The second article by Glynn and colleagues, published in Pain in 1993, investigated the effect of morphine injection around the stellate ganglion. They reported neither a modulatory effect on the sympathetic nervous system, nor an effect on pain relief in patients with RSD of the upper extremities; but the most important conclusion of this modeling research seems that valid and high quality evidence to treat RSD / CRPS with narcotics is still missing.
As Dr. Kirkpatrick stated before, RSD / CRPS is classified as a neuropathic pain state.
Let us first take a look at the data existing for opioids in the treatment of neuropathic pain.
Up until the late 1980's, pain treatment with opioids have been reserved for acute pains; and in chronic pain medicine for the treatment of cancer pain. Then this particular stigma changed and today it is generally accepted that opioids may be of promise for non-malignant pain; for example, often neuropathic pain states.
We selected a few exemplary studies reflecting the current knowledge of opioids for neuropathic pain. Cherny and colleagues published in 1994 in Neurology described that neuropathic pain apparently is less sensible to opioids, meaning higher doses are required compared to known deceptive pains. Thus, observation that higher doses of opioids are needed in neuropathic pain has been confirmed by many other studies. For example the work of Portenoy and colleagues published in 1990 in Pain, and colleagues in 1998, also published in Pain, only to name a few studies support the use of opioids for neuropathic pain. In a very well designed and conducted study by Rowbotham published this year in the New England Journal of Medicine, demonstrated that higher doses of narcotics produce a better effect on pain relief in neuropathic pain, but also high dosages are associated with a higher incidence of adverse and side effect.
Let's now take a closer look at the most common side effects, which are typically seen when taking narcotics.Most of the side effects are clinically seen when the treatment with opioids is started, and many of them improve or even disappear in the course of treatment.
The clinically most common side effects are:
Nausea and vomiting, constipation, sedation and other unspecific central nervous system symptoms. Nausea and vomiting is a direct effect of opioids on the chemo receptive trigger zone, or the so-called emetic trigger zone in the brain. Nausea and vomiting are specific side effects of all opioids.
One of the most important side effects of narcotics is constipation, which can lead to severe clinical problems. Opioids directly impair the motility, thus the normal function of the stomach and the entire intestines and leads to an increase in tone in the gastrointestinal sphincter, altogether, leading to constipation. In this matter it is most important to realize that the effect of narcotics on the gastrointestinal system apparently does not show any tolerance, therefore, bowel function cannot be expected to improve during the course of therapy.
Opioids may also cause urinary retention mostly by increasing the tone smooth muscles in the urinary pathways and the sphincters of the urinary bladder. This problem seems to be more significant when opioids are used by intraspinal injection. Commonly, patients also report unspecific central nervous system effects. These include tiredness and fatigue, impairment of cognitive function, such as the ability to think, sometimes dysphoria, or impairment of the mood, significant confusion and dizziness.
Clinically and legally important is an impaired reaction capacity above all when starting for therapy with opioids; therefore, patients in our country (Germany) are not allowed to drive a car when the therapy with narcotics is started. In patients with a good response to opioids, these adverse effects are intermediate and may improve or even disappear after about one week of treatment. Apart from these common side effects other rare side effects occur.
The side effects listed in this slide are either uncommon or the exact prevalence is not known. Pruritis or a severe itching feeling is currently thought to be an effect on the central nervous system. It is rarely seen when opioids are given orally, but is very common after epidural and intrathecal use. Dahl and colleagues reported in 1999 in Anesthesiology, an incidence of pruritis of 51% after the use of spinal morphine. Unclear are data concerning the effects of opioids on diuresis. The existing data were reported in the 1950's to 1970's, mostly collected peri-operatively and most of the reported effects are currently thought to relate to inadequate peri-operative fluid management, rather than to a specific opioid effect.
Diaphoresis, or increased sweating, is reported by some patients, but the underlying mechanisms remain unclear. Myoclonic involuntary contractions of muscles are also seen in some patients. Mechanisms underlying these myoclonic movement and opioid-induced muscle rigidity, however, remain unclear. Seizures have also been reported with the use of opioids, specifically after the use of meperidine.
In recent years it has also become clear that opioids have neuroendocrine effects. Clinically very important and relevant are the patient's effects on sexual functions. Opioids apparently negatively effect libido, but also may lead to erectile dysfunction. This depression of sexual function seems to be more common in men than in women. Interference with the female menstrual cycle also has been reported. For spinal opioids in young women, amenorrhea, or the stopping of the period, and galactorrhea, or the production and flow of milk, have been reported.Last, but not least, there remains some very rare side effects of opioids resulting from single or very small case reports. These include: edema, or the accumulation of fluid, above all in the lower extremities, probably caused by a peripheral venous pooling that occurs under opioid therapy. Other psychiatric symptoms, mainly hallucinations and psychotic symptoms have been reported. Respiratory depression is known to be a specific effect of opioids. However, in the presence of severe pain, which is a strong respiratory stimulus, respiratory depression is clinically almost irrelevant when opioid therapy is used at the right indications and carried out correctly.
Polyarthralgia's are severe pains in numerous joints appearing after opioids has been reported, after the use of spinal opioids, mostly in young women. So far, the mechanism is unclear, but the suppression of the cortisol-release is suspected. Asthma or so-called analgesic asthma is a very rare condition following opioid administration. Again, the mechanisms are not fully understood.
Recently, a growing number of reports suggest that treatment with narcotics under certain conditions, for example, long-term administrations with larger doses may lead to pathological pain stage, such as hyperalgesia or allodynia. Basic research suggests that opioids may lead to formation of a spinal pathway, resulting in these symptoms.
In conclusion, we would like to state the following:
The adverse effects of narcotics or opioids seem to occur in dose-dependent manner. Clinical experience and published evidence suggests that the rate of adverse effects with opioids is high with non-responders and partial responders compared to patients showing a clear benefit under the treatment with narcotics. Apart from dosage, the rate of rise of blood concentrations of opioids is very important. Thus, immediate release formulations will be more likely to produce adverse effects than sustained or slow-release formulas.
Clinically, it is most important for physician's to realize that when patients experience severe side effects, patients are often not willing to continue opioid therapy. Thus, detailed information on the patient is very important to gather during the course of treatment with an understanding that many initially observed side effects will disappear in the course of treatment.
Also, it seems very important for us to state that in the case of persistent and intolerable side effects, this may be indicative of a lack of opioid sensitivity. If this is suspected, it seems mandatory to check the opioid sensitivity and to prove that the patients clearly benefit from opioid therapy. Should severe side effects nonetheless persist, however, together with a significant pain relief, then a so-called opioids rotation, that is, changing the type of opioid, might be of promise.
Please allow us to emphasize a last issue. Be careful to closely monitor patients treated with opioids. Before starting long-term therapy with narcotics, a significant pain reduction following opioid treatment needs to be clearly demonstrated. Side effects have to be recognized early and treated consequently. Constipation prophylaxis should be given in all patients routinely. After all, it should not be forgotten that the therapy with narcotics only represents one piece in the puzzle of a multi-disciplinary approach in the sufficient treatment of chronic pain.
We hope that we were able to give you a short impression about the adverse effects in the use of narcotics in chronic pain disorders. And thank you very much for your interest and attention.
Dr. Kiefer, thank you very much for that very scholarly, very comprehensive review of the potential adverse effects of opioids. Now we're going to open this up to a further discussion. We have a total of eight (8) physician experts distributed in the United States and around the world to comment on this topic. For the sake of efficiency, however, I'm going to ask the speakers at these different sites, and including in the studio here, to try to limit their presentations to one or two minutes. We have an individual sitting here who is going to keep score and let us know if we're exceeding these time limits. We want to give as many people as possible an opportunity to offer different views on this topic. Now, fortunately we have with us at a remote site a Dr. Stephen Butler.
Dr. Butler began his career as a pain management specialist at the University of Washington. There, he ran the Pain Management Program. For those of you that are experts in the field of pain, you know that is where John Bonica started a pain management program. That program is highly regarded all over the world as being a leader in pain management. From there, he went to Sweden, and there at Uppsala University, he's now the director of their Pain Management Program. One of the areas of his current research is focusing on the impact of immobilization on exacerbating the syndrome reflex sympathetic dystrophy. Dr. Butler, are you with us here?
Dr. Steve Butler:
Yes, I am.
Let me also clarify. Dr. Butler, it was very thoughtful for you to join us today, because, you know, Dr. Butler is on vacation right now. He's not in Sweden, he happens to be in Canada. And from what I understand, Dr. Butler, you're in some cabin someplace over looking a lake, and the only thing you've got is a telephone. Is that pretty much the picture here?
That's right. But today we also have the rain, so this is a nice way to pass the time when I can't be outside.
Dr. Kirkpatrick: Well, listen. I just personally want to thank you for taking time out of your vacation to share with us your skill, your experience with this audience. On the topic of adverse effects, is there something that you would like to emphasize or to comment on or to question us on in that particular area?
Well I think Dr. Kiefer did a wonderful job about going through the side effects of opioids and I don't have too much too add. One thing that surprises me is the limitation of driving with opioids in Germany, and there's some new research underway in Finland that shows that in pain patients, untreated pain, has a greater effect on driving ability than does opioids, and patients performance improves when their on opioids. That's just a small side-light. The other thing I would like to talk about is long-term opioids.
One of my colleagues has been doing some research that shows that it's not only libido that's decreased with long-term opioids, but they seem to depress the hypothalamic pituitary axis, and there's a depression of a lot of endocrine function including thyroid and adrenal on chronic high-dose opioids. And this is something that might account for a lot of the side effects in a broader sense, why patients feel generally unwell on high-dose opioids for a long time.
Dr. Butler, I would like to raise another area that's of interest. As you know, Dr. Kiefer mentioned the idea of switching from one opioid to another by sequencing the medications. We do know there's one clear-cut example of an opioid, a very commonly used opioid that has some unique properties that the others don't have, and that happens to be methadone.
As you know, methadone has this NMDA-antagonist activity. For those of you that may not be familiar, we believe the NMDA receptor is very important in neuropathic pain. And what's been reported in literature. When you look at the conversion tables for methadone, going from morphine for example, you find that you get a higher analgesic effect, in other words, more than what you would expect. This has been attributed to the NMDA-antagonistic effects of methadone. Methadone really is a racemic mixture, it has a D-isomer. It's the D-isomer in there that seems to be the active antagonist of the NMDA receptor. And so what I would like to ask you is what role in Sweden do you have for methadone besides, well just tell us in terms of in addiction programs, recovery programs as opposed to treating pain?
The Swedish government is very restrictive in the use of methadone, and most physicians think that it can only be used for treatment of addiction, of opioid addiction. This isn't exactly true and we've been using more and more methadone over the last 5 years because we found in some patients that this has a much better effect than any other opioid. Many of the patients like it also because they feel more stable than when they've been using shorter-acting agents. We now have more longer-acting agents on the market in Sweden and so there are other options. Personally, I think methadone is probably underused in chronic, non-malignant pain and that we need more studies to look at its specific uses in neuropathic pain and probably in complex regional pain syndrome.
OK. Now, there's another area that I feel compelled to bring up and that has to do with this constipation problem that we see in these patients when they're on chronic opioids. I don't know how many other physicians that are speaking today have had this experience, but I have had some unbelievable, great experiences with using opioids in patients, literally transforming their lives, and we're primarily talking about treating reflex sympathetic dystrophy. On the other hand, I have to tell you about one patient because I think it's relevant to this story.
A relatively young lady, 28 years old, has RSD of the upper extremity and right lower extremity, sympathetically independent pain, so the nerve blocks, the sympathetic blocks, really weren't that effective. So, we're really running out of treatment options here, and so we put her on a trial of opioids; and it literally changed her life. She went back to work; she was more active, engaged with her family and so forth and so on.
Five years later she comes back to me and she has this scar from here, well basically from here, down to here (Dr. Kirkpatrick demonstrates from the upper to the lower abdomen); and I asked her what that scar was about, from here down to here, in case you missed that. And she said that she had a swollen abdomen and that they brought her in to the hospital and they did an ultrasound, ruled out that she was pregnant, and determined that she had a fecal impaction. She didn't think that was very alarming because she actually had diarrhea on occasion. So they went in there and removed it because they were afraid of getting an ischemic bowel. And when they took it out and weighed it, it weighed 22 lbs. (pounds). 22 lbs! And she enjoyed 5 years, but then she ended up with this as a problem.
I would like to ask our panel here in the studio if they've had this type of experience. What do you think Dr. Wilson? Have you run into the narcotic bowel syndrome?
Dr. Maria Carmen Wilson:
I have, but fortunately not to that extreme.
It was less than 22 lbs.?
Definitely. And I really haven't had anybody that actually needed surgery. I am very aggressive with prophylaxis of that. I put everybody on a very aggressive bowel regimen, but once in a while people still have problems.
Dr. Marsha Brown:
I actually haven't had that problem in any of the patients, but I don't treat...I'm on the opposite end in terms of addiction, and looking at trying to get people off at times, or whether they need to be on or not. But certainly I have heard of a lot of folks having that difficulty, and particularly in the methadone clinics where they're being treated with methadone, that's one of their common complaints is that they have constipation.
Good! Now - let's talk a little more about these NMDA receptors because this has a lot to do with neuropathic pain syndromes. Dr. Kiefer?
Yes, I'm still on the line.
Good! Dr. Kiefer, you and Dr. Rohr have been doing some very cutting-edge research on high-dose ketamine. That is where you put patients under general anesthesia, you intubate them, and have them in Intensive Care Unit for 5 or 7 days; but you've also done some work on low-dose ketamine. Could you bring us up to date Dr. Kiefer. I know you've been doing this in collaboration with Dr. Schwartzman, (as I indicated earlier he had to leave for Philadelphia on short notice), but bring us up to date of where you are at in your studies in both the high dose ketamine patients and in the low dose ketamine patients, and compare those two different treatment protocols, if you would please.
OK. I would like to start with the low-dose ketamine. Actually, we started working with ketamine, as you mentioned correctly, is one of the strongest or the strongest currently available NMDA-antagonist. We actually started this work in 1998, and you mentioned also the treatment of high-dose Ketamine, which actually is the result of our experiences with the low-dose ketamine. So, let's start with the low-dose ketamine.
Low dose ketamine is basically infusion therapy with increasing doses of ketamine over a prolonged period of time, normally between 6 (six) and 10 (ten) days. The ketamine is administered IV. And what we can say in summary is that if you have patients with RSD / CRPS that come to the clinic in very early stages, the onset of disease should not be longer than 6 months, and the disease is still localized, it means that the disease is not spreading to other than the primary effected extremity, then you see some success with low-dose ketamine. The problem with low-dose ketamine is to maintain pain relief.
We recently performed a series in very severe affected patients, who all had long standing disease between 4 and 6 years of CRPS, most of them with entire body RSD. We performed a trial of low-dose Ketamine on these patients. And we are seeing that these patients basically did not profit much from the ketamine. However in measurements you could detect that their touch sensitivity, or allodynia, got better, but the clinical outcome was that the pain in those patients was mainly not changed.
Now if you go to the high-dose ketamine. The high-dose ketamine treatments were invasive treatments, as you said; it's basically Intensive Care treatment with the patients being intubated, and mechanically ventilated for a period of 5 days with high-doses of ketamine, together with midazolam to prevent the patients from showing the typical ketamine side effects, such as agitation and involuntary movements. Up to today we performed this treatment in 13 (thirteen) patients, together with Dr. Schwartzman. Those patients all had intractable patients with worsening RSD / CRPS, who had many treatments attempts with no prior success. And in those patients we saw always, meaning all of the patients, a primary response, which was very, very promising. All those patients were being pain-free for some period of time. The problem in the high-dose Ketamine treatment also is maintaining of this primarily very effective pain reduction over longer time periods. Up to today we would say that about 50% to 60% of the patients of the high-dose ketamine, can you still read me?
Yes, oh yes! We're sitting on the edge of our seats!
OK. So I'll proceed! There was just a click in the line. OK. Today we can say that about 50% to 60% of the patients have longer time periods, months, up to the longest pain-free patient is now 4 1/2 years (four and a half years) without any problems, and we see that in about 50% to 60% of the patients. Some patients, about 40%, they have a relapse of pain symptoms, and we are not sure what causes those problems. In some patients we could locate a triggering pathology, such as a chronic arthritis in the foot, which seems to re-trigger the neuropathic pain. In 2 out of those 13 patients, we had a real CRPS relapse to the intensity of pain that existed before treatment.
Dr. Kiefer. Thank you so much. That's really putting us right up to date with what's going on with NMDA-antagonists in managing neuropathic pain, and I thank you very, very much for that information.
Dr. Kiefer, please stand by. Towards the end of this program we're going to invite you back because we're asking all the speakers to come up with some take-home messages, and we'll be asking you to help us out with that.
OK. I'm on standby.
Now, we're going to move on to the second topic here which is addiction, aberrant drug behavior, that sort of thing while on opioids.
Fortunately, we have with us today, a world-renowned expert on that at a remote site. It's Dr. Seddon Savage at Dartmouth Medical School. Dr. Savage has been investigating primarily in the context of a patient who is a known addict, and how do you manage their pain. And some of her work is being done in collaboration by someone else that we all know, and that's Russell Portenoy, in New York. So I can't think of someone that is better at giving us an up-to-date current picture of what to do with a patient who is an addict, or has a propensity to be in that situation. Dr. Savage?
Dr. Seddon Savage:
Yes! Thank you very much Dr. Kirkpatrick and I want to thank you and your colleagues for putting together this conference, which I think, is extremely valuable and very innovative and exciting. Thank you very much for inviting me.
When we consider addiction issues in the use of opioids for the treatment of chronically painful conditions, including such conditions as CPRS/RSD, it's important for us to be very clear in our use of terminology.
Confusion regarding terms such as addiction, physical dependence and tolerance contribute significantly to the under treatment of pain and to the trivialization of addiction when it does occur.
Physical dependence and tolerance are both expected physiological consequences that may occur when opioids are used over time. This is in contrast to addiction that is a disease state, not an expected consequence of appropriate therapeutic opioid use. Physical dependence and tolerance are not usually clinical problems. They can usually be easily managed when they occur, and their presence does not mean an individual is addicted to his or her medication.
As defined by the American Society of Addiction Medicine and also accepted by the American Pain Society and the American Academy of Pain Medicine addiction is a primary, chronic, neuro-biologic disease that has genetic, psychosocial and environmental factors influencing its development and its manifestation. Addiction is characterized by behaviors that include one or more of the following:
Impaired control over drug use, compulsive use of medications or drugs, continued use of the drug despite harm and craving for purposes other than pain relief when we're referring to opioids.
It is important that we distinguish addiction from a number of other states that may generate some of those behaviors, however. For example, when pain is inadequately treated, a patient may appear to seek opioids when their really seeking relief of pain, some instances referred to as pseudo-addiction. Or a person may have anxiety, depression, other mood issues or sleep problems and they may misuse their opioids prescribed for pain in an attempt to treat these other problems. But in order to address those problems it's usually more effective if we identify their misuse, why they're using them, and institute more effective and appropriate treatments, and reserve the use of the opioids for the treatment of pain.
Now, thinking about the causes in the etiology of addiction, both biogenetic vulnerability and a pattern of drug use that produces a rush or a high by stimulating limbic reward systems are believed to be important factors in triggering addiction. Psychological and social factors are also important, but primarily as they shape, encouraging or discouraging risky patterns of drug use. In addition, they are important in recovery from addiction, shaping the psychological and social factors. Stress, the physiologic effects of stress, may also play a role in the development of addiction in vulnerable persons.
