Fibrowendy,

I just wanted to say thanks for the info on the book....Fibromyalgia and Chronic Myofascial Pain: A Survival Manual by Devin J. Starlanyl and Mary Ellen Copeland

I ordered this book from Amazon...I also read tonight in another book an interesting statement about Fibro and Rheumatiod Arthritis...

"Twenty years ago Rheumatoid arthritis was considered a psychological illness, its symptoms exacerbated by stress and life changes. Today we know that stress has nothing to do with it. Fibro is undergoing the same changes."

I made mention to the one RA doc that since there was no definitive test for Fibro how could she give a diagnosis. She said that they have done studies of the brain and that areas of the brain "light up" and show as pain on MRI of the brain.

I found this in one study...Interesting..and since I just started to post here do not know if this information was already posted, but found it interesting none-the-less...


Medscape: There is some evidence from MRI studies that neurotransmitters are involved in the pathophysiology of fibromyalgia. Can you comment on some of these studies and their findings?

Dr. Clauw: There are studies showing that certain substances in the spinal fluid, like substance P, are much higher in patients with fibromyalgia than in those without fibromyalgia. And there are also imaging studies that show that if you give a fibromyalgia patient a stimulus that a normal patient generally would not feel as pain, not only do the fibromyalgia patients say they feel pain but you can see on functional MRI of the brain that they're actually sensing that pain, even though it's at a level of pressure that a patient without fibromyalgia does not sense on the MRI. In fact, there are many other objective abnormalities that can be identified in people with fibromyalgia.

This is the entire article....:

http://www.medscape.com/viewarticle/544596?src=mp

Diagnosing and Treating Fibromyalgia in a Patient With Rheumatoid Arthritis. An Expert Interview With Daniel J. Clauw, MD
Posted

Daniel J. Clauw, MD

Editor's Note:

Fibromyalgia is a chronic musculoskeletal pain disorder of unknown etiology. It is characterized by chronic widespread musculoskeletal pain, fatigue, poor sleep, and mood disturbances, as well as a multitude of associated symptoms. Approximately 2% of the general population in the United States suffer from fibromyalgia and it is more common in women (3.4%) than men (0.5%). Although it may occur at any age, fibromyalgia is most common in adults aged 40-75 years. Currently there are no FDA-approved treatments for fibromyalgia.

Because of the diverse nature of its presentation as well as the current lack of guidelines for its diagnosis and treatment, there is no consensus among physicians regarding the diagnosis and management of fibromyalgia. In this interview conducted by Helen Fosam, Editorial Director of Medscape Rheumatology, Daniel J. Clauw, MD, presents valuable insight into the current state of knowledge on fibromyalgia. Dr. Clauw is Professor of Medicine in the Division of Rheumatology at the University of Michigan; he also serves as Assistant Dean for Clinical and Translational Research, Director of the Chronic Pain and Fatigue Research Center, and Director of the Center for the Advancement of Clinical Research.

Medscape: There is some evidence from MRI studies that neurotransmitters are involved in the pathophysiology of fibromyalgia. Can you comment on some of these studies and their findings?

Dr. Clauw: There are studies showing that certain substances in the spinal fluid, like substance P, are much higher in patients with fibromyalgia than in those without fibromyalgia. And there are also imaging studies that show that if you give a fibromyalgia patient a stimulus that a normal patient generally would not feel as pain, not only do the fibromyalgia patients say they feel pain but you can see on functional MRI of the brain that they're actually sensing that pain, even though it's at a level of pressure that a patient without fibromyalgia does not sense on the MRI. In fact, there are many other objective abnormalities that can be identified in people with fibromyalgia.

But that doesn't mean that patients should feel the need to get an objective test to prove that they have pain. There are a large number of different conditions diagnosed entirely on the basis of what people report to us (ie, there are no abnormal findings on examination or X-ray) and fibromyalgia is one of these. I don't think we should be recommending that people do spinal taps and look at levels of substance P to diagnose fibromyalgia when they can just talk to the patient for a couple of minutes and come up with that diagnosis.

Medscape: Is it possible that fibromyalgia is simply an alternative name for pain?

Dr. Clauw: It is really sort of one of many names for pain. It's the name for widespread musculoskeletal pain which cannot be identified with a specific causal factor. The equivalent names for this type of nondescript pain in the gastrointestinal region is irritable bowel syndrome, noncardiac chest pain, or nonulcer dyspepsia.

