New release from our founder of this site on cause of Fibro

Discussion in 'Fibromyalgia Main Forum' started by sues1, Sep 12, 2006.

  1. sues1

    sues1 New Member

    This also could explain while my hands and feet sometimes tremble like I have Parkinson's disease. My mother had it.
    ================Why it is important tos sign up for the news letter from this site.

    Critical New Piece of Fibromyalgia Puzzle Found?

    Pieces of the Fibromyalgia puzzle are slowly falling into place, and researchers are moving toward a unified theory that explains the etiology and pathogenesis of the disease.

    While the conviction among the majority of Fibromyalgia researchers is that Fibromyalgia represents a significant sensitization of the brain and spinal cord, some leading researchers have recently formed a theory that takes the "Sensitization Theory" a step further, to what can be called the "Hippocampus Hypothesis" or "Dopamine Hypothesis." This fascinating theory states that FM is primarily a brain dysfunction resulting from stress-induced physiological changes to a part of the brain called the hippocampus and to the important neurotransmitter that it regulates - dopamine.

    Specifically, the hippocampus is extremely sensitive to stress, and in fact is the brain organ that enables us to respond to environmental stressors in a way that helps us avoid danger. The best example of the beneficial stress response is when our ancestors crossed paths with a saber tooth tiger - an immediate "fight or flight" response was mandatory to ensure survival. Studies have shown that chronic stress, however, can contribute to a disruption of normal hippocampus function. The hippocampus plays a major role in pain perception and memory formation, and it is involved in controlling the production of that crucial brain neurotransmitter, dopamine. Dopamine abnormalities have been linked to "restless leg syndrome," increased pain, and feelings of self doubt, anxiety, and problems with memory formation.

    If the "Dopamine Hypothesis" is correct, then it is reasonable to assume that drugs that restore normal dopamine levels and activity in the brain should have a therapeutic effect when administered to Fibromyalgia patients.

    And this is where the "Dopamine Hypothesis" picks up steam. Andrew Holman, MD, recently conducted a controlled, double blind study of the drug pramipexole with several Fibromyalgia patients. Pramipexole, sold under the brand name Mirapex™, is approved for treatment for Parkinson's disease - a primary dopamine disorder. Patients experienced significant improvement in their symptoms. Another drug that affects dopamine and has been approved by the FDA as a treatment for restless legs syndrome - ropinirole - also met with remarkable success in another recent Fibromyalgia study conducted by Dr. Holman.

    All told, the Dopamine Hypothesis looks promising for several reasons. It ties in nicely to the pathogenesis of the disease - that the onset of Fibromyalgia frequently occurs during times of prolonged or intense emotional or physical stress, when the hippocampus may become overworked and become dysfunctional as a result. And it ties into the fact that dopamine, which is largely regulated by the hippocampus, may cause many of the symptoms of Fibromyalgia when its levels are unregulated.

    I would like to acknowledge Patrick B. Wood, MD, and Dr. Holman for their brilliant work with brain imaging, neurotransmitter physiology, and creative pharmaceutical approaches to normalizing/regulating dopamine in Fibromyalgia. Their work has proven beneficial to many Fibromyalgia patients and may hold promise for treatment of millions more. I applaud their bold, creative, and compassionate work.

    Dr. Wood explains the Dopamine Hypothesis in easy-to-understand language, using computer generated graphics and patient and doctor interviews in the acclaimed Fibromyalgia DVD "Fibromyalgia: Show Me Where It Hurts" To purchase a copy of this DVD, please visit the ProHealth store.

    Wishing you health and hope,

    Rich Carson
    ProHealth Founder and CFS Patient

  2. Marta608

    Marta608 Member

    "If the "Dopamine Hypothesis" is correct, then it is reasonable to assume that drugs that restore normal dopamine levels and activity in the brain should have a therapeutic effect when administered to Fibromyalgia patients."

    Isn't this great news? I hope they continue to pursue this theory and that doctors will prescribe at least a trial dose of Mirapex for FM patients.

    Now. I wonder how this affects those of us with more CFS symptoms of the illness?

  3. Cromwell

    Cromwell New Member

    I am both pleased and concerned as I recall Michael J Fox saying he does not take the drug much due to the side effects from it.