The risk of developing addiction when using opioids on a long-term basis for the treatment of pain is not really known.
Available data suggests that the risk of the development of addiction or serious drug abuse problems in medical patients, who use opioids on a short-term basis for pain control, is very low, probably in the range of 1(one) in 10,000 (ten thousand) persons. However, when we treat pain in individuals who have complex regional pain syndrome, we often require long-term opioid use and we need to be aware that many of our patients may have histories of addictive disorders, so we can't rely on these very low estimates of risk.
Now, the most common estimate of the prevalence of addictive disorders in the general population, including alcoholism is about 10% (ten-percent), though studies range from about 3 to 18% (three to eighteen-percent) depending on the methodologies and definitions that are used. However, studies consistently show much higher rates of additive disorders in hospital patients, ranging between 20 and 25% (twenty and twenty five-percent). And for patients who present to hospitals or emergency rooms with significant trauma, the rates are between 40 and 60% (forty and sixty-percent), this is consistent over many, many studies.
We have to be aware then, particularly when we're treating patients who have complex regional pain syndrome that began with significant traumatic injury, that the group we're treating may have a higher prevalence rate than the general population of addictive disease.
Now, while patients with addictive disorders may be more at risk for developing abuse or addiction problems when opioids are used for pain, clearly such problems are not inevitable.
There is likely a spectrum of risk in terms of the vulnerability to developing addiction when opioids are used therapeutically, that includes both host, or patient factors, and drug use factors. Based on our understanding of addiction in general, individuals with no personal or family history of any form of addictive disorder are likely at lowest risk. While those who have a family history, but no personal history, may have a slightly increased risk, though there are no good studies that evaluate this. The little data that we do have suggests that persons with a history of opioid addiction themselves, a personal history of opioid addiction, have a greater risk of developing addictive patterns of behavior when using opioids on a long-term basis for chronic pain than persons who are in recovery from alcoholism or other non-opioid addictions, though those persons may have a somewhat increased risk over individuals with no history of addiction. Now, medication use patterns may also impact addiction risk when opioids are used for pain and some factors include the routes of administration, schedules of administration and certain receptor effects. It is well understood by Addictionists that the more rapid the increase in blood/brain levels of a drug, the more likely it is to cause a rush or a high, which is often termed a reward which may, with repetition, trigger addiction in vulnerable individuals that theoretically, we'd expect opioids use by rapid IV (intravenous) bolus to propose more risk for vulnerable individuals than the use of oral opioids.
And we'd expect the use of a slower onset long-acting opioid, such as methadone or a sustained release preparation, morphine or oxycodone or fentanyl, when used as directed to pose less risk than frequently repeated doses of quick onset short-acting opioids. However, I think we're all aware that persons who want to abuse sustained release preparations can adulterate them to get a quick onset high bolus dose that may be very rewarding and potentially addictive.
Finally, mu opioid receptors appear to be more involved in stimulation of psychic reward, that rush and high, than kappa or other opioid receptors. Therefore, kappa analgesic agonists such as pentazocine and butorphanol may pose less risk than mu opioid receptors, but of course the use of these for pain is limited by their ceiling effects, and because they may reverse mu analgesia in persons who are dependent on mu opioid analgesics. Partial mu agonists such as tramadol or buphinorphene may also have less abuse potential, though their use as analgesics is also fairly limited. Importantly, some studies suggest that pain may actually interfere with the reward effects of opioids so that the risk of addiction to administered opioids may be lower when pain is present then in the absence of pain.
In summary, looking at things from a clinical perspective, it's helpful to view the risk of addiction when opioids are used for pain as an interaction of host vulnerability and pattern of medication use. From the patient perspective, if one has no personal, no family history of addiction, one can generally feel confident that opioids are safe and effective when used as directed, and that the risk of becoming addicted to the medications is low. For patients who do have an addictive disorder, or known risk of an addictive disorder, these patients can also achieve relief with opioids, but it is important that they and their doctors' use special care. It is important that individual lets their physician know of their addiction history, pays close attention to cultivating addiction recovery, takes special care to use medications only as directed, and consider in some circumstance having a partner monitor their use of the medication.
From a physician perspective, since risk of abuse and addiction can never be 100% (one hundred percent) certain prospectively, it is best practice to use care and vigilance in prescribing opioids to all patients. We need to screen our patients for personal and family history of substance use problems and inquire about current patterns of drug and alcohol use. Encourage recovering patients to be involved in active recovery programs and support their recovery. We need to treat pain aggressively, but when faced with a patient who may be at high risk for relapse, try and use less rewarding forms and schedules of opioid medications, when these meet their needs for analgesia.
We need to apply a clear agreed upon structure that often may include a written opioid contract when it's appropriate. We need to monitor not only pain, but also function, mood, sleep, and the patient's ability to comply with our structure of use, to assure that opioids are helping rather than leading to a spiral of abuse or addiction that may be harmful to the patient. It's often helpful to monitor patients with urine drug screen using care to interpret them appropriately, as such monitoring can be an important support to recovery and can detect early relapse.
Finally, for patients with a history of opioid addiction, who appear to have difficulty controlling use of opioids, participation in a methadone maintenance program to achieve blocking doses of opioids, then providing additional opioids or other pain treatment for pain control, as needed, may be the best option. In those circumstances, however, close communication between addiction treatment providers and pain treatment providers is really critical.
see ADDENDUM on Methadone HYPERLINK \l "Methadone"
Dr. Savage, thank you very much. That was just a fantastic review of the issue of addiction with medications. I'm going to ask you if you would please stand by, because I want to come back to you here, because I know there are going to be some questions for you. But before we do that...Dr. Brown. I know you've been treating patients with addictive problems and pain problems going on at the same, time for a couple of decades, and, you know, tell us what you're perspective is on the addiction problem as it relates to this topic. We have outpatient, we have a contract you can give the patient, we have outpatient ways to get control with these patients and then we have inpatient programs. Can you give us some perspective on when you have a patient in pain, where they go to get the proper treatment in this situation?
Dr. Martha Brown:
I think it's a very difficult issue. And I think that over the years we have certainly had a lot of conversations with pain management specialists and with addictionologists. I think that Dr. Savage did a wonderful job in terms of distinctly putting down some of the issues I think we need to look at. Sometimes what I find is that some patients don't do well as outpatients, and there's a lot of miscommunication, sometimes not on the Dr.'s part but purposely on the patient's part, because they may have that addiction potential or may have the disease of opiate dependency. Yet, on the other hand they have pain, and they have legitimate pain, and how do you put those two together in terms of that?
One of the things certainly, I have done is work very closely with the pain management specialists in developing a program. First, if we can do it on an outpatient basis, looking at all the different methods that we can do and going through different processes working up to the opiates, particularly if they have a problem. Contracts, setting up a contract in terms of only one doctor prescribing a medication, you know. Monitoring urine drug screens --- I think all of those things work together and only as a last resort, sometimes then we put somebody in an inpatient unit to work out what's the plan going to be.
Thank you Dr. Brown. Dr. Wilson, I know you have also been at this also for a couple of decades and I know you have an inpatient program at Tampa General Hospital, which is outstanding. What would you add to this, I mean, because your focus is on the pain, but also sensitive to the addiction issues and how do you handle that in a hospital setting?
Well, I am very fortunate that I have a wonderful team that helps me out. I have nurses that are excellent in keeping track of medications. And actually developing a relationship with the pharmacists and the family members is like a combined effort. And we find that the urine drug screens, the contracts and close monitoring, close monitoring are truly, truly invaluable. So, I think that, ditto to what they both said, and then I do have a question, however, for Dr. Savage and Dr. Brown.
We know that rotating opioids helps tolerance issues, but are there any data as to rotating opioids having a positive effect, minimizing addiction issues on those that are at high risk?
Dr. Savage: We're not aware of any data regarding opiates, rotating opioids to avoid addiction. I think selecting opioids may make a difference. As I suggested before, theoretically, there's reason to believe that slow onset, more continuous stable blood levels, are really less likely to stimulate that reward, that rush and that high, that in a recovering patient may trigger relapse or lead to it. I had a patient who once referred to using one of his short-acting medications, his opioids, as dancing with an old lover. I thought that was in solid recovery, but he didn't like using those short-acting opioids because it just was like dancing with an old lover, and I really appreciated that characterization.
Certainly, you know, methadone is used for the treatment of opioid addiction, and I haven't seen studies comparing it to slow onset morphine, or, I mean sustained release morphine or sustained release oxycodone, in terms of risk, but it's not adulterable in the same way. It's easy for patients if they have a slip and want to chew up a tablet of the sustained release formulation and get a buzz to do so, where as with methadone, there's not much you can do to increase the rapidity of onset. So, those are my thoughts.
Dr. Savage. Since you opened up the "dancing with lover" theme...
...let me follow up with that with you, just to make sure I understood you. Are you suggesting that it is an absolute that you can't have a patient on short-acting opioids chronically for pain?
Not at all, not at all!
OK. So, some patients like that exquisite control, that sense if they have an exacerbation they can hit it.
Right! And thank you, thank you for pointing that out. I did not mean to say that any person whose at risk for an additive disorder or has a history, can't use opioids when they're needed, short-acting opioids for chronic pain. I think it has to be an individualized decision and talk about what the effects of the opioids are. In some patients they're very clear; it just relieves the pain and they don't feel the psychic effects from it. And some patients don't need around the clock medications. They have pain and they need a short-acting medication when they're doing an activity that they value that causes significant pain. So there are a lot of variables that have to be weighed against each other, I think in decision making.
OK. I would like to turn back to another subject that you touched on, obviously you can only touch on it in a short presentation that you gave, but I feel it's worth going back over, and that's this whole concept of pseudo-addiction. In other words, under-prescribing the opioids in someone who has pain. As you know, one of your colleagues, Dr. Russell Portenoy has done some studies on patients under-prescribed their medication, in two patient populations; cancer patients and HIV patients. And I believe on average in the cancer population, even today, the data suggests that maybe 50% (fifty-percent) of them are not being adequately medicated with opioids. In the HIV patient population it's like 85% (eighty five-percent). And what they have found, and what they have reported is, that, pseudo-addiction sort of sets in motion behaviors that actually trigger or produce real addiction. And the examples they use are in the female population where some women had HIV, who were not getting adequately medicated, would actually exchange sex for drugs, obviously a major health problem. So, I think our audience really wants to know what you think about that and I'm going to ask Dr. Brown to comment on that as well. Pseudo-addiction...a little bit more on that, please.
OK. While I certainly think pseudo-addiction does occur, I think the best way we manage that is after we've done a thorough evaluation to try and sort out as best we can whether there's under-treated pain or that there may be abuse or addiction of medication. If we consider under-treated pain part of one of the strong possibilities, a trial of carefully structured, effective, aggressive pain treatment is appropriate with careful monitoring to assure safety in case there is abuse or an addiction problem that puts the patient at risk for having medications. So, giving doses of medications that the patient states relieve their pain and watching what happens to their function; their ability to work or do activities of daily living; what happens to their relationships; to their mood; to their sleep; if all of it improves, and their pain is reported to be improved, and, then we've treated pseudo-addiction in most circumstances.
One of my colleagues raised, or...made the observation that in some cases when we...if someone truly has and opioid addiction and we do supply them with, or prescribe to them larger doses of opioid medications, we may in fact be blocking their craving and blocking their addictive disorder, just as methadone maintenance therapy would, and therefore allowing them to return to a better level of function and normalize their lives and improve their quality of life. From a clinical point of view that's really a moot point. We've provided a medication that has treated an underlying disorder, be it pain or opioid craving, provided it safely and allowed them to return to a higher quality of life. That's our goal as clinicians. From a legal point of view, of course we need to be licensed appropriately if we are treating opioid addictions with opioids.
Dr. Brown, would you like to add something to the issue of pseudo-addiction?
I would certainly agree with Dr. Savage in terms of her comments. I think that it's a very difficult issue, particularly at lower levels of opiates, when you have a patient who has that craving and has the pain, and you don't want that patient to be in pain. And so you really do need to adequately treat it and see what happens having taken a good history, and looked at their family history; and also the issue of loss of control, because if somebody hasn't, that's one of the cardinal symptoms of addiction, that's in terms of a loss of control so if they're maintaining and taking as prescribed you're less likely to get into problems.
I would like you to stand by. We're going to have an opportunity for you to share with us, what you might say a take-home message.
Dr. LeBel, thank you very much. I think what you've really helped us do is put the whole problem of chronic pain into a much, much broader perspective, looking at multiple modalities in managing these patients.
We're very fortunate to have with us today at a remote site, at Johns Hopkins University, Dr. Sabine Kost-Byerly. Dr. Kost-Byerly has probably seen some of the worst-of-the-worst in children that have chronic pain syndromes, in particular patients with reflex sympathetic dystrophy. And I've asked her to join us today because, I think we really want to make sure we explore all of the potential treatment options, and that we look at where the opioids fit in...into the bigger picture. And I think if we can understand children, which are the most challenging, with all the problems they have from an emotional standpoint and so forth, I think the adults become a piece of cake. Dr. Kost-Byerly?
Yes! I wanted to first thank you for this wonderful opportunity to participate in this symposium. I think it's an exciting new tool and I think it's something that should be explored further in the future as well.
I listened carefully to Dr. LeBel's presentation and I would agree with her and most of it. I think the patients I've seen in Boston are similar to what we see here. This is a Tertiary Care Medical Center, so most of the patients that I would see in the clinic or for in-patient therapy are rather complex and might have failed therapy in other locations.
We use a multi-disciplinary approach to the treatment of RSD. The primary tools are as Dr. Lebel said, physical therapy, behavioral intervention; and they will lead to an improvement in the majority of patients. We do use opioids as adjuncts to the therapy, though not as the first pharmacological intervention, but usually as the third, fourth or fifth.
I see that there are essentially three forms for the treatment of opioids. The one that we use probably most frequently and intermittently is to facilitate physical therapy, or to treat acute increases in pain due to other activities throughout the day. We will use, in a certain patient population, long-acting opioids at night if the patients report to me that they have poor sleep due to pain. This is not as a sleep agent, but really it's a poor initiation of sleep, or poor...they do wake up in the middle of the night because of pain; and then we will attempt to treat them with a long-acting opioid to see whether this will improve.
Finally, there is the around-the-clock treatment. This is really a very small sub-group of patients. In this population, the goal is an increase in function activity and the quality of life. For a child that usually means the child will be able to return to school; participate in activities with a peer group; that should be the goal. When around-the-clock opioids are used, then the treatment should be re-assess at regular intervals, then every few months to check for the continued need and the effect. As I said, that is a small sub-group.
For my in-patients, it's not unusual, because a lot of them have severe pain, are very hesitant to participate in physical therapy programs. It's not unusual then that we will use a peri-spinal infusion, like a lumbar epidural catheter with local anesthetic and opioids and try to alleviate some of the fears of this patient so that they will participate in physical therapy more easily and a little bit more ready to do this.
There is one point that has not been mentioned by previous speakers, but I think it is important in the pediatric population. I'm a little bit hesitant to provide long-term opioid therapy in children adolescents, not necessarily because of development of tolerance or the development of addiction, which I think is pretty rare; but I'm worried in this population particularly about the long-term effects of opioids in the developing body. Opioid therapy, as Dr. Kiefer in Germany said, can result in abnormal endocrine effects and can result in hypogonadism, and lead to low levels of testosterone and estrogen. And, we don't really know what this means for an adolescent, a child going through puberty. So, the risk of osteoporosis or mood changes, or how this will influence the immune system...there are really still many questions, so I think I would be very hesitant to provide long-term opioid therapy in an adolescent patient.
This is what I have to add to this discussion at this point.
Dr. Kost-Byerly, thank you very much. I know that there's nothing like experience in trying to navigate through this, through all of the treatment modalities that are available, especially in children. At this point, what I would like to ask Dr. LeBel to please standby. ...Dr. Lebel, could you please stand by here?
Because I'm going to come back to you in just a second here.
TAKE HOME MESSAGE
What I'd like to do at this point is to go ahead and try to put together, start to put together, construct a "Take-Home Message" thing.
And, what I want to do I guess, first of all, is to kind of weigh in with my two-cents. So, I was taking notes as we went through these presentations and here's what I got out of it, and then I'm going to invite each of our speakers to contribute something more to that.
First, opioid therapy should be considered in anyone with moderate to severe pain. There is no evidence that there is any characteristic in a given patient that imparts a total resistance to the analgesic effects of opioids. But, every case requires the physician to weigh the factors that would influence opioid therapy sooner, rather than later, after other treatment modalities have been tried. We've heard a beautiful discussion of that with Dr. LeBel and Dr. Kost-Byerly about how they've tried to navigate in placing, positioning the opioid in the proper clinical context.
Point number 2 (two). Opioid therapy is not easy; and you said that (Dr. Kirkpatrick speaking to Dr. Marsha Brown), it's not easy, it's very difficult. What does it really require? It requires us starting with a comprehensive assessment of the patient, which includes looking at the issue of potential addiction, aberrant behavior and so forth as part of our assessment. It requires a certain knowledge base about the adverse effects of opioids, and we have to have knowledge about addiction medicine, that's important. We have to have certain skills, certain experience in order to navigate our way most effectively with these patients.
Documentation was noted, the importance of documentation...Dr. Savage brought that up; Dr. Brown, you brought that out as being very, very important...contracts with the patients.
Communication, very important. Communicating with the patient, communicating with the primary care physician. As pain experts, we depend on them to care for these patients. We have to consider their preferences, their resources and so how do we do that? We educate them. that's our job. We have to do that. And of course, the patient can't make an informed decision without being informed about some of these potential problems we've talked about... as Dr. Kost-Byerly pointed out, what about the long-term effects in children on the pituitary axis? So, all of these things are important.
A third point that I think needs to be pointed out here is that, although there's nobody that's resistant, chronic therapy with opioids but opioid therapy might unmask problems. And we've talked in great detail about those things: intolerable side effects; unmanageable side effects; addictive disease. We've discussed the importance to always be aware of the problem, the potential problem of pseudo- addiction.
And we also talked about that not all opioids are the same: methadone is really, really quite different than the other opioids; transdermal fentanyl: there's some patient's where this drug has been a Godsend at 400 mcg patches changed every 2 (two) to 3 (three) days, being required to make them functional. So, they're not all the same and this was something, of course, that Dr. Kiefer brought to our attention.
Dr. Savage at Dartmouth pointed out the potential advantages of long-acting opioids and the fact that you have the slow onset and that you have less risk of this rush, this dancing with the medicine, and of course, it's a little easier to comply in that situation. But I think the point that was made that's very important, there are very few absolutes; each patient is an individual. Maybe a short-acting opioid on a chronic basis for chronic pain would be more appropriate in some patients.
Now, I think what the audience really wants to hear from us today, I really believe this, if I'm sitting out there this is what I want to know: How do I use these opioids, particularly long-acting opioids? So, I'm going to highlight very quickly here, what I think some basic...what a basic roadmap might look like, and I'll invite all of you to comment on this.
I would suggest that maybe when you're starting a long-acting opioid that you may increase the dose until you get adequate pain relief, or, you get intolerable or unmanageable side effects. I would suggest that you increase the dose by 25% to 100% every two to four days. There is no maximum dose! There is no maximum dose for these medications. I think that's a very important concept. You increase the dose until you're limited by toxicity, or one of these other problems related to addiction medicine that would limit you in your prescribing. Now I would like our speakers to offer their take-home messages and I'd like to start with Dr. Kiefer. Are you still with us in Germany?
Yes. I am still with you.
