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Neuroinflammation in Patients with CFS/ME: PET study

Discussion in 'Latest ME/CFS Research' started by RustyJ, Mar 26, 2014.

  1. lnester7

    lnester7 Seven

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    I beg to disagree, if it would be the inflammation the factor then 100% of us who have inflammation would have the psy issues too.

    I am 100% sure I have brain inflammation. I do not have anxiety and I have never been depressed (evaluated by neuropsy and all).
  2. anciendaze

    anciendaze Senior Member

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    lnester7, I believe that 100% do have neuroinflammation, but many are able to cope. Part of the reason would be that the inflammation affects different nerves, and part that some are more careful about checking themselves before they act on impulses. This would go along with evidence that cognitive processing is slower in ME/CFS patients. Those who don't check as carefully probably end up in a different category with a more solid psychiatric label.
    NK17 likes this.
  3. Sea

    Sea Senior Member

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    I think it depends entirely on where the damage is done. People with brain injuries from accidents have variable outcomes (including depression) depending not only on the extent of damage but also which part of the brain is damaged.
    WillowJ, Marlène, Kati and 5 others like this.
  4. Marco

    Marco Old blackguard

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    Further coverage in Science Daily

    http://www.sciencedaily.com/releases/2014/04/140404085538.htm
    WillowJ likes this.
  5. alex3619

    alex3619 Senior Member

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    To date I have seen no evidence in ME that I recall of damage to the myelin around nerves. There is evidence of brain-associated inflammation and immune infiltration however. Should the myelin sheaths be damaged then it would most likely be a diagnosis of MS not ME.

    However, myelitis does not have to involve damage to myelin according to wikipedia, maybe someone should look into this further:

    http://en.wikipedia.org/wiki/Myelitis
    SOC likes this.
  6. lansbergen

    lansbergen Senior Member

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    I think myelitis can be transient and does not always cause demyelination.

    Not every itis causes large amount of tissue destruction.
    NK17 likes this.
  7. Gijs

    Gijs Senior Member

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    Many people with ME have UBO's showing up in MRI. Little white leasies. This can be due to inflamation.
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  8. alex3619

    alex3619 Senior Member

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    Exactly. In MS its often due to demyelinization, but that is not the only cause.
  9. alex3619

    alex3619 Senior Member

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    Yes, that is my understanding. Myelitis may involve functional impairment of myelin, or neuronal action, but not necessarily demyelinization.

    PS On M.E. there is another reason its not a good acronym, although the name is fine. I had Measles Encephalitis when I was 7. That is also M.E.

    I think @SOC pointed out that Encephalitis might be a better term than Encephalomyelitis.
  10. Hip

    Hip Senior Member

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    The ME/CFS neuroinflammation study discussed in this thread found microglia and/or astrocyte activation in the brain, indicating state of brain inflammation; the interesting thing is that you also get this inflammatory state of chronic microglial activation in other diseases, including:

    Hepatitis C [1]
    Lyme neuroborreliosis [1]
    Systemic lupus erythematosus [1]
    Schizophrenia [1]
    Bipolar disorder [1]

    The first three, hep C, Lyme and lupus, have fairly similar symptoms to ME/CFS, such as fatigue and brain fog.


    Russell L. Blaylock has written an accessible overview on how chronic microglial activation raises glutamate and generally causes problems in the brain:

    Microglial Activation and Neurodegeneration by Russell L. Blaylock, MD

    @Marco has written an article about how raised glutamate from neuroinflammation may be the cause of many ME/CFS symptoms, especially the sensory gating symptoms of ME/CFS, like increased sound sensitivity:

    Glutamate - One More Piece in the Chronic Fatigue Syndrome Puzzle?
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  11. Hide

    Hide

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    I heard this test cost about 1 million yen.
  12. alex3619

    alex3619 Senior Member

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    That would be about ten thousand dollars or in the vicinity. That sounds a little high, though it might not be high for cutting edge research testing. Its not like existing facilities would be structured to do experimental tests cheaply.

    If this becomes a standardized commercial test it should be much cheaper.
  13. biophile

    biophile Places I'd rather be.

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    Anthony Komaroff on the E in ME

    I was going to start another thread, but what I wanted to post is an implication of this thread.

    http://www.meactionuk.org.uk/Komaroff-Summary-San-Francisco-March-2014.htm

    Based on this video:



    Some good bits, but I found this comment interesting:

  14. Marco

    Marco Old blackguard

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    @Hip

    Thanks Hip. That early blog kicked off a long (and ongoing) series of blogs considering a possible neuroinflammatory basis for ME/CFS.

    A key issue I had to ponder was mechanisms whereby a wide range or peripheral 'stressors' (given the reported heterogenous onset in ME/CFS) could result in the same chronic, low grade and difficult to detect central neuroinflammation.

    One potential mechanism is the model of 'spreading neuroinflammation' in complex regional pain syndrome (CRPS) :

    Plus autoimmunity may be a key mechanism to explain why only a small minority of patients develop CRPS (or ME/CFS following a common viral infection) :

    http://www.cortjohnson.org/blog/201...lgia-mecfs-spreading-neuroinflammation-model/
    Hip likes this.
  15. RustyJ

    RustyJ Contaminated Cell Line 'RustyJ'

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    Why has the possibility of myelin damage been ruled out? Just because there is no corroberating evidence in the case of ME doesn't mean it doesn't happen. There really hasn't been much effort to research neurological issues in ME.

