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Brodmann 38, current research, and possibilities for treatment?

Discussion in 'General ME/CFS Discussion' started by Jesse2233, May 24, 2017.

  1. Jesse2233

    Jesse2233 Senior Member

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    Dr Byron Hyde states that ME is a clearly defined disease caused by damage to the brain (akin to polio but in a different area). The primary area of brain damage he singles out is Brodmann 38, a part of the temporal cortex (although he finds damage in other areas as well).

    He believes that damage is caused by an enterovirus infection and is diagonsable via SPECT scan and gut biopsy.

    This strikes me as both an elegant and sobering definition given that the brain influences everything downstream. And while Dr Hyde's results have not been independently verified, he has seen thousands of patients, and meticulously documented his work.

    He states that the nature of the damage is microvascular and neuronal, and hence does not often show up on MRIs. This meshes fairly well with Dr Jared Younger's work on migcroglial inflammation and LDN.

    Some questions that have been discussed before...
    • How can we contextualize these findings with current findings on metabolomics and autoimmunity? Are these simply the downstream results of limbic brain damage?
    • If the brain damage is severe as he says, how do we account for temporary spontaneous recoveries where cognitive and physical function are fully restored?
    And some new thoughts...
    • Do the 6 months delay in responses to Rituximab and Ampligen actually reflect the time it takes the brain to heal (once stressors have been removed)?
    • Are there other diseases or research on damage to Brodmann 38 that give us any clues?
    • What happens to the brain damage when you treat whatever "x-factor" has been shown in the blood (as demonstrated by Ron Davis)?
    • Can this kind of brain damage be partially treated with things like stem cells, HBOT, and neurofeedback? Or is it more treatment resistant because there's an ongoing precipitating cause?
     
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  2. halcyon

    halcyon Senior Member

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    Personally I think Hyde should be a bit more clear when he talks about injury. Clearly, we're not talking about gross structural damage here, or we'd all have abnormal MRI/CT brain scans and this disease would be taken a lot more seriously.

    I think the subject was was covered well by Richardson and Costa in 1998. The way they talk about it makes a lot more sense. This is a functional rather than structural injury (though I think Hyde may be correct that there is actual structural microvascular damage, e.g. cuffing, expanded Virchow-Robin spaces). The areas that are hypoperfused are not structurally damaged, but are instead hypometabolic. I've not been able to square the current hypothesis about the disease being caused by global hypometabolism with these findings of regional brain hypometabolism. To me, the latter has virus and viral tropism written all over it, and is more in line with what Richardson hypothesized, and is backed up by autopsy data.

    If we take these issues as functional rather than structural, then spontaneous recovery becomes a lot more reasonable.
     
    Last edited: May 24, 2017
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  3. Jesse2233

    Jesse2233 Senior Member

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    @halcyon I like your thinking on spontaneous remission, but if there is long term hypoperfusion, wouldn't that cause areas of the brain to permanently die? And did polio patients ever spontaneously remit or should that analogy not be taken too far?

    I have the same confusion regarding regional vs global hypometabolism. Perhaps the abnormalities found in the blood are caused by specific damaged metabolic regulating regions in the brain. If the causality went the other way wouldn't the entire brain show hypoperfusion?
     
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  4. halcyon

    halcyon Senior Member

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    We know there is white and grey matter loss over time in ME brains. I'm not sure if the regions where the loss is found correlates with the SPECT research.The hypoperfused areas aren't getting no blood, they're just taking up less than the surrounding areas due to lower metabolic demand. That's the hypothesis anyways. Poliovirus affects a very specific region of motor neurons in the spinal cord, and the effects are pretty obvious when a muscle gets cut off from the brain. Perhaps the tropism of the enteroviruses that cause ME is a bit broader and the initial encephalitic damage isn't as striking or catastrophic. Once the infection becomes chronic, there is very little or no lytic action so there won't be ongoing damage directly from the virus, just whatever dysfunction occurs due to immune response in the area of the infected cells.
     
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  5. Jesse2233

    Jesse2233 Senior Member

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    I hadn't heard this, wonder what causes it. Do you know the specific studies?

    That makes sense

    Got it, this seems to correlate with the positive anti-inflammatory effects of low dose naltrexone. Makes me wish we could high dose with that specialty LDN variant (w/o the opioid blocking, can't remember/find the name)
     
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  6. halcyon

    halcyon Senior Member

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  7. Jesse2233

    Jesse2233 Senior Member

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  8. Woolie

    Woolie Senior Member

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    Ah, Brodmann 38 my old friend, we meet again!

    This area supports the retrieval of stored long-term knowledge, like what a tiger looks like, where you find them, what the capital of Sweden is.

    If this guy has found hypoperfusion here during a task or activity, he might be measuring a behaviour, not a brain abnormality. PwMEs may be drawing on various cognitive resources less effectively than healthy folks, due to malaise, brain fog. etc. That would mean - nothing wrong with the brain, we're just not thinking all that straight.

    Some methods - like fMRI - aren't very good at detecting activity in the poles - and Brodmann's 38 is at the pole of the temporal lobe (the tip). So I'd wanna be sure the findings aren't just due to that.
     
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  9. Jesse2233

    Jesse2233 Senior Member

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    I believe he used SPECT scans to identify Brodmann 38
     
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  10. Sancar

    Sancar Sick of being sick ~ and so is my walking buddy

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    @halcyon ~ Thnak you for listing these references. I found it quite relavent that the first reference you listed, NMR in Bio Medicine ~ noted that "Astrosyte dysfunction" could be the driver in this senerio. It makes so much sence.

    ~~The Astroglia are star shaped cells in the brain AND spinal cord. They are responsible for the support of "Endotheial cell" that form the blood brain barrier, provision of nutrients to the nervous tissue, maintenance of extracellular ion balance, and a role in the repair and scaring process of the brain and spinal cord following tramtic injuries.~~ Wikipedia

    I started "blacking out" cold in '97. A couple of random times after. I went down like I tree, (so I'm told). I had horrible headaches after. Dah- Lots of test and Drs. Everyone said it was an 'anomaly'. In 2010 I then really had a bout, 8 black outs in 11 months. Not an anomaly. But no answer. I would love to have a Doctor who would appreciate these detailed reports.

    My MRI's, 3 or 4? all state "abnormalities in punctuated white matter". I was told by one Dr that I had "White matter disease". I was given Namenda. It made my head feel 'heavy' and I was so tired on it. Needless to say I couldn't take it. So that was that.

    As I said it would b amazing to find a Doctor that would respect and respond to those reports.
     
  11. Sancar

    Sancar Sick of being sick ~ and so is my walking buddy

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    @Jesse2233 ~ Thank you for starting this thread! I hope you benefit from this info!
     
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  12. Sancar

    Sancar Sick of being sick ~ and so is my walking buddy

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    @Jesse2233 ~? for you ~ Did you find out the name of a he "LDN variant" that you mentioned above. That could be a real help. Do think it would be more effective for thos of us eh have no reaction good or bad to LDN?
     

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