So, you tell me what you think the take-home message should be from this conference.
OK. We think that the take-home message should be that nobody should be withheld opioids if the patient needs opioid treatment. However, we would like to emphasize that it's very important to show that opioid treatment for the individual patient results in a clear benefit, that is a significant pain relief for the patient. We would also like to emphasize that neither the physician's nor the patient should fear adverse side effects. We would point out that opioid therapy has to be monitored very closely and physician's need to watch for those side effects and treat and sufficiently, and above all, very early.
And our last remark is that everybody involved should be stimulated to work on providing sufficient evidence to perform scientific studies to finally provide some high quality evidence in the treatment of opioids for neuropathic pain and especially CRPS. Thank you.
Dr. Kiefer, thank you very much. Dr. Butler?
Did you go out sailing while we were talking, or did you hear the discussion we were having?
Oh, no, no! I've been listening to the discussion, very interesting.
OK, good. Well listen, give us your perspective, give us your take on the take-home message, please.
Well, I think if we think of about complex regional pain syndrome use of opioids, you have to think of two uses. One is an acute use to facilitate therapy, and that's probably the best use. The second is chronic long-term use when therapies haven't been very helpful. I'm a little more conservative than you are in use of opioids. You're recommendations sound to me like those for pain in cancer patients, and my experience over time is that we always have been sent the patients on high-dose opioids with the problems, and had to deal with that. And many of those patients on detoxification were significantly better than they were on the high-dose opioids, so you have to be a little careful in how far you go with high-dose opioids.
Another thought is that if you do embark on opioids, especially high-dose opioids for long term treatment, then you marry that patient, because no other practitioner will take over that care. And so, you have to think about not only what's going to happen next week or next month, but in five years. And so, you need to have a short-term plan as well as a long-term plan. But, it has been a wonderful conference, and I've gotten a lot of very good information from the presentations and thank you for having me there with you.
And Dr. Butler, thank you for letting us disrupt your vacation. While you were talking, some of your comments resonated pretty heavily here among our panelists in the audience here, so I'm going to ask them to comment a little about...especially about marrying patients. They were both kind of nodding their head a little bit here. Dr. Brown, what is your take-home message from this? Dr. Brown:
Well, I think there's several. One is obvious, communication. I do think that we have to take a good history and look at the addiction potential, because some of our patients will do quite well on high-dose opioids and they don't have that addiction potential. The one's that do will be the ones that you truly marry and will increase their dose and ultimately, unfortunately, some of those people die in terms of it and so there's always, again, weighing the issues there, I think from the addiction standpoint. It's certainly...I urge all my patients who are in recovery, if they have chronic pain, to let me talk with their physician whose managing their pain, so that we communicate and we talk about what's going on and we form a plan, because we don't want them to be in pain.
Hold on for a moment, Dr. Wilson, I'm going to go over to Dr. Savage to follow up on this theme, and then I'm going to come back to you and ask you a question or two. Dr. Savage?
You've been hearing some of these comments; tell us, what do you think? What would you like the audience to take home?
Well, I'll give you my take-home messages from the point of view of the issues that I've been asked to cover, which are more the addiction and abuse issues. So my take-home messages would be first, that we look at the pain associated with CPRS/RSD and at addiction both as medical conditions, which have potential to cause considerable suffering, and we need to attend very closely to each of them. We need to treat pain aggressively and most often that means an interdisciplinary approach, using cognitive/behavioral approaches, physical therapy, perhaps interventionalist procedures and a variety of medications. But when opioids are used, we need to pay close attention to the potential or risk for developing addiction; monitor patients, not only their pain, but their level of function, their mood, their sleep; to be sure that the medications are helping them and improving their quality of life; and to detect abuse or addiction early because these are life threatening problems, detect them early if they occur. If we need to continue opioid therapy in somebody who does develop addiction, we need to partner with somebody who understands the disease of addiction and work together to help that patient receive the pain relief that they need and to monitor their recovery or help get them into recovery.
One final brief comment. I agree with your recommendation to increase 25 to 100% dose of opioids if you're titrating aggressively, if it's appropriate to titrate aggressively, for most opioids, but I would be very cautious titrating methadone that way. We need to start low and go very, very slowly. It takes 7(seven) to 10 (ten) sometimes even 14 (fourteen) days to get stable state of methadone, so we need to titrate a little more slowly. Thank you.
Thank you Dr. Savage. Dr. Wilson, what is the take-home message here today?
Well, the take-home message, I think that it should be like we're doing. More education at all levels. I think that education is of paramount importance because part of the reason why we have to marry so many patients is because doctors in Primary Care are not comfortable. I mean, in part it's because they don't have appropriate knowledge of opioids, and rightfully so, they should not be doing things that they are not really well informed and prepared and ready to do. But I think it's very important that they get the message that we educate primary care physicians so we can work together, that way our clinics would not be filled with so many patients that we have gotten to be stable, and all we do for a lot of those people is just continue to prescribe and perpetuate prescriptions every 30 days. And then, if we're lucky enough that they take them back, then if the primary care physician is not educated about opioids, in no time the patient is back to us full of problems.
Right, right. Well, it looks like everybody is resonating to that as well. Dr. LeBel?
Tell us what you think from your perspective, particularly as it relates to the pediatric population.
Well I think for pediatrics, as emphasized, this is a population that has a generally favorable prognosis, and therefore, opioids as an intervention in this group do adhere more to Dr. Butler's acute use to facilitate functional rehabilitation in all ways, both as in-patients and out-patients and are usually brief courses of intervention and not sustained long term except in very, very, very rare cases. I want to emphasize that we have a chance in pediatrics because of the favorable prognosis, to intervene early and effectively, pushing forward the rehabilitative strategies, adequately treating the pain to allow the child to pursue that type of rehabilitation, and we have the opportunity as practitioners to prevent these patients from going on to having chronic pain disorders, which is a very important mandate. And I would just echo the need for additional research in all type populations, elderly, pediatric and most adults in the use of chronic opioids and acute opioids in neuropathic pain.
Thank you for letting me participate. It has been very educational for me.
Again, thank you Dr. LeBel. Dr. Kost-Byerly?
Yes, I would agree with Dr. LeBel. I think although opioids are not the first choice of treatment for RSD / CRPS in children, they should be considered as a part of a pharmacological approach within a multidisciplinary management. I also couldn't agree more with Dr. Kiefer in Germany, Dr. LeBel, that more research is needed. I particularly feel that more research is needed for the subgroup of patients that, pediatric patients, that do not respond favorably to the most common physical therapy or behavioral intervention. I feel it is very much in need so we can prevent potentially years of suffering in these patients.
I wanted to say thank you that I was able to participate and I think it was a very exciting symposium.
Well, thank you very much Dr. Kost-Byerly, we're privileged to have you join us today.
QUESTIONS & ANSWERS
Now, please everybody stand by because, I went back and picked up some of these faxes, some of these questions and, boy, there's some tough questions here. So, I'm going to have to just say just jump right in. Those that are at remote sites and we want to see whose the bravest. This question is asked over and over again, so are you ready for the big question? Here it is.
You have a patient that is on a contract, they break the contract. They have chronic pain, they're suffering. On occasion they may be writhing in pain. They've been into a rehab program, a recovery program and they relapse... you see the question, what do you do? What do you do? Now, don't raise your hands all at once.
Let's take the people at the remote sites first. Is anybody at one of our remote sites either here in the United States or abroad, does anyone want to weigh in on that question?
I can stick my neck out on that one.
This is Dr. Butler talking. I've had several patients like that and I just sit down and talk to them quite frankly and tell them what the problem is: I think you're abusing these medications and I'm not sure you're getting any help from them. And I'll tell them if they fail the contract once, I have the talk; if it happens a second time I warn them, then you've got two options. One is that you can go back to drug treatment program. The second is I will do detox myself and then you have to find another physician if you're going to, if you want to continue taking these medications, because I can't do it under this situation. I don't think they're helpful and I think that the problem is not the pain; it's the drug abuse that's the major problem. And that's what I've done. But, sometimes tough love is what these patients need.
Dr. Butler, once again, what can I tell you. If you had eyes here you'd see that you're getting a lot of people shaking their head in agreement with you. Does anybody else want to weigh in on that question?
Yes, I would. This is Dr. Savage.
Yes, Dr. Savage.
I agree with essentially all of what he has said. I would add though, that it's highly variable the reasons that people break contracts. We have to make an individual assessment of what the reasons for breaking the contract is, and what the facts were, I mean what actually happened. If the person is relapsed into addiction and they have an active addiction disorder, it's probably not safe for them to be using opioid medications, and we need to help them get back into recovery, and be aggressive about doing that and then once in recovery be highly structured in re-providing opioids if we elect to do that, sometimes dispensing even on a daily basis we have done.
The bottom line is to protect the patient, but in the end I think we have to recognize that we can't help all people, and there may be safety issues that are beyond our control. That means that we need to taper people off of opioids, and I would not refer them to somebody else necessarily unless they chose to go to somebody else, but to continue to follow them aggressively with non-opioid approaches to treatment and provide them with support they need for recovery and for pain.
If I'm hearing you right Dr. Savage, you're saying that...you almost have to...if you want to play this game; you have to anticipate that some of these patients are going to relapse, and you better have a program, you better have a plan in place. Is that what I'm hearing?
Yes, and that pain treatment, the promise and offer of pain treatment, effective pain treatment, may actually be a support for helping them get into recovery.
Good. We have time for one more question. Well, we have a lot of questions, but I think this is a very important question, so I'm going to just lay it out here.
The question is: Patients who develop tolerance to the analgesic effects of opioid, is that a lifetime thing? If they later decide to wean themselves from opiates, do they remain tolerant? Do we have any empirical scientific information, anything that would help us understand that?
And also another question which is related is: What about...what about...do we know...are there some individuals, or some characteristics of individuals that develop tolerance more quickly than others to the opioids? So there's really a 2-part question. Let's take one at a time.
The question is: Is it a permanent change in your body when you develop tolerance to opioids, or do you have a return of your sensitivity to the analgesic effects later on? Who would like to weigh in on that one, anyone either at a remote site or here at the University of South Florida?
I could answer this; this is Dr. Byerly from Johns Hopkins.
Thank you Dr. Kost-Byerly.
As a Pain Specialist and an Anesthesiologist, I can tell you this from my experience, that when we have trauma patients, other patients on high-dose opioids for a long period of time, who eventually come back to the operating room later, their requirement, if they have been off the medication for a period of time, pretty much is back to normal, so they will have a normal analgesic requirement. Of course, if they are still taking high-dose opioids, that has to be considered and they will have a higher requirement for surgery, potentially.
I think from an addiction medicine perspective, I would give the same response. We know that many people who have been detoxified from illicit opioids say during a jail term, who then go back out on the street, are at a very high risk for overdosing because their tolerance has diminished significantly.
Thank you Dr. Savage. This is very, very important. It is not only important for Pain Specialists, but for the Anesthesiologist that has to provide anesthesia for these patients. Does anybody know if there's a certain characteristic of person who is more likely to develop tolerance than others either in terms of, well for example, age or in terms of other co-existing medical problems, they develop tolerance more quickly? I don't know of anything. Does anybody at any of our remote sites have any data to share on that question?
I don't have any data, but........
We're with you Dr. Butler. We hear you.
I don't have any data, but my experience is that the patients who are treating things like anxiety are ones that are more likely to develop rapid tolerance. If they have a pain problem, but they have an underlying anxiety problem that hasn't been well addressed, they're the ones that tend to escalate doses much, much quicker.
Well that certainly makes a lot of sense and I think that some of our panelists here are agreeing with you that in their clinical experience as well, they see the same thing, for sure. So, pain in a way, treating pain itself, is somewhat protective to the developing tolerance to medications, I think that's what I'm hearing from you?
Well, in patients, I know that in patients who are treated say, with fentanyl infusions in the ICU, the development of tolerance can be rather rapid. More recently though, that would agree with...I think with Dr. Savage...I think it was Dr. Savage said, the quicker rise in the analgesic blood level, the CSF level, might lead to a higher development, maybe to a quicker development of tolerance. Though more recent studies did not support that for remifentanil, which is even shorter-acting and even more rapid in onset. So, I think it might, if at all, it might depend on the analgesic itself, less so is it on the patient.
Thank you very much Dr. Kost-Byerly. I think we're ready to close this symposium, but before I do, I really, really want to thank the faculty from around the world. I want to thank the staff here at the University of South Florida, this has been a Herculean team effort to make this happen in real time and be interactive the way it has been. And, last but not least, I want to thank the audience for participating in this. We hope that you have gained as much as we have from this experience.
Thank you very much.
WARNING ABOUT METHADONE USE
Physicians must be aware of the particulars of methadone. When switching from opioids with a relatively short half-life (such as hydrocodone and MS-Contin) to methadone, the physician must be aware that methadone has an unusually long half-life and that it might take several days before the patient's blood levels become stabilized. The maximum analgesic AND respiratory depressant effects of a dosing regimen of methadone cannot be determined until a steady state is achieved. Therefore, days of drug accumulation may occur after a period of rapid dose titration. In some cases, this may lead to profound respiratory depression and death. For this reason, methadone is considered a poor choice for patients who are difficult to monitor.
When administering methadone, start low and go slow! For example, the initial rate of titration of methadone could be no more than by 2.5 mg TID for 7 days since there is such a long half-life, blood levels continue to rise during this period. After seven days, the dose could be increased to 5 mg per day for another seven days. IF SEDATION OCCURS OR IF THERE IS A PROBLEM WITH AROUSABILITY, METHADONE SHOULD BE HELD UNTIL THIS CLEARS AND RESTARTED AT A LOWER DOSE. Other shorter acting opioids may be used in the interim to compensate for the slow titration of methadone.
Converting to methadone from other opioids needs to be done with caution. Some researchers propose that methadone is almost 10 times more potent than opioids such as MS-Contin and hydrocodone when treating chronic pain. Calculating a morphine equivalent of methadone is essential for patient safety. Let's assume that prior to switching to methadone, the patient was taking 60 mg of MS-Contin per day plus up to 20 mg of hydrocodone per day for a total of 80 mg of morphine equivalents per day. If the patient was switched to 80 mg of methadone per day, the patient's dose, in effect, would have been abruptly increased from 80 mg per day to 800 mg of morphine equivalents per day.
In addition, when switching an opioid-tolerant patient to an alternative opioid drug, it is wise to assume that cross-tolerance will be incomplete. This means that a patient who has developed tolerance to one opioid analgesic may not be equally tolerant to another. Therefore, when switching to a new opioid, opioid-tolerant patients should be started on a lower dose of the new opioid.
Here is a link to a site where the use of methadone has been subject to a consensus process by a US government health agency:
"Methadone Dosing Recommendations for Treatment of Chronic Pain"
ALERT FROM THE FDA ON METHADONE
FDA ALERT [11/2006]: Death, Narcotic Overdose, and Serious Cardiac Arrhythmias
FDA has reviewed reports of death and life-threatening side effects such as slowed or stopped breathing, and dangerous changes in heart beat in patients receiving methadone. These serious side effects may occur because methadone may build up in the body to a toxic level if it is taken too often, if the amount taken is too high, or if it is taken with certain other medicines or supplements. Methadone has specific toxic effects on the heart (QT prolongation and Torsades de Pointes). Physicians prescribing methadone should be familiar with methadone’s toxicities and unique pharmacologic properties. Methadone’s elimination half-life (8-59 hours) is longer than its duration of analgesic action (4-8 hours). Methadone doses for pain should be carefully selected and slowly titrated to analgesic effect even in patients who are opioid-tolerant. Physicians should closely monitor patients when converting them from other opioids and changing the methadone dose, and thoroughly instruct patients how to take methadone. Healthcare professionals should tell patients to take no more methadone than has been prescribed without first talking to their physician.
This information reflects FDA’s current analysis of data available to FDA concerning this drug. FDA intends to update this sheet when additional information or analyses become available
Where i found this information ... http://www.rsdfoundation.org/en/opioids_transcript/en_use_of_opioids_transcript.html
Living Life With RSD / CRPS
Living with rsd/crps isnt always an easy thing to do , altho we try our hardest to be as normal as possible . The flair ups tell us another thing . With everything we go through Pain , Swelling , Tears , Flair -ups . Makes our lives a living hell . I wonder sometimes what did i do in my lifetime to deserve this , Was i a bad person and this is the result of anything i ever did ? Was it not enough that i didnt do ? When your in bed because of a bad flair up all kinds of things run through your mind ( besides the pain your going through ) Life with rsd/crps certainly changed me forever , It stole my life and now suffer in pain on a daily bases . The meds i take help but not always , when a bad flair up hits nothing seems to help , I prayer for everyone who has it , who dont deserve it , I never pray for myself , There are other out there more deserving of a miracle then me. If this is gods plan for me then so be it . But i dont have to like it ... Take Care & Soft Hugs
An Injury and Subsequent Experiences Living with RSD
Written by Michelle Lyons
I suffer from Reflex Sympathetic Dystrophy (RSD) which started as a result of all the wrong things being done after a fall in which I suffered broken fingers, wrist, elbow, three part humeral head break, scapular, clavicle, twisted leg and ankle sprain, all on the right side. Add to all that fibromyalgia, osteoporosis and hyperparathyroid problems.
If all that wasn't enough, what I went through afterwards is a nightmare that no one should ever have to endure. I was released from the ER five hours after I was brought there. I should have never have been released from the hospital. I hadn't even been examined by an orthopaedic doctor. The one that was supposed to be coming in to see me was told not to by the ER doctor. After all those hours there, all they did for me was to inject me with demerol and some other painkiller, along with taking x-rays. No one who has never suffered could even imagine the excruciating pain I had to endure. All I had to take for the pain was Excedrin. I couldn't even walk or lie down. I could only sit.
The rest is a nightmare. I never saw an orthopedic doctor until 8 days later. When I saw him, he looked at the x-rays, took some more. clucked about the extent of broken bones, grabbed my arm, twisted it and put a cast on. Remember, I had many broken bones. That was the only medical
treatment I ever received. Within weeks I developed RSD. The only medication I even had was Excedrin. I was sent for physical therapy and it was there that the therapist noted the problem. He called the doctor to advise him that he thought I was developing RSD. I had just seen him the day before and he never mentioned it. So, back I went to this doctor who confirmed the therapist's diagnosis and he ordered more aggressive therapy. The doctor did not refer me to a neurologist when I mentioned seeing one. He said you don't need one, the physical therapy will take care of it.
By this time my fingers were swollen and looked like rigormortis had set in. They were purple and mottled. My therapy consisted of pulling my fingers almost off me and soaking my hand in cold and hot water. By this time I couldn't even tell the difference between hot and cold. Also. inserting my hand in paraffin. As a result of all the wrong things being done, I am left with an RSD problem that my doctors' deny even exist, because as I'm told constantly, RSD doesn't spread. This, as we know, is completely ludicrous. Mine is a constant burning and disabling condition that has left me permanently injured as a result. Not too mention the fact that all the bones that were broken mended angled and my hand, arm and shoulder are in constant pain. Too deny is too destroy and that is exactly what has been done to me. I certainly would like too know of doctors' who are specialists in a disorder that destroys the sympathetic nervous system along with causing osteoporosis.
Unfortunately, all work injured and doctor destroyed victims of Workers' compensation are involved in a tyranny that is perpetrated on victims of work related injuries. Had I been able to see a trauma specialist immediately after my work related accident. I would not be writing this letter today. I am appalled and outraged that this evil exists. I am even more outraged that we are denied our constitutional and human rights daily. Hence the feelings of being overwhelmed while dealing with the terrorists that make our 'medical determination' for us. Isn't it amazing how someone can know how we feel. If we had the ability to do pain transference, I would be only too happy to have them take on my pain and see how well they could cope. It is easy to be a critic when your only an observer.