    Have to research this.

    Love Anne
  4. IntuneJune

    IntuneJune New Member

    Rich, thank you for putting this "out there."

    Sue, thank you for bringing it to our attention.

    And a thank you to the doctors who are willing to research our cause!!

    ".......recently conducted a controlled double blind study of the drug pramipexole with several Fibromyalgia patients."

    "several" is a very limited study. I will take a very cautious approach. Having transcribed medical reports for over 30 years now, I cannot caution folks enough about drugs and their side effects.

    If a new and better drug is patented for CSF/FMS someone will have to be willing to test it. Unfortunately at this point in time, I will not step up to that plate.

    I must run to teach my aquatics class, but there recently have been other posts that may address somewhat this issue, but it is not as easy. I wish I had more time.

    Thank you again, June
  5. StephieBee

    StephieBee New Member

    That was a great article. Thank you sues!

    I am on Mirapex and it has controlled my RLS significantly. Keep in mind though that it will not help the leg pain everyone, I know that first hand.

    I never actually have read anything about a relation between Parkinson's and Fibro...but I knew there was a connection between the two.

    Sometimes I feel like I have a very mild case of Parkinson's because I get trembling. When I drive into work in the morning, my legs will tremble and shake very badly. It scares me because Im driving on the highway and my foot is on the gas pedal. I used to have to dissolve my valium under my toungue to get a quick effect, but now Ive been rx'd Soma for the spasms during the day. It doesnt seem to have a sedating effect on me. The Zanaflex I take at night knocks me out though!

    Thanks again!

  6. peas

    peas New Member

    I emailed a reply to this site regarding the article on dopamine. Easier for me to just copy it than try explaining again, sorry for the length of it here.

    Giving a drug to people who have similar problems to those experienced by people with adverse effects of psych drugs - and one in which the most common adverse side effects includes DYSKINESIAS alongside other predictable and dangerous and disabling adverse effects of psychotropic drugs - is that a good idea? The drug hasn't even been on the market long enough to show the full blown extent of how much dyskinesia will show up, it can often take a long time to develop. Once its there as in Tardive Dyskinesia there's a big problem, and withdrawal from the drug can even make it worse. The facial actions in Tardive Dyskinesia are often mistaken by onlookers as some form of 'mental retardation' which is an added horror for the person inflicted with this drug-induced suffering. This painful adverse effect happens to HEALTHY people on psych drugs - how much more likely is it to happen to people already with problems? A few studies do NOT make for reliable evidence as is proven over and over and over again where warnings (and sometimes removal from the market) are issued by drug regulatory bodies many years after the emergence of a drug on the market (clinically 'proven' to be safe), when the effects on people are too many too ignore and long after very many people have been disabled or died from those effects.

    Please see below, and note that with prolonged exposure to dopamine-affecting medication 50% of people will develop Tardive disorders (No. 6 in the list). No 'short-term' clinical studies are going to show those risks, tardive means LATE ONSET. Giving this drug which causes neurological (brain) damage to another set of people for another set of symptoms is another future catastrophe in the making and its very worrying to me to see an article suggesting that a drug with a propensity to cause so much damage has been published where many people who have no idea of the harm that can be done and who may therefore seek treatment by that or similar drugs might end up with iatrogenic disabilities as a result. I hope some thought will be given to the following:


    "...The most commonly reported adverse effects with pramipexole treatment were constipation, nausea and dyskinesias. Sudden onset of sleep during daily activities has been reported in rare cases. The Summary of Product Characteristics recommends that patients being treated with pramipexole who experience somnolence and/or sudden onset of sleep must be informed not to drive and to avoid other potentially dangerous activities until such effects have resolved...."


    In the three double-blind, placebo-controlled trials in early Parkinson’s disease, hallucinations were observed in 9% (35 of 388) of patients receiving MIRAPEX, compared with 2.6% (6 of 235) of patients receiving placebo. In the four double-blind, placebo-controlled trials in advanced Parkinson’s disease, where patients received MIRAPEX and concomitant levodopa, hallucinations were observed in 16.5% (43 of 260) of patients receiving MIRAPEX compared with 3.8% (10 of 264) of patients receiving placebo. Hallucinations were of sufficient severity to cause discontinuation of treatment in 3.1% of the early Parkinson’s disease patients and 2.7% of the advanced Parkinson’s disease patients compared with about 0.4% of placebo patients in both populations.

