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A Little Poisoning Along the Road to ME/CFS
Looking at my symptoms, many of which are far less these days and some are gone, it would be easy to figure that I'd just been dealing with some heavy-duty menopausal issues.
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First Direct Evidence of Neuroinflammation - 'Encephalitis' - in ME/CFS

Discussion in 'Phoenix Rising Articles' started by Phoenix Rising Team, Apr 28, 2014.

  1. soofke

    soofke

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    Dutchy
    Thank you for your reply, I'm asking because inflammation would mean celldeath (right?) and I know it sounds (and looks, I sent you the link to a video) ridiculous but I think mine are recuperating which wouldn't be possible if...well.....dead. The same thing is happening throughout my body but it manifests differently (brain; májor pressure, eyes; trembling, and so on).
     
  2. MeSci

    MeSci ME/CFS since 1995; activity level 6

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    or a gliopathy, as described here?
     
  3. Snow Leopard

    Snow Leopard Senior Member

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    Good question, I'd like to know how the findings of this study compare to that of other medical conditions.
     
  4. N.A.Wright

    N.A.Wright Guest

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    Simon, excellent survey of the terrain !

    I'm cautious about what the Osaka study actually found - as I wrote on another thead:

    "The Osaka City University study is promising but even that need not require actual inflamation of the brain, merely that the usual products of inflammation be present and caused by some as yet unexplained disease process. There's also the possibility that this small Japanese study has revealed something specific to a localised gene variant and replication needs to be done in diverse populations to address that, along with the usual prcesses of replication."

    Of course one would hope that nature is abiding by Occam's Razor and the simplest explanation of 'evidence of inflamation = inflamation' is the right one, but in the case of ME I don't think that we can be certain without some very weighty numbers. It's become a sort of accepted coda amongst patients that - "the answer is out there" - and if only researchers had been looking in the right place then 'the answer' to ME would have been found years ago. And again of course that would be ideal because good, focussed and sustained research should be certain of getting the answer. But it may not be like that - ME may just be something that is very difficult to get at, something where there is an awful lot of evidence to be found, but where little or none of the evidence quite means what it is expected to mean.
     
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  5. Simon

    Simon

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    Thanks :). And if you are talking about mecfs research on neuroinflammation, I totally agree it should be a priority.

    Great question

    I think for all of this, the first step needed is replication by the original authors using their improved design, which I understand has already started or will soon do so. Then other Qs come into play, including how it compares with other chronic illnesses and with acute infection. As Tony Komaroff said, what's needed is independent confirmation by multiple different labs. I wouldn't normally blog on such a small study, but as the findings tie in with so many other theories, and as an improved version of the study is already planned, I think this study deserves more attention.

    Re encephalitis, I took my cue from Tony Komaroff:

    As for encephalomyelitis, the microglial and astrocytes that showed up as activated in the brain PET scan are also present in the spinal column, so it's plausible they too are activated - that would need a different PET scan to investigate. Again, this would be low-grade which as I understand it is not what is normally meant by encephalomyelitis. There again, my understanding was that Ramsay used encephalomyelitis because he thought that would explain the clinical symptoms he found (he didn't have direct evidence).

    If the neuroinflammation evidence checks out Ramsay may have been on exactly the right lines - that's the only point I'm trying to make. I wouldn't want to push it too far, esp as this is a study on only 9 patients and didn't even look at the spinal column.

    We must talk before I write my next blog! Hugh Perry's hypothesis is about microglial priming, so that people have an exaggerated immune response.

    got a link for that, would like to follow up?

    still working on replies to others, got to go lie down and rest....
     
    Last edited: Apr 29, 2014
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  6. A.B.

    A.B. Senior Member

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    Will this happen within a year or two though? How much importance does the medical community attribute to these findings? Is this a mere curiosity or highly significant?
     
  7. Marco

    Marco Old blackguard

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    Yes indeed.

    I appreciate that and I agree that its an 'itis' but this type of neuroinflammation is also found in conditions such as post concussion syndrome, complex regional pain syndrome, in normal aging (as previously mentioned) neurodegenerative diseases and in what were considered 'classic' psychiatric disorders such as major depression, bipolar and OCD. It may just be semantics but I doubt few would refer to these conditions as reflecting 'encephalitis' even if neuroinflammation is now recognised as playing a central role.

    http://www.molecularneurodegeneration.com/content/4/1/47

    Good idea! :)
     
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  8. Simon

    Simon

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    :thumbsup:

    Fair point. Just found Charles Shepherd's quote on this:
    So to avoid confusion I will stick with neuroinflammation. However, I do think that Ramsay's implicit point, that the symptoms indicated a problem in the brain, may eventually prove right.