Our Legislators' must take responsibility and correct the statutes that allow the predators' carte blanche to manipulate and destroy the victims' of work related accidents. Who is accountable to us for the denial of our constitutional and civil rights; not too mention human rights. No one should ever have to endure the pain and body destruction that has happened to all of us. Why are we subjected to this
persecution? Remember, we are this way because of what wasn't done for us. Not only are we dealing with the pain, we also live with the bias.
Take away the immunity from the IME doctors' and make them accountable and responsible just like the rest of the world. The IME is one of the biggest fraudulent issues that is perpetrated against the injured worker. Denial is their credo. Think about it? Why would anyone want to live in this odyssey. We are hurting and we want someone too hear our complaints and stop the pretense and suggestive
findings. All of us are the victims' of the total and wanton disregard of our rights' to Life, Liberty and the Pursuit of Happiness. Many of our ancestors' gave their lives for this freedom. We are entitled to
the same rights' as any other citizen. Who decided that we were to be treated differently? Something to think about, isn't it!
Our lives are forever changed as a result of what wasn't done for us at the time of our work related accident. What has happened to all of us is a travesty of justice. We have been forever more subjected to a life of pain and disabling limitations. This is our reality.
All I can say is God help all of us who are living the tyranny.
where i found this information ... http://www.workerscompensationinsurance.com/articles/rsd_story.htm
Living With RSD--When the Only Constant in Your Life Is Pain
Imagine sustaining a minor injury, like a sprained ankle, but the pain from the injury is much worse than you would expect, and, to your horror, it doesn't go away. Instead, the pain worsens, the ankle swells, and the skin around your ankle suddenly seems to develop a mind of its own. It gets cold and turns blue, then gets hot and turns red. You think you're losing your mind, and your family and coworkers are inclined to agree.
You probably haven't lost your mind, but you may well have developed a disease known as RSD, or Reflex Sympathetic Dystrophy (also known as CRPS, or Complex Regional Pain Syndrome).
where i found this information ... http://www.outwittingstress.com/content/view/8/2/
Living Together With RSD
My wonderful hubby, JD, has full body RSD. He was first injured when he was a U.S. Marine. He fell about 12 feet from an obstacle and was caught beneath his right arm as he landed. At first his arm was completely numb with a tingling sensation. Intense burning pain from within the limb followed later that same day. He had not broken any bones. There was no explanation for the onset of intense pain. The discoloration and swelling followed within days, and his RSD was diagnosed before the week was over. It has progressed to the fourth stage in his right arm at this time. His RSD has since spread throughout his body. The other areas are affected at various levels. This spreading may have been due to failure to gain proper control of his RSD and many surgical procedures by well meaning doctors. His body hurts everywhere all the time.
I hate watching him in pain, of course. However, I never knew JD before the pain. He had been suffering from RSD for 5 years when we met. He's now had it for nearly 10. He has always made it clear how emphatically he wants me to disregard his pain. He emphasizes how it is not his focus. I don't focus on it all the time, because it is always there. We have both accepted that we cannot live our lives revolving around the pain. However, I admit this is not always a simple thing to do. It's always there lurking in the background. Many times I find it impossible not to think about it. I upset him, because there are moments when I get "a little" overprotective. Then there are the times I have to step in, because he's not thinking clearly. It can be like being stuck between a rock and a hard place for me. It is much worse for him. I am sure of that. I would say that we try to take life one day at a time, but with RSD it can literally be moment by moment. Although, we know neither one of us could overcome all the pain and fear of this disease in and of ourselves. We have a very strong faith in God. It's His strength that fills us.
He has been through a battery of treatments. We have learned that some RSD experts advise avoiding many of the treatments that were used in JD's care. To summarize it all, his physicians at the VA began with many Bier blocks and Stellate Ganglion blocks. They attempted to immobilize his arm by various means and pack it in ice. This caused a tremendous increase in pain. JD put a stop to it quickly. He has since developed the motto: "use it or loose it!" He uses his arm as much as possible and many times past the point I would have stopped trying were it me. His doctors then put him on high doses of Morphine, and later combined the Morphine with Methadone. We have since read that this can be a lethal combination. JD decided of his own volition that life on those types of narcotics was no life at all. He used his last dose of these in Nov. of 99 and has never used them since. These medications only took a fraction of the pain away, and often left him in a confused state of mind. His doctors continue to try prescribing such drugs. JD simply turns it down. He feels that it is easier to combat the pain with a clear and focused mind. They have put him on many other medications too numerous to list. None of these have been of much benefit that we have noticed.
He has also been through many surgical procedures. His doctors have preformed 4 Sympathectamies, a Dorsalectomy, and implanted two Spinal Cord Stimulators (SCS) just to list a few of the major ones. Some RSD experts feel these surgeries could be responsible, at least in part, for the spread of RSD. We tend to agree with that opinion. Dr. Hooshmand, a leading expert in RSD with over 40 years experience in its treatment, advises strongly against having an SCS implanted. He has made a wealth of advice and knowledge on RSD available on line athttp://rsdrx.com .
However, JD did not research the device before he began using it. A team of neurologists and neurosurgeons presented it to him as his last and only hope. His first SCS was removed quickly due to a life threatening infection. Many RSD sufferers experience failure of the immune system of this type. It had worked for pain control initially, but was fraught with false hope as the pain and many other new pains crept in quickly within the first few weeks.
The second SCS did not become infected. They prepared him with high doses of antibiotics. It worked for pain control very well when they first put it in. That was May of 99. That kind of miraculous pain control only lasted a few weeks. Its efficiency began to decline right away. This SCS has leads that go down his right arm, along his spinal cord, and through a hole they've drilled into the back of his neck up into his brain. It not only helped with pain control, but it actually regulated his respiration and heart rate. It also assists with the motor functions of his right arm. Initially, he could not move the arm when the implant was switched off. Following its implantation, my husband suffered seizures for about 6 months. The seizures seemed to be related to the leads going into his brain. When he seized, we could actually stop the seizures by maneuvering the leads in the back of the neck. He would often pass out right afterward. Many times, he would have episodes of amnesia following the seizures and black outs. During this amnesia, he would not know who I was or where he was. It would last for anywhere from a half-hour to a few hours. He would often come in and out of consciousness during this. Of course, it was very scary. Then, miraculously all of the seizing stopped in Dec. of 99. The doctors never explained why any of it happened or why it stopped. He rarely has a black out now. He hasn't seized since then.
For the past several years his doctors have been convinced that he is going to die soon. They've been giving him predictions like "6 months left to live" for the last several years. I used to constantly wonder how long he would live. I married him in fear of becoming a widow within the first year. JD feels that a life lived in continual expectation of death is no life at all. I have learned how true that is, and refuse to focus on the opinions of these doctors.
During the last surgery to implant the current SCS, JD had a near death experience. He flat lined for 3 minutes. He came home from that surgery with a new motto: "Live Life to Its Fullest." It was after developing that attitude that he stopped dating me and asked me to marry him. We have been "living life" together ever since.
where i found this information ... http://www.rsdalert.co.uk/stories/Patsy_Adams.htm
Having sex and dealing rsd/crps
i dont know about everyone else bad due to my injury site i cannot have sex , or at least i havent found away to deal with and the pain , no amount of pain meds will allow me to have sex . And sex is apart of having a realtionship with your partner . Thank god i have an understanding partner ! This is something i have to deal with so i decided to search and see if i was the only one like this .I have spoke with a few who take pain meds before having sex so they say it helps but can still feel a little bit of pain , just not as bad ......
Take Care & Soft Hugs
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~Journal Article Excerpt
by Vern L. Bullough
The more I study the development of modern sexuality, the more I believe in the importance and significance of Alfred Kinsey. Although his research was on Americans, it came to be a worldwide source of information about human sexuality and set standards for sex research everywhere. In America and much of the world, his work was a decisive factor in changing attitudes toward sex. Within the field of sexuality, he reoriented the field, moving it away from the medical model and medical dominance, to one encompassing a variety of disciplines and approaches. In short, his work has proved revolutionary.
To understand what Kinsey wrought, one must look at the field of sexuality when Kinsey began his studies. One must also look briefly at Kinsey as an individual to understand his accomplishments.
SEX RESEARCH, 1890-1940
The modern study of sexuality began in the nineteenth century, and these early studies were dominated by physicians. It was assumed that since physicians were the experts on body functions, they should be the experts regarding sexual activities. In a sense, this was a divergence from the past, when sexuality had been regarded almost entirely as a moral issue. And although there were still moral issues involved, physicians were also...
where i found this information .... http://www.questia.com/googleScholar.qst;jsessionid=JsWLBLCqNjmtHynQv6P2dkRBQd5bvTpvqGBcYv0pSTLJtzDlJn6V!1153215274?docId=5001347048
RSD, Opioids and Sex
You have asked if sex is good for RSD or not. Sex is very beneficial for RSD. RSD is a disturbance of the sympathetic system, the immune system, and the hormonal system of the brain. The sympathetic system regulates the immune system. The tools in this regulation consist of the white blood cells and their protective function, hormones such as ACTH, sex hormones, growth hormones and endorphins, as well as monoamine such as norepinephrine, serotonin, and acetylcholine.
Exercise, sex, rest and relaxation improve the function of the above mentioned immune system.
On the other hand, stress of any form, be it emotional or physical, traumatic or due to infection or toxins such as alcohol or narcotics, disrupt the function of the immune system.
In RSD natural and pleasant sex raises the threshold of pain because it also elevates sex hormones, endorphins and growth hormone. On the other hand, high doses of pain medication, especially the opioid agonist type of medication flood the hormonal system of the brain. Physical trauma such as unnecessary surgical procedures also causes the same adverse effect.
Among other benefits of a proper, natural sexual relationship, is the excellent natural REM sleep that ensues the sexual activity. The REM is essential for regeneration of the monoamine such as serotonin, which is an excellent anti-depressant, and Dopamine, which is an important monoamine in protection against stress.
Large doses of opioid agonist pain medications causes lack of desire for sex, as does an overdose with serotonin. Such an overdose of Serotonin at the cerebral level is a byproduct of SSRI anti-depressants such as Prozac, Paxil or Zoloft. This is the reason for lack of libido in over 1/5 the patients who take SSRI anti-depressants, such overdose can be corrected by periodic "drug holiday" such as stopping the SSRI intake on Friday, Saturday and Sunday and restarting it on Monday. Lack of libido is not just a lack of luxurious desire, but also the sign that other hormonal system and monoamine system are dysfunctional as well.
In the late stages of RSD (stages III and IV ), especially after surgical procedures or after insertion of infusion pump or spinal stimulator, there is such as suppression of sex hormones in the brain and spinal cord that two phenomena are noted. One is tenacious lack of libido, erection, and any other form of desire for sex. Another is the problem of severe fatigue and depression. Both of these problems can be corrected in men by testosterone replacement and in women by estrogen replacement. As a matter of fact, the infusion pump patient almost invariably require such hormonal replacement. Without the hormonal replacement, the depression and fatigue aggravate the chronic pain and result in failure of beneficial pain relief.
H. Hooshmand, M.D.
where i found this information ... http://rsdrx.com/rsdpuz4.0/puz_91.htm
Q..OK, I need some honest and serious answers/comments. Since I am fairly new to RSD, what kind of effect has it had on your sex life? I know some of you have had RSD for years, and some of you are fully involved, so I hope you can relate some info to me. I know others want to hear your comments, but may be too shy to ask! My love-making has been a VERY great part of my marriage over the years...I surely hope THAT won't be taken away from me, too?!:circlelove:
A...My rsd started when I was 23, I got married when I was 19. Obviously at that age I didn't want my rsd to get in the way of that part of our marriage either. We've had our ups and downs, but I always try to make sure we don't go too long between times. :wink: I think you both have to accept that it won't be the same as before, for example if you can't bear your weight on your arms anymore, so you have to find different ways to do it, and it may end up being that it can only happen one way and thats it.
where i found this information ... http://neurotalk.psychcentral.com/archive/index.php/t-18962.html
Pelvic Pain and Complex Regional Pain Syndrome
where i found this information ... http://www.rsds.org/3/education/pelvic_pain_gerwin.htm
Abdominal Wall Pain
Female Pelvis/Male Groin
Pain in the pelvic or rectal region may affect women and men of all ages. This pain can be seen acutely or chronically. Pelvic pain may be due to endometriosis and gynecologic disorders, testicular and urologic disorders, scar tissue from radiation or surgery and ligament injury. Patients may experience burning with urination, painful intercourse, or a burning, electric-like pain that is present at rest or with activity.
Headache Pain and Migraine Pain
Neck pain can be a significant source of discomfort for many patients. The source of pain in the cervical (neck) region may be multi-factorial and relate to muscle, nerve, bone, joint or disk problems. Patients may experience discomfort in the neck area or radiating down the arms and hands.
Disc pain may occur when a patient has a symptomatic degenerated disc (one that causes neck, mid or low back pain or other symptoms). It is the disc itself that is painful and is the source of pain. This type of pain is typically called axial pain.
Herniated disks may cause headache, neck, arm, mid-back, chest wall, low back or leg pain and/or numbness. Usually patients will not need surgery for herniated disks.
Chest Wall Pain
where i found this information ... http://www.illinoispain.com/conditionstreated.php
Conditions We Treat
Arthritis can cause misalignment of the bones which strains the muscles. The muscle then forms trigger points which tighten the muscle and increase the arthritis pain. Treating trigger points can significantly decrease the pain associated with arthritis.
There are many causes of back pain. Any cause of back pain can make the back muscles form trigger points. This can cause persistent back pain even after the original cause of the pain has resolved.
Bursitis is an inflammation of the tissue surrounding a joint. The inflammation can cause the muscle to form trigger points. Also, trigger points in the muscle can cause pain that feels like bursitis.
CARPAL TUNNEL SYNDROME
Arm muscle trigger points are a frequent cause of carpal tunnel syndrome.
COMPLEX REGIONAL PAIN SYNDROME
Complex regional pain syndrome, also known as reflex sympathetic dystrophy, may result from trigger points causing tight muscles which pinch nearby nerves.
Fibromyalgia is a condition of widespread pain and tenderness throughout the body, sleep problems and fatigue. Most fibromyalgia patients have trigger points as part of their problem. Treating the trigger points can significantly decrease the pain associated with fibromyalgia and improve function in daily activities. Many doctors and patients think of fibromyalgia as a "final diagnosis" of a poorly treatable, permanent, incurable disease. We consider a fibromyalgia diagnosis as a starting point to search for treatable problems to decrease pain and improve function. We see fibromyalgia as the starting point of a journey to a better life, not as a life sentence of pain.
Frozen shoulder refers to painful, limited shoulder motion. Shoulder pain from any source (such as arthritis, bursitis, rotator cuff tendinitis or tears) will cause trigger points to develop. This keeps the muscle tightened and unable to move normally. Treating the trigger points helps to restore normal movement and reduce pain.
LOW BACK PAIN
Low back pain can result from herniated discs, arthritis, spinal stenosis and other causes. Any cause of low back pain can induce trigger point formation in the muscles of the back which then aggravate and prolong the back pain. Although treating the trigger points does not cure the underlying problem, it can reduce pain and improve mobility. If back pain develops after a fall, trigger points may be the only source of pain.
MYOFASCIAL PAIN AND DYSFUNCTION
Myofascial pain is pain in the muscles, tendons, ligaments and fascia (connective tissue). This pain results from trigger points which are abnormally contracted muscle fibers which stress these tissues. Dysfunction means that the muscles are not moving normally. This can cause abnormal stress on nearby or distant muscles, spreading the pain and dysfunction.
PELVIC PAIN OR PAINFUL INTERCOURSE
This can be caused by tight and tender pelvic muscles with trigger points. This can result from ovarian cysts, endometriosis, pelvic inflammatory disease, fibroids, childbirth, surgery, trauma or other problems that occurred recently or many years ago. The trigger points may persist long after the initial disease or event. Treating the trigger points may reduce or eliminate the pain.
where i found this information ... http://themusclepaincenter.com/conditions/index.html
Studies being done on rsd/ crps people
I always look for new studies , 1. to always be updated , 2. to know whats being done to help us , 3. to feel someone is trying to do something in new studies of this terrible thing . As always Take Care & Soft Hugs .....
Complex Regional Pain Syndrome (CRPS)
Synonyms (commonly used interchangeably although they are not strictly speaking all the same entity): reflex sympathetic dystrophy, causalgia, Sudeck's atrophy, post traumatic dystrophy, shoulder hand dystrophy, reflex neurovascular dystrophy.
CRPS I - formerly known as reflex sympathetic dystrophy (RSD), this is pain which develops in the absence of identifiable nerve injury.
CRPS II - formerly known as causalgia (literally meaning 'hot pain') develops after injury to a major peripheral nerve.
However, the difference may be academic for patients who experience the same pain in both conditions and for whom treatment options are the same.
Incidence - CRPS can affect any age but is more common between the ages of 40 and 60 with a mean age of onset is 46 years, although the number of CRPS cases among adolescents and young adults is increasing.
It may occur as often as 5% of all injuries. It occurs in up to 15% of peripheral nerve injuries and following 10-30% of fractures.
Prevalence - based on the single population study available, it seems to be more common in females (male:female is 1:4) with an estimated prevalence of 20.57 cases per 1,000,000. However, the true prevalence is hard to establish as many cases are not diagnosed and resolve spontaneously.
The word 'complex' was added to the terms RSD and causalgia to reflect the variety of symptoms and signs that these patients can present with, in addition to pain.
The characteristic symptom is that of pain - typically burning in nature and out of proportion to the severity of the injury. It is chronic, gets worse rather than better with time and the affected area may have associated features such as:
Sensitivity to touch
Allodynia - perception of pain from a non-painful stimulus
Abnormal vasomotor activity - spontaneous temperature changes
Abnormal sudomotor activity - spontaneous sweating
Abnormal pilomotor activity - 'goose bumps'
The symptoms of CRPS vary in severity and duration. There is often a history of trauma - this may be very minor such as a cut to the finger. The symptoms do not appear to be related to the magnitude of the injury which may not be remembered (if it occurred at all). Other entities that have led to CRPS include:
Operative procedures e.g.carpal tunnel release
Brachial plexus pathology
There are not always objective findings in these patients who may be accused of malingering. However, the following may occur:
About 80% of cases have temperature differences between opposite sides. They may be warmer or cooler and this may be a fluctuating sign (sometimes occurring within a few minutes) depending on room temperature, local temperature of the skin and emotional state. Occasionally it may occur spontaneously. This may be associated with a change in skin colour.
Other skin changes include a shiny, dry or scaly appearance. Hair may be coarse initially, then become thin, nails become brittle and grow faster (initially) then slower and there may be associated rashes, ulcers or pustules which may become infected. Abnormal and spontaneous vasomotor, sudomotor and pilomotor activity as described above, also occur.
Hard, pitting oedema may occur diffusely over the painful region. There is often a well demarcated boundary along the skin line - almost diagnostic of the condition although similar findings occur when patients tie a band around the limb for comfort.
Movement may be limited both because of the pain and because joints are often described as stiff, with difficulty in initiating movements particularly. (The stiffness disappears after a sympathetic nerve block). Disuse atrophy can ensue. Other muscular disorders include sudden and severe spasms, tremors and involuntary severe jerking and
Symptoms and signs may spread over time in one of three manners:
Continuity type spread - the symptoms gradually spread out from the initial source.