    Age appears to increase the risk of hallucinations attributable to pramipexole. In the early Parkinson’s disease patients, the risk of hallucinations was 1.9 times greater than placebo in patients younger than 65 years and 6.8 times greater than placebo in patients older than 65 years. In the advanced Parkinson’s disease patients, the risk of hallucinations was 3.5 times greater than placebo in patients younger than 65 years and 5.2 times greater than placebo in patients older than 65 years.



    A single case of rhabdomyolysis occurred in a 49-year-old male with advanced Parkinson’s disease treated with MIRAPEX Tablets. The patient was hospitalized with an elevated CPK (10,631 IU/L). The symptoms resolved with discontinuation of the medication.


    Since pramipexole is eliminated through the kidneys, caution should be exercised when prescribing MIRAPEX to patients with renal insufficiency (see DOSAGE AND ADMINISTRATION).


    MIRAPEX may potentiate the doparninergic side effects of levodopa and may cause or exacerbate preexisting dyskinesia. Decreasing the dose of levodopa may ameliorate this side effect. ..."


    Dyskinesia refers to an impairment of voluntary movement. The resultant tics and other movements are often referred to as dyskinesias. Dyskinesia is sometimes caused by long-term use of anti-psychotic drugs or other dopamine antagonists like the antiemetic metoclopramide. The effect of these drugs can be tardive, meaning the dyskinesia continues or appears even after the drugs are no longer taken (see Tardive dyskinesia). In context of Parkinson's disease, dyskinesias are often the result of chronic levodopa therapy. These motor fluctuations occor in more than half of PD patients after 5 to 10 years of levodopa therapy, with the percentage of affected patients increasing over time.[Obeso JA, et al. The evolution and origin of motor complications in Parkinson's disease. Neurology. 2000;55(suppl 4):S13-S20.]


    "...What is Tardive Dyskinesia?
    Tardive dyskinesia is a neurological syndrome caused by the long-term use of neuroleptic drugs. Neuroleptic drugs are generally prescribed for psychiatric disorders, as well as for some gastrointestinal and neurological disorders. Tardive dyskinesia is characterized by repetitive, involuntary, purposeless movements. Features of the disorder may include grimacing, tongue protrusion, lip smacking, puckering and pursing, and rapid eye blinking. Rapid movements of the arms, legs, and trunk may also occur. Involuntary movements of the fingers may appear as though the patient is playing an invisible guitar or piano.

    Is there any treatment?

    There is no standard treatment for tardive dyskinesia. Treatment is highly individualized. The first step is generally to stop or minimize the use of the neuroleptic drug. However, for patients with a severe underlying condition this may not be a feasible option. Replacing the neuroleptic drug with substitute drugs may help some patients. Other drugs such as benzodiazepines, adrenergic antagonists, and dopamine agonists may also be beneficial.

    What is the prognosis?

    Symptoms of tardive dyskinesia may remain long after discontinuation of neuroleptic drugs; however, with careful management, some symptoms may improve and/or disappear with time..."


    "...Tardive dyskinesia is a syndrome involving dysfunctional, involuntary movements associated with long-term, chronic use of neuroleptic medications, such as Haldol, Prolixin, and Thorazine. These drugs lead to an apparent general calming or sedative effect on the individual and are considered major tranquilizers.

    Tardive dyskinesia may appear anywhere from three months to several years after initial use of these medications, and withdrawal from neuroleptics often exacerbates the symptoms..."


    "...Tardive Syndromes
    Tardive (meaning "late onset") dyskinesia (meaning "abnormal involuntary movement") is a term used to describe a syndrome occurring as a result of treatment with medications that block the receptors for the neurotransmitter dopamine in the brain. Dopamine is involved in producing movement. If the receptors are blocked over a period of time, some individuals may develop uncontrolled involuntary movements. Onset of symptoms can range from a few months to several years after initiation of drug therapy. In contrast to a tardive syndrome (which as the name implies occurs only after extended exposure to a causative agent), symptoms may also occur within a few hours to days after initiation of drug therapy. This is called an acute reaction. Acute reactions are more easily managed and usually completely resolve within a few days.

