Brain inflammation

Bill said:
What do you think is accountable for the incredible brain-fog so many of us experience?

By many measures, I was once considered a person of very high intelligence. Many days now I feel highly compromised. As if the impulses in my mind have to swim across synapses of heavily viscous fluid. And my head feels "pressurized."

I feel like something is very wrong with my brain. Not sure what that is, but it's not right.

I'm glad that there are clear thinking scientist-physicians like yourself helping us out and speaking the truth as you see it. I'm grateful for that.

Bill
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It could all just be down to energy supply, all of our bodily processes consume energy the brain especially, if we can't we can't supply enough energy to our legs to work properly maybe the same is true of our brains.
 
I think that the Good thing is there’s atleast some neuro-imaging research happening now so we don’t have to hypothesise forever. Whether microglia are activated, active or not and how much is possible to explore
 
Laboratory of Persistent Viral Diseases, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT 59840, USA. bchesebro@niaid.nih.gov.
https://www.ncbi.nlm.nih.gov/pubmed/30650564

Neuroinflammation, Microglia, and Cell-Association during Prion Disease.

Our current understanding is that microglia are beneficial during prion infection and critical to host defense against prion disease.
 
lansbergen said:
Rocky Mountain Laboratories,
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Interesting location. (@chrisb)

lansbergen said:
On the positive side, recent findings suggest that therapeutic strategies modulating microglial activation and function may have merit in prion disease.
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I think often times when it comes to brain inflammation people conflate the appearances of acute brain inflammation, like in encephalitis, with brain inflammation in chronic conditions which I suspect is less overt. I think this holds true with many commonly accepted markers that ME/CFS patients may inadvertantly fall in-range. This holds true for cognitive testing as well.

As a medical community, broadly speaking, we don't calibrate well for the chronically ill.
 
lansbergen said:
Laboratory of Persistent Viral Diseases, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT 59840, USA. bchesebro@niaid.nih.gov.
https://www.ncbi.nlm.nih.gov/pubmed/30650564

Neuroinflammation, Microglia, and Cell-Association during Prion Disease.

Our current understanding is that microglia are beneficial during prion infection and critical to host defense against prion disease.
Click to expand...
lansbergen said:
https://www.ncbi.nlm.nih.gov/pubmed/28714865

Microglia in prion diseases.

On the positive side, recent findings suggest that therapeutic strategies modulating microglial activation and function may have merit in prion disease.
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I'm not an expert on prions, but the above 2 posts seem contradictory to me.

1. Microglial are beneficial during prion infection and
2. Modifying/reducing their activation may be a good thing in prion disease.

which, in my mind, reduces down to

1. Microglial activation is an important part of the response to infection, so
2. Lets disable them as it reduces pesky symptoms.
 
Wonko said:
which, in my mind, reduces down to

1. Microglial activation is an important part of the response to infection, so
2. Lets disable them as it reduces pesky symptoms.
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In conclusion, microglial activation during prion disease progression is a complex and multistep process, with activated microglia comprising a heterogeneous population with diverse functions. At early stages of prion infection, microglia respond to PrPSc deposits and consequently increase their phagocytic capacity to remove PrPSc. However, this phagocytosis is insufficient, and sustained PrPSc accumulation leads to neuronal damage, which could in turn trigger the microglia to switch to a proinflammatory phenotype and exert detrimental effects in the brain (Figure 1).
 
Jonathan Edwards said:
No need. That was the sort thing I was referring to - empty vessels.
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Lot of empty vessels out there. A lot. As far as I can tell, they float just fine.

But hey, I know all too well what passes as opinion - or even dogma - in some areas can be crap, so I hear your concerns.
 
A recent Dutch article writes about long-term symptoms following COVID-19 and makes the connection to CFS.