    Terrific, another highly relevant paper I need to digest. Thanks ;)
     
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  9. Sean

    Sean Senior Member

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    Thanks for this, Simon.

    Could be wrong, but I have a vague memory that Ramsay actually wasn't so enamoured with that name, but reluctantly went with it for various reasons.
     
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  10. Firestormm

    Firestormm Guest

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    It was Post-viral Fatigue Syndrome he regretted :)
     
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  11. Sean

    Sean Senior Member

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    Thanks, Firestorm.
     
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  12. Simon

    Simon

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    I agree with that, but there are other possibilities. Certainly, if you can treat the underlying cause of the chronic inflammation that would be best, but people have suggested tackling the 'downstream' neuroinflammation with microglial inhibitors. I can't remember where I saw that but did find this recent study:
    Antiviral drug ganciclovir is a potent inhibitor of microglial proliferation and neuroinflammation

    I'm not suggesting this is a treatment for ME/CFS or any other case of neuroinflammation, but it does suggest another route to treatment, even if it wasn't treating the cause.

    Another possibility is that the chronic neuroinflammation is chronic because of a problem with the microglia, and not because of any stimulus outside the brain, and again in that case a microglial inhibitor might be appropriate. Though of course, you need your microglia to get active some of the time, that's what they are there for.

    Guess we need the 'Big If' of replication sorted first!
     
  13. wdb

    wdb Admin

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    I'm a little concerned about this bit, do you know if the scans were analyzed blind ?
     
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  14. Dolphin

    Dolphin Senior Member

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    Another great article, Simon.

    Small point:
    What the study found was:
     
  15. Legendrew

    Legendrew Content team

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    I'd imagine you would compare the scans of controls and patients alongside one another and it would allow you to clean up a lot of the 'noise', it's far from a perfect way to analyse this kind of data but it lets you see on a qualitative level whether there is any significant difference which is what I believe this study is reporting.
     
  16. lauluce

    lauluce as long as you manage to stay alive, there's hope

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    It seems that the pieces of the puzzle are starting to fit
     
  17. Simon

    Simon

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    Not sure, but they did prespecify which areas they considered:
    Does this help? there is more like it....

    Thanks on both counts. I was finishing the blog off yesterday and was having a rough one - I was sure the figure was around 12% but could only find one suggesting 20% so lazily went with that. Blog now corrected.

    Activation of the microglia (or astrocytes) themselves does not cause their cell death. Their activation will lead to other changes which may or may not lead to cell death/apoptosis for other cells - I think it would depend on other things too, such as other signalling molecules in the micro environment.
     
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  18. heapsreal

    heapsreal iherb 10% discount code OPA989,

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    its worth looking into memantine as a treatment for inflammation in ME as this drug has been around awhile and can be repurposed, so no having to wait for long trials and studies for its approval, possibly get a doctor now to prescribe it off label.

    Memantine has effects on lowering tnf as well as nmda/glutamate, another cause of inflammation. It also helps increase dopamine which is useful for increasing mood and energy, decreasing pain and many other functions. Its also known to increase cortisol in certain parts of the brain which would also enhance energy. The nmda antagonist effects can also improve gaba sensitivity, so maybe help those with that tired wired feeling??

    I think its an interesting drug that could be very useful in this reguard??

    cheers!!
     
  19. alex3619

    alex3619 Senior Member

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    I think the evidence of neuro-inflammation, whether or not you consider that to be encephalitis, goes back to 1955. After the outbreaks in Adelaide, Australia, in the late 1940s they did some research. One line of research injected patient blood into animals. In 1955 it was published that the blood in monkeys resulted in particular kinds of spinal lesions, with immune infiltration. That is, I think not coincidentally, the kind of thing they have found in ME autopsy results.

    In inflammation there is growing evidence that brain cells do not so much die as become dormant. So long as inflammation persists they do not function. Remove the inflammation and they have restored function. This is still a new and controversial area though.
     
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  20. Womble

    Womble

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    I also had a normal MRI. Should I ask my doctor for a PET scan now?

    Also, what are the implications for treatment once this inflammation is discovered?

    Is this an article I should be showing to my neurologist or pain management doctor?
     

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