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FM in the Brain or Muscles or Both

Discussion in 'Latest ME/CFS Research' started by Cort, Jul 12, 2009.

  1. Cort

    Cort Phoenix Rising Founder

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    Most research in FM has focused on the central nervous system but the questions remain whether problems in the muscles are also contributing to the pain. We know that FM patients suffer from central sensitization - increased activity of the pain circuits of the brain - but is that activity partially results of increased messages from the muscles to the brain? Or does the brain simply interpret the messages from the muscles incorrectly.

    Staud, one of the biggies of the field, recently published a study on the muscles contributions to the disease. He put an anesthetic, lidocaine, on the tender points in FM and healthy controls - stimulated the muscles and then measured pain levels. The pain levels dropped in both FM and healthy patients indicating that at least part of the pain in FM is due to increased nervous system traffic from the muscles to the brain.

    Essentially these overactive nerves in the muscles seem to be maintaining the state of central sensitization present in the brain. FM researchers have two battles to fight; turning down the overactive nervous system activity both in the brain and the body.

    http://www.ncbi.nlm.nih.gov/pubmed/19540671?ordinalpos=34&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum
     
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  2. Michelle

    Michelle Decennial ME/CFS patient

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    This study reminds me of one that came out in April that suggested muscle modification in patients with FMS. Using surface electromyography they found that "patients might have a different fiber recruitment or a possible atrophy of type II fibers suggesting that they are not able to reach muscle relaxation." Perhaps there is some sort of pathological synergy between muscle and brain at work?

    When I was a kid (11 or so) and started having pain in my right leg after breaking my right ankle (and frequently re-injuring it), I remember thinking then that it was like there was a "pain memory" in my leg. Except then I dismissed the idea because it sounded silly. Now it sounds like I was probably right.
     
  3. Cort

    Cort Phoenix Rising Founder

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    Not able to reach muscle relaxation! That sounds so right on to me. That's a fascinating study. Too bad I'm spending so much time trying to learn computer programing. That is me to a T; if I 'exercise' it seems like my muscles just lock up; they feel tight and contracted.

    A few studies have show evidence of increased oxidative stress in ME/CFS patients muscles but just a few small groups are studying it; one in Italy and one in the UK, I believe; they publish a study every couple of years - it takes FOREVER to prove anything that way. Where are the teams of researchers pouring over our muscles? Such a shame.....It certainly 'feels' like those muscles are involved.
     
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  4. Rosalie

    Rosalie

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    mucsles

    HI Cort
    My one doctor keeps telling me the reason my muscles hurt so much is because i'm not exercising enough, its a catch 22 for me, If I exercise I spend the next 2 days prone. My arms and legs ache and now I find the muscles are jumping. What type of muscle pain do you experience and do you have the jumping?

    Thanks
    Rosalie
     
  5. roxie60

    roxie60 Senior Member

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    Yes, the more exertion the more 'jumping', I also call it vibrating, nerve explosions in th muscles. It is not usually painful but takes my energy.
     
  6. SickOfSickness

    SickOfSickness Senior Member

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    Sounds like me too.
     
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  7. Xandoff

    Xandoff Michael

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    Hi Cort,

    I transcribed Dr. Kenny De Meirleir's video on ME & PAIN that you posted on HR. I think this is a good place to post it again because he talks about Mitochondrial pain and other pain we can't control in ME. I have been off pain meds for 17 months so I really know understand the pain of Me, whether it be from muscles or dysfunctions in the brain. His descriptions really hit the mark with me. Thanks Cort!


    ME & PAIN Transcribed from Youtube video

    Prof. Dr. Kenny De Meirleir
    Produced March 2013,

    The Pains change during the disorder.

    Most patients, who recall how they felt before the run-up of this disease, remember they were free of pain in the beginning. The fatigue and the lack of recovery often occur before the start of Pain. The various possible causes are of a central nature. That is, cytokines, which are particles produced by our own white blood cells, can affect certain receptors and induce pain.

    This concerns mainly the so-called inflammatory cytokines, with one specific pointer to interleukin 1. They also occur in other disorders and animal models and are accompanied by pain of central origin.