    Tardive dyskinesia was first described in the 1950s in patients treated with antipsychotic medications. The tardive syndromes can affect anyone exposed to medications that block dopamine receptors; however, women, the elderly and persons with psychiatric disorders (particularly affective disorders) are at increased risk. The incidence is difficult to estimate as symptoms and severity can vary widely and many cases are probably undiagnosed, but it is believed that up to 50 % of persons with prolonged exposure to medications that block dopamine receptors will develop a tardive syndrome. The tardive syndromes include classic tardive dyskinesia, tardive dystonia, and tardive akathisia.

    Classic tardive dyskinesia most commonly appears as repetitive, somewhat rhythmical involuntary movements. Typical involuntary movements include tongue thrusting, lip smacking, lip pursing, grimacing and chewing movements, rocking of the trunk, pelvic thrusting, rotation of the ankles or legs, marching in place, irregular respirations, and repetitive sounds such as humming or grunting.

    Tardive dystonia may also be seen as part of the tardive syndrome. Dystonia is characterized by sustained muscle spasms causing involuntary movement and abnormal postures of the affected area. Some examples include torticollis (the head and neck are turned to the side), retrocollis (the head and neck are pulled back between the shoulder blades) and blepharospasm (the eyelids are squeezed forcefully shut). It can also cause excessive arching of the back. Tardive dystonia clinically appears identical to idiopathic or primary dystonia (meaning "of unknown cause") but is classified as a secondary dystonia since it is the result of a known agent.

    Tardive akathisia is the third type of tardive syndrome. Akathisia refers to a feeling of restlessness often accompanied by anxiety. In milder cases, the individual may complain of a sensation of inner restlessness and be unable to sit quietly without fidgeting . In more severe cases, the individual may actually be unable to remain seated and must pace or march around the room. Their sense of anxiety increases if they are unable to move about.

    While the above tardive syndromes are characterized by excessive movements, individuals may also experience a drug-induced parkinsonism which appears clinically like Parkinson’s's disease. With drug-induced parkinsonism, there is an absence of movement. Individuals have slow movements with rigid or stiff muscles and tremor. When walking, a shuffling gait is present with a stooped posture and diminished arm swing. Facial expression is blunted causing a very solemn appearance. Of all the tardive syndromes, drug-induced parkinsonism is the most reversible. It resolves after the medication is stopped, but this may take up to 18 months...."


    ... In these phase 1 studies [re SSRI antidepressants], the companies generally code akathisia to agitation or to hyperkinesis. The critical point that emerges from these studies is how the market authorization holders can argue that their drugs do not lead to suicide against a background of their drugs causing agitation severe enough to lead to drop-outs from clinical trials at an up to 5% rate - in addition to all the less severe forms of agitation caused – and to agitation at an approximately 25% rate, occurring in a dose dependent fashion, in healthy volunteers...."

    "... a link between akathisia and suicide has been recognized by DSM-IV and company reviewers. It has been long recognized in the medical community that akathisia can cause suicidality and this fact has been extensively documented in the medical literature..."

    8) (A sufferer's view)

    "Then why are there people that have had dyskinisia lawsuits and won? It could be said that I could do such a thing, especially since when this happened, I had no doctor for a month, no one to talk to about what I am supposed to do with this medicine. I told the older doctor before I stopped seeing her that I was getting twitching and that I was scared, but she didn't believe me and didn't give me any advice as to what to do.

    And how about misdiagnosing and it's product causing much needless sufferring? The fact that I have been suffering with this for over a year and a half before getting diagnosed properly? Or the fact that I was on antipsychotics without having anything psychotic happening, or manic-depression? How about the fact that I can never work again? Or go to school? How about that it destroyed my life? Or the fact that doctors never warned me about these tardive things, or about withdrawal? Or how about when I was at this hospital for a week, and that I had passed out and was bleeding, and that no one did anything about for over an hour? Or when I had passed out for low blood pressure, and they were forcing me to get up and move? Or the fact that the antipsychotics they were giving me forcibly sedated me for hours, and that when I brought this up they told me it was because I wasn't "doing anything"?