Mirror image type spread - the symptoms spontaneously start up in the opposite limb.
Independent type spread - this may be spontaneous or following another trauma.
The diagnosis is clinical and may be tricky, particularly in the early stages of the syndrome where there may be little, if any, physical evidence of a problem (particularly in CRPS I).
Generally, the diagnostic criteria is accepted as being a history of a noxious event or immobilisation (CRPS I) or a nerve injury (CRPS II) of the affected area associated with pain that is disproportionate to the inciting event
Abnormal function of the sympathetic nervous system
Evidence of swelling at some point in time since injury
Changes in tissue growth (dystrophy and atrophy)
Absence of any condition that could cause this degree of pain or dysfunction
However, patients may present in complex and varied ways, the one common factor being pain. This may result in the patient being labelled as a malingerer or there may be suspicion that it is a ploy to obtain opiate analgesia. The bizarre nature of themovement disorders can be erroneously diagnosed as a psychogenic. Diagnosis may be aided by the spreading nature of the problems but on the other hand, if a mirror image type spread occurs, there is no normal limb to compare to. There are often psychological sequelae (see below) which may be interpreted as the cause rather than the consequence of the symptoms. Careful history taking and a systematic look for evidence of the signs outlined above is crucial as early diagnosis and intervention is important for a positive outcome.
Key screening features to look for4
Patients do not feel that the limb belongs to them - a lack of self ownership. This is not a concrete denial as you may see in stroke, as they know logically it is part of their body so should feel that it belongs to them.
Some have or have had a desire to amputate the limb. This desire often fluctuates with symptom activity. Some repeatedly request physicians to amputate despite knowing that this is medically inadvisable.
Patients perceive the affected limb as feeling different to how it looks i.e. as being much larger (more swollen) or less commonly, smaller than it actually objectively appears.
Poorly placed splint or cast
Carpel tunnel syndrome
This is essentially a clinical diagnosis as there is no blood test to confirm it. There is no inflammation and ESR, plasma viscosity and CRP are all normal. X-rays can show patchyosteoporosis in due course in up to 70% of cases3 (Sudeck's atrophy or post-traumatic osteoporosis) and a bone scan may show increased or decreased uptake of technecium 99m. Thermography may detect changes in body temperature that are common in CRPS. It is worth noting that X-rays, EMG, nerve conduction studies, CT scans and MRI studies may all be entirely normal.
There has been some debate over whether these patients have a predisposingpersonality disorder. The current general consensus is that this is not the case but that the severity of the pain and the disruption that it can cause to a patient can lead to depression and anxiety which may resemble a personality disorder.5
Traditionally, CRPS was seen as a three stage disease:
Stage I or early CRPS - there is onset of severe pain at the site of the injury associated with hyperaesthesia. At the outset, the skin is usually warm, red and dry but this may change to a blue (cyanotic) appearance when it becomes cold and sweaty (
Stage II or established CRPS - the pain becomes more severe and diffuse. Oedematous tissue becomes indurated. Skin becomes cool with hyperhidrosis andlivedo reticularis or cyanosis. Hair may be lost and nails become ridged, cracked and brittle. Hand dryness becomes prominent and atrophy of skin and subcutaneous tissues becomes noticeable. Pain remains the dominant feature. It usually is constant and is increased by any stimulus to the affected area. Stiffness develops at this stage and muscle wasting begins. X-rays may show diffuse osteoporosis. The 3-phase bone scan is usually positive. Duration is 3-12 months from onset.
Stage III or late CRPS - pain spreads and although it may diminish in intensity, it remains a prominent feature. Flare-ups may occur spontaneously. Irreversible tissue damage occurs. Skin is thin and shiny. Oedema is absent. Contractures may occur. X-rays indicate marked demineralisation.
However these stages are increasingly being seen as theoretical as all the features may not be present and the speed of progression varies hugely between patients. Some patients never actually progress to stage III whilst others get to stage III and lose some of the symptoms of the earlier stages.
The key approach is to provide adequate pain relief in order to undertake rehabilitation with the primary aim of restoring function.
Good progress can be made in treating CRPS if treatment is begun early, ideally within three months of the first symptoms. Early treatment often results in remission so consider early referral (see below).
It will usually resolve spontaneously. However, if treatment is required but delayed, the disorder can quickly spread to the entire limb and changes in bone and muscle may become irreversible.
Therapeutic goals should include:
Minimisation of pain and determination of the contribution of the sympathetic nervous system to the patient's pain.
Physical therapy to encourage normal use of the limb.
Education and psychological support.
Minimisation of pain
Drug therapy6,7 - introduction of analgesic drugs is done gradually and sequentially with an optimal dose determined on an individual patient basis. Drugs tend to be prescribed for pain that is:
Inflammatory or due to recent tissue injury
Spontaneous and jabbing in nature (paroxysmal dysesthesias and lancinating pain)
Sympathetically maintained pain (SMP)
Due to muscle cramps
Drugs used includeNSAIDs for mild to moderate pain, anti-convulsants or other sodium channel blockers for significant allodynia or hyperalgesia, anti-depressants and opiates. The latter is debated owing to the obvious disadvantages but is useful where pain is refractory to less aggressive therapies, particularly during flare-ups.3 Sympathetically mediated pain responds well to clonidine patching and benzodiazepines may be used in muscle cramps. Steroids may be used in swelling and inflammation and calcitonin or bisphosphonates may be added where osteopaenia and trophic changes have occurred.
Sympathetic blockade - generally, sympathetic nerve blocks are used less commonly as they only provide an effective medium term analgesic effect for some, no benefit to others and can exacerbate the pain in certain cases. However, sympathetic blockade may provide a solution in some individuals and selective blockade provides a further insight into the cause of the pain. There is the added benefit that it has a prognostic value as the patient's response will help determine the likely success of other treatment modalities.
Reversible blockade: injections - these can be performed with or without intravenous sedation and are performed in a setting where vital signs can be monitored throughout the block. A sympathetic block of the upper extremity is called a stellate ganglia block. A sympathetic block of the lower extremity is called a
Surgicalsympathectomy - only those patients with SMP are considered for surgical treatment. Surgical intervention will only provide as much relief as a chemical block (with the benefit that it is permanent) so those who have only experienced a modest improvement may not be suitable as it is a relatively invasive procedure with potential complications. Post-sympathectomy pain (neuralgia) is one potential complication. Motor cortex stimulation is another surgical option that is being investigated.6
Other treatment modalities - spinal cord stimulation may be a useful treatment for some of the more severely affected patients (it is costly and can have technical drawbacks).9 Acupuncture has been investigated and found to work well in children.3 Some patients respond to placebo treatment but the beneficial effect tends to be weaker and last less long.
Physical and occupational therapy
One of the cornerstones of therapy is re-establishing use of the affected limb. Physical therapy exercises, occupational therapy interventions, use of hydrotherapy and aTENS machine can all be key in this process.
Patient education and psychological support6
A useful initial approach is to establish a written protocol covering various aspects of the patient's care: procedures (e.g. nerve blocks), medications, physical/occupational therapy, psychosocial issues and new laboratory tests or consults. A psychological evaluation by an expert in chronic pain should be carried out to outline contributory factors which might be addressed. Patients with CRPS commonly report the following psychological issues:
Inappropriate/ineffective coping strategies
Difficulty accessing/accepting social support
Psychological interventions (including cognitive behavioural therapy andrelaxation techniques) can help the patient to address these issues.
Depression is common.
Immobilisation may aggravate pain and stiffness.
Skin infections can occur and occasionally may be very severe.
The duration of CRPS varies: in mild cases it may last for weeks followed by remission; in many cases the pain continues for years and in some cases, indefinitely. Some patients experience periods of remission and exacerbation. Periods of exacerbation may last for weeks, months (50% of cases have pain for > 6 months) or years. Paediatric cases tend to do better.3
Investigators are studying new approaches to treat CRPS and intervene more aggressively after traumatic injury to lower the patient's chances of developing the disorder. Scientists are studying how signals of the sympathetic nervous system cause pain in CRPS patients and there is evidence that there might be a role for sympathetic blocks in preventing CRPS. Researchers hope to discover the mechanism that causes the spontaneous pain of CRPS and that discovery may lead to new ways of blocking pain. Meanwhile, it would appear that patients suffering from fractures are well advised to maintain a good intake of vitamin C.10
where i found this information ... http://www.patient.co.uk/showdoc/40001759/
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~RSD Advisory- Where Chronic Pain & Mental Illness Collide New Rechargeable SCS Systems Offer Advantages in CRPS Treatment
New Rechargeable Spinal Cord Stimulator Systems Offer Advantagesin CRPS Treatment By Joshua P. Prager, MD, MSIn April, 2004, the Food and Drug Administration (FDA) approved the first rechargeable spinal cord stimulator (SCS) system. This system, called Precision™, produced by Advanced Bionics, is the first in a new generation of SCS systems that offers a significant improvement in stimulation to people with CRPS. In early 2005, Advanced Neuromodulation Systems rechargeable system, the Eon™, was approved and shortly thereafter Medtronic, the largest producer of neurostimulator systems, received FDA approval for its Restore™ System. This article will briefly review the use of SCS for treatment of CRPS and then describe the potential of the new systems in improving care and outcomes.
SCS as Part of the CRPS Treatment Algorithm
In 1995, the International Association for the Study of Pain (IASP) brought together a group of international experts to address treatment of CRPS. This was one of four meetings the IASP has held in the last two decades regarding various aspects of CRPS. Stanton-Hicks published results of the 1995 meeting as a treatment algorithm, which indicates that the mainstay of CRPS/RSD treatment is physical therapy, and that nerve blocks or SCS as adjuvant treatment are important for patients who are not adequately progressing with physical therapy alone. The important point of this article is that SCS can significantly enhance CRPS treatment by facilitating physical therapy as part of the entire rehabilitation process.
Stanton-Hicks suggested that the beneficial effect of SCS relates not only to pain relief, but it also to inhibits or modulates the sympathetic outflow to the region where the tingling produced by the stimulation is experienced.
SCS and CRPS
There have been numerous studies of SCS for the treatment of CRPS. These studies have been both retrospective and prospective randomized. In 1982, Broseta reported the use of SCS for CRPS-2 patients with 72 percent having experienced excellent results. Barolat reported a 73 percent success rate of pain in 18 patients with CRPS-1. Kumar discussed 12 patients treated with SCS for CRPS. Robaina compared SCS with TENS in 35 patients with late-stage CRPS-1; 66 percent of patients reported good results with SCS, experiencing rapid relief of pain and reduction in swelling. Bennett examined not only the effect of SCS on CRPS, but also looked at the effect of different lead arrays. He found that patient satisfaction was markedly improved with dual octapolar leads as opposed to traditional quadripolar leads.
There have been four prospective studies published of spinal cord stimulation in CRPS. The first, Calvillo in 1998, examined 31 patients with CRPS affecting the upper extremity with a significant reduction in pain scores compared to baseline. Oakley and Weiner observed statistically significant reduction in pain and an 80 percent success rate with SCS for CRPS. The largest prospective study in CRPS was that of Kemler , in the New England Journal of Medicine in 2000; 54 patients with CRPS-1 of one extremity were randomized to SCS plus physical therapy or physical therapy alone. A significantly greater number of patients with SCS plus physical therapy had a much improved global perceived effect than the physical therapy group alone. Most recently, Kemler published a two-year followup of the randomized trial. The mean pain score in the 24 implanted SCS patients was significantly reduced compared to those receiving physical therapy alone; 63 of the SCS patients reported improvement in their global perceived effect.
Thus, there is significant literature demonstrating the success with SCS in treating CRPS. This brief discussion above was not meant to thoroughly review or evaluate this literature, but merely to call attention to its presence and provide a reference list where one can review this information in greater detail.
Rechargeability and its Implication toward the Treatment of CRPS with SCS
The advent of rechargeability, being able to recharge the SCS battery, creates new opportunities. Previously, when a battery failed, the entire pulse generator needed to be replaced, which required expensive surgery and was uncomfortable for the patient. Rechargeability may significantly reduce the need to replace internal pulse generators.
Many CRPS patients with SCS systems have needed to use a lot of power to achieve the pain relief necessary to function. In order to reduce the need to replace the internal pulse generator, patients have often rationed the amount of stimulation by either reducing the power or turning the unit off some of the time. Thus, both patient and physician have attempted to manage the battery while compromising treatment. Rechargeability offers the opportunity to manage the patient instead of managing the battery.
Bennett notes that large arrays produce greater satisfaction than traditional quadripolar leads. Rechargeability offers the opportunity to use many contacts simultaneously, which uses a significantly greater amount of energy. Previously, this increased power consumption would have been prohibitive in some patients. Rechargeability allows the use of a greater number of electrodes at a given time to provide better coverage with stimulation.
There are some reports that increased frequency improves stimulation in patients with CRPS. Although this not been well documented, it is important to note that higher frequency produces higher energy consumption. Higher frequency potentially compromises battery life. Thus, rechargeability provides an opportunity to fully utilize the potential of any system without needing to worry about battery failure.
Conventional SCS four-and eight-contact leads were placed relatively far apart. Oakley and Prager in their discussion of SCS, indicate that when SCS leads are placed closer together the result is deeper penetration of the spinal cord, which provides a stronger effect. New lead configurations have been and will be designed specifically for rechargeable systems because the more-effective configurations will use more energy. Thus, once again, rechargeability provides a platform to allow for a more effective form of stimulation that conventional primary cell internal pulse generator source would not support.
Cost-Effectiveness of SCS
Taylor et.al recently reviewed the cost effectiveness of SCS for treating chronic pain. They conclude that in the medium to long term, SCS is economically favorable compared to other therapies for people with CRPS. Taylor indicates that pay back ranged from 15 months to five years after the SCS was implanted. The pay back period was sensitive to the efficiency level of the battery/electrode life and the amount of patient usage. However, this review was performed before rechargeable batteries. Considering the advantages of rechargeability, it is possible that pay back will be shortened and that the costs of SCS plus physical therapy will be lower than the cost of physical therapy alone. SCS initial costs are offset by a reduction in healthcare expenditures after the implant.
The Future with Rechargeability
The release of rechargeable systems has prompted the development of many new lead configurations that will enhance the effectiveness of SCS for the CRPS patient. New leads and extensions are currently in development. In particular, one product that will be available in the near future will allow four limbs to be treated simultaneously from a single-pulse generator. For patients with advanced four-limb CRPS, this eliminates the need for multiple systems; four limbs can be treated with a rechargeable single-pulse generator that, despite high energy consumption, will not require frequent replacement.
Spinal cord stimulation has a demonstrated efficacy in treating patients with CRPS when it is used in conjunction with a comprehensive rehabilitation program. Rechargeability enhances the ability to perform stimulation without requiring as frequent internal pulse generator battery replacements. SCS is cost effective in CRPS and future developments will enhance its effectiveness.
where i found this information ... http://rsdadvisory.wordpress.com/new-rechargeable-scs-systems-offer-advantages-in-crps-treatment/
TWO NEW STUDIES SUPPORT NEUROLOGIC BASIS FOR CHRONIC REGIONAL PAIN SYNDROME.
Where is the pathophysiologic origin of neuropathic pain - is it in the skin, the brain, the psyche, or somewhere in between? The question is nowhere more puzzling - and the answers potentially various - than when the subject is complex regional pain syndrome (CRPS), a cluster of symptoms that includes chronic pain, somatosensory, autonomic, and sometimes motor systems. The syndrome was formerly called reflex sympathetic dystrophy.
Typical features of CRPS can include changes in the color and temperature of the skin over affected limbs and body parts accompanied by burning or aching pain, skin sensitivity, sweating, and swelling. Like other conditions, there is a spectrum of severity. Some patients with intense pain have had affected limbs amputated, and suicides have been reported. Secondary depression is common as in all chronic pain syndromes.
Weir Mitchell described this syndrome (causalgia or CRPS-II) after major nerve injuries, but it has been unclear why other patients with sometimes trivial-seeming injuries report similar pain and disability. Some patients experience long-lasting pain and crippling changes in spite of often radical and invasive treatments, others experience spontaneous remission of symptoms.
In some cases - which have been dubbed CRPS II - there is clear evidence of previous neurological trauma; in other cases (CRPS I, the more common syndrome) there is no apparent trauma that would account for the pain.
Various explanations have been proposed, with passionate believers on all sides. Some say CRPS is psychogenic and that some patients are malingerers or neurotic. Others say the condition involves initial triggering and subsequent over-stimulation of the sympathetic nervous system resulting in characteristic inflammatory signs. Still others suspect a complex interaction of peripheral and central systems along with psychological factors.
About all that everyone agrees on is that CRPS is controversial. Cases are not infrequently litigated for workmen's compensation, but because of the difficulty of proving the biological existence of the condition - and because of the suspicion of malingering - claims are typically turned-down. Now, two papers in the journal Pain seem to show evidence of neurological damage in patients with CRPS.
FOCAL SMALL-FIBER AXONAL DEGENERATION
In one study, led by Anne Louis Oaklander, MD, PhD, results from quantitative mechanic and quantitative sensory testing (QST) and skin biopsies of 18 patients with CRPS-I were compared to seven symptom-matched individuals experiencing chronic pain as a result of trauma or osteoarthritis (Pain 2006;120:235-243).
Dr. Oaklander, Associate Professor of Neurology at Harvard and Director of the Nerve Injury Unit at Massachusetts General Hospital in Boston, and colleagues assessed three sites on CRPS-affected and matching contralateral limbs - the CRPS-affected site, and nearby unaffected ipsilateral and matching contralateral control sites.
They reported evidence of focal small-fiber axonal degeneration in CRPS patients, a surprising number of whom had had previous medical procedures. Axonal densities at the CRPS-affected sites were diminished in 17 of the 18 patients by an average of 29 percent. In contrast, the control subjects with similar symptoms from osteoarthritis had no painful-site neurite reductions. Moreover, QST revealed mechanical allodynia and heat-pain hyperalgesia at affected sites in the CRPS patients. Data from the control group suggest that small fiber damage is not merely a consequence of limb swelling, disuse, or pain, Dr. Oaklander said.immunofluorescence photomicrograph of a skin biopsy from the arm of a patient with complex regional pain syndrome type-1. The loss of epidermal endings is shown in green dye; disrupted vascular endothelial cells in red; and nuclei of the various types of skin cells in blue. previously healthy young scientist underwent routine bunionectomy in 2004 that left her with chronic left foot pain and focal autonomic changes.
Dr. Oaklander told Neurology Today that the study demonstrates that CRPS I, like CRPS II, is a neurological condition associated with damage to small-diameter axons caused by major, or sometimes seemingly insignificant trauma, such as needlesticks or mild injuries.
And because typical EMG and nerve conduction tests measuring function are insensitive to small-fiber damage, the neurological basis of the symptoms goes unrecognized, she said.
These are post-traumatic neuralgias, said Dr. Oaklander. The injuries that precede symptom onset may seem mild, but we have shown that they are sufficient to have damaged underlying small-nerve fibers. Since most neurologists focus on motor signs and electrodiagnostic abnormalities to diagnose nerve injuries, these subtle sensorineural injuries are often missed.
She added: We were also dismayed to see that medical procedures, including surgery, casting, and even routine phlebotomy are perhaps the most common cause of this syndrome in our arena.
Dr. Oaklander said that the study is not the first to show neurologic injury in patients with CRPS-I, and she said the use of a control group of chronic pain patients demonstrates a specific association between small-fiber damage and CRPS.