So every subspecialty has at least one name for people [who present] with pain in the region of the body which that doctor is responsible for, where there is no clear inflammatory process or damage in that area of the body that's responsible for the pain.

Medscape: How can a diagnostic assessment for fibromyalgia be made in a patient who presents to a rheumatologist?

Dr. Clauw: Fibromyalgia doesn't need to be diagnosed by a rheumatologist, but if there is any confusion with the diagnosis of different rheumatologic conditions (eg, lupus, rheumatoid arthritis [RA]) the person should certainly see a rheumatologist. Otherwise, there are no universally agreed-upon criteria for diagnosing fibromyalgia. I feel that it should be diagnosed when someone has widespread and diffuse musculoskeletal pain, with no alternative cause. Usually patients also have many other symptoms, including tenderness, fatigue, sleep problems, memory problems, etc.

Some people feel uncomfortable that there is not a "diagnostic test" for fibromyalgia, but there are a number of conditions in medicine in which clinicians feel entirely comfortable making a diagnosis in the absence of physical findings or abnormal lab tests. In the spectrum of neurology, there are at least 6 different conditions for which there is no diagnostic test, including migraine headache, tension headache, and dyslexia. Orthopaedists very commonly see people with pain in their back or pain in their neck and all they do is say that this is chronic low back pain. They don't deny the existence of the pain. They just use a label that is, if you will, sort of a nondescript label that says that the person has pain without trying to say why the person has pain.

So every subspecialist in medicine has several diagnostic categories that are identical to fibromyalgia in that there is pain and other symptoms and there is no "abnormal" test. It is not entirely clear to me why fibromyalgia is sometimes singled out as being an entity that has these properties when, in fact, there are 50 or 60 diagnoses that people very comfortably make in routine clinical practice that are identical to fibromyalgia and are based on subjective symptoms with no definitive diagnostic test.

Medscape: Should fibromyalgia be suspected if a patient with RA presents with generalized pain? If so, what tests should be performed in order to diagnose fibromyalgia?

Dr. Clauw: It really depends almost entirely on the history that the patient presents, both with and without RA. If any patient has had relatively recent onset of widespread musculoskeletal pain, then fairly extensive diagnostic testing is essential to [rule out] an early case of lupus or RA or some other disease that can at the initial stages look just like fibromyalgia. But if someone comes in with the exact same symptoms which they've had for 5 or 6 years, and there is no damage to their joints nor are there other features that on physical exam or during the patient history are indicative of RA, lupus, or other conditions that early on can present like fibromyalgia, then it is likely that this person has fibromyalgia and not much more testing is necessary. So it is quite difficult to define a set of standardized tests in order to diagnose fibromyalgia in any given patient with generalized pain. However, a combination of disease presentation and longevity of the disease can help with diagnosis. These tests to a large part are dictated by how long the patient has had the symptoms and whether there are any abnormalities on physical exam or any findings in the history that are inconsistent with fibromyalgia.

For someone who has RA and then subsequently develops widespread pain, we would first be concerned about a flare of RA or infection, but once those are excluded then coexisting fibromyalgia is both possible and common. I would strongly recommend to a rheumatologist who has patients with inflammatory joint diseases like RA or noninflammatory joint diseases like osteoarthritis, who are not responding optimally to treatment with a nonsteroidal anti-inflammatory drug or to immunosuppressives, to immediately consider that they may also have fibromyalgia. And if they think the person does have fibromyalgia, then they would have to use an entirely different class of drugs, such as drugs that were initially developed as antidepressants, and some of the nondrug therapies, like exercise and cognitive behavioral therapy, to manage that aspect of the individual's disease.

Medscape: The current diagnostic criteria for fibromyalgia are a series of subjective tests recommended by the American College of Rheumatology (ACR) guidelines. How should physicians use these guidelines?

Dr. Clauw: We actually don't recommend that people use the ACR diagnostic criteria to diagnose individual patients. Those criteria were initially intended to be used as a standardized test in clinical research studies in fibromyalgia. The latter is really what they were designed for and how they function best. The criteria have helped tremendously in allowing imaging studies to be done as well as studies of neurotransmitter levels in spinal fluid, which have led to the current level of understanding about the neurobiology of fibromyalgia.

The application of these criteria in routine clinical practice actually does not work very well. It is important for practicing physicians to understand that the current ACR criteria for diagnosing fibromyalgia were not designed to be used in routine clinical practice and probably should not be used in routine clinical practice to diagnose patients. It is important to educate clinicians that these criteria were never intended for the purpose that they are sometimes currently used, and that they do not work very well for that purpose.