    How about the fact that I am in debt now because of this, this writhing pain in my body. It has left me completely destroyed. All I want is justice, these things aren't merely side-effects, they are permanent life destroyers, this demands justice..."


    "...Why Most Published Research Findings Are False
    John P. A. Ioannidis

    There is increasing concern that most current published research findings are false. The probability that a research claim is true may depend on study power and bias, the number of other studies on the same question, and, importantly, the ratio of true to no relationships among the relationships probed in each scientific field. In this framework, a research finding is less likely to be true when the studies conducted in a field are smaller; when effect sizes are smaller; when there is a greater number and lesser preselection of tested relationships; where there is greater flexibility in designs, definitions, outcomes, and analytical modes; when there is greater financial and other interest and prejudice; and when more teams are involved in a scientific field in chase of statistical significance. Simulations show that for most study designs and settings, it is more likely for a research claim to be false than true. Moreover, for many current scientific fields, claimed research findings may often be simply accurate measures of the prevailing bias. In this essay, I discuss the implications of these problems for the conduct and interpretation of research.

    John P. A. Ioannidis is in the Department of Hygiene and Epidemiology, University of Ioannina School of Medicine, Ioannina, Greece, and Institute for Clinical Research and Health Policy Studies, Department of Medicine, Tufts-New England Medical Center, Tufts University School of Medicine, Boston, Massachusetts, United States of America. E-mail:

    Competing Interests: The author has declared that no competing interests exist.

    Published: August 30, 2005..." [The author goes on to explain - please visit the url).

  7. IntuneJune

    IntuneJune New Member

    Exercise also increases the dopamine (feel good) hormone with less side-effects and a lot more benefit.

    Please refer to the "Healing Principals" thread.

    This is not a cure....

    of course.....

    Just a way to help ourselves.....


  8. sues1

    sues1 New Member

    For myself, I feel that this is part of the puzzle and an important one. I have been researching for a long time. That is hard as my eyes tire and my brain shuts down and it is hard to process the information, and to remember it!

    I have told my DH and others that I feel it is a "Head problem" for a very long time. We all know our own bodies, even though we do not understand it.

    My mother had Parkinson Disease. I remember looking up meds on it. Some said that if you give "this med or that one" to a person with Parkinson, they could hallucinate by seeing or hearing things that was not there.

    This is something that has to be approached carefully and needs much research, but I do feel that at least....part of the answer is there.......right in our heads.

    I feel that we must not push at our Drs. to try some of the meds, as we need to study this more. We can do more harm by
    trying unchartered methods.

    I am feeling positive on this though. Thanks Rich,

    God Bless us all..and he does..................Susan
  9. StephieBee

    StephieBee New Member

    I feel that some people are trying to give Mirapex a bad rap.

    The fact is, ALL medication, both OT and Rx have side effects. It is up to you and your doctor to decide if taking a certain medication is worth chancing the side effects or possible risks.

    For example, a very good and effective drug (for me atleast)...Lamictal (as mentioned by haleycole) has a very severe risk behind it. Some people get Stevens-Johnson Syndrome from it. It is a very low percentage, but if you take Lamictal, who is to say you wouldnt be one to get it. To learn more about it you can search it. But ultimately you could very well die from it.

    I am not commenting on the little research that has been done, although any reasearch is a good ting, I am commenting on Mirapex specifically. It has made my life alot better. I can actually sleep without writhing, thrashing and kicking my legs around at night. My RLS is very severe, and Mirapex has been a godsend. Along with my doctor, I ultimately decided it was worth the risk to try it...nothing else was working.

    It has been said that Mirapex may become the first drug to be approved for Fibro.

    Also, on the compulsiveness side effect...I have heard that it is extremely rare, and usually occurs in Parkinson's patients.


    Take Care,
  10. anches

    anches New Member

    I read the research and thought it interesting, so I showed it to my doctor so she let me try the Mirapex.

    For me it made my FM pain worse and I started dropping things abnormally.

    It did help a high percentage of people in the clinical test, though. I think it's worth more study for it's potential.