She added that the loss of axonal density of 29 percent suggests that trauma preceding the onset of symptoms can be mild. You don't have to have severe damage to get this syndrome, she said. That is one of the reasons it is so difficult to diagnose. The neurologist has a critical role in the diagnosis of this syndrome, Dr. Oaklander said. Only neurologists have the training in careful examination and neuroanatomical localization that will enable these patients to get a diagnosis, and then perhaps definitive treatment.
NEUROPATHIC ALTERATIONS WITH CLINICAL SYMPTOMS
A second paper also appearing in Pain analyzed glabrous and hairy skin samples from an arm and a leg amputated from two CRPS patients (Pain 2006;120:244-266). Using a battery of antibodies directed against neural-related proteins and mediators of nociceptive sensory function, they found a wide range of neuropathic alterations corresponding with clinical symptoms.
Lead author Frank L. Rice, PhD, acknowledged that there is no way of knowing what the initiating event triggering the neurological changes was, and that the amputation itself may be involved. But he said the results, in tandem with Dr. Oaklander's report, at least suggest the possibility of underlying neurologic damage in some cases of CRPS. Dr. Rice is Professor at the Center for Neuropharmacology and Neuroscience at Albany Medical College in New York.
In the study, Dr. Rice and colleagues reported the presence of abnormal axons innervating hair follicles; a decrease in epidermal, sweat gland, and vascular innervation; loss of expression of calcitonin gene-related peptide on remaining innervation to blood vessels and sweat glands; and a loss of vascular endothelial integrity and extraordinary vascular hypertrophy.
Everywhere you look, the norm of how nerve endings look was disrupted, including nerve fibers that we didn't view as pain-mediating to begin with, Dr. Rice told Neurology Today.
Dr. Rice emphasized that the changes correlate directly with clinical symptoms. For instance, nerve endings around hair follicles were disrupted in patients who had experienced extreme allodynia associated with the light movement of air over hairy skin. We detected an appropriate set of nerve endings that have been deranged and that fit to the symptoms, he said.
Neurologist Paola Sandroni, MD, PhD, who reviewed the papers for Neurology Today, said they would do little to clarify a condition that remains a clinical conundrum. She authored a landmark study of incidence and prevalence of CRPS in Pain (2003;103:199-207). In that report she found an incidence rate of 5.46 per 100,000 person-years at risk, and a period prevalence of 20.57 per 100,000, with a female-to-male ratio of four-to-one.
Seventy-four percent of patients underwent remission, often spontaneously. She and fellow researchers concluded that CRPS I is of low prevalence and that invasive treatment of CRPS may not be warranted in most cases.
Dr. Sandroni, a neurologist at the Mayo Clinic in Rochester, MN, said the study led by Dr. Oaklander was intriguing, but offered little that was conclusive. A lot more work needs to be done, he said. These are small numbers and I still don't know whether the changes Dr. Oaklander detected are secondary to endogenous substances and treatments that may have been applied. A little bit of reduction [in small nerve fibers] in the affected painful site - is that the whole story?
Dr. Rice agreed that CRPS remains a catch-all syndrome that may offer different explanations for different patients. We can't say carte blanche that there is always real injury, he said. That may not always be the case.
But he noted that many patients report experiencing the most extreme form of pain, and often take drastic measures to relieve themselves. And he said that both Pain papers suggest that nerves may be more fragile - and damage to them more consequential - than previously recognized.
ARTICLE IN BRIEF
✓ Two papers in the journal Pain report neurological evidence of chronic regional pain syndrome. But an expert in pain management commented that the evidence may not be conclusive.
where i found this information ... http://www.neurotodayonline.com/pt/re/neurotoday/fulltext.00132985-200605160-00010.htm;jsessionid=JvGJwnYF0JgLt2b62tG6y59Wbkb3QdGy2GdWpMNz1BNbhVylqMLW!-234910483!181195629!8091!-1
Epidemiological studies of RSD/CRPS using well-defined diagnostic criteria.
where i found this information ... http://www.crpsadvisory.com/crpsa_research.html
Objective Correlates of CRPS:
Utility for Diagnostic Criteria
Official Satellite Meeting of the 12th World Congress of Pain
August 13-15, 2008
The complex regional pain syndrome (CRPS) is an uncommon, chronic condition that usually occurs secondary to fractures, sprains, and soft tissue injury. CRPS has identifiable signs and symptoms. If diagnoses at an early stage, treatment can successfully treat the syndrome; however, if unrecognized, the symptoms can become disabling.
This 2-day satellite symposium will review the latest scientific research regarding the pathology, diagnosis, and management of CRPS. Join this internationally recognized faculty of experts in an evidence-based discussion of research findings conducted in both human and animal models as well as an analysis of their implications for clinical practice.
The symposium is directed to physicians and allied health professionals with an interest in the complex regional pain syndrome.
Upon completion of this activity, the participant will be able to:
Review the latest diagnostic criteria.
Recommend treatments based on new diagnostic approaches.
Relate the new diagnostic information for interventional and noninterventional treatments to clinical practice.
( there is alot more to read , It is a pdf file )
where i found this information ... http://www.clevelandclinicmeded.com/live/courses/2008/CPRS08/index.asp
NINDS Complex Regional Pain Syndrome Information Page
Complex regional pain syndrome (CRPS) is a chronic pain condition. The key symptom of CRPS is continuous, intense pain out of proportion to the severity of the injury, which gets worse rather than better over time. CRPS most often affects one of the arms, legs, hands, or feet. Often the pain spreads to include the entire arm or leg. Typical features include dramatic changes in the color and temperature of the skin over the affected limb or body part, accompanied by intense burning pain, skin sensitivity, sweating, and swelling. Doctors aren’t sure what causes CRPS. In some cases the sympathetic nervous system plays an important role in sustaining the pain. Another theory is that CRPS is caused by a triggering of the immune response, which leads to the characteristic inflammatory symptoms of redness, warmth, and swelling in the affected area.
Is there any treatment?
Because there is no cure for CRPS, treatment is aimed at relieving painful symptoms. Doctors may prescribe topical analgesics, antidepressants, corticosteroids, and opioids to relieve pain. However, no single drug or combination of drugs has produced consistent long-lasting improvement in symptoms. Other treatments may include physical therapy, sympathetic nerve block, spinal cord stimulation, and intrathecal drug pumps to deliver opioids and local anesthetic agents via the spinal cord.
What is the prognosis?
The prognosis for CRPS varies from person to person. Spontaneous remission from symptoms occurs in certain individuals. Others can have unremitting pain and crippling, irreversible changes in spite of treatment.
What research is being done?
The National Institute of Neurological Disorders and Stroke (NINDS) and other institutes of the National Institutes of Health (NIH) conduct research relating to CRPS in laboratories at the NIH and also support additional research through grants to major medical institutions across the country. NINDS-supported scientists are studying new approaches to treat CRPS and intervene more aggressively after traumatic injury to lower the chances of developing the disorder.Select this link to view a list of studies currently seeking patients.
where i found this information ... http://www.ninds.nih.gov/disorders/reflex_sympathetic_dystrophy/reflex_sympathetic_dystrophy.htm
CHRONIC PAIN DRAINS THE BRAIN
The means by which persistent or chronic pain affects an individual’s ability to live a ‘normal’ life has been clarified by investigators at Northwestern University’s Feinberg School of Medicine.
People with persistent pain live a life that often includes coping with a host of symptoms beyond the non-stop sensation of throbbing pain. They also have trouble sleeping, are often depressed, anxious and even have difficulty making simple decisions.
In the new study, researchers identified a clue that may explain how suffering long-term pain could trigger these other pain-related symptoms.
Scientists found that in a healthy brain all the regions exist in a state of equilibrium. When one region is active, the others quiet down. But in people with chronic pain, a front region of the cortex mostly associated with emotion "never shuts up," said Dante Chialvo, lead author and associate research professor of physiology at the Feinberg School.
"The areas that are affected fail to deactivate when they should." They are stuck on full throttle, wearing out neurons and altering their connections to each other.
This is the first demonstration of brain disturbances in chronic pain patients not directly related to the sensation of pain. The study will be published in The Journal of Neuroscience.
Chialvo and colleagues used functional magnetic resonance imaging (fMRI) to scan the brains of people with chronic low back pain and a group of pain-free volunteers while both groups were tracking a moving bar on a computer screen.
The study showed the pain sufferers performed the task well but "at the expense of using their brain differently than the pain-free group," Chialvo said.
When certain parts of the cortex were activated in the pain-free group, some others were deactivated, maintaining a cooperative equilibrium between the regions. This equilibrium also is known as the resting state network of the brain. In the chronic pain group, however, one of the nodes of this network did not quiet down as it did in the pain-free subjects.
This constant firing of neurons in these regions of the brain could cause permanent damage, Chialvo said. "We know when neurons fire too much they may change their connections with other neurons and or even die because they can’t sustain high activity for so long," he explained.
‘If you are a chronic pain patient, you have pain 24 hours a day, seven days a week, every minute of your life," Chialvo said. "That permanent perception of pain in your brain makes these areas in your brain continuously active. This continuous dysfunction in the equilibrium of the brain can change the wiring forever and could hurt the brain."
Chialvo hypothesized the subsequent changes in wiring "may make it harder for you to make a decision or be in a good mood to get up in the morning. It could be that pain produces depression and the other reported abnormalities because it disturbs the balance of the brain as a whole."
He said his findings show it is essential to study new approaches to treat patients not just to control their pain but also to evaluate and prevent the dysfunction that may be generated in the brain by the chronic pain. Source:Northwestern University
where i found this information ... http://jesdenm.livejournal.com/
RSD/CRPS How much can it take over your body . As you know each person is different and acts differently in each person . What happens to one may never happen to another person . But it can take over your whole body or many parts of it .Also copin skills . So i decided to take a look around to see just how much it can do to us .......... Take Care & Soft Hugs ............
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~Complex regional pain syndrome (CRPS)
Complex regional pain syndrome (CRPS) is an uncommon, chronic condition that usually affects your arm or leg. Very rarely, the disease can affect other parts of your body. You may experience intense burning or aching pain along with swelling, skin discoloration, altered temperature, abnormal sweating and hypersensitivity in the affected area.
The nature of CRPS is puzzling, and the cause isn't clearly understood. The condition may result from disturbances in the sympathetic nervous system, the part of the nervous system that controls blood flow and your sweat glands. The disease commonly follows an acute problem. Most often, CRPS is preceded by a major injury to an arm or a leg, but it may also be triggered by an illness such as a heart attack or a minor injury you can't even recall
Dramatic improvement and even remission of CRPS is possible if treatment begins within a few months of your first symptoms. Your doctor may initially suggest:
Pain relievers. Over-the-counter nonsteroidal anti-inflammatory drugs such as aspirin, ibuprofen (Advil, Motrin, others) and naproxen sodium (Aleve) may ease pain and inflammation. Prescription pain relievers may be recommended in some cases.
Applying heat and cold. Applying cold may relieve swelling and sweating. If the affected area is cool, applying heat may offer relief.
Physical therapy. Gentle, guided exercising of the affected limbs may improve range of motion and strength. The earlier the disease is diagnosed, the more effective exercises may be.
If the above treatments aren't effective, your doctor may recommend:
Corticosteroids. Use of the corticosteroid prednisone may reduce inflammation.
Sympathetic nerve-blocking medication. Injection of an anesthetic to block pain fibers in your affected nerves may relieve pain.
Vasodilators. These medications, traditionally used to treat high blood pressure, may help relieve pain in affected areas by easing blood vessel constriction.
Transcutaneous electrical nerve stimulation (TENS). Chronic pain is sometimes eased by applying electrical impulses to nerve endings.
Biofeedback. In some cases learning biofeedback techniques may help. In biofeedback, you learn to become more aware of your body so that you can relax your body and relieve symptoms of pain.
Surgical sympathectomy. In rare cases, your doctor may recommend surgically cutting the nerves in your affected area. This procedure may also destroy other sensations and is controversial.
If CRPS isn't diagnosed and treated at an early stage, the disease may progress to more disabling signs and symptoms. If you avoid moving an arm or a leg because of pain, or if you have trouble moving a limb because of stiffness, your skin and muscles may begin wasting (atrophy). You may also experience tightening of your muscles as they lose their tone. This may lead to a condition in which your hand and fingers or your foot and toes contract into a fixed position.
The illness may also spread from its source to elsewhere in your body in these patterns:
Continuity type. The symptoms may migrate from the initial site of the pain — for example, from your hand — to your shoulder, trunk and face, affecting a quadrant of your body.
Mirror-image type. The symptoms may spread from one limb to the opposite limb.
Independent type. Sometimes, the symptoms may leap to a distant part of your body.
where i found this information ....
Complex regional pain syndrome (CRPS) is an uncommon, chronic condition that usually affects your arm or leg. Very rarely, the disease can affect other parts of your body. You may experience intense burning or aching pain along with swelling, skin discoloration, altered temperature, abnormal sweating and hypersensitivity in the affected area.
The nature of CRPS is puzzling, and the cause isn't clearly understood. The condition may result from disturbances in the sympathetic nervous system, the part of the nervous system that controls blood flow and your sweat glands. The disease commonly follows an acute problem. Most often, CRPS is preceded by a major injury to an arm or a leg, but it may also be triggered by an illness such as a heart attack or a minor injury you can't even recall.
If CRPS isn't diagnosed and treated at an early stage, the disease may progress to more disabling signs and symptoms. If you avoid moving an arm or a leg because of pain, or if you have trouble moving a limb because of stiffness, your skin and muscles may begin wasting (atrophy). You may also experience tightening of your muscles as they lose their tone. This may lead to a condition in which your hand and fingers or your foot and toes contract into a fixed position.
The illness may also spread from its source to elsewhere in your body in these patterns:
Continuity type. The symptoms may migrate from the initial site of the pain — for example, from your hand — to your shoulder, trunk and face, affecting a quadrant of your body.
Mirror-image type. The symptoms may spread from one limb to the opposite limb.
Independent type. Sometimes, the symptoms may leap to a distant part of your body.
~*~*~ Pain & Depression ~*~*~
This seems to happen to each of us at one time or another . How we cope with it different . I lost 3 friends with rsd / crps due to this and i hope to never see or feel it again . There has to be away out all we have to do is find it , Like a mouse in a maze , courage and stergth is what we have to keep telling ourselves . Take Care & Soft Hugs ........
Depression and pain
Hurting bodies and suffering minds often require the same treatment.
(This article was first printed in the September 2004 issue of the Harvard Mental Health Letter. For more information or to order, please go to http://www.health.harvard.edu/mental.)
Pain, especially chronic pain, is an emotional condition as well as a physical sensation. It is a complex experience that affects thought, mood, and behavior and can lead to isolation, immobility, and drug dependence.
In those ways, it resembles depression, and the relationship is intimate. Pain is depressing, and depression causes and intensifies pain. People with chronic pain have three times the average risk of developing psychiatric symptoms — usually mood or anxiety disorders — and depressed patients have three times the average risk of developing chronic pain.
Medicating pain and depression
Almost every drug used in psychiatry can also serve as a pain medication. Relieving anxiety, fatigue, depression, or insomnia with mood stabilizers, benzodiazepines, or anticonvulsants will also ease any related pain. The most versatile of all psychiatric drugs, the antidepressants have an analgesic effect that may be at least partly independent of their effect on depression since it seems to occur at a lower dose.
The two major types of antidepressants, tricyclics and selective serotonin reuptake inhibitors (SSRIs), may have different roles in the treatment of pain. Amitriptyline (Elavil), a tricyclic, is one of the antidepressants most often recommended as an analgesic, partly because its sedative qualities can be helpful for people in pain. SSRIs such as fluoxetine (Prozac) and sertraline (Zoloft) may not be quite so effective as pain relievers, but their side effects are usually better tolerated, and they are less risky than tricyclic drugs. Some physicians prescribe an SSRI during the day and amitriptyline at bedtime for pain patients.
Both drug classes act in brain pathways that regulate mood and the perception of pain. Tricyclics heighten the activity of the neurotransmitters norepinephrine and serotonin; SSRIs act more selectively on serotonin. Some researchers and clinicians believe that a newer antidepressant which acts strongly on both neurotransmitters, the so-called dual action drug venlafaxine (Effexor), is superior to both tricyclics and SSRIs for treating pain. So far, the evidence is inconclusive.
Physicians and psychiatrists are also considering the uncertain potential of the anticonvulsant drug gabapentin (Neurontin) and drugs that block the activity of substance P, another neurotransmitter involved in the regulation of both pain and depression. Electroconvulsive therapy, a standard treatment for severe depression, may have independent analgesic effectsBrain pathways
The convergence of depression and pain is reflected in the circuitry of the nervous system. In the experience of pain, communication between body and brain goes both ways. Normally, the brain diverts signals of physical discomfort so that we can concentrate on the external world. When this shutoff mechanism is impaired, physical sensations, including pain, are more likely to become the center of attention. Brain pathways that handle the reception of pain signals, including the seat of emotions in the limbic region, use some of the same neurotransmitters involved in the regulation of mood, especially serotonin and norepinephrine. When regulation fails, pain is intensified along with sadness, hopelessness, and anxiety. And chronic pain, like chronic depression, can alter the functioning of the nervous system and perpetuate itself.
The mysterious disorder known as fibromyalgia may illustrate these biological links between pain and depression. Its symptoms include widespread muscle pain and tenderness at certain pressure points, with no evidence of tissue damage. Brain scans of people with fibromyalgia show highly active pain centers, and the disorder is more closely associated with depression than most other medical conditions. Fibromyalgia could be caused by a brain malfunction that heightens sensitivity to both physical discomfort and mood changes.
Depression, disability, and pain
Depression contributes greatly to the disability caused by headaches, backaches, or arthritis. People in pain who are also depressed become extremely heavy consumers of medical services, even if they have no severe underlying illness. But that doesn’t mean they receive better treatment; studies show that they actually use fewer mental health services than other patients with mood disorders. According to some estimates, more than 50% of depressed patients who visit general practitioners complain only of physical symptoms, and in most cases the symptoms include pain. Some studies suggest that if physicians tested all pain patients for depression, they might discover 60% of currently undetected depression.
Pain slows recovery from depression, and depression makes pain more difficult to treat; for example, it may cause patients to drop out of pain rehabilitation programs. Worse, both pain and depression feed on themselves, by changing both brain function and behavior. Depression leads to isolation and isolation leads to further depression; pain causes fear of movement, and immobility creates the conditions for further pain. When depression is treated, pain often fades into the background, and when pain goes away, so does much of the suffering that causes depression.
Treating pain and depression in combination
In pain rehabilitation centers, specialists treat both problems together, often with the same techniques, including progressive muscle relaxation, hypnosis, and meditation. Physicians prescribe standard analgesics — acetaminophen, aspirin and other nonsteroidal anti-inflammatory drugs, and in severe cases, opiates — along with a variety of psychiatric drugs (see "Medicating pain and depression" box above).
Physical therapists provide exercises not only to break the vicious cycle of pain and immobility but also to help relieve depression. Cognitive and behavioral therapies teach pain patients how to avoid fearful anticipation, banish discouraging thoughts, and adjust everyday routines to ward off physical and emotional suffering. Psychotherapy helps demoralized patients and their families tell their stories and describe the experience of pain in its relation to other problems in their lives.
Pain specialists can improve their practice by learning more about the interactions among psychological, neurological, and hormonal influences that link pain and depression. Why do some people recover from injuries without pain while others develop chronic symptoms, and how is that process related to depression and anxiety? How do psychotherapy and antidepressant drugs affect brain function in depressed people with chronic pain? What kinds of psychotherapy are helpful for them, and how long should psychotherapy continue? In investigating these questions, and in all treatment of both pain and depression, the goal is not just comfort or the absence of symptoms but restoring the capacity to lead a productive life.
where i found this information ... http://www.health.harvard.edu/newsweek/Depression_and_pain.htm
This post is part of the Health and Wellness Channel’s monthly theme day. This month, it’s hosted by Alicia over atMental Health Notes.