Having said that, there are currently no alternative criteria developed for use in routine clinical practice. So what ends up happening is that clinicians apply the current criteria in combination with their intuitive sense to arrive at a diagnosis of fibromyalgia.

This diagnostic process is somewhat not different from almost all other rheumatologic diseases. For example, although the ACR has criteria for diseases including RA vasculitis and lupus, it is extremely unusual that clinicians only use the criteria to diagnose the disease. In most cases, clinicians apply the criteria to their clinical experience and judgment as well as their intuitive sense to arrive at a diagnosis.

Medscape: What about a test for genetic polymorphisms? Is this an important test, and can it be ordered by a rheumatologist?

Dr. Clauw: Research is ongoing, but these tests are not yet available. I think in 5 or 10 years these tests will be extremely important in clinical practice. We're learning that genetic polymorphisms do in part predict sensitivity to pain. It is likely that many different genetic polymorphisms can make people more sensitive to pain. Furthermore, 1 or more of these genetic polymorphisms in a given individual can be responsible for the fibromyalgia.

Right now, there is nothing that can be done with respect to genetic testing that would in any way help either confirm the diagnosis of fibromyalgia or help with decision-making on the treatment plan. However, in 5 or 10 years, I very much believe that we will be using these tests.

Medscape: There is some evidence for association between prior sexual trauma and fibromyalgia. Can you comment on this relationship and whether it should be routinely explored during patient clinical history?

Dr. Clauw: It appears as though people with any kind of early-life abuse, whether it's physical abuse or sexual abuse, might be more likely to develop fibromyalgia. There are also some recent data to suggest that individuals with a history of early-life physical or sexual abuse who develop fibromyalgia may have a different form of fibromyalgia, compared with those with no evidence of abuse, especially with respect to how the hypothalamic-pituitary-adrenal axis and cortisol secretion appear to change in the setting of early-life trauma.

Research on the latter is ongoing, and perhaps in 3-5 years we may understand this phenomenon well enough to better individualize the treatment plan. Right now, we do not really know how and whether we should treat someone differently if they have had a history of early-life trauma.

With regard to exploring sexual trauma during patient clinical history, it is safe to say yes — we should. But this may not be as simple as it may appear, because early-life sexual and physical abuse is extremely common even in non-fibromyalgia patients. Depending on how clinicians ask the question, up to a quarter or a third of people in the general population who do not have fibromyalgia will report early-life sexual or physical abuse. A further 10% to 15% more people with fibromyalgia will report the same history. This leads us to believe that perhaps early-life trauma can actually trigger the development of fibromyalgia in some individuals.

To put this in perspective, though, it is important to realize that most fibromyalgia is not triggered by early-life trauma, and that most people who have early-life trauma do not develop fibromyalgia.

Medscape: There is some evidence that fibromyalgia is comorbid with depression and is therefore a clinical symptom of depression.

Dr. Clauw: The simple answer to that is "no," because, even in a tertiary care setting where people with fibromyalgia do have a high rate of comorbid depression, depression is seen in about 50% of individuals. This means that 50% of people with fibromyalgia do not have depression. In a primary care setting, only 20% or 25% of people with fibromyalgia will have comorbid depression.

So at one level, labeling fibromyalgia as a subcategory of depression would be the same as labeling diabetes as a subcategory of depression because 25% of people with diabetes are depressed. Most chronic medical illnesses will lead to a higher rate of depression than in the general population. In terms of psychological impact, fibromyalgia is really not different from chronic low back pain or a variety of other chronic pain states. A significant percentage of people with any kind of chronic pain or illness will be depressed, and that does not mean that the depression and the chronic illness are the same disease.

Medscape: Can antidepressants be used to manage patients with fibromyalgia?

Dr. Clauw: Many of the drugs currently used to treat fibromyalgia are drugs that were initially developed as antidepressants. But only some types of antidepressants help improve fibromyalgia and other pain syndromes, and the response to these drugs is totally independent of whether the recipient is depressed. Theoretically, if antidepressants were working to make fibromyalgia better, then they should work better in someone with depression than in someone without depression. However, this is not the case; the effect of antidepressants on fibromyalgia appears to be totally independent of depression.

A possible explanation for this is that some of the neurotransmitters that are responsible for depression, such as serotonin and norepinephrine, also play a role in fibromyalgia. And so some medications that treat depression also happen to work in fibromyalgia. This phenomenon is also seen in other diseases, such as restless leg syndrome. For example, some of the antipsychotic drugs are effective for treating restless leg syndrome; however, it does not mean that psychosis and restless leg syndrome are the same disease.

