News From Jarred Younger / Neuroinflammation, Pain, and Fatigue Laboratory at UAB, From Aug 2020

Think it's beyond doubt there is brain inflammation since patients all complain of the horrible inflammed head feeling, it's basically my worst symptom.

It is unlikely that an inflamed feeling comes from inflammation in the head any more than a sugary taste comes from sugar in the head or a burning smell comes from burning in the head. The brain's job is to paint pictures that describe what is happening elsewhere. The components of the brain are, more or less, completely unaware of their own state. If you stick an electrode in an awake person's brain and fire electricity at it they may remember the house their grandmother lived in or see a green flash or anything pretty much except an electric shock.

There are parts of the brain that are there to pick up signs of inflammation elsewhere - just as eyes pick up sunlight on the grass. Those areas may actually use some of the same signals the inflamed tissues use. So for those areas to have some signals associated with inflammation in ME/CFS makes sense. But I don't see a scrap of evidence so far for inflammatory signals in other parts of brain. The only data we had was Nakatomi and it didn't really look like a pathological state because it had no specific pattern different from normals. It looked like the same pattern with the gain setting on the scan turned up a bit.

If Younger has specific patterns for glial activation in all the areas he talks of then that would be very interesting. But he didn't show a single picture of his own findings.
 
It is unlikely that an inflamed feeling comes from inflammation in the head any more than a sugary taste comes from sugar in the head or a burning smell comes from burning in the head. The brain's job is to paint pictures that describe what is happening elsewhere. The components of the brain are, more or less, completely unaware of their own state. If you stick an electrode in an awake person's brain and fire electricity at it they may remember the house their grandmother lived in or see a green flash or anything pretty much except an electric shock.

There are parts of the brain that are there to pick up signs of inflammation elsewhere - just as eyes pick up sunlight on the grass. Those areas may actually use some of the same signals the inflamed tissues use. So for those areas to have some signals associated with inflammation in ME/CFS makes sense. But I don't see a scrap of evidence so far for inflammatory signals in other parts of brain. The only data we had was Nakatomi and it didn't really look like a pathological state because it had no specific pattern different from normals. It looked like the same pattern with the gain setting on the scan turned up a bit.

If Younger has specific patterns for glial activation in all the areas he talks of then that would be very interesting. But he didn't show a single picture of his own findings.
That's fair, I like that actually as it kind of aligns with my experience where when my blood pressure increases/pumps harder that 'inflamed' feeling goes away.

So it feels like an illusion, unless the coffee is actually dialing down whatever is causing the "inflamation"..
 
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Isn't that in disagreement with Wirth/Scheibenbogen?

Maybe dear old Ron is sensible enough to see that the minuscule difference between antibody levels in patients and controls in the Scheibenbogen study doesn't amount to 'specific elevated antibodies' in the books of any seasoned scientist.

And the study did not indicate specificity - patients and controls had antibodies to various things and there were no blinded controls testing for differences in antibodies to other things as far as I know.
 
Yeah some of Cort’s reporting strikes me a bit like, “What if every biological claim a researcher made about ME was true at once”
I find he can be helpful in explaning how things are supposed to work or purported mechanisms behind this or that study, and that's a useful service. But as indicated above, he seems to go beyond that and assume that all is as described. it's one thing to explain how something is supposed to happen, and another to essentially assume that is in fact happening.
 
ME/CFS doesn’t look anything like the brain damage diseases or conditions.
But it sure can feel that way at times. I wouldn't discount some brand of damage simply because our technology is not up to snuff. Personally, I'd like to see more SPECT efforts, but that seems to have fallen out of favor since the turn of the millennium. Don't know why that particular spigot got turned off, especially with its reveals relative to blood flow in the brain.
 
But it sure can feel that way at times.

The "at times" concerns me, though.

It's plausible a damaged or diseased brain is better at compensating under some conditions than others, so the person's level of function would vary.

But I'm not sure they'd see the huge changes that some moderately ill people get between their least-worst day and brutal PEM. That seems more like a normal brain that sometimes has to drive with a faulty HT lead.
 
But I'm not sure they'd see the huge changes that some moderately ill people get between their least-worst day and brutal PEM. That seems more like a normal brain that sometimes has to drive with a faulty HT lead.
But I fear the brain isn't normal in many pwME. From head pressure and headaches to issues with balance and gait to deficits in multiple cognitive domains, we can sense our brains are in many ways not normal (makes me think of the Mel Brooks line Abby Normal).

Does the fact that we have wild gradations in severity negate the overt reality that, for many, our brains can't - routinely or in a sustained fashion - function remotely at pre-morbid levels?
 
But I fear the brain isn't normal in many pwME. From head pressure and headaches to issues with balance and gait to deficits in multiple cognitive domains, we can sense our brains are in many ways not normal (makes me think of the Mel Brooks line Abby Normal).

Does the fact that we have wild gradations in severity negate the overt reality that, for many, our brains can't - routinely or in a sustained fashion - function remotely at pre-morbid levels?
Problems with the brain just doesn't have to mean there is *brain damage*. Obviously there is something going on in there.
 
But I fear the brain isn't normal in many pwME. From head pressure and headaches to issues with balance and gait to deficits in multiple cognitive domains, we can sense our brains are in many ways not normal (makes me think of the Mel Brooks line Abby Normal).

Does the fact that we have wild gradations in severity negate the overt reality that, for many, our brains can't - routinely or in a sustained fashion - function remotely at pre-morbid levels?
I think we might have to separate between permanent damage and/or death of neurons, and other factors that might affect how the brain functions.

The lack of clear permanent damage indicates that there are one or more transient mechanisms that are more or less permanently activated due to something else.

While we can’t generalise from anecdotes, the people that do recover generally don’t complain about cognitive issues afterwards.
 
While we can’t generalise from anecdotes, the people that do recover generally don’t complain about cognitive issues afterwards.
Didn’t one of the only studies on recovered people find that people who described themselves are “recovered” were still quite limited ability wise compared to people who never had ME. (I don’t have the energy to dig and confirm so relying on my dysfunctional brain memory for this…)
 
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