    There is some evidence that hypoperfusion (well-documented in ME) leads to myelin damage; also leads to neuroinflammation (in rats):

    Permanent, bilateral common carotid artery occlusion in the rat: a model for chronic cerebral hypoperfusion-related neurodegenerative diseases.

    Also a possible treatment option?:

    Huperzine a improves chronic inflammation and cognitive decline in rats with cerebral hypoperfusion.
  16. Marco

    Marco Old blackguard

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    Prasher et al (1990) used evoked potentials to show that sensory nerve conduction (which is impaired in demyelinating diseases such as MS) is normal in 'ME' whereas event related potentials (the cortical response to stimuli) show abnormalities related to 'gating in' or attentional processes which may reflect cognitive problems.

    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1014138/pdf/jnnpsyc00513-0063.pdf

    Not necessarily definitive but I don't see the need to demonstrate gross structural abnormalities when discussing neuroinflammation.
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  17. RustyJ

    RustyJ Contaminated Cell Line 'RustyJ'

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    I agree. However my response was intended as a contribution to the discussion on the aptness of using the term 'myelitis'. It may well be that there is not only different damage sites in the brain, but different causes, in patients.

    Further to this, Richard A. Van Konynenburg mentions that in me/cfs the body's capacity to repair normal degradation of myelin is hampered. Also he mentions that the myelin damage causes “white spots” in MRI examination of the brain. I don't know what his references were.

    With respect to me/cfs it appears to be more accurate to say that not enough research has been done to determine if there is myelin damage or not, rather than to say there is no damage.
    NK17 likes this.
  18. Hip

    Hip Senior Member

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    Note that the term myelitis does not mean inflammation of myelin, but rather means inflammation of the spinal cord.

    Myelitis derives from Greek word myelós which refers to the spinal cord.

    Similarly:
    Encephalitis = inflammation of the brain.
    Encephalomyelitis = encephalitis + myelitis = meaning inflammation of the brain and spinal cord.

    Though of course damage to myelin can occur as a result of inflammation such myelitis or encephalitis.



    This is an interesting list of Greek and Latin medical prefixes and suffixes:

    List of medical roots, suffixes and prefixes - Wikipedia, the free encyclopedia

    Once you learn a few of these, you can often half guess the meaning of medical terms.

    You can see from this list that the prefix myel(o)- actually means "of or relating to bone marrow or spinal cord." So this prefix in fact has two meanings.

    Not to be confused with the prefix my(o)- which means "of or relating to muscle," as in the term myalgic, meaning muscle pain.
    Last edited: Apr 6, 2014
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  19. Marco

    Marco Old blackguard

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    Hi Rusty (and thanks to Hip for clarifying the full interpretation of 'myel').

    Correct me if I'm wrong but wasn't the term myalgic encephalomyelitis first coined following the Royal Free outbreak? From the few original papers I've read I don't recall any physiological/histological evidence to support 'myelitis' in these folks.

    Very happy to be told otherwise though.
    rosie26 and RustyJ like this.
  20. Hip

    Hip Senior Member

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    That's a good point: how did they know in the 1950s that there was brain and spinal cord inflammation in ME/CFS, so as to be able to call it "myalgic encephalomyelitis"?

    In two published studies about the Royal Free Hospital outbreak in London 1955, the authors already described the condition as "encephalomyelitis" (but without using the "myalgic"), so even in this 1955 outbreak, they must have known it involved brain and spinal cord inflammation. The two Royal Free Hospital outbreak papers are these:

    Epidemiological aspects of an outbreak of encephalomyelitis at the Royal Free Hospital, London, in the summer of 1955

    An Outbreak of Encephalomyelitis in the Royal Free Hospital Group, London, in 1955

    From the second paper cited above, I quoted a text extract below which seems to provide possible physical evidence of brain inflammation: it details a postmortem brain examination of one of the Royal Free ME/CFS patients who committed suicide using the barbiturate drug Carbrital.

    In the brain of this patient they actually found demyelination; however they diagnosed this as the patient having an early stage of multiple sclerosis, in addition to simultaneously having what we now call ME/CFS.

    In this brain autopsy, the main abnormality they found, in addition to the typical multiple sclerosis brain lesions, was to quote: "one section taken from the hypothalamus which showed intense perivascular cuffing."

    Perivascular cuffing means the accumulation of lymphocytes or plasma cells in a dense mass around the blood vessel, and this perivascular cuffing is indicative of inflammation or of an immune reaction.

    So this is possible evidence of brain inflammation in ME/CFS, back in the 1950s. Although the authors stated that it is more probable than the intense perivascular cuffing in the hypothalamus represents an unusual reaction associated with multiple sclerosis.

    Presumably though there must have been other good indicators of brain and spinal cord inflammation in these Royal Free outbreak patients for this outbreak to be described as encephalomyelitis.


    It is interesting that another ME/CFS brain autopsy published in 1994 found what appeared to be coxsackievirus B infection in the hypothalamus and brainstem of the patient. So here we see a hypothalamus infection again implicated in ME/CFS. Reference: here. Full paper here.

    @Marco, from the perspective of sensory gating dysfunction, the brainstem infection is very relevant, since "studies on rats show the brain stem, thalamus, and primary auditory cortex play a role in sensory gating for auditory stimuli." Reference: here.



    Here is the text from the Royal Free Hospital ME/CFS 1955 outbreak study (terms in bold are defined in the glossary below):
    Last edited: Apr 7, 2014

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