    Bacterial neurotoxins also play a part. When the immune system has been seriously disrupted, all kinds of bacteria can no longer be eliminated. Or intestinal bacteria pop up, because the intestines are less capable of holding them back. Bacterial toxins can also cause central pain. Moreover there are a lot of other substances such as nitrogen oxide, which play a role. We know for example that if we reduce the effects of nitrogen oxide, pain is reduced.

    The same applies to a number of antibiotics that inhibit certain bacteria and also reduce pain. There is also a problem with opiate receptors. Endogenous opiates play a part in the brain, and with those receptors there seems to be a problem too. An English group is engaged in manipulating those opiate receptors, as to also reduce pain in patients.

    Perhaps the most important cause of pain is metabolic pain, pain from the metabolism. It is cause by a poor delivery of oxygen to the organs and also by mitochondrial dysfunction. The mitochondria are responsible for the release of ATP to let all our organs function.

    This is the most difficult pain to combat and the biggest problem, because there is no medicine for it. We can try to ensure the peripheral parts of the body getting more oxygen. We can do that artificially. But the release of several substances causing the large vessels to expand automatically causes a contraction of the small blood vessels which is the cause of cold feeling in the peripheral organs like fingers and feet, because the blood vessels themselves contract.

    This is a result of an altered sympathetic nervous system that is more active as compensation, but still can’t prevent H2S, NO and other vasoactive substances….to cause the expansion of large blood vessels. To such an extent that the small blood vessels are contracting. I think many organs suffer from a chronic oxygen shortage. And this will also, in the peripheral nerves…which contain blood vessels as well-cause a shortage of oxygen. So we have a mixture of neuropathic and metabolic pain.

    In my experience metabolic pain is the biggest problem because you can’t cure it, simply because there’s an imbalance in the blood circulation. Then there are all kinds of other factors. With this condition the red blood cells aren’t functioning normally, and there is also a problem with oxygen supply. I could mention an entire list of different mechanisms which all come down the to the same. We call them ischemic pains, due to a shortage of oxygen to form energy.

    The result is of course, the production of much lactic acid. We and others have found that while resting, the concentration of lactic acid in the blood to be up to three times the normal value. In normal blood 0.6 to 1 mmol lactic acid per liter is found. In a ME patient it is not uncommon to find 2 to 2.5 mmol per liter. And that a normal value in the blood of someone running the marathon of Rotterdam at considerable speed.

    In ME patients this is a normal value when at rest. That lactic acid comes from the tissues, which must convert all their glucose in lactic acid as a final product with much less energy supply. On the other hand there are also intestinal bacteria, as we have shown in a publication which produce both left as right turning lactic acid.

    Often the disintegration of D-lactate is more difficult with ME patients because they lack the enzymes to do so. That is animal lactic acid. So there are a lot of factors which cause the aerobic metabolism to shift to a more anaerobic metabolism and to me this is also an important element in the occurring pain.

    That’s why pain management must be performed with an overall vision on pain. Often one can’t cure this with one particular medicine, but with a more integrated approach one can usually cause a serious relief from the pains.
     
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  8. Allyson

    Allyson *****

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    Thanks indeed for the transcription Xandoff; interseting indeed.

    ischemic means lack of blood supply of course

    and one thing the blood and muscles both have in common is a potential lack of blood supply during upright exercise, especially if we have OI...and many PWME have this and do not know it and or have not been tested for it.

    I would like to see studies done where the subjects remain recumbant for a couple of weeks - asn so stay crash-free form OI - and do exercise to see if that impacts on - lessens - ie the PEM and pain.

    thanks again for the transcript,

    A
     
  9. Valentijn

    Valentijn Activity Level: 3

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    PEM hits just as bad when lying down doing the same exercises.
     
  10. Allyson

    Allyson *****

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    Oh thanks Val - what studies have been done into it please? I was not aware of any.


    cheers,

    ALly
     
  11. Valentijn

    Valentijn Activity Level: 3

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    Extensive personal experience.
     
  12. Allyson

    Allyson *****

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    He he ....nice one Val !

    I am amazed you have not published that - such a rigorous academic appproach.

    I am sure all the major journals will be fighting to publish - such a large sample size for one thing!
     
  13. Valentijn

    Valentijn Activity Level: 3

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