What came first, the chicken or the egg? Or - what comes first depression or chronic pain?
It’s a legitimate question that many people have asked and are still asking. Many people with chronic pain have been diagnosed with depression; people with depression who have chronic pain seem to have more severe pain or more complaints of pain than do those who don’t have depression.
It may seem simple. If you have chronic pain, it’s easy to understand how you can become depressed. As you become more depressed, you can feel your pain more intensely and the vicious cycle has begun. But if it’s so simple, how do we find out what is causing what
where i found this information ... http://www.helpmyhurt.com/2008/05/15/more-pain-and-depression-stuff/
Patients with chronic pain, when compared to those with almost all other medical conditions, suffer dramatic reductions in physical, psychological, and social well being, and theirHealth Related Quality of Life is lower (Atkinson et al. 1991; Becker et al. 2000; Skevington 1998). Many factors can interfere with the successful treatment of chronic pain including undiagnosed diseases, mental disorders, emotional distress, personality traits, and personal beliefs. These factors must be addressed directly to ensure that every barrier to the relief of chronic pain is addressed. Depression is one of the most common problems experienced by patients with chronic pain.
Signs, Symptoms, and Prevalence
In several studies of patients presenting to clinics specializing in the evaluation of pain, the prevalence of psychiatric conditions was systematically assessed. Affective and anxiety disorders were the most commonly found (Reich et al. 1983). For example, the prevalence of major depression in patients with chronic low back pain is 3-4 times greater than in the general population (Sullivan et al. 1992). However, the causal relationship between these syndromes remains controversial.
Physical symptoms are common in patients suffering from major depression (Lipowski 1990). Approximately 60% of patients with depression report pain symptoms at the time of diagnosis (Magni et al. 1985; von Knorring et al. 1983). In a study of 1,016 members of an HMO, persons with moderate to severe depression at baseline were more likely to have developed headache and chest pain 3 years later (Von Korff et al. 1993). The presence of a depressive disorder has also been demonstrated to increase the risk of developing chronic musculoskeletal pain (Leino and Magni 1993; Magni et al. 1993; Magni et al. 1994). Older age increased the risk for neck, back, and hip pain even more. Even after 8 years, depressed patients remained twice as likely to develop a new chronic pain condition compared to non-depressed individuals.
In patients with chronic pain referred for evaluation to comprehensive pain programs, 8-50% have been reported to have current major depression (Smith 1992). In another analysis of the 1,016 HMO members, the prevalence of depression was 12% in individuals with 3 or more pain complaints compared to only 1% in those with one or no pain complaints (Dworkin et al. 1990). The U.S. Center for Health Statistics conducted an 8 year follow-up survey and found 32.8% of the general population reported chronic pain symptoms. Depression was the most important variable associated with persistent chronic pain (Magni et al. 1993). If pain resulted in a loss of independence or mobility that decreased an individual’s participation in social activities, the risk of depression was significantly increased (Williamson and Schulz, 1992).
Individuals with chronic physical complaints also have higher rates of lifetime major depression. In groups of patients with medically unexplained symptoms such as chronic back pain and chronic dizziness, 66% of patients have a history of recurrent major depression compared to less than 20% of control groups with medically explained symptoms (Atkinson et al. 1991; Katon and Sullivan 1990; Sullivan and Katon 1993). Katon and colleagues have demonstrated a linear relationship between lifetime depression and anxiety disorders and the number of medically unexplained symptoms including pain complaints (Katon et al. 1991).
Family studies have also supported the increased risk for depression in patients with chronic pain. Compared to the general population, patients with chronic pain had more first degree relatives with depression and depressive disorders (Magni 1990). Even in patients with chronic pain without a personal history of depression, significantly higher rates of depression have been found in family members (Magni et al 1987). A biological vulnerability to affective disorder in patients with chronic pain is also supported by studies of biological markers. Decreased REM latency, decreased serum melatonin and lower density of 3H-imipramine binding sites on platelets have been found in patients with chronic pain (Blumer et al. 1982; Magni et al. 1987; von Knorring and Ekselius 1994; von Knorring et al. 1983).
The diagnosis of depression in patients with chronic pain is controversial. Many of the criteria traditionally used to diagnose major depression overlap with the symptoms experienced by patients with chronic pain. It is important to distinguish these manifestations of a chronic pain condition from the general distress such a condition provokes and the psychiatric diagnosis of a mood disorder. In a comparison of measures of emotional distress, self-reported depressive symptoms, and the presence of major depression in 211 patients with chronic pain in a university pain clinic, major depression was significantly related to self-reported disability and negative thoughts about pain (Geisser et al. 2000). Self-reported depressive symptoms were also highly related to the evaluative or cognitive component of pain but affective distress was uniquely related to the sensory or emotional component of pain.
Alternative sets of diagnostic criteria for major depression in patients with chronic pain have been proposed and include: 1) disregarding symptoms that are caused by medical problems, 2) replacing somatic symptoms with non-somatic alternatives, and 3) including all symptoms regardless of presumed cause (Wilson et al. 2001). The prevalence of major depression ranged from 19 to 36% with disregarding symptoms producing the lowest rate. However, patients who were excluded from diagnosis by this method were comparable to those patients diagnosed with depression across all methods. These findings support the use of inclusive criteria for major depression to avoid neglecting patients who have significant distress and disability.
Depression is not simply a comorbid condition but interacts with chronic pain to increase morbidity and mortality. Depressed chronic pain patients report greater pain intensity, less life control, and more use of passive-avoidant coping strategies. They also describe greater interference from pain and exhibit more pain behaviors than chronic pain patients without depression (Haythornthwaite et al 1991; Herr et al. 1993; Weickgenant 1993). The presence of preoperative depression in patients undergoing lumbar discectomy was predictive of poorer surgical outcome at 1 year follow-up (Junge et al. 1995). In patients with rheumatoid arthritis, depressive symptoms were significantly associated with negative health and functional outcomes as well as increased health services utilization (Katz and Yelin 1993). Depression has been shown to be the best predictor of application for early retirement at 6 month follow-up in a study of 111 patients with acute radicular pain and lumbar disc prolapse/protrusion (Hasenbring et al. 1994).
The consequences of unrecognized and untreated major depression are substantial. The most severe consequence of major depression is suicide. For example, patients suffering from chronic pain syndromes including migraine, chronic abdominal pain, and orthopaedic pain syndromes report increased rates of suicidal ideation, suicide attempts, and suicide completion (Fishbain 1999; Fishbain et al. 1991; Magni et al. 1998). In a study of patients who attempted suicide, 52% suffered from a somatic disease and 21% were taking analgesics daily for pain (Stenager et al. 1994). In another similar study, patients with chronic pain completed suicide at 2-3 times the rate in the general population (Fishbain et al. 1991).
Oncology patients with concomitant pain and depression were significantly more likely to request assistance in committing suicide as well as actively take steps to end their lives. In contrast, those with pain in the absence of depression were unlikely to request the interventions of euthanasia and physician-assisted suicide (Emanuel et al. 1996). Depression, not suicidal status, consistently predicted lower levels of functioning, higher pain severity, more pain-related disability, less use of active coping, and more use of passive coping in patients with chronic pain on a university inpatient unit (Fisher et al. 2001). If a patient with chronic pain expresses suicidal ideation, he/she should receive immediate assistance to ensure safety and ensure evaluation for depression. Depression should be treated aggressively and not simply "understood" as an expected outcome of chronic pain.
Antidepressants as Analgesics
The effectiveness of antidepressants for the treatment of major depression is well documented; however, the analgesic properties of this class of medication are under-appreciated. It is important for the patient to understand for which of these applications an antidepressant is being prescribed. Likewise, it is important that the physician understand that antidepressants can treat both pain and depression.
In 1960, the first report of imipramine use for trigeminal neuralgia was published (Paoli et al. 1960). Since then, the antidepressants, and in particular the tricyclic antidepressants (TCA), have been commonly prescribed for the treatment of many chronic pain syndromes, especially neuropathic pain. Animal models have been established for the study of nociception and neuropathic pain (Ollat and Cesaro 1995). Current research suggests that the analgesic effect of antidepressants is mediated by the blockade of reuptake of norepinephrine and serotonin. The resulting increase in the levels of these neurotransmitters enhances the activation of descending inhibitory neurons (King 1981; Magni 1987). Other aspects of monoaminergic systems have been implicated in the analgesic action of antidepressants. Beta-adrenoceptors have been demonstrated to mediate the analgesic effects of desipramine and nortriptyline (Mico et al. 1997). Imipramine demonstrated differential hypoalgesic effects depending on the experimental paradigm used to assess pain (Poulsen et al. 1995). TCA’s may reduce hyperalgesia but not tactile allodynia because different neuronal mechanisms underlie different manifestations of neuropathic pain (Jett et al. 1997). Generally, amitriptyline or TCA’s with a similar pharmacological profile are considered most effective analgesic agents but randomized controlled trials have not demonstrated consistent differences between the TCA’s (Bryson and Wilde 1996).
In a review of 39 placebo-controlled studies, antidepressants were reported to be superior to placebo in 80% (Magni 1991). The findings in a number of these studies have been challenged however because of poor study design and variable protocol criteria (Goodkin et al. 1995). A recent systematic review of randomized controlled trials and meta-analysis concluded that tricyclic antidepressants (TCA) are the only agents proven to benefit post-herpetic neuralgia (Volmink et al. 1996). Tricyclic antidepressants have been most effective in relieving neuropathic pain and headache syndromes (Gruber et al. 1996; MacFarlane et al. 1997; Max et al. 1987; McQuay et al. 1996; Vrethem et al. 1997; Wesselmann and Reich 1996). The analgesic efficacy was not dependent on mood elevation. A recent placebo-controlled, double-blinded, randomized clinical trial of nortriptyline for chronic low back pain in patients without depression demonstrated significant reduction in pain intensity scores (Atkinson et al. 1998).
A variety of treatment studies of post-herpetic neuralgia and painful diabetic peripheral neuropathy have employed TCA’s in mean daily doses ranging from 100-250 mg (Max 1994; Onghena and Van Houdenhove 1992). Over 60% of patients reported improvement usually beginning in the third week of treatment and serum levels of TCA’s were in the low end of the therapeutic range for the treatment of depression. The results of investigations to determine drug concentrations needed for pain relief remain contradictory and no clear guidelines have been established (Kishore-Kumar et al. 1990; Sindrup et al. 1989). In a study of TCA utilization, 25% of patients in a multidisciplinary pain center were prescribed these medications. However, 73% of treated patients were prescribed only the equivalent of 50 mg or less of amitriptyline suggesting the potential for additional pain relief (Richeimer et al. 1997). While tertiary amines have been used most commonly, they are metabolized to secondary amines that are associated with fewer side effects such as decreased GI motility and urinary retention. Desipramine and nortriptyline had significantly fewer side effects and led to discontinuation of the drug less frequently than clomipramine, amitriptyline, and doxepin. Nortriptyline, the major metabolite of amitriptyline, causes less sedation, orthostatic hypotension, and falls than imipramine and has been demonstrated to be as effective as amitriptyline in treating chronic pain (Roose et al 1981; Watson et al. 1988). The cost of TCA’s for pain treatment is generally much lower (less than $5.00 per month) than other antidepressants and medications with analgesic activity (Adelman and Von Seggern 1995).
The selective serotonin reuptake inhibitors produce weak antinociceptive effects in animal models of acute pain (Gatch et al. 1998; Paul and Hornby 1995; Schreiber et al. 1996). This antinociception is blocked by serotonin receptor antagonists and is enhanced by opioid receptor agonists. A large number of studies have investigated the potential role of serotonin receptor subtypes in both nociceptive and hyperalgesic mechanisms of pain but no definitive conclusions have been delineated. In human clinical trials, the efficacy of serotonin reuptake inhibitors (SRI’s) in chronic pain syndromes has been variable and inconsistent (Belcheva et al. 1995; Tokunaga et al. 1998). For example, desipramine was superior to fluoxetine in the treatment of painful diabetic peripheral neuropathy (Max et al. 1992).
However, paroxetine was not beneficial in a study of patients with diabetic neuropathy (Sindrup et al. 1990). In other studies, fluoxetine significantly reduced pain in patients with rheumatoid arthritis and was comparable to amitriptyline (Rani et al. 1996). Recently, the SRI’s were shown to be effective in the treatment of headache, especially migraine, and were well tolerated by patients (Bank 1994; Foster and Bafaloukos 1994; Saper et al. 1994). In contrast, in a study of chronic tension type headache, amitriptyline significantly reduced the duration of headache, headache frequency, and the intake of analgesics but citalopram, an SRI, did not (Bendtsen et al. 1996). Until the results with SRI’s are more consistent, they are not recommended as first choice medications unless a specific contraindication exists for TCA’s (Max et al. 1991).
Biogenic amines are the neurotransmitters of neurons from the cortex and hypothalamus responsible for descending inhibition of nociception at the level of the spinal cord. This mechanism for the neurobiology of pain suggests potential efficacy for all antidepressants, despite their different pharmacological actions, in the treatment of chronic pain. Norepinephrine and dopamine reuptake inhibitors such as buproprion produced antinociception in studies of thermal nociception (Gatch et al. 1998). Monoamine oxidase inhibitors have been found to decrease the frequency and severity of migraine headaches (Merikangas and Merikangas 1995). Buspirone has been found to be effective in the prophylaxis of chronic tension type headache however, buspirone-treated patients used more rescue analgesics for acute treatment of headache than those patients treated with amitriptyline (Mitsikostas et al. 1997). Protriptyline compared to placebo decreased chronic tension type headache frequency by 86% in a study of women with this condition (Cohen 1997). Trazodone was ineffective in decreasing pain in a double-blind, placebo-controlled study of patients with chronic low back pain (Goodkin et al. 1990; Marek et al. 1992). Venlafaxine inhibits the reuptake of both serotonin and norepinephrine with fewer side effects than TCA’s and SRI’s. In an animal model of neuropathic pain, venlafaxine reversed hyperalgesia as well prevented its development (Lang et al. 1996). Nefazodone possesses both the actions of analgesia and potentiation of opioid analgesia in the mouse hotplate assay (Pick et al. 1992). Other antidepressants that inhibit serotonin reuptake and block certain serotonin receptor subtypes such as mirtazapine will need to be studied in the treatment of pain (Galer 1995).
Chronic pain is an intrapersonal experience not a specific diagnosis. Patients with chronic pain should receive treatment for underlying medical conditions, and should be evaluated for anxiety and distress. Major depression is a common psychiatric comorbidity of chronic pain, is associated with severe consequences, and is very responsive to treatment. In addition to being a primary treatment for depression, antidepressants are effective in the treatment of many chronic pain syndromes such as neuropathic disorders. The complexity of chronic pain requires an extensive knowledge of the potential actions of many pharmacological agents. The physician should always think about the innovative application of medications regardless of how they are traditionally classified.
where i found this information ... http://www.hopkins-arthritis.org/patient-corner/disease-management/depression.html
4 Tips to Help Cope With Chronic Pain and Depression
By: William Deardorff, PhD, ABPP
Chronic pain and depression cycle
It is not uncommon for those who suffer from chronic pain to feel stressed and depressed at times. This is no surprise, given the fact that "chronic pain" usually means pain that lasts more than three to six months. Prolonged pain appears to set up a pathway in the nervous system that sends pain signals to the brain, even in the absence of an underlying anatomical problem.
Some chronic pain may be due to a diagnosable anatomical problem, such as degenerative disc disease or spinal stenosis, that can cause continual pain until successfully treated. More often, the chronic pain has no clear anatomical cause, as in failed back surgery syndrome or chronic back pain without an identified pain generator. In such cases, the pain is itself the disease. Click here for moreDepression Symptoms For some people, the stress and depression resulting from chronic pain can become consuming, and can even worsen and prolong the pain. (More information on Depression Causes.) Increased pain can, in turn, lead to increased stress and depression, creating a cycle of depression and pain that can be difficult to break. There are things a person with pain can do, however, to prevent or manage the chronic pain and depression that may develop:
Minimize the chances of developing chronic pain
Talking to a physician about symptoms of depression or stress, or a history of depression, while still in the acute pain phase can alert a physician to the need for consideration of both conditions in creating a treatment plan for the patient’s spine health. While one patient may demonstrate a full recovery from the initial injury, a patient who is more prone to depression and stress, shows signs of depression and/or stress, or who has a history of clinical depression may be more vulnerable to developing a chronic pain problem that persists beyond the initial acute pain complaint. An informed physician can suggest a treatment plan early on that treats the patient’s mental state as well as their physical pain, minimizing the chances of the patient developing a chronic pain problem.
It is advisable for patients to talk with their doctors if they experience any of the following common symptoms of depression:
Changes in sleep patterns
Changes in appetite
Feelings of anxiety.
Stress can manifest itself in several ways.Patients should talk with their doctors if they believe they exhibit symptoms characteristic of stress-related back pain, which are similar to those of fibromyalgia:
Back pain and/or neck pain
Diffuse muscle aches
Muscle tender points
Sleep disturbance and fatigue
In many stress-related back pain cases, patients complain of the pain "moving around"
Chronic pain can also be exacerbated by things such as physical de-conditioning due to lack of exercise and a person’s thoughts about the pain. Patients can help thwart their pain from developing into or minimizing chronic pain by engaging in an appropriate exercise program and practicing distraction, guided imagery and other cognitive techniques.
Identify stress triggers that can increase chronic pain
Patients can monitor how their own stress and anxiety affects their back pain by keeping a diary of when their back pain changes and what kinds of stress could be triggering the pain. This exercise can redirect a patient’s focus from the pain to the elements in their life that affect their pain. Identifying stress triggers or emotional triggers that affect the pain will give the patient the opportunity for better pain relief through avoiding or eliminating these stress triggers. Recognizing how depression and stress affect their pain can lessen anxiety by giving patients more control over their chronic pain problem.
Communicate about depression
Depression and an emotional reaction to chronic pain are normal. Many patients do not speak to their physicians about their depression because they believe that once the initial pain problem is resolved, the depression, anxiety, and stress they are feeling will go away. However, secondary losses from a chronic pain problem, such as changes in the ability to do favorite activities, disrupted family relationships, financial stress, or the loss of a job, can continue to contribute to feelings of hopelessness and depression.
Talking to a physician about feelings of depression will keep the physician better informed and better able to provide appropriate care. Depression can affect the frequency and intensity of pain symptoms, and the healing rate. Getting simultaneous back pain treatment and depression treatment will give the patient a better chance of a full recovery.
Seek multi-disciplinary care for pain and depression
Informing a physician of depression can create an opportunity for a multi-disciplinary course of treatment involving both a physician and a mental health professional. With a team approach, both the pain problem and the depression are monitored simultaneously, and both doctors can communicate about how each area affects the other. It’s important for physicians to understand that changes in the physical symptoms of pain can also be related to changes in a patient’s mental state.
In addition, some common treatments for pain, including opioid pain medication, can actually make depression worse. This worsening depression can then affect the physical presentation of the pain. If both physical and mental well-being are being monitored closely by medical experts, treatment and medication recommendations, including antidepressants, can be made that take both the physical pain and the emotional health of the patient into account.