Jos van der Meer, one of the Dutch researchers who helped develop the CBT-model for CFS in collaboration with Bleijenberg, is interviewed. The interesting thing is that this article writes that Van Der Meer suspects CFS is due to undetected inflammation in the brain. It writes (translated with DeepL):
Van der Meer suspects that CFS patients suffer from a simmering inflammation of the brain, in which the immune cells of the nervous system continue to produce more inflammatory substances than necessary. Everything indicates that something is going wrong in the brain, but that is so difficult to substantiate, the abnormalities are subtle and it is impossible to biopsy the brain.
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The article is titled: "Ook maanden na corona nog extreem moe: ‘Dit is een nieuwe ziekte. En een buitensporige'" en published in de Volkskrant.
https://www.volkskrant.nl/wetenscha...JbeVZm3dlTDzzh-EBj-Zq-bi8PoM1cdboqFfVR9zvNflo
 
While that's interesting to hear, I suspect he would fit into the "bio"-psycho-social side. And, perhaps argue CBT helps undue this ongoing inflammation by calming the brain, reducing negative thoughts and resetting normal patterns.

I had heard the NIH or OMF or perhaps both we're collecting brains for autopsy - but I haven't heard anything since. I wish it was just inflammation, but I'm afraid that's something every patient has tried and failed to some degree. Steriods and the like. Seems like just a simple non-info "inflammation you can never detect". I can't believe that's true today.
 
I don't entertain the idea that he has changed his opinions since:
https://www.researchgate.net/public...ort_in_Patients_With_Chronic_Fatigue_Syndrome

The whole discussion section simply assumes (as a bias) that there is no peripheral issues, particularly with regard to afferent input and places the blame solely on dysfunctional effort beliefs and symptom focusing, as influenced by this paper:
https://pubmed.ncbi.nlm.nih.gov/22641838/

Also, they made this claim in their conclusion:

van der Meer & colleagues said:
Finally, it remains to be seen whether changing dysfunctional beliefs, as achievable with cognitive behavioural therapy(28-30, 51-55), leads to corresponding changes in DLPFC/vACC activity and/or SMA connectivity during feedback processing. We are testing this hypothesis in an ongoing randomized controlled trial(36).
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Their trial was first registered in December 2013, protocol published in 2015 they've had two years to test the hypothesis, and well, nada...
 
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Danish BPS proponents also argue something is wrong in the brain and use it to justify the biology part of the bio-psycho-social model of functional illnesses (they have no evidence obviously, and are as vague about it as possible to avoid being proven wrong).
 
one of the premises of 'psychoneuroimmunology' is geared towards 'inflammation of the brain' for numerous mental health issues. This is just an extension of that.
The other 'favourite' is cortisol which bPS proponents claim to be able to alter with CBT.

Psychoneuroimmunology: Psychology's Gateway to the Biomedical Future
https://journals.sagepub.com/doi/10.1111/j.1745-6924.2009.01139.x
https://sci-hub.tw/10.1111/j.1745-6924.2009.01139.x#

while there may be something in it on a purely biological level (eg VanElzakkers work), the danger comes when psychologists use it to justify psychotherapies with no directly related biomedical evidence.
 
Sly Saint said:
one of the premises of 'psychoneuroimmunology' is geared towards 'inflammation of the brain' for numerous mental health issues. This is just an extension of that.
The other 'favourite' is cortisol which bPS proponents claim to be able to alter with CBT.

Psychoneuroimmunology: Psychology's Gateway to the Biomedical Future
https://journals.sagepub.com/doi/10.1111/j.1745-6924.2009.01139.x
https://sci-hub.tw/10.1111/j.1745-6924.2009.01139.x#

while there may be something in it on a purely biological level (eg VanElzakkers work), the danger comes when psychologists use it to justify psychotherapies with no directly related biomedical evidence.
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However it is approached, the two things should not be conflated by anyone:
  • Physiological inflammation in the brain, versus
  • Hotchpotch notions of how CBT might supposedly fix such things.
Wonder they've not suggested CBT as a fix for meningitis (or maybe they have?).
 
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