I think the antidepressants are working because there are neurotransmitter imbalances in fibromyalgia. And the way I explain these drugs to my patients is that these neurotransmitter imbalances can be corrected by these drugs and that makes pain better and fatigue better and sleep better and all of the other symptoms better. The fact that these drugs also can treat the neurotransmitter imbalances associated with depression is almost irrelevant.

Although research is ongoing, currently there are no drugs approved for fibromyalgia. My guess is that in 1-2 years there will be several drugs specifically approved for fibromyalgia.

We also have to keep in mind the benefit of nondrug therapies for managing patients with fibromyalgia. I'm a tremendous advocate of especially exercise and cognitive behavioral therapy. And I think that one of the biggest mistakes that is used in routine clinical practice in management of fibromyalgia is that people underuse these nondrug therapies.

For many patients with fibromyalgia who have had the condition for 5, 10, 15 years, it's really naive to think that simply giving them a drug will bring them back to their baseline state of health. The most a drug can do is to undo whatever is wrong with the way that person's nervous system is processing pain. I think many people in clinical practice are also using the wrong types of drugs for this type of pain (eg, anti-inflammatory drugs and narcotics do not work well in fibromyalgia pain), and they are also often underutilizing nondrug therapies such as exercise and cognitive behavioral therapy.

Medscape: It has been noted that fibromyalgia is comorbid with some autoimmune disorders, such as Sjögren's syndrome and systemic lupus erythematosus, and perhaps less likely to be associated with RA. How true is this?

Dr. Clauw: It appears that fibromyalgia plays a greater role as a comorbid condition in lupus and Sjögren's than it does in RA. The reason for this is not entirely clear.

Studies do confirm that, in lupus for example, the presence of comorbid fibromyalgia affects quality-of-life scores more than how active the person's lupus is with respect to the inflammatory component of their lupus. So it seems as though the fibromyalgia comorbidity really does dramatically affect the quality of life of a lupus patient, even more so than the lupus does. Again, the reason is unclear and may be due to a combination of biological, cognitive, psychological, and behavioral effects.

Medscape: What do you see as the future for managing patients with fibromyalgia?

Dr. Clauw: Well, in terms of diagnosis, we theoretically could be using functional imaging tests or testing for genetic polymorphisms in 5 or 10 years to help us determine whether someone has fibromyalgia or not. But where these tests will likely be more useful is in identifying different subsets of fibromyalgia that might respond differently to different classes of drugs or different classes of nondrug therapies. From a diagnostic standpoint, I think functional imaging and genetic testing will have some utility. But where the biggest advances will be is on the treatment side. There are many drugs for fibromyalgia currently in development, and in 5 years, there might be 4 or 5 drugs that are specifically approved for fibromyalgia whereas right now there are none. I think part of the benefit, from a treatment standpoint, will be the new drugs under development. There are 3 or 4 compounds currently in phase 3, and another compound is currently entering phase 2. If the current trials yield positive results, it will be at least 4 or 5 years before these products are approved and on the market.

Suggested Readings
Bennett R. Fibromyalgia: present to future. Curr RheumatolRep. 2005;7:371-376.
Hudson JL, Pope HG Jr. The relationship between fibromyalgia and major depressive disorder. Rheum Dis Clin North Am. 1996;22:285-303.
Le Goff P. Is fibromyalgia a muscle disorder? Joint Bone Spine. 2006;73:239-242. Epub 2005 Nov 9.
Mease P. Fibromyalgia syndrome: review of clinical presentation, pathogenesis, outcome measures, and treatment. J Rheumatol Suppl. 2005;75:6-21.
Wolfe F, Ross K, Anderson J, et al. The prevalence and characteristics of fibromyalgia in the general population. Arthritis Rheum. 1995;38:19-28.
Wolfe F, Smythe HA, Yunus MB, et al. The American College of Rheumatology 1990 Criteria for the Classification of Fibromyalgia. Report of the Multicenter Criteria Committee. Arthritis Rheum. 1990;33:160-172.


Daniel J. Clauw, MD, Professor of Medicine; Assistant Dean for Clinical and Translational Research, University of Michigan Medical School, Ann Arbor, Michigan


Disclosure: Daniel J. Clauw, MD, has disclosed that he owns stock, stock options, or bonds in, and has served as an advisor or consultant for, Cypress Biosciences.