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where i found this information ... http://www.spine-health.com/conditions/depression/4-tips-help-cope-chronic-pain-and-depression
~*~*~ Stress & Pain ~*~*~
Have you ever noticed the more you stress out the more pain you feel . These two go hand & hand , With each other . It happens to me all the time when i,m stressed out , Then here comes the flair up .Some things work for me and sometimes not . What works for you ? How can you not get stressed out over dealing with the pain . Sometimes its likes vicious circle. Until you find an opening to let you out . So i decided to see what i could find to not only help myself but others as well .
Take Care & Soft Hugs
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~There is no direct reason for stress at work to impact on the RSD. On the other hand, your RSD will increase your feelings of stress. In both cases, the fundamental problem is one of self esteem and feeling that you are understood. After the pain, the biggest problem I hear about from RSD sufferers is loneliness. This is a time when you need friends to support, endorse and encourage you. If you have a good network of friends around you, you should talk with them about how you feel and what you fear. If your friends are not up to this kind of thing (or anyway, because of your specific needs) I suggest that you join a Support Group. You will find several groups listed on the RSD Alert "Help Groups" pages.
"Emotional issues and loneliness are huge issues, and can increase duress. However, since RSD/CRPS is a nervous system as well as a neurological disorder, stress heightens the pain triggers throughout the body (the brain and the spinal cord), and is therefore a huge factor. That is why relaxation and mediation are recommended to keep stress levels down, to try and keep stress managed, continually under control, and to reduce flare ups. The connection between duress and pain physiologically is not mentioned at all in Derrick's answer, and is a key factor in the understanding of trying to control mind and body and one method of pain management for those living with RSD/CRPS.
where i found this information ... http://www.rsdalert.co.uk/FAQ/canstressatwork.htm
IT'S NOT IN MY HEAD!
"Just pull yourself up by your bootstraps!" " It can't be that bad!" "You don't look sick to me!" "You're just imagining it!" "Just don't think about it, IT'S ALL IN YOUR HEAD!"
These are some of the comments that many RSD sufferers have come to loathe. The only common experience in suffering from RSD seems to be an uncommon lack of understanding about the disease and its potentially devastating effects. Many times, it seems as if our society simply cannot accept that a "simple pain" can be so all-consuming. Some even question whether the pain is real at all. There is no doubt that RSD is a physical disease. It usually develops as a complication of a minor injury or operation. There is real anatomical damage. It responds, in its early stages at least, to pharmacological and physical treatment. Examination of a limb affected by RSD leaves only one conclusion - this disease is physical - every bit as physical as heart pain from angina or the breathing difficulties of asthma.
But many physical diseases are impacted by emotion. Angina sufferers get pain under stress. Heart attacks are most common on a Monday morning when the victim is driving to work, especially if there is low job satisfaction. Some forms of asthma are triggered by emotional stress, and can be physically life-threatening. The association between stress and symptoms is widely recognized in many diseases. Many physicians have adopted methods that address the patient's reaction to stress along with their physical needs. For example, programs helping asthma sufferers deal with stress without developing bronchospasm have existed for decades. Dean Ornish's program for cardiac rehabilitation emphasizes meditation and stress reduction together with good nutrition and proper exercise.
Just because a physical disease is affected by stress does not mean it is a "mental" problem. It does however, suggest additional directions for treatment, and for some, even a way to complete recovery.
In RSD, these emotional aspects are especially important since the sympathetic nervous system, which is responsible for maintaining the pain of RSD, also regulates emotions. This is why many RSD patients find symptoms worsen with emotional upset - psychological stress aggravates an already-stressed sympathetic system, and may be one reason RSD is so misunderstood. If a person has more physical symptoms when stressed, people may think that the root of the problem is "really" psychological. Since living in chronic pain is itself highly stressful, many RSD patients find themselves in a vicious cycle - the stress of RSD makes the symptoms worse which, in turn, increases the stress! For this reason, emotional support from family, support groups and others is particularly important while treating RSD. In our work at The Pain Institute, we have seen that the intense and incapacitating physical symptoms of RSD, can, for many patients, be diminished significantly with supportive, stress-management psychotherapy. In addition to stress reduction, many people can learn to use psychological techniques to actually control sympathetic activity.
Using psychological techniques to treat physical problems is not new. For example, some people with high blood pressure can use relaxation and visualization techniques to control their disease. Recent studies have also shown that immune response, hormone production and a host of other sympathetic-related functions can be positively controlled using psychological techniques. These recent advances promise exciting treatment options for RSD.
The staff of The Pain Institute have been working since 1989 to integrate specific psychological therapies with conventional medicine, physical therapy and advanced neuromuscular retraining to directly control the symptoms of RSD. Using these techniques, many of our patients with established and apparently intractable disease have achieved long-term remission.
For many RSD patients, the suggestion of psychotherapy seems to validate the statement: "it's all in your head." Our hope at The Pain Institute is that more RSD patients will be able to benefit from an integrated treatment program that meets all their physical and psychological needs.
where i found this information .... http://www.medhelp.org/www/piic2.htm
Facing the Storm
Mental Health, a most fascinating area of study, but are all diagnosis’ correct? A diagnosis relies on symptoms, or should I say, for a doctor to give a diagnosis, he must rely on symptoms and underlying factors before making such a determination. Can a doctors determination of said illness be based simply on assumption? How about a pre conceived idea or notion that the symptoms are obvious to a specific illness or disorder? Perhaps you know someone that experiences mood swings, altered behavior, or sudden changes in personality with bouts of highs and lows without notable warnings and you probably never even see it coming. This seems to be a tell tale sign of a widely known and diagnosed disorder and before I mention it, many of you will already know where I’m heading.
Depression is defined as sadness, gloom, dejection. A condition of feeling sad or despondent. In Psychiatry it is defined as a condition of general emotional dejection and withdrawal; sadness greater and more prolonged than that warranted by any objective reason. A disorder characterized by an inability to concentrate, insomnia, loss of appetite, anhedonia, feelings of extreme sadness, guilt, helplessness and hopelessness, and thoughts of death. Also called clinical depression. In Pathology, a low state of vital powers or functional activity.
Mania is defined as excessive excitement or enthusiasm; craze. An excessively intense enthusiasm, interest, or desire. In Psychiatry, manic disorder. A manifestation of bipolar disorder, characterized by profuse and rapidly changing ideas, exaggerated sexuality, gaiety, or irritability, and decreased sleep. Violent abnormal behavior. Insanity. Excitement of psychotic proportions manifested by mental and physical hyperactivity, disorganization of behavior, and elevation of mood; specifically : the manic phase of bipolar disorder. An irrational but irresistible motive for a belief or action. A mood disorder; an affective disorder in which the victim tends to respond excessively and sometimes violently.
Lets take a look at this again. Depression equals low and mania equals high. Common sense would lead us to believe that a "normal" mood would be at the center of both and in studying mental illness and Bipolar disorder, we would be correct. Imagine a pole, any pole, even a telephone pole. At the top is mania, in the middle is an even stabalized mood and at the bottom is depression.
Lets take a peek at hypomania. A mild to moderate level of mania is called hypomania, which generally does not impair a persons daily functioning and includes an enhanced mood and productivity.
A manic depressive is called Bipolar 1, the less severe form of Bipolar 1 is Bipolar 2, who’s characteristics include hypomania, instead of full blown manic episodes and then there is Unipolar, which by definition means that there is a depressive phase only.
Hmm! Wouldn’t that simply be depression? Lets review for a moment. Bi means two, Uni means 1. Bipolar 1 and 2 move up and down the pole, Unipolar means 1, it stays at the bottom. It’s said that mixed episodes do not exist in Bipolar 2, on the contrary, they do exist. It is but a mixed state of being, fluctuating, deflating and back again.
Have you wondered by chance where I might be going with all this? Let me introduce you to pain.
Pain is defined as physical suffering or distress, as due to injury illness, etc. A distressing sensation in a particular part of the body. Pain and ache usually refer to physical sensations (except heartache); agony and anguish may be physical or mental. Pain suggests a sudden sharp twinge. Agony implies a continuous, excruciating, scarcely endurable pain: in agony from a wound. Anguish suggests not only extreme and long-continued pain, but also a feeling of despair. A pang, twinge, stitch. afflict, torment; trouble, grieve. An unpleasant sensation occurring in varying degrees of severity as a consequence of injury, disease, or emotional disorder. Suffering or distress. A physical discomfort associated with bodily disorder (as disease or injury). A state of physical, emotional, or mental lack of well-being or physical, emotional, or mental uneasiness that ranges from mild discomfort or dull distress to acute often unbearable agony, may be generalized or localized, and is the consequence of being injured or hurt physically or mentally or of some derangement of or lack of equilibrium in the physical or mental functions (as through disease), and that usually produces a reaction of wanting to avoid, escape, or destroy the causative factor and its effects. Basic bodily sensation that is induced by a noxious stimulus, is received by naked nerve endings, is characterized by physical discomfort (as pricking, throbbing, or aching), and typically leads to evasive action. A symptom of some physical hurt or disorder. A somatic sensation of acute discomfort.
Now I’m going to propose a thought for others to think upon. When physical pain developes in a person, at some point emotional distress will take over. This is not an assumption, but fact. I don’t even need to get into information explaining the chemical imbalances that play a part in mental illness. Of course, it’s true. What I want to discuss is that when someone is in pain, acute, severe, mild to extreme, it takes so much energy inside ourselves that mental dilemma’s will develop. This can happen over a short period of time or a longer period of time. It might depend on strength, hope, the will to live, the ability to fight off the discomfort, attitude and a minimal level of stress. Stress increases pain, pain increases instability, instability creates lack of peace of mind. Thoughts of no longer wanting to live and exist expand and increase, however, there is a difference between suicidal ideation and suicidal intent.
On a good pain day the individual may have their high, creativity, feel happiness, smile and laugh, bounce around in a positive manner, demonstrate self esteem, feel excitement, desire, feel optimistic with the emotion that "no one can hold me back". Mania?
On a bad pain day the person may feel hopeless, worthless, no longer have the will to live that they had on their "good pain day". Lose hope, cry, feel agony, sadness, have no drive to get out of bed because either the physical pain or emotional pain has them beat. It is that the physical and emotional has grabbed them up once again. Depression?
On a so so day, he or she may feel fatigued, but flash a smile, hurt, but want to survive, their mood may be that of feeling "okay" considering what they endure through their day to day lives and hope flows through them. A stabalized mood? The center of that pole!
I am at the belief that pain is misunderstood and since many pain syndromes currently have no cure that many people are mis-diagnosed with a mental illness, namely Bipolar disorder as a means to justify that which cannot be accepted or explained.
I urge you all to think about this, I certainly do.
where i found this information .... http://rsdadvisory.wordpress.com/facing-the-storm-pain-and-mental-illness-by-twinklev/
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~Put Your Stress into Perspective and Lower your Pain with RSD- Sunday's Post
When you’re in allot of pain, even everyday things can be overwhelming. This is especially true with RSD/CRPS. It is our sympathetic nervous system that is "short circuited", so the more stress we have, the more our pain increases. The more stress we can eliminate, the better our focus and the lower our pain will be. The better our medications will work to control the pain, and decrease swelling, etc.
To see how stress might affect your RSD symptoms and increase your pain or how to understand how it is all conected,lets look at what the body goes through while you are under stress:
When you are worried, angry, anxious your heart rate increases, your breathing increases, more blood is pumping faster through your circulatory system, adrenalin is released preparing you to "take flight" should you need to (the fight or flight system) blood pressure goes up, vasoconstriction (blood vessels clamping down becoming narrow) occurs in the extremities so the heart can have more blood, this makes the extremities cold tingling because of increased breathing not enough O2 to the extremities.
When the even is over, and your body goes back to a "semi-state of normal" because you are still on a heightened state of awareness because of stress and pain:
You have vasodilatation (blood vessels opening wider) occurring in your extremities. The excess fluid because you did not "take flight" run anywhere, it has pooled in the lower extremities.
You may have increased swelling in the legs and feet, hands. Muscles become tender from adrenalin and other hormones released during stressed out episodes, some are turned into lactic acid and deposited n the muscles.
Some may experience a drop in blood pressure or blood glucose and feel dizzy or light headed or chest is tight if they have asthma.
There may not be a cure for RSD, but you have control over some very basic things that control your pain levels. You have control over who pushes your "stress" buttons.
You need to ask yourself a few questions before you hand over your power to another person and give them control over your pain.
Is this really going to matter or be of importance a month from now, 2 months from now, a year from now?
If you can honestly answer yes, then you need to address the subject of your stress.
Here is a tool you can print or draw and use it to help you identify which stressors you can cross off your list and which stressors you need to address.
This is a tool you can use to help look at stress realistically.
Here is how to use the diagram:
1. On a piece of paper in the center draw a circle, label it as my stress.
Draw lines coming from it creating a picture of a child like sun.
2. At the end of each line draw another circle with more lines branching out. Draw smaller circles at the end of these lines and make lines coming off from them also.
3. Label each circle with what is stressing you at the moment.
Break each stress down as far as you can, by using/drawing more lines and circles.
4. Sit back look at your stress diagram.
What are you NOT able to do anything about?
An example being: my pet has just died.
Ask yourself, can I change this in any way? (only how I react/emotions etc)
If you can not change or do anything about a stress
You draw a big X over it and let it go.
If you CAN change something,
An example being: the bill collectors are calling me-
Again ask yourself, can I do anything to eliminate this stress?
At the end of each line around the smaller circles, break it into each bill collector, write things that you can actually do to resolve this stress,
- Change your number?
- Work out a solution by calling?
- Contact a debt specialist for assistance?
- Are there programs at church, your community etc, that can help?
After breaking all of your stresses down using the diagram, look at the stresses remaining after drawing X's through the ones you can't change.
Hopefully you will have more X's than you have remaining stresses!
Pick the stressor (circle) that is causing you the most stress.
This is the one you need to focus on.
Only focus on one stress at a time.
There is time to work on the other stressor's
after you finishing resolving the first one.
One day at a time! One Step at a Time!
I hope everyone has a low pain week.
May you be surrounded by a warm healing light of positivity and love. We are all here for you if you need us!
Stress is phenomenon that we must learn to cope with. It is a turbulent storm between your mind and body. Stress occurs when there is either emotional or physiological tension that creates an imbalance in our nervous systems. During stress, the sympathetic nervous system in our brain, which is part of the autonomic nervous system, responds by increasing our heart rates and the number of breaths we take per minute, increasing the production of certain hormones, and by sending signals that activate damaged pain nerves, worsening our pain even more. This leads to a vicious cycle of pain leading to stress leading to more pain. I am living with an illness that is called complex regional pain syndrome ([CRPS], formerly known as reflex sympathetic dystrophy [RSD]) that has created a hurricane inside me, increasing the stress in my life. Anyone living with chronic pain has a heightened level of stress because of the tension between our minds and bodies.
Our bodies respond to stress with a "fight or flight" defense mechanism. This causes the adrenal and pituitary glands to release different hormones. It's our bodies own way of combating the storm while living with chronic pain. Stress can affect your over all well being, sending a tidal wave of signals throughout your body. This becomes a catch-22 because disease causes stress and stress can weaken your body's' immune system, exposing you to other health-related conditions. I'm stressed just thinking and writing about it.
Stress can change our blood pressure, heart rate, and breathing. It creates tension in our muscles and can affect our body temperature. These reactions are a direct order from the central command post in our brains! But we can develop a line of defense against STRESS and the storm within our bodies.
Developing your Defenses
There are many different sensory responses to living with chronic pain and stress. Many times, I can feel a storm or the change in barometric pressure before weather changes actually occur. My muscles get very tight and stiff, sending me into a tailspin of pain.
I now realize that I can slow down my breathing when I become overly anxious about the pain. So I stop to think and try to relax, inhaling and exhaling slowly. This is a learned behavior that I have acquired by going to yoga classes for years. Deep breathing allows me to stretch at my own pace and connect my mind with my body, which helps me onto the path of healing. My yoga teacher speaks profoundly to us while we are doing our breathing, relaxation, and mediation during class. The comment that really strikes a nerve with me is "try to just smile at the thoughts as your mind fills with chatter and anxiety." She is always suggesting that we try to let go of the negative thoughts. Our minds are very powerful and we can directly take action against some of the stress and stressors in our daily lives.
When you live with chronic pain, there is a constant storm of emotions and reactions due to the stressful situations we inadvertently find ourselves in. Exercising helps to increase the levels of endorphins in our body, which creates a healthy response to stressors. This does not mean you have to participate in strenuous exercise. If you are not able to exercise vigorously, you can do restorative activities like yoga, mat Pilates, Feldenkrais or small, concentrated movements that help release endorphins, creating a healthy response to stressors.
I do not compare myself to others — I just concentrate on my own abilities and disabilities and find a comfortable venue to pursue movements. It's like taking small baby steps before we learned to walk. I realized that I can benefit more from these activities if I try to focus in on the positive and let go of the negative.
I was very athletic and used to exercise daily before I developed CPRS/RSD. It has taken years for me to work toward wellness — now I am finally able to do some physical activities. I cross-train my body by doing a variety of tolerable activities that I enjoy or that help my pain. Swimming, walking or even laying down and learning to do small, isolated rhythmic movements can help our minds connect more with our bodies. Try some movement exercises and tailor them to your own needs and limitations..
So when the storm comes — whether it is pain or everyday stress — I try to go with the flow. I revel in the moments when I feel good and I use these as a resource in my memory bank to refer back to when I need a reminder that I do have good days. I have developed hobbies that are relaxing to help combat the stressors. When my ability to move or my activities are limited by my pain, I can write in a journal or even color in a Mandela book. A Mandela book contains different abstract-like maze patterns that help to stimulate different sides of the brain for functioning and patterning. I call it thinking outside of the box. Another favorite activity is when I spend time outside in my backyard with my dog — she is very loving and has brought me unconditional happiness. I collect orchid plants and I spend time watering them a few times a week — it's a very relaxing way to move around when I'm feeling stressed.
Now I know stress comes in many different shapes and sizes and we all respond differently. But we can be diligent about how we choose to respond to stress by choosing and learning new behaviors and creating new patterns. Try to stimulate your brain and the different senses. Looking at artwork and listening music are great sensory stimulators. Maybe you like crossword puzzles or books — develop new hobbies or pursue old ones. Be aware of what stressors set you off while you tune in and try to stay calm. I have a good support system of family and friends to talk to about my daily stressors. There are many support groups as well that can help because they are experiencing the same tidal wave of events caused by living with chronic pain.
There are stressors that are totally out of our control. Travel and extreme changes in weather, for example, can create treacherous conditions for us. So be prepared by keeping things simple — always have your prescriptions filled and contact your doctor, therapists, drugstore or whomever in advance. This will ease the burden of unnecessary stress. I always take extra medicines, special foam pillows, heating pads, a hot water bottle and whatever items I feel will help me get through the trip or the storm. I live in South Florida, and you can rest assured I have done this drill many times over. Stress is an endless storm in each of our lives — try to soothe your soul when the storm of stress moves in.
Wishing you wellness,
where i found this information ... http://www.nationalpainfoundation.org/MyTreatment/Spotlight_Zuckerman4.asp
Take Care & Soft Hugs
Hello Everyone , after so many prescription recalls i decided to search to see what i could find . I happen to run across an FDA recall site . Maybe you would like to look up your meds and speak with your doctor about it . I,m NOT telling you to toss them away i am asking that you talk with your doctor about it and what you read ...... Take Care & Soft Hugs ......
Here is the web site with clickable link
If you would like to contact us , Please feel free to e mail us at email@example.com
If you cannot get through using this please copy and paste to you email .... Take care ....