    I didn't feel any compulsive behavior. Just thought I'd put in my experience!
  11. sues1

    sues1 New Member

    You mentioned on this thread to see the thread on "Healing Principals"

    I have been searching and not finding it. Are you speaking of "Principles of Healing in Fibromyalgia CFS" ? Posted by jlh today?

    Wow, Everyone who has responded to this posting is marvelous. You are giving us good info and also opening our minds on this subject.

    [This Message was Edited on 09/13/2006]
  12. IntuneJune

    IntuneJune New Member

    Yes, YOU have it correct.


    I'm sorry for the confusion especially if you spent a lot of time hunting that that!!!!

    I plead fibrofog. :)
  13. StephieBee

    StephieBee New Member

  14. Daisys

    Daisys Member

    I was on mirapex (.50mg) for RLS for quite awhile. I heard that at .75mg, there was an appetite control component for some. Since I was starting to need to take it earlier in the day, I asked my Dr. if I could go up to .75 and it worked. I went from being always hungry to having a normal appetite.

    I also heard that going to 4.5mg was helping some with the muscle pain of FM.

    I stopped taking mirapex when I started on xyrem, since it resolves RLS too.

    The one negative that I noticed for me, while on mirapex, was that after awhile the twitching started earlier in the day, I think it's called augmentation?

    I never got an urge to gamble.
  15. StephieBee

    StephieBee New Member

    I had no idea that Xyrem resolves RLS.

    As you know (because you have replied to my posts regarding this subject), I am leaning towards Xyrem instead of Provogil.

    If it does get rid of the RLS, I would go off the Mirapex. But for now Ill keep with it!

    I just wish it got rid of the pain also!

  16. cjcookie

    cjcookie New Member

    in case there was anyone who didn't see it.
  17. Daisys

    Daisys Member

    I'm biased toward xyrem because I don't need anything to keep alert while on it. I'm wide awake all day.

    I've had a lot less muscle stiffness and pain. When I do get sore, most of the time it's a lot better in the morning. The other day I wore the wrong shoes and ended up walking a lot and had really sore feet. I was expecting the usual several day recovery time, but the next day I even forgot I had expected them to be sore!

    I had heard that xyrem would take care of the RLS and so went off the mirapex. I did have twitches real bad for a few days and then it resolved.

    I'm sure I've said this before, and you've most likely heard it from others too: The best way to make sure xyrem will work for you is to start out low and slowly work up to the best dose for you. If you let your body get used to it before it even is strong enough to get you good sleep, you'll have less chance of bad side effects.

    I'm a little more sore these last couple of weeks, because my life has gotten stressful, busy, and my days are longer than usual. I couldn't have done it before starting on xyrem. I sure hope it gets approved for the alpha wave intrusion sleep disorder of FM. Then insurances would have to cover it for everyone with FM.

  18. vixiechix

    vixiechix New Member

    I'm just beginning to research this theory, but it does seem to make sense. Can you recommend any other articles that I should read? My fibro started after I was VERY ill in 1992 with viral encephilitis. This certainly increased STRESS throughout my entire body/central nervous system.
    Thanks for any other info. you could direct me to.

  19. Daisys

    Daisys Member

    It's been 3 months now since I last posted on this thread, so I'm glad to see it bumped.

    When I began taking the higher dose of mirapex, my sleep got so much worse I ended up going off it. Even xyrem couldn't overcome the effect. I got down to 3 hours sleep at night before I tried backing off the mirapex. As soon as I stopped the mirapex, my sleep went back to 8 hours.

    I researched a little and found sleeplessness is a very common side effect of mirapex.

    Everyone is different, of course. I have CFS/FM/RLS. Xyrem controls RLS as well as mirapex did, plus it gives me the deep, restorative sleep.
  20. sues1

    sues1 New Member

    Well......I really do not have anything new to speak of on this. BUT..

    My Dr. put me on sinemet (for Parkinson's aka PD), as he thinks I might have it.

    I am taking a low doseage and it has helped me. I did start out with two a day but now on just one pill. My mind seemed to race with two of them, yet getting one helped me and did not have that side effect. I checked with him first of course.

    Rather I have PD or not is unknown, but I am thinking that I do not. Just another one of the CFIDS/FM quirks. But I would hate not to have this med